modulação hormonal

Transcription

modulação hormonal
SOBRAF
DIRETRIZES PARA A UTILIZAÇÃO DE HORMÔNIOS
HOMÓLOGOS HUMANOS POR MÚLTIPLAS
ESPECIALIDADES MÉDICAS NA PRÁTICA CLÍNICA
A- INTRODUÇÃO:
As diretrizes aqui elencadas representam a posição oficial da Sociedade
Brasileira Para Estudos da Fisiologia – SOBRAF - com relação ao uso de
hormônios homólogos humanos por múltiplas especialidades médicas na prática
clínica, e estão fundamentadas no Projeto Diretrizes, iniciativa conjunta da
Associação Médica Brasileira e Conselho Federal de Medicina, que tem por
objetivo conciliar informações da área médica a fim de padronizar condutas que
auxiliem o raciocínio e a tomada de decisão do médico.
As informações contidas neste documento devem ser submetidas à avaliação e à
crítica do médico, responsável pela conduta a ser seguida, frente à realidade e ao
estado clínico de cada paciente.
B- DESCRIÇÃO DO MÉTODO DE COLETA DE EVIDÊNCIA:
A revisão bibliográfica de artigos científicos destas diretrizes foi realizada na
base de dados MEDLINE.
A busca de evidências partiu de cenários clínicos reais, e utilizou palavras-chaves
(MeSH terms): (aging hormone replacement therapy) OR (gynecology hormone
replacement therapy) OR (endocrinology hormone replacement therapy)
(hormones OR Estradiol OR Testosterone OR Progesterone OR Thyroid Hormones
OR DHEA OR Pregnenolone OR Melatonin OR Growth Hormone OR IGF-1 OR
deficiency OR therapeutic OR replacement) AND quality of life AND risk factors
AND bone density AND osteoporosis AND osteopenia, (hormone replacement
therapy OR hormones) AND (cancer) AND (Monitoring) AND (sexual function) AND
glucose metabolism AND plasma lipids AND inflammatory factors AND visceral fat)
AND cardiovascular disease AND antioxidant activity AND immune function AND
fatigue AND depression AND sleep disorders AND anxiety AND hypertension AND
obesity AND body composition AND lean mass AND muscle mass AND sarcopenia
AND longevity AND alzheimer´s disease AND cancer risk AND cancer prevention
AND low hormone levels .
C- GRAU DE RECOMENDAÇÃO E FORÇA DE EVIDÊNCIA:
A: Estudos experimentais e observacionais de melhor consistência.
B: Estudos experimentais e observacionais de menor consistência.
C: Relatos de casos (estudos não controlados).
D: Opinião desprovida de avaliação crítica, baseada em consensos, estudos
fisiológicos ou modelos animais.
D- OBJETIVOS:
Estabelecer a definição, interferências do uso de hormônios no metabolismo
lipoproteico, na vida sexual, na baixa densidade mineral óssea, nas mamas, na
redução do percentual de gordura corporal, na redução dos riscos de
hipertensão arterial sistêmica, na redução dos riscos de diabetes, na redução do
risco de demência de Alzheimer, na melhora da massa muscular, na promoção
de bem estar físico e mental, na redução dos riscos de doenças, na melhora da
qualidade de vida, na prevenção das perdas funcionais da velhice, na melhora da
capacidade laboral, física e funcional, na melhora da libido, na melhora da
qualidade do sono, na melhora da depressão, na melhora da ansiedade, na
melhora do estresse, na atenuação da formação de espécies oxigênio-reativas, na
redução do estresse oxidativo celular, na preservação da integridade celular, na
preservação da integridade mitocondrial, na otimização metabólica, na
otimização imunológica, na redução e ou reversão da placa ateromatosa, na
redução do risco cardiovascular, na prevenção de doenças crônicas, na
prevenção do câncer, na redução do risco de câncer e na promoção de um
envelhecimento saudável e determinar as indicações da terapêutica hormonal
baseadas nas melhores evidências atuais.
E- CONFLITO DE INTERESSE:
Nenhum conflito de interesse declarado.
1. MENOPAUSA
a. Quadro clínico
i. Amenorréia secundária em mulheres com mais de 35 anos
ou amenorréia secundária em mulheres, por período
superior a seis meses;
ii. Fogachos, sudorese noturna, insônia, labilidade emocional,
secura vaginal, dispareunia, declínio cognitivo, fragilidade
imunológica, ressecamento da pele, queda de cabelos,
aumento do peso total, aumento do percentual de gordura,
perda de massa magra, perda de massa óssea, redução da
libido e comprometimento da qualidade de vida.
b.
Quadro Laboratorial
i. FSH > 15 u/L
ii. LH > 8 u/L
c.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da menopausa. Por outro lado,
nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico de menopausa será confirmado
tomando-se como referência as manifestações e o quadro
clínico apresentados pelo paciente e devidamente avaliados
e registrados pelo médico. Tal conduta se justifica pela
baixa acurácia dos métodos de diagnóstico laboratorial das
deficiências hormonais, falhas de técnicas intrínsecas aos
métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a menopausa, a SOBRAF recomenda que seus médicos associados
utilizem-se do termo de consentimento padrão adotado pela
mesma e que deverá ser devidamente assinado pelo médico e pelo
seu paciente.
e.
CONSENSO DA SOBRAF PARA O TRATAMENTO
HORMONAL DA MENOPAUSA
i. Após criteriosa revisão da literatura científica, discussões
com médicos representantes de todos os continentes e
discussões entre médicos brasileiros, todos profissionais
versados e adequadamente qualificados em utilizar e
prescrever hormônios em seres humanos com a
finalidade primária de promoção da saúde e, ainda, em
total consonância com os preceitos e diretrizes da
Sociedade Brasileira Para Estudos da Fisiologia – SOBRAF,
da International Hormone Society e da World Society of
Anti-Aging Medicine, nós, médicos membros da SOBRAF,
concluímos haver chegado o momento de reconsiderar os
conceitos atualmente vigentes acerca da reposição
hormonal na menopausa.
A presente controvérsia acerca da reposição hormonal na
menopausa, teve início após a publicação dos resultados
do chamado estudo WHI ( Women’s Health Iniciative ),
publicado em 2002, bem como do British One Million
Women Study, publicado em 2003. Em ambos os estudos,
o uso de hormônios em mulheres na pós-menopausa foi
associado a uma maior incidência de câncer de mama,
quando comparadas ao grupo placebo-controle ou ao de
não usuárias. No estudo WHI, o uso de hormônios em
mulheres foi associado a um aumento no risco de doenças
cardiovasculares e cerebrovasculares. Para os médicos
membros da SOBRAF, ambos os estudos apresentam,
dentre outras, duas falhas graves de desenho que
consistem, respectivamente, em primeiro lugar: estas
mulheres estavam utilizando estrogênios conjugados de
urina equina. Consiste em um coquetel de 38 hormônios
obtidos da urina de éguas prenhes, portanto, um dejeto
animal, sendo que nenhum destes hormônios existe em
seres humanos ou é produzido pelos mesmos, tendo,
portanto, propriedades farmacológicas e comportamento
completamente distintos do 17-beta-estradiol, hormônio
que deixa de ser produzido por mulheres na fase pósmenopausal. Em segundo lugar, à esta combinação, foi
associado o acetato de medroxiprogesterona, molécula
que consiste em um progestogênio sintético, igualmente
não existente em seres humanos, e, consequentemente,
substância com propriedades químicas e fisiológicas
diferentes da progesterona humana.
Revisando
cuidadosamente a literatura científica existente, é
possível encontrar vários outros estudos que
demonstram, de maneira inquestionável, a potencial
toxicidade e os riscos inerentes ao uso destas substâncias.
De acordo com as recentes recomendações de um grupo
cada vez maior de sociedades médicas ao redor de todo o
mundo, nós, igualmente, não recomendamos o uso de
hormônios não-homólogos humanos a reposição
hormonal da menopausa. Em contraste com as
recomendações de algumas sociedades, que não
recomendam a reposição hormonal na menopausa, ou
ainda, algumas outras que a recomendam por um período
limitado a cinco anos, no máximo, nós recomendamos o
uso de hormônios em mulheres antes e após a
menopausa, por tanto tempo quanto se fizer necessário,
desde que as indicações e as necessidades clínicas
justifiquem e que nenhum evento adverso ocorra que
contraindique o seu uso.
Contudo, nós recomendamos o uso da combinação de
estradiol e estriol homólogos humanos, associados à
progesterona homóloga humana para a correção da
deficiência ovariana da menopausa, exceto para casos
específicos e bem pontuais e por um período de tempo
limitado, aonde o uso de hormônios não-homólogos
humanos possa apresentar resultados clínicos melhores,
com é o caso de algumas metrorragias e sangramentos da
perimenopausa. A via de administração , é, igualmente,
parâmetro de considerável importância. A via
transdérmica, é, sem dúvida bem mais segura e fisiológica
do que a via oral. Esta via não oferece risco de elevação
do câncer de mama, e, quando se associa progesterona
homóloga humana à reposição de estradiol e estriol,
vários estudos, na verdade, demonstram uma clara
redução dos riscos para aquela patologia.
A mulher que teve câncer de mama, pode fazer reposição
hormonal? A tendência observada na atualidade é de se
evitar a administração de hormônios em mulheres que
tiveram câncer de mama. Esta observação pode não se
justificar nas mulheres em que a lesão foi removida
cirurgicamente de
forma completa. Revendo
cuidadosamente todos os estudos científicos atuais que
envolvem mulheres que tiveram câncer de mama e
receberam reposição hormonal na menopausa, nenhum
risco de recorrência foi reportado ou identificado. Ao
contrário, a reposição hormonal na menopausa está
associada a uma notória redução do risco de recorrência
do câncer, bem como uma clara diminuição das taxas
gerais de mortalidade na maioria dos estudos. Mesmo a
despeito de fartas evidências em contrário, ainda é muito
cedo para recomendar-se a reposição hormonal para
mulheres em menopausa portadoras de câncer de mama.
Nós recomendamos que estudos em larga escala placebocontrole sejam efetivados com a finalidade de identificar
com a maior clareza possível, em quais mulheres que
tiveram câncer de mama a terapia de reposição hormonal
da menopausa estaria mais indicada.
Nós recomendamos aos médicos que fazem a reposição
hormonal da menopausa, que submetam suas clientes à
propedêutica e monitoração mamária periódicos, antes e
durante o período de duração da reposição, obedecendo
aos intervalos regulares preconizados e consensuados,
consistindo de inspeção, palpação e mamografia de alta
resolução,
acompanhada
de
ultrassonografia
complementar de alta resolução. Importante, igualmente,
ressaltar a necessidade de vigilância periódica do
endométrio, através de monitoramento ultrassonográfico
transvaginal.
CONCLUSÃO DO CONSENSO:
Tendo em vista as enormes repercussões biopsicossociais
da menopausa e os crescentes e exorbitantes gastos para
o tratamento e controle das doenças chamadas
“inevitáveis” da velhice, nós recomendamos aos médicos
estimularem a reposição hormonal da menopausa,
sempre observando os bons preceitos da prática médica e
utilizando-se de hormônios homólogos humanos,
preferencialmente administrados pela via transdérmica,
no caso da associação estradiol-estriol, e, no caso da
progesterona, via transdérmica ou transvaginal. Para os
casos anteriores, a via oral também pode ser uma
alternativa, desde que os hormônios administrados sejam,
igualmente, homólogos humanos.
São Paulo, 12 de Novembro de 2012
Grupo de Consensos da SOBRAF
1.
2.
3.
4.
5.
6.
7.
Professora Doutora Ana Cristina Vendramini, PhD
Professora Doutora Andreia Conceição Milan B. Antoniolli, PhD
Professora Doutora Andrea Thomaz Soccol, PhD
Professor Doutor Eduardo Faria, PhD
Professor Doutor Marcelo Alexandre de Mattos, PhD
Professor Doutor Marcos Renato Scholz, PhD
Dr. Ítalo Emmanuel Valeriano Rachid
2. ANDROPAUSA
a. Quadro clínico
i. Cansaço, redução da libido e do desempenho sexual,
redução da força muscular, adinamia, fragilidade
imunológica, ginecomastia, redução da capacidade física,
ressecamento da pele, déficit de memória, aversão ao
convívio social, aumento da circunferência abdominal,
queda de cabelos, aumento do percentual de gordura
corporal, alterações do sono, alterações do humor, perda
de massa óssea, e comprometimento da qualidade de vida.
b.
Quadro Laboratorial
i.
ii.
iii.
iv.
v.
FSH > 5 u/L
LH > 8 u/L
Testosterona Total < 700 ng/dL
Índice de Androgênio Livre < 0,7
Testosterona livre < 2%
vi. Testosterona biodisponível < 400 ng/dL
c.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da andropausa. Por outro lado,
nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico de andropausa será confirmado
tomando-se como referência as manifestações e o quadro
clínico apresentados pelo paciente e devidamente avaliados
e registrados pelo médico. Tal conduta se justifica pela
baixa acurácia dos métodos de diagnóstico laboratorial das
deficiências hormonais, falhas de técnicas intrínsecas aos
métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a andropausa, a SOBRAF recomenda que seus médicos associados
utilizem-se do termo de consentimento padrão adotado pela
mesma e que deverá ser devidamente assinado pelo médico e pelo
seu paciente.
e.
CONSENSO DA SOBRAF PARA O TRATAMENTO
HORMONAL DA ANDROPAUSA
Após criteriosa revisão da literatura científica, discussões com
médicos representantes de todos os continentes e discussões
entre médicos brasileiros, todos profissionais versados e
adequadamente qualificados em utilizar e prescrever
hormônios em seres humanos com a finalidade primária de
promoção da saúde e, ainda, em total consonância com os
preceitos e guidelines diretrizes da Sociedade Brasileira Para
Estudos da Fisiologia – SOBRAF, da International Hormone
Society e da World Society of Anti-Aging Medicine, nós,
médicos membros da SOBRAF, concluímos haver chegado o
momento de considerar a deficiência hormonal masculina, e o
conseqüente
andropausa.
tratamento
de
reposição
hormonal
da
Desde que a estrutura química da testosterona e a técnica de
obtê-la de forma sintética foram descobertos na década de 30,
um grande número de estudos têm demonstrado, de forma
indubitável, ser a testosterona um hormônio indispensável
para a manutenção de um estado ótimo de saúde na população
masculina. Na medida em que os homens envelhecem, as
frações biodisponíveis da testosterona e de outros androgênios
declinam crônica e cumulativamente. O declínio gradual da
testosterona biodisponível responde por uma vasta e
multivariada gama de sinais e sintomas, tais como fadiga,
depressão, mudanças do humor, labilidade emocional,
irritabilidade, perda de massa muscular, aumento da gordura
corporal total, aumento da gordura intra-abdominal, perda do
desejo e da performance sexual, fragilidade imunológica,
ginecomastia, perda de massa óssea e muitas outras
manifestações que são, invariavelmente, atribuídas a achados
normais da idade. A persistência da deficiência hormonal
masculina pode aumentar os riscos das comorbidades
associadas ao envelhecimento, tais como obesidade, depressão,
diabetes, osteoporose e doenças cardiovasculares. Embora o
declínio hormonal não afete de maneira tão aguda e incisiva os
homens como a queda hormonal da menopausa, de todo modo,
compromete, pela sua cronicidade e efeito cumulativo, a sua
qualidade de vida, sua saúde e, muito provavelmente, a sua
própria expectativa de vida. O declínio androgênico masculino
recebe uma vasta sinonímia: distúrbio androgênico do
envelhecimento masculino (DAEM ), andropausa, climatério
masculino, menopausa masculina, partial androgen deficiency
in aging men ( PADAM ), hipogonadismo relacionado à idade,
penopausa, dentre outros tantos.
A quantidade de homens que recebe atenção e tratamento no
transcurso da deficiência hormonal é incomparavelmente
menor do que a quantidade de mulheres que recebe reposição
e tratamento na menopausa. Isto se deve, principalmente, ao
fato de que, ao contrário do declínio feminino, o declínio
hormonal masculino ainda não é um fato plenamente aceito
por boa parte da medicina tradicional. Com base na fisiologia
do envelhecimento hormonal, nós acreditamos não haver
qualquer justificativa válida para tal discriminação.
Os oponentes da reposição hormonal da andropausa amparamse em estudos conflitantes e com sérios erros de desenho
existentes na literatura, que demonstram diferenças não
significativas entre os níveis séricos hormonais de homens
jovens e homens velhos, outros sugerem que a testosterona
pode aumentar a incidência de câncer de próstata, enquanto
outros sugerem que a reposição de testosterona não apresenta
efeitos clínicos significativos. Estes estudos atípicos são
fartamente contrapostos por um imenso número de estudos
que são claros e unânimes em demonstrar exatamente o
oposto, destacando-se, principalmente, um indubitável efeito
protetor da testosterona contra o câncer de próstata.
Uma revisão global da literatura corrente não consegue
fornecer qualquer evidência de que a reposição com
testosterona ou seus derivados possa aumentar os riscos de
câncer de próstata in vivo. Ao contrário, homens com baixos
níveis de testosterona biodisponível são exatamente os que
apresentam não só os maiores riscos de câncer de próstata,
como a ocorrência de tumores de comportamento muito mais
agressivo, aumento do processo de deposição aterosclerótica
das artérias e piora gradual e cumulativa da qualidade de
saúde. Além do mais, pacientes portadores de câncer de
próstata que têm os seus níveis circulantes de testosterona
drasticamente reduzidos por conta das terapias antiandrogênicas, não apresentam qualquer aumento ou melhora
da sobrevivência.
Com a finalidade de detectar com o maior grau de precisão
possível a deficiência hormonal masculina, nós recomendamos
não somente uma detalhada avaliação clínica, levando-se em
conta os sinais e sintomas físicos e mentais sugestivos do
declínio masculino, como a realização de testes laboratoriais
que auxiliem e quantifiquem o diagnóstico, dentre os quais:
dosagem da testosterona total, testosterona livre, SHBG,
proteinograma, DHT, testosterona biodisponível, FSH, LH, e o
índice de androgênio livre. Igualmente importante é avaliar os
níveis séricos de estradiol, uma vez que a elevação destes
níveis pode provocar um bloqueio da ação da testosterona nos
homens.
Levando-se em consideração o enorme impacto para a saúde
masculina oriundo da queda de testosterona, nós
recomendamos aos médicos que estimulem o tratamento desta
deficiência para todos os casos, utilizando-se da testosterona
homóloga humana ou de seus derivados quimicamente mais
semelhantes possíveis, excetuando-se alguma contraindicação
absoluta. Todos os homens que avançam na idade, devem
expectar, cedo ou tarde, declínio dos seus níveis ótimos de
testosterona, sendo, portanto, potenciais candidatos à terapia
de reposição. A maioria dos homens irá experimentar declínio
entre os 30 e 45 anos de idade. Vale, entretanto, salientar, que
exceções a esta regra podem ocorrer, fazendo com que alguns
homens venham a necessitar da reposição hormonal abaixo ou
acima daquela faixa etária.
Somente doses fisiológicas de testosterona devem ser
administradas, objetivando-se manter os níveis séricos
comparáveis ao de adultos jovens e saudáveis, na faixa etária
dos 25 a 30 anos.
As melhores vias de administração para este hormônio são a
transdérmica e a intramuscular.
Níveis excessivos de estradiol devem ser evitados durante o
tratamento de reposição com testosterona, por conta do efeito
biológico neutralizador e além de responder pela ocorrência de
ginecomastia, hipertrofia prostática benigna e, possivelmente
infarto agudo do miocárdio. Ajustes no padrão alimentar, evitar
álcool e cafeína, além da prática regular de atividade física são
importantes medidas de suporte para redução dos níveis
excessivos de estradiol. Evitar a obesidade é um ponto
importantíssimo neste contexto, uma vez que o tecido adiposo
é rico em aromatase, enzima que catalisa a transformação de
testosterona em estradiol. Quando estas medidas não surtirem
o efeito desejado, o uso de inibidores da aromatase ou de
pequenas doses de progesterona podem estar indicados. A
progesterona aumenta a transformação de estradiol em
estrona, diminuindo, portanto, as suas concentrações séricas.
O câncer de próstata em atividade pode ser considerado como
uma contraindicação para o uso de testosterona. Contudo, ao se
rever cuidadosamente a literatura atual, parece haver uma
inconsistente base de evidências para dar suporte a esta
afirmação. Muitos estudos, ao contrário, demonstram que
portadores de câncer de próstata que também possuem
deficiência hormonal masculina têm a sua qualidade de saúde
severamente comprometida e podem ser beneficiados com a
reposição de doses pequenas de testosterona, trazendo
benefícios suplementares que em muito superam qualquer
suposto risco de estimulo ao crescimento tumoral.
CONCLUSÃO DO CONSENSO:
Nós não conseguimos identificar na literatura atual qualquer
evidência de que repor doses fisiológicas de testosterona
deponha contra ou traga riscos à saúde de homens portadores
de declínio nos níveis daquele hormônio. Ao contrário. Uma vez
que são múltiplos e multivariados os benefícios advindos da
reposição hormonal masculina, nós recomendamos o uso de
doses fisiológicas de testosterona ou de seu derivado químico
mais próximo possível, com o intuito de corrigir esta
deficiência, submetendo este homem em reposição a um
programa de acompanhamento clínico periódico e regular.
São Paulo, 12 de Novembro de 2012
Grupo de Consensos da SOBRAF
1. Professora Doutora Ana Cristina Vendramini, PhD
2. Professora Doutora Andreia Conceição Milan B. Antoniolli, PhD
3. Professora Doutora Andrea Thomaz Soccol, PhD
4.
5.
6.
7.
Professor Doutor Eduardo Faria, PhD
Professor Doutor Marcelo Alexandre de Mattos, PhD
Professor Doutor Marcos Renato Scholz, PhD
Dr. Ítalo Emmanuel Valeriano Rachid
3. SOMATOPAUSA
a. Quadro clínico
i. Deterioração da composição corporal, redução da massa
muscular, aumento do percentual de gordura corporal
total, aumento do percentual de gordura visceral, cansaço,
redução do desempenho sexual, redução da força muscular,
adinamia, fragilidade imunológica, redução da capacidade
física, ressecamento e enrugamento da pele, déficit de
memória, baixa autoestima, alterações do sono, alterações
do humor, perda de massa óssea, e comprometimento da
qualidade de vida.
b.
Quadro Laboratorial
i. IGF-1 < 300 ng/dL em homens
ii. IGF-1 < 280 ng/dL em mulheres
c.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da somatopausa. Por outro
lado, nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico de somatopausa será
confirmado tomando-se como referência as manifestações e
o quadro clínico apresentados pelo paciente e devidamente
avaliados e registrados pelo médico. Tal conduta se justifica
pela baixa acurácia dos métodos de diagnóstico laboratorial
das deficiências hormonais, falhas de técnicas intrínsecas
aos métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a somatopausa, a SOBRAF recomenda que seus médicos
associados utilizem-se do termo de consentimento padrão adotado
pela mesma e que deverá ser devidamente assinado pelo médico e
pelo seu paciente.
e.
CONSENSO DA SOBRAF PARA O TRATAMENTO
HORMONAL DA SOMATOPAUSA
Após criteriosa revisão da literatura científica, discussões
com médicos representantes de todos os continentes e
discussões entre médicos brasileiros, todos profissionais
versados e adequadamente qualificados em utilizar e
prescrever hormônios em seres humanos com a finalidade
primária de promoção da saúde e, ainda, em total
consonância com os preceitos e guidelines da Sociedade
Brasileira Para Estudos da Fisiologia – SOBRAF, da
International Hormone Society e da World Society of AntiAging Medicine, nós, médicos membros da SOBRAF,
concluímos haver chegado o momento de considerar a
reposição com o hormônio do crescimento humano
recombinante não só em adultos portadores de patologias
que impeçam ou dificultem a sua produção, como nos
adultos que estão envelhecendo e decaindo a sua
capacidade inata de síntese endógena. Nós concordamos e
aprovamos os consensos já estabelecidos e consagrados em
muitos países, que aconselham a reposição com o hormônio
do crescimento humano recombinante em adultos
portadores de patologias que impeçam ou dificultem a sua
produção. Nestas situações, existe história pregressa de
remoção, trauma, radiação, tumores ou severa inativação
da hipófise, fatos que impedem a produção endógena do
hormônio do crescimento.
Pensamos já haver na literatura científica atual uma base
suficiente de dados que demonstram e confirmam os
múltiplos benefícios e segurança do uso clínico do
hormônio do crescimento. Desta forma, tornou-se uma
necessidade médica estendermos a indicação de reposição
também aos adultos que estão envelhecendo e decaindo a
sua capacidade inata de síntese endógena, por conta da
progressiva redução funcional, consequente ao processo de
envelhecimento.
A evidência é de que o hormônio do crescimento é essencial
não apenas para o crescimento de crianças, mas também
essencial para a saúde física e mental de adultos,
particularmente na manutenção da integridade dos
sistemas muscular, adiposo, ósseo, imunológico e
cardiovascular. A deficiência do hormônio do crescimento é
frequentemente acompanhada de fadiga, ansiedade e
depressão, além de um progressivo e cumulativo
comprometimento da qualidade de vida. Por outro lado, a
reposição com o hormônio do crescimento nestes casos tem
demonstrado ser capaz de promover a parada e, por muitas
vezes reversão da progressão de todos aqueles processos.
A falta da reposição do hormônio do crescimento nos
adultos que estão envelhecendo e decaindo a sua
capacidade inata de síntese endógena, ao contrário do que
se imagina, pode trazer consequências verdadeiramente
desastrosas. Aumento considerável da velocidade de
deposição da placa ateromatosa, aumento das taxas de
mortalidade cardiovascular, deterioração da composição
corporal através da perda de massa muscular e
concomitante aumento da deposição de gordura corporal
total e gordura intra-abdominal, fragilidade imunológica,
perda de massa óssea, depressão, distúrbios progressivos
do sono e redução da síntese de proteínas são, dentre
outros, alguns dos fenômenos que se sucedem ao declínio
da capacidade de manutenção da síntese de níveis
fisiológicos do hormônio do crescimento, e que são parcial
ou totalmente reversíveis através da reposição do mesmo.
Nós recomendamos aos médicos submeterem os clientes
em uso do hormônio do crescimento a um regime de
avaliações regulares e aprazados. Isto inclui: anamnese,
exame físico e exames laboratoriais complementares
obedecendo a um intervalo de um a doze meses,
dependendo da necessidade individual de cada cliente.
Em relação a um eventual aumento no risco de
desenvolvimento de certos tipos de câncer com o uso do
hormônio do crescimento, os estudos mais sérios e
respeitados realizados em pacientes que receberam o
hormônio, comparados ao grupo controle de indivíduos
não-tratados,
mostram
uma
clara
redução
de
aproximadamente 50% na incidência de câncer e na
mortalidade por câncer no grupo de indivíduos que
receberam o hormônio. Na realidade, inexiste qualquer
argumento consistente ou fundamentação razoável para se
acreditar que repor o hormônio do crescimento possa
elevar o risco de câncer.
De qualquer forma, uma pesquisa de rotina a cada seis a 12
meses para o câncer de próstata e mama, complementadas
por ultrassom e mamografia quando necessário, constitui
conduta essencial, segundo este grupo de consenso. Além
do mais, nós também recomendamos que o tratamento de
reposição seja programado de modo a se respeitar as doses
fisiológicas preconizadas. Em casos clínicos muito
específicos e pontuais, como, por exemplo, os grandes
obesos e indivíduos com grande superfície corporal, pode
ser justificável o uso de doses maiores, que deverão ser
mantida por período de tempo não superior a 90 dias.
Doses acima dos limites fisiológicos não são recomendadas
por esta sociedade e fogem t ao escopo deste protocolo de
consenso.
Desta forma e seguindo estes princípios, o médico estará
assegurando não só a eficácia como a segurança do
tratamento.
CONCLUSÃO DO CONSENSO:
Na atualidade inexiste qualquer base científica de dados
que contraindique a reposição do hormônio do crescimento
humano recombinante em adultos que estão envelhecendo
e decaindo a sua capacidade inata de síntese endógena. Ao
contrário, uma multiplicidade de sinais, sintomas e
problemas adversos e deletérios à saúde humana tem sido
abundantemente reportada em indivíduos portadores de
níveis endógenos infra fisiológicos do hormônio do
crescimento, bem como tem sido fartamente reportada
melhora, desaparecimento ou mesmo reversão dos
problemas aludidos ao se promover a adequada reposição
do mesmo.
Ressaltamos, mais uma vez, a importância de se observar as
doses fisiológicas do hormônio, bem como a realização de
avaliações clínico-laboratoriais periódicas.
São Paulo, 12 de Novembro de 2012
Grupo de Consensos da SOBRAF
1.
2.
3.
4.
5.
6.
7.
Professora Doutora Ana Cristina Vendramini, PhD
Professora Doutora Andreia Conceição Milan B. Antoniolli, PhD
Professora Doutora Andrea Thomaz Soccol, PhD
Professor Doutor Eduardo Faria, PhD
Professor Doutor Marcelo Alexandre de Mattos, PhD
Professor Doutor Marcos Renato Scholz, PhD
Dr. Ítalo Emmanuel Valeriano Rachid
4. TIREOPAUSA
a. Quadro clínico
i. Deterioração da composição corporal, redução da massa
muscular, aumento do percentual de gordura corporal
total, aumento do percentual de gordura visceral, cansaço,
depressão marcadamente matinal, apatia, incapacidade de
concentração, dificuldade de perder peso, unhas fracas,
queda de cabelos, dislipidemia, hipercolesterolemia,
ateromatose precoce, intolerância ao frio, adinamia,
fragilidade imunológica, constipação, redução da
capacidade física, zumbidos, ressecamento e enrugamento
da pele, déficit de memória, alterações do sono, alterações
do humor, e comprometimento da qualidade de vida.
b.
Quadro Laboratorial
i.
ii.
iii.
iv.
c.
TSH ultrassensível > 2,0 pg/mL
T3 livre < 0,37 ng/dL
T4 livre < 0,7 ng/mL
Média da Temperatura Basal < 36,5o C em cinco aferições
matinais consecutivas.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da tireopausa. Por outro lado,
nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico de somatopausa será
confirmado tomando-se como referência as manifestações e
o quadro clínico apresentados pelo paciente e devidamente
avaliados e registrados pelo médico. Tal conduta se justifica
pela baixa acurácia dos métodos de diagnóstico laboratorial
das deficiências hormonais, falhas de técnicas intrínsecas
aos métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a tireopausa, a SOBRAF recomenda que seus médicos associados
utilizem-se do termo de consentimento padrão adotado pela
mesma e que deverá ser devidamente assinado pelo médico e pelo
seu paciente.
e.
CONSENSO DA SOBRAF PARA O TRATAMENTO
HORMONAL DA TIREOPAUSA
Após criteriosa revisão da literatura científica, discussões
com médicos representantes de todos os continentes e
discussões entre médicos brasileiros, todos profissionais
versados e adequadamente qualificados em utilizar e
prescrever hormônios em seres humanos com a finalidade
primária de promoção da saúde e, ainda, em total
consonância com os preceitos e guidelines da Sociedade
Brasileira Para Estudos da Fisiologia – SOBRAF, da
International Hormone Society e da World Society of AntiAging Medicine, nós, médicos membros da SOBRAF,
concluímos existir um sólido conjunto de evidências de
ordem clínica, prática e teórica que já permitem expandir o
tratamento do hipotireoidismo além dos parâmetros
correntes convencionais.
Existe, na atualidade, uma controvérsia entre grupos de
médicos. Um grupo essencialmente define o diagnóstico do
hipotireoidismo baseado em testes de laboratório,
enquanto o outro toma como base parâmetro
essencialmente clínicos. Uma sólida base de evidências
científicas não dá suporte à ideia de que o diagnóstico do
hipotireoidismo deva ou possa ser baseado apenas em
testes laboratoriais. Isto implica em que a existência do
hipotireoidismo só se confirma quando os níveis séricos de
TSH encontram-se acima dos limites superiores atuais de
referência, e os níveis séricos de tiroxina (T4) e
triiodotireonina (T4), encontram-se abaixo dos limites
inferiores atuais de referência, negligenciando os sinais e
sintomas clínicos.
Esta sociedade adota a posição intermediária. A decisão de
iniciar a reposição com o hormônio tireoidiano deve ser
baseada tanto em achados clínicos quanto laboratoriais, e
não somente em resultados de um simples teste
laboratorial, como se encontra atualmente expresso nos
jornais JAMA e Thyroid, conduta que representa o atual
consenso da Sociedade Americana de Tireoide.
Entendemos que achados e informações clínicas são
essenciais no diagnóstico de deficiências hormonais. Os
dados necessários ao diagnóstico do hipotireoidismo
incluem a pesquisa das queixas físicas e emocionais dos
pacientes, sinais físicos e coleta de história pregressa
pessoal e familiar sugestivas de deficiência tireoidiana, bem
como eventuais anormalidades no volume glandular,
expressos pela presença de hipertrofia ou bócio e/ou
tireoidite autoimune.
As seguintes evidências dão suporte à existência de
hipotireoidismo clínico, em indivíduos erroneamente
considerados laboratorialmente normais, e que são
candidatos ao tratamento de reposição hormonal
tireoidiana:
Os níveis de referencia da normalidade são excessivamente
largos e ignoram e existência dos níveis ótimos de
referência. Estes níveis incluem largas margens de
referência de normalidade para os níveis de T3, T4 e TSH,
que são, na realidade, plenamente compatíveis com
múltiplas disfunções tireoidianas. Não existe qualquer
evidência atual que dê suporte à persistência do uso destes
parâmetros, uma vez que são completamente incapazes de
definir e diferenciar de maneira clara e adequada os
estados de eutireoidismo e hipotireoidismo. A base de
dados atuais sugere que sejam utilizados níveis de
referencia incomparavelmente mais estreitos e específicos
para esta situação. Os níveis convencionais de referência
para detecção do hipotireoidismo sofrem variação de mais
de 30 vezes ( 0.2 a 6.5 mUI/L ).
Em muitos estudos clínicos atuais, níveis séricos de TSH
acima de 1.5 a 2.0 mUI/L tem sido associados com
dislipidemia, inflamação crônica subclínica, níveis elevados
de homocisteína, proteína C reativa, hipercolesterolemia,
depressão, pobre resposta ao tratamento com
antidepressivos, maiores índices de massa corpórea, maior
incidência de hipertensão arterial sistêmica, elevação dos
triglicérides e hiperglicemia. Do mesmo modo, aqueles
níveis tem sido associados a anormalidades cardíacas e
vasculares, que incluem ateromatose acelerada e perda da
elasticidade vascular. Neonatos com baixo peso e partos
prematuros tem sido relatados em mães com TSH acima de
2.0 mUI/L. Mais importante, iniciar o tratamento do
hipotireoidismo nestes casos, tem demonstrado ser uma
medida capaz de minimizar ou reverter aqueles problemas.
Com base ainda nestes múltiplos estudos, existem
evidências que dão suporte a adoção de níveis de referencia
bem mais estreitos para o TSH, cujos valores devem se
situar entre 0.4 a 2.0 mUI/L. Torna-se importante ressaltar
que 95% da população de indivíduos saudáveis e com a
atividade tireoidiana normal exibem níveis séricos de TSH
dentro do intervalo de 0.4 a 2.0 mUI/L.
Um outro ponto de capital importância, é que os estudos
demonstram resultados clínicos incomparavelmente
superiores quando se utiliza no tratamento a associação
entre T3 e T4, ao invés do tratamento isolado com T4. Isto
se deve ao fato de que uma boa parte do T4 administrado
isoladamente, sofre conversão para T3 reverso, forma
hormonal inativa biologicamente. Além do mais, para que o
estado de eutireoidismo seja alcançado, o organismo
humano necessita de ambos os hormônios, T4, que tem a
finalidade principal de atrair moléculas de TBG ( thyroid
binding globulin ) e T3, que, livre do atrelamento da TBG,
pode ligar-se rapidamente aos receptores celulares do
hormônio tireoidiano nas células-alvo. A combinação
fisiológica entre T3 e T4, obedecendo às proporções de uma
parte de T3 para cinco partes de T4 , produz resultados
clínicos inequivocamente superiores.
Nós recomendamos aos médicos que excluam
cuidadosamente outras patologias ou estados clínicos que
produzam sintomatologia semelhante ao hipotireoidismo
antes de iniciar a reposição do hormônio tireoidiano. Ao se
iniciar o tratamento, utilizar doses menores e programar
elevação gradual, de acordo com a necessidade clínica,
visando evitar a presença de superdosagem, e,
consequentemente,
um
possível
quadro
de
hipertireoidismo iatrogênico, efeito adverso mais frequente
no tratamento do hipotireoidismo.
Intolerância ao
tratamento pode ser causada por excessiva conversão de T4
em T3, acelerando, desta forma, a atividade tireoidiana.
Devemos lembrar que a principal causa deste problema é a
deficiência não diagnosticada de outros hormônios,
principalmente a hipocortisolemia e a deficiência de
estradiol na menopausa. Os médicos devem dedicar
especial atenção aos níveis de cortisol. A fadiga adrenal
crônica, que leva à queda excessiva dos níveis de cortisol
provoca uma baixa tolerância ao tratamento do
hipotireoidismo, principalmente quando a opção foi pela
combinação T4/T3. A deficiência de cortisol provoca
hiperatividade do sistema nervoso ortossimpático e uma
excessiva e rápida conversão de T4 em T3. Desta forma, em
pacientes com fadiga adrenal crônica, nós recomendamos
que os médicos tratem a deficiência de cortisol antes de
iniciarem o tratamento do hipotireoidismo ou, no mínimo,
de forma concomitante ao início do mesmo. A segurança do
tratamento do hipotireoidismo pode ser aumentada se o
iniciarmos com doses menores, promovendo um aumento
gradual nos casos em que tais ajustes se fizerem
necessários.
CONCLUSÃO DO CONSENSO:
Hipotireoidismo clínico, em indivíduos erroneamente
considerados laboratorialmente normais, constitui, sem
nenhuma dúvida uma racional justificativa para se
promover a inclusão destas pessoas no grupo de candidatos
ao tratamento com os hormônios tireoidianos. Estes
indivíduos podem se beneficiar com um programa de
reposição com baixas dosagens, em que estejam associados
T4 e T3 em proporções fisiológicas. Avaliação clínica e
laboratorial aprazados, utilizando-se parâmetros mais
estreitos para os níveis de referência do TSH, além de um
cuidadoso monitoramento individual de cada caso, são as
bases que conduzem a resultados clínicos favoráveis.
São Paulo, 12 de Novembro de 2012
Grupo de Consensos da SOBRAF
1.
2.
3.
4.
5.
6.
7.
Professora Doutora Ana Cristina Vendramini, PhD
Professora Doutora Andreia Conceição Milan B. Antoniolli, PhD
Professora Doutora Andrea Thomaz Soccol, PhD
Professor Doutor Eduardo Faria, PhD
Professor Doutor Marcelo Alexandre de Mattos, PhD
Professor Doutor Marcos Renato Scholz, PhD
Dr. Ítalo Emmanuel Valeriano Rachid
5. FADIGA ADRENAL CRÔNICA
a. Quadro clínico
i. Cansaço marcadamente matinal, apatia, incapacidade de
concentração,
adinamia,
fragilidade
imunológica,
compulsão massas e doces, irritabilidade, intolerância ao
estresse, déficit de memória, alterações do sono, alterações
do humor, e comprometimento da qualidade de vida.
b.
Quadro Laboratorial
i. Cortisol matinal < 15 mcg/dL
ii. Cortisol livre < 10 ng/ml
iii. Transcortina > 30 mg/L
c.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da fadiga adrenal crônica. Por
outro lado, nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico da fadiga adrenal crônica será
confirmado tomando-se como referência as manifestações e
o quadro clínico apresentados pelo paciente e devidamente
avaliados e registrados pelo médico. Tal conduta se justifica
pela baixa acurácia dos métodos de diagnóstico laboratorial
das deficiências hormonais, falhas de técnicas intrínsecas
aos métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a fadiga adrenal crônica, a SOBRAF recomenda que seus médicos
associados utilizem-se do termo de consentimento padrão adotado
pela mesma e que deverá ser devidamente assinado pelo médico e
pelo seu paciente.
e.
CONSENSO DA SOBRAF PARA O TRATAMENTO
HORMONAL DA FADIGA ADRENAL CRÔNICA
Após criteriosa revisão da literatura científica, discussões
com médicos representantes de todos os continentes e
discussões entre médicos brasileiros, todos profissionais
versados e adequadamente qualificados em utilizar e
prescrever hormônios em seres humanos com a finalidade
primária de promoção da saúde e, ainda, em total
consonância com os preceitos e guidelines da Sociedade
Brasileira Para Estudos da Fisiologia – SOBRAF, da
International Hormone Society e da World Society of AntiAging Medicine, nós, médicos membros da SOBRAF,
concluímos ter chegado o momento de reconsiderar os
conceitos atualmente vigentes acerca do tratamento da
deficiência adrenal, em particular a deficiência de cortisol,
não apenas nas pessoas afetadas por severas deficiências,
mas também nos portadores de fadiga adrenal crônica.
Nós concordamos plenamente e aprovamos o consenso
mundial que foi atingido no que concerne ao tratamento
com glicocorticoides para adultos portadores de severa
deficiência de cortisol. Geralmente, naquela condição, existe
uma deficiência total ou quase total da produção de cortisol,
que ocorre por conta de remoção total ou parcial ou
inativação total ou parcial das glândulas adrenais, as
estruturas responsáveis pela produção de cortisol.
Acreditamos que a quantidade de evidências existentes na
atualidade demonstrando os efeitos benéficos do cortisol,
bem como os seus eventuais efeitos adversos é suficiente
para promover a extensão da recomendação da reposição
de cortisol também para os portadores da condição clínica
conhecida como fadiga adrenal crônica.
Entre os quadros de deficiência de cortisol deve também
ser incluído a forma que incide ao longo do processo do
envelhecimento, ocasionada pela progressiva deterioração
do eixo hipofisário-adrenal.
A evidência é de que o cortisol é essencial não só para os
portadores de estados de severa depleção, como também
para a manutenção do equilíbrio físico e mental dos adultos
que estão envelhecendo e declinando a sua capacidade de
produção. Uma quantidade adequada de cortisol é essencial
para o normal funcionamento de uma multiplicidade de
órgãos e sistemas: cérebro, pele, articulações, músculos,
trato digestório, sistemas imunológico e cardiovascular. A
deficiência de cortisol encontra-se clinicamente relacionada
com fadiga, baixa tolerância ao estresse, confusão mental e
comprometimento da qualidade de vida. O tratamento com
glicocorticoides tem se mostrado capaz de melhorar a
qualidade de vida, humor e status mental dos pacientes.
Consequências adversas da deficiência de cortisol variam
desde potenciação dos efeitos debilitantes de doenças
inflamatórias ( artrite reumatoide, gastrenterite, colite,
desordens imunológicas e alergias ), até o aumento da
mortalidade em condições de alto risco como o choque
séptico. Os estados de deficiência leve de cortisol podem,
igualmente, causar mais repercussões danosas à saúde
humana do que se imaginava antes.
Como a suplementação de cortisol e de outros
glicocorticoides tem sido associada com importantes efeitos
adversos, dentre os quais: imunossupressão, osteoporose,
ganho de peso, atrofia cutânea, hipertensão, supressão
adrenal e fácies cushingóide, nós recomendamos aos
médicos que a reposição de cortisol deva ser pautada pela
observância de guidelines de segurança. Acreditamos
firmemente que os efeitos colaterais são consequentes ao
uso de doses excessivas, bem como pelo fato de que a
reposição de cortisol não pode ocorrer na ausência da
correção dos desequilíbrios nos níveis de hormônios
anabólicos (pausas humanas ), principalmente a queda dos
níveis de DHEA. e T3. A presença de níveis fisiológicos de
hormônios anabólicos pode bloquear os efeitos catabólicos
da presença de doses excessivas de glicocorticoides. Em
vários casos de deficiência de cortisol, reposição de
derivados sintéticos produz efeitos clínicos muito menos
efetivos do que a reposição do cortisol na sua forma
homóloga humana.
Em termos de diagnóstico laboratorial, pode-se lançar mão
das dosagens séricas de cortisol total matinal, cortisol livre,
transcortina ( CBG= cortisol binding globulin ), ACTH, bem
como dosagens dos 17-hidroxiesteróides em urina de 24
horas, pela técnica de cromatografia a gás.
O tratamento de reposição com cortisol nas formas leves
pode ser feito observando-se os limites diários das doses
fisiológicas. Em casos mais severos, as doses recomendadas
podem sofrer um acréscimo de até 30-50%.
Lembramos que os homens necessitam de doses maiores
porque fisiologicamente secretam quantidades diárias
cerca de 50% maiores do que as mulheres. Apenas 50 % da
dose diária administrada é absorvida pelo trato
gastrintestinal. Em situações de agravamento das condições
de estresse, como: infecções, procedimentos cirúrgicos e
abalo emocional intenso, recomendamos que as doses
sejam temporariamente aumentadas.
Importante lembrar que a reposição com cortisol pode
agravar deficiências já existentes na produção dos
hormônios tireoidianos e DHEA. Desta forma,
recomendamos aos médicos corrigirem concomitantemente
aquelas deficiências.
CONCLUSÃO DO CONSENSO:
Com base na literatura científica atual, inexistem quaisquer
justificativas
plausíveis
que
contraindiquem
ou
desestimulem o tratamento de reposição com cortisol em
adultos com baixos níveis. Efeitos colaterais adversos
podem ser evitados seguindo-se os guidelines já propostos,
bem como utilizando-se doses fisiológicas da forma
homóloga humana do cortisol. Novamente ressaltamos a
capital importância da correção concomitante de outras
deficiências na produção de hormônios anabólicos,
particularmente DHEA e o hormônio tireoidiano. Monitorar
os pacientes através de um programa regular de
acompanhamento clínico-laboratorial.
São Paulo, 12 de Novembro de 2012
Grupo de Consensos da SOBRAF
1.
2.
3.
4.
5.
6.
7.
Professora Doutora Ana Cristina Vendramini, PhD
Professora Doutora Andreia Conceição Milan B. Antoniolli, PhD
Professora Doutora Andrea Thomaz Soccol, PhD
Professor Doutor Eduardo Faria, PhD
Professor Doutor Marcelo Alexandre de Mattos, PhD
Professor Doutor Marcos Renato Scholz, PhD
Dr. Ítalo Emmanuel Valeriano Rachid
6. ADRENOPAUSA
a. Quadro clínico
i. Depressão e cansaço em pessoas jovens, adinamia, apatia,
fragilidade imunológica, ateromatose, irritabilidade, déficit
de memória, alterações do sono, alterações do humor,
ressecamento vaginal, queda de cabelos, rarefação de pelos
pubianos, redução da libido, hipercolesterolemia,
dislipidemia, perda de massa óssea e comprometimento da
qualidade de vida.
b.
Quadro Laboratorial
i. SDHEA < 350 ug/mL em homens
ii. SDHEA < 300 ug/mL em mulheres
c.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da adrenopausa. Por outro lado,
nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico de adrenopausa será
confirmado tomando-se como referência as manifestações e
o quadro clínico apresentados pelo paciente e devidamente
avaliados e registrados pelo médico. Tal conduta se justifica
pela baixa acurácia dos métodos de diagnóstico laboratorial
das deficiências hormonais, falhas de técnicas intrínsecas
aos métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a adrenopausa, a SOBRAF recomenda que seus médicos associados
utilizem-se do termo de consentimento padrão adotado pela
mesma e que deverá ser devidamente assinado pelo médico e pelo
seu paciente.
e.
CONSENSO DA SOBRAF PARA O TRATAMENTO
HORMONAL DA ADRENOPAUSA
Após criteriosa revisão da literatura científica, discussões
com médicos representantes de todos os continentes e
discussões entre médicos brasileiros, todos profissionais
versados e adequadamente qualificados em utilizar e
prescrever hormônios em seres humanos com a finalidade
primária de promoção da saúde e, ainda, em total
consonância com os preceitos e guidelines da Sociedade
Brasileira Para Estudos da Fisiologia – SOBRAF, da
International Hormone Society e da World Society of AntiAging Medicine, nós, médicos membros da SOBRAF,
concluímos ter chegado o momento de considerar a
deficiência de dehidroepiandrosterona, bem como a sua
reposição.
Até o presente momento, as sociedades médicas
convencionais relacionadas à endocrinologia, ainda não
reconheceram a necessidade e a importância clínica de
tratar
e
repor
a
deficiência
adrenal
de
dehidroepiandrosterona
(DHEA).
Algumas
poucas
sociedades médicas convencionais ao redor do mundo, tem
expressado de forma pontual e tímida a importância da
reposição de DHEA. Em geral, se identifica a conclusão de
que ainda não existe base de dados suficiente que dê
suporte à reposição deste hormônio. Eles são da opinião de
que a literatura cientifica sobre o DHEA ainda é muito
escassa e sua eficácia clínica ainda não está suficientemente
comprovada.. Eles, igualmente, expressam a preocupação
de que a reposição de DHEA poderia estar relacionada a
uma maior incidência do câncer genital e a uma redução do
HDL – colesterol.
Após uma cuidadosa e exaustiva revisão da literatura
cientifica atual, bem como ler e discutir os relatórios
negativos institucionais, concluímos não existir qualquer
base de dados científica razoável que dê suporte à ideia de
que o uso de DHEA possa trazer riscos à saúde humana.
Nós reconhecemos e corroboramos um grande número de
estudos aonde homens e mulheres com deficiência de
DHEA tem sido tratados e tem apresentado significativa
melhora em múltiplos aspectos físicos e mentais.
Ao nos detalharmos com estudos que demonstram efeitos
“pouco significativos” no tratamento com DHEA é possível
observar que uma falha de desenho importante é
frequentemente perceptível: o tempo excessivamente curto
em que estas pessoas tem passado recebendo o hormônio,
períodos inferiores a duas semanas, em boa parte das
vezes, tempo notoriamente insuficiente para que resultados
consistentes sejam alcançados.
Ao lado de uma minoria de estudos que demonstram
resultados negativos ou não significativos, existe um grande
número de estudos que atesta de maneira inquestionável a
importância e, mais ainda, uma multivariedade de
benefícios oriundos da reposição com DHEA. Além do mais,
estes estudos não só confirmam a eficácia como chegam à
conclusão que a reposição de DHEA, o mais abundante
hormônio esteroide produzido no corpo humano, é uma das
formas de reposição mais seguras e eficientes que existem.
Estudos randomizados, placebo-controle e duplo-cego,
confirmam inexistirem quaisquer efeitos danosos à saúde
humana, quando níveis fisiológicos de DHEA são
suplementados. Efeitos colaterais porventura existentes,
encontram-se completamente vinculados ao emprego de
doses excessivas. Os sinais mais característicos de doses
excessivas de DHEA são: pele oleosa, acne e leve hirsutismo,
efeitos reversíveis através do devido ajuste nas dosagens.
Em muitos estudos que analisam a reposição de DHEA,
significativos benefícios foram obtidos no ganho de massa
óssea, qualidade da pele, sistema imunológico,
sensibilidade à glicose, sensibilidade à insulina e perfil
lipídico. Benefícios também foram evidenciados na
performance mental e emocional, qualidade de vida, fadiga,
depressão, redução do risco cardiovascular, diabetes e
obesidade.
É a opinião deste grupo que os seguintes argumentos dão
suporte e justificam plenamente o tratamento de reposição
com DHEA em adultos com baixos níveis séricos:
1. DHEA é um hormônio natural aos seres humanos,
está plenamente configurado para atender às nossas
demandas metabólicas, e, na verdade, é o hormônio
presente em maior quantidade no corpo humano.
2. DHEA exerce mais de 150 funções anabólicas no
metabolismo humano.
3. Apresenta uma multiplicidade de benefícios quando
usando em indivíduos adultos que apresentam
baixos níveis, sendo uma valiosa ferramenta no
combate
às
doenças
relacionadas
ao
envelhecimento.
4. Reposição de DHEA é segura.
5. Reposição de DHEA tem um custo acessível.
Com o intuito de elevar a segurança do tratamento de
reposição com DHEA, nós recomendamos que os médicos
submetam seus clientes a um programa de avaliações
periódicas, incluindo anamnese, exame físico e exames
laboratoriais complementares a cada 3 a 12 meses,
dependendo das necessidades individuais de cada um.
Entendemos ser igualmente relevante promover uma
rotina de avaliações clínico-laboratoriais para o câncer de
próstata e mama, obedecendo a um intervalo de seis a 12
meses, dependendo de cada caso.
Na nossa experiência, os melhores métodos para o
diagnóstico da deficiência de DHEA são a avaliação sérica
dos níveis do sulfato de dehidroepiandrosterona e a
avaliação da excreção dos metabólitos 17-cetoesteróidesDHEA em urina de 24 horas, pela técnica de cromatografia
a gás.
As doses de segurança são as chamadas doses fisiológicas,
que devem ser seguidas e observadas pelos membros da
sociedade.
Ressaltamos que nos casos em que é clinicamente
relevante evitar a conversão de DHEA para Testosterona
ou Estradiol, pode-se lançar mão da reposição de 7-KetoDHEA, principal metabólito ativo do DHEA, que possui
exatamente as mesmas propriedades do DHEA, porém, não
sofre conversão para outros hormônios. Neste caso, devese, igualmente, observar as doses fisiológicas de segurança.
CONCLUSÃO DO CONSENSO:
Com base na literatura científica atual, inexistem
justificativas
plausíveis
que
contraindiquem
ou
desestimulem o tratamento de reposição de DHEA em
adultos com baixos níveis, exceto para as mulheres que
encontram-se na pós-menopausa e não estão fazendo a
reposição hormonal da menopausa. Ao contrário, benefícios
em quantidade e intensidade suficientes já tem sido
demonstrados e servem como base para nos permitir
recomendar o uso de doses fisiológicas de DHEA para
corrigir as deficiências bem estabelecidas e previamente
diagnosticadas em adultos, submetendo-os, daí por diante,
a um programa regular de acompanhamento clínicolaboratorial. A reposição de DHEA encontra-se
especialmente justificada em indivíduos portadores de
condições de saúde tratadas com corticoides, uma vez que o
seu uso pode neutralizar com segurança os efeitos
catabólicos excessivos da corticoterapia.
São Paulo, 12 de Novembro de 2012
Grupo de Consensos da SOBRAF
1.
2.
3.
4.
5.
6.
7.
Professora Doutora Ana Cristina Vendramini, PhD
Professora Doutora Andreia Conceição Milan B. Antoniolli, PhD
Professora Doutora Andrea Thomaz Soccol, PhD
Professor Doutor Eduardo Faria, PhD
Professor Doutor Marcelo Alexandre de Mattos, PhD
Professor Doutor Marcos Renato Scholz, PhD
Dr. Ítalo Emmanuel Valeriano Rachid
7. MELATOPAUSA
a. Quadro clínico
i. Depressão, cansaço, adinamia, apatia, fragilidade
imunológica, irritabilidade, déficit de memória, alterações
do sono, alterações do humor, alterações gastrointestinais e
comprometimento da qualidade de vida.
b.
Quadro Laboratorial
i. 6-Sultatoxi-Melatonina < 40 ng/dia em urina de 24 horas
c.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da melatopausa. Por outro lado,
nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico de melatopausa será
confirmado tomando-se como referência as manifestações e
o quadro clínico apresentados pelo paciente e devidamente
avaliados e registrados pelo médico. Tal conduta se justifica
pela baixa acurácia dos métodos de diagnóstico laboratorial
das deficiências hormonais, falhas de técnicas intrínsecas
aos métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a melatopausa, a SOBRAF recomenda que seus médicos associados
estarão, concomitantemente, utilizem-se do termo de
consentimento padrão adotado pela mesma e que deverá ser
devidamente assinado pelo médico e pelo seu paciente.
e.
CONSENSO DA SOBRAF PARA O TRATAMENTO
HORMONAL DA MELATOPAUSA
Após criteriosa revisão da literatura científica, discussões com
médicos representantes de todos os continentes e discussões
entre médicos brasileiros, todos profissionais versados e
adequadamente qualificados em utilizar e prescrever
hormônios em seres humanos com a finalidade primária de
promoção da saúde e, ainda, em total consonância com os
preceitos e guidelines do Grupo Longevidade Saudável, da
International Hormone Society e da World Society of AntiAging Medicine, nós, médicos membros do Grupo de Consenso
do Grupo Longevidade Saudável, concluímos ter chegado o
momento de considerar o tratamento da deficiência de
melatonina em adultos.
Até o presente momento, nenhuma sociedade médica
convencional no mundo reconheceu a necessidade e a
importância de tratar a deficiência da glândula pineal através
da reposição de melatonina.
Como é de costume quando se trata do assunto reposição
hormonal, a controvérsia também não foge à regra na
reposição de melatonina. Para algumas escolas constitui-se em
um hormônio essencial, com importantes repercussões para a
saúde humana. Já para outras escolas, não passa de um placebo
sem qualquer importância clínica. Em contraste com esta
controvérsia, existe uma unanimidade completa acerca da
segurança e importância da reposição de melatonina entre
pesquisadores renomados e médicos ao redor de todo o mundo
que acumularam vasta experiência no uso e aplicações clínicas
deste hormônio em seres humanos. A melatonina tem se
mostrado tão segura, que até o presente momento não foi
possível determinar os limites de doses tóxicas para humanos e
para animais. Doses extremamente elevadas tem sido
utilizadas em experimentos com animais com o intuito de
estabelecer aqueles níveis, sem que se consiga produzir efeitos
danosos ou mesmo a morte dos animais.
Após exaustiva revisão da literatura e troca de experiências
entre grupos versados no emprego clínico da melatonina, o que
se pode concluir é que a sua reposição é capaz de produzir
consistentes e significativos benefícios à saúde humana. Os
efeitos mais notórios são observados na qualidade do sono,
controle do Jet Lag, varredura de radicais livres, metabolismo
da glicose, ossos, sistema cardiovascular, metabolismo
cerebral, melhora do perfil lipídico e manutenção da ciclicidade
e responsividade dos receptores celulares para hormônios
anabólicos.
Foram revistos mais de 350 estudos sobre o uso de melatonina
e o sono, sendo que a quase totalidade dos mesmos (98,6%)
deixa evidente uma notória melhora da qualidade do sono, por
ser a melatonina capaz de encurtar o tempo de indução do
sono, encurtar o início da fase REM do sono profundo e
provocar um relaxamento muscular e nervoso através da
estimulação do sistema parassimpático. O conjunto destas
ações facilita o sono e melhora a sua qualidade, além de
contribuir diretamente para o processo de reparo e
recuperação metabólica ao longo do período de permanência
no sono.
Com base na literatura e experiência mundial atuais, inexistem
quaisquer justificativas plausíveis de ordem científica ou
médica que contraindiquem ou desestimulem o tratamento de
reposição com melatonina. Sua segurança e eficácia clínica são
motivos mais do que suficientes para ressegurar às autoridades
de saúde a validade e aceitação do seu uso, desde de que tal
seja feito sob criteriosa prescrição e supervisão médica.
As doses de segurança são as chamadas doses fisiológicas, que
devem ser seguidas e observadas pelos membros da sociedade.
Lembramos que a melatonina pode reduzir a atividade do
cortisol, de modo que, em casos de fadiga adrenal crônica devese iniciar o tratamento com doses menores e também corrigir a
deficiência de cortisol de forma concomitante.
Na opinião deste grupo, os seguintes argumentos dão suporte e
fundamentam o tratamento de reposição de melatonina em
adultos:
 Melatonina é uma substância natural ao organismo
humano e sua presença é abundante, principalmente no
período noturno.
 Melatonina está completamente adaptada ao corpo
humano.
 Melatonina exerce uma multiplicidade de benefícios na
manutenção da saúde física e mental, bem como contra
o desenvolvimento das doenças degenerativas da
velhice.
 Melatonina é segura.
 Melatonina tem custo acessível.
O diagnóstico da deficiência de melatonina é baseado
em critérios essencialmente clínicos. Pode-se,
entretanto, em casos que se façam necessários, recorrer
à dosagem da excreção em urina de 24 horas da 6sulfatoxi-melatonina,
principal
metabólito
da
melatonina, como parâmetro diagnóstico laboratorial.
CONCLUSÃO DO CONSENSO:
Com base na literatura científica atual, inexistem
quaisquer justificativas plausíveis que contraindiquem
ou desestimulem o tratamento de reposição com
melatonina em adultos com baixos níveis. Ao contrário,
uma vasta base de dados e evidências dão suporte e
validam o seu emprego em indivíduos com deficiência e
com baixos níveis, submetendo-os a um programa
regular de acompanhamento médico.
São Paulo, 12 de Novembro de 2012
Grupo de Consensos da SOBRAF
1.
2.
3.
4.
5.
Professora Doutora Ana Cristina Vendramini, PhD
Professora Doutora Andreia Conceição Milan B. Antoniolli, PhD
Professora Doutora Andrea Thomaz Soccol, PhD
Professor Doutor Eduardo Faria, PhD
Professor Doutor Marcelo Alexandre de Mattos, PhD
6. Professor Doutor Marcos Renato Scholz, PhD
7. Dr. Ítalo Emmanuel Valeriano Rachid
8. ELETROPAUSA
a. Quadro clínico
i. Depressão, cansaço, adinamia, apatia, fragilidade
imunológica, irritabilidade, déficit de memória, alterações
do sono, alterações do humor e comprometimento da
qualidade de vida.
b.
Quadro Laboratorial
i. Dosagem do Sulfato de Pregnenolona no líquor
ii. Sulfato de pregnenolona < 90 ng/mL.
c.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da eletropausa. Por outro lado,
nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico de eletropausa será confirmado
tomando-se como referência as manifestações e o quadro
clínico apresentados pelo paciente e devidamente avaliados
e registrados pelo médico. Tal conduta se justifica pela
baixa acurácia dos métodos de diagnóstico laboratorial das
deficiências hormonais, falhas de técnicas intrínsecas aos
métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a eletropausa, a SOBRAF recomenda que seus médicos associados
utilizem-se do termo de consentimento padrão adotado pela
mesma e que deverá ser devidamente assinado pelo médico e pelo
seu paciente.
REFERÊNCIAS BIBLIOGRÁFICAS COMPLEMENTARES
1- ATIVIDADE ANTI-OXIDANTE
MODULAÇÃO HORMONAL
MEDIADA
PELA
Atividade Antioxidante da Melatonina
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5.
6.
7.
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Rodriguez MI, Escames G, López LC, García JA, Ortiz F, López A, AcuñaCastroviejo D. Melatonin administration prevents cardiac and diaphragmatic
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CONTROLE DA ANSIEDADE ATRAVÉS DA
MODULAÇÃO HORMONAL
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ATRAVÉS DA MODULAÇÃO HORMONAL
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104 ESTUDOS PLACEBO-CONTROLADOS DEMONSTRANDO OS BENEFÍCIOS
E CONTROLE EXERCIDOS PELA REPOSIÇÃO DE MELATONINA NOS
MECANISMOS E QUALIDADE DO SONO EM CRIANÇAS E ADULTOS
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Distúrbios do Sono: A Correlação Com Baixos Níveis de Testosterona
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-
CONTROLE DA PRESSÃO ARTERIAL
ATRAVÉS DA MODULAÇÃO HORMONAL
6
Hipertensão Arterial: A Associação Com Baixos Níveis de Melatonina
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Fraturas do Quadril: A Prevenção Com a Reposição de Estradiol e
Progesterona
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of hip fracture protection after estrogen cessation: evidence from the National
Osteoporosis Risk Assessment. Obstet Gynecol. 2004 Mar;103(3):440-6
Osteoporose: A Associação Com Baixos Níveis de Testosterona
1- Clapauch R, Mattos TM, Silva P, Marinheiro LP, Buksman S, Schrank Y.
Total estradiol, rather than testosterone levels, predicts osteoporosis in aging
men. Arq Bras Endocrinol Metabol. 2009 Nov;53(8):1020-5
2- Deutsch S, Benjamin F, Seltzer V, Tafreshi M, Kocheril G, Frank A. The
correlation of serum estrogens and androgens with bone density in the late
postmenopause. Int J Gynaecol Obstet. 1987 Jun;25(3):217-22
3- Garnero P, Sornay-Rendu E, Claustrat B, Delmas PD. Biochemical markers
of bone turnover, endogenous hormones and the risk of fractures in
postmenopausal women: the OFELY study. J Bone Miner Res. 2000
Aug;15(8):1526-36
4- Lau EM, Suriwongpaisal P, Lee JK, Das De S, Festin MR, Saw SM, Khir A,
Torralba T, Sham A, Sambrook P. Risk factors for hip fracture in Asian men
and women: the Asian osteoporosis study. J Bone Miner Res. 2001
Mar;16(3):572-80
5- van den Beld AW, de Jong FH, Grobbee DE, Pols HA, Lamberts SW.
Measures of bioavailable serum testosterone and estradiol and their
relationships with muscle strength, bone density, and body composition in
elderly men. J Clin Endocrinol Metab. 2000 Sep;85(9):3276-82
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mineral density and cardiovascular risk factors. Bone. 1996 Feb;18(2):11-7
3- Katznelson L, Finkelstein JS, Schoenfeld DA, Rosenthal DI, Anderson EJ,
Klibanski A. Increase in bone density and lean body mass during testosterone
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1996 Dec;81(12):4358-65
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Effect on phospho-calcium metabolism of testosterone administration in
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6- Diamond T, Stiel D, Posen S. Effects of testosterone and venesection on
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7- Kenny AM, Prestwood KM, Gruman CA, Marcello KM, Raisz LG. Effects of
transdermal testosterone on bone and muscle in older men with low
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May;56(5):M266-72
8- Snyder PJ, Peachey H, Berlin JA, Hannoush P, Haddad G, Dlewati A,
Santanna J, Loh L, Lenrow DA, Holmes JH, Kapoor SC, Atkinson LE, Strom
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Staley J, Santanna J, Kapoor SC, Attie MF, Haddad JG Jr, Strom BL. Effect
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Fraturas do Quadril: A Associação Com Baixos Níveis de Testosterona
1- Leifke E, Wichers C, Gorenoi V, Lucke P, von zur Muhlen A, Brabant G. Low
serum levels of testosterone in men with minimal traumatic hip fractures. Exp
Clin Endocrinol Diabetes. 2005 Apr;113(4):208-13
-
PREVENÇÃO DO CÂNCER E REDUÇÃO DO
RISCO DE CÂNCER ATRAVÉS DA MODULAÇÃO
HORMONAL
10
Proteção na MENOPAUSA:
o
Raghvendra K et al. Cardiovascular pharmacology of estradiol
metabolites. Journal of Pharmacology and Experimental Therapeutics.
2004; 308-403-409.
 Replace E2 = presence of catecholestradiols and
methoxyestradiols = not activation of the nuclear estrogen
receptors = protection against cancer and other diseases
o
Liu ZJ et al. Selective insensitivity of ZR-75-1 human breast cancer
cells to 2-methoxyestradiol: evidence for type II beta-ydroxisteroid
dehydrogenase as the underlying cause.
Cancer
Res. 2005 Jul 1;65(13):5802-11
 Metabolism of E2 after replacement by P450 produce 2ME2
and confer protection


2ME2 decreases tumor growth, angiogenesis and growth of
cancer cells
2ME2
has strong antiproliferative, apoptotic and
antiangiogenic action
o
Fournier A. et al. Breast cancer risk in relation to different types
of hormone replacement therapy in the E3N-EPIC cohort study.
International Journal of Cancer .2005 Apr 10;114(3):448-54
 Progesterone protects, progestins worsen cancer risk
 The risk was significantly greater ( p < 0.001) with HRT
containing synthetic progestins than with HRT containing
bioidentical Progesterone
 The RR respectively 1.4 and 0.8
 20% decrease in risk with bioidentical progesterone
o
Fournier A. et al. Unequal risks for breast cancer associated with
different hormone replacement thearpies: results of the E3N-EPIC
cohort study.
Breast Cancer Research Treat .2007 Feb
10;104(13):373-91
 80.377 postmenopausal women
 No increase in breast cancer in women on E2 and
Progesterone
 CEE+MPA had RR of 1.69 or 69% increase in risk of breast
cancer
 These findings prove that bioidentical hormones are
undoubtedly safer
o
Campagnoli C. et al. Progesterone and Progestins in relation to
breast cancer risk. Journal of Steroid Biochemistry amd Molecular
Biology.2005 441-450
 Progesterone decreases breast cancer risk
 Synthetic progestins increase BC risk
 Higher P4 during menstrual cycle, 50% reduction risk
 Higher P4 HRT, 78% reduction in risk
Proteção na ANDROPAUSA:
o
Morley, J. et al., “Testosterone replacement and the physiologic
aspects of aging in men”, “ Mayo Clinic Proc 2000; 75(suppl):583-7
 There is absolutelly no clinical evidence that the risk of either
prostate cancer or BPH increases with transdermal
testosterone replacement.
o
Stattin, P. et al., “High levels of circulating testosterone are not
associated with increased prostate cancer risk: a pooled prospective
study”, “ Intl J Cancer 2004 Jan 20; 108(3):418-24.
 Higher T less prostate cancer.
 Higher E2 more prostate câncer
o
Basaria, A. et al., “Anabolic androgenic steroid therapy in the
treatment of chronic diseases”, “ The Journal of Clinical Endocrinology
and Metabolism 2004; Vol 86. No. 11:5108-5117

The increase of prostate cancer is not increased by
Testosterone administration
o
Rhoden, W. et al., “High levels of circulating testosterone are not
associated with increased prostate cancer risk” . New England Journal
of Medicine 2004 Mar; 163(3):824-7
 No compelling evidence at present to suggest that men with
higher testosterone levels are at great risk of prostate cancer
or that treating men who have hipogonadism with exogenous
androgens increases this risk. In fact, it should be recognized
that prostate cancer becomes more prevalent exactly at the
time of a man’s life when testosterone levels decline.
o
o
TESTOSTERONE therapy in men with untreated PCa
Morgentaler et al, J Urol 2011
 All men experienced symptomatic benefit
 No increase in PSA
 No increase in prostate volume
 No definite cancer progression
 54% of biopsies- no cancer seen!
o
Muller M, van der Schouw YT, Thijssen JH, Grobbee DE. Endogenous
sex hormones and cardiovascular disease in men. J Clin Endocrinol
Metab. 2003; 88 (11): 5076-86.
 A report in The Journal of Clinical Endocrinology and
Metabolism (November 2003) sheds more light on the
beneficial effects of testosterone supplementation in
andropausal men. The study authors conducted a rigorous
database search of testosterone’s effect on heart disease in
men, and identified multiple studies showing that men with low
testosterone levels had higher blood pressure, LDL cholesterol
levels, triglyceride levels, and body mass index compared to
men with optimal testosterone levels. Discussing the potential
side effects of testosterone supplementation in elderly men,
the authors noted, “the scientific basis for these concerns is
scarce.”*
HORMÔNIO DO CRESCIMENTO E CÂNCER:
o
Vance M, CJ. et al., “GH Therapy in Adults and Children. The New
England Journal of Medicine. October 14, 2000
 “No evidence that GH replacement therapy affects the risk of
cancer”
o
Molitch ME. et al., “Diagnosis of GH deficiency in adults – how good
the criteria need to be ? J Clin Endocrinol Metab 2002 Feb;
87(2):473-6
 Although there has been concerns about an increased risk of
cancer, reviews of existing well-maintained databases of
treated patients have shown this theoretical risk to be
nonexistent.
o
Fiebig HH et al. No evidence of tumor growth stimulation in human
tumors in vitro following treatment with recombinant human growth
hormone. Anticancer Drugs J 2000 Sep; 11(8):659-64
 GH improves cancer cachexia
 No evidence of tumor growth stimulation
o
Growth Hormone Research Society. J Clin Endo Metab, May 2001.
 There is no data to suggest that IGF-1 and IGFBP 3 modulate
cancer risk in GH treated patients.
 There is no data to support that active malignancy is a
contraindication for GH supplementation.
 No evidence that GH increases cancer recurrence or de novo
cancer or leukemia.
o
Swerdlow A. et al. Growth Hormone Treatment of Children with Brain
Tumors and Risk of Tumor Recurrence. The Journal of Clinical
Endocrinology and Metabolism Vol 85, No. 12, December 2000.
 Children with brain tumors  180 treated with GH
 891 not treated with GH
 In treated patients
 Decreased risk of recurrence: 60%
 Decreased risk of mortality: 50%
o
Murray R.D. et al. GH-Deficient Survivors of Chidlhood Cancer: GH
Replacement During Adult Life. The Journal of Clinical Endocrinology
and Metabolism 2002 Jan;87(1):129-35
 GH Replacement and Cancer
 Improved QOL
 “Importantly, during the 12-24 months of GH replacement
therapy, there was absolutely no clinical suggestion of tumor
reccurence.
o
Hong J et al. IGFBP 3 mutants that do not bind IGFs stimulate
apoptosis in human cancer cells. Journal of Bio Chem 2002 Jan 9.
 IGFBP 3 Independent Anti-Cancer Actions
 IGFBP 3 triggers cell cycle and stimulates apoptosis.
 IGFBP 3 independent mechanisms are major contributors to
IGFBP 3 induced apoptosis in cancer cells.
 IGFBP 3 plays a wider hole in the anti-proliferative and antitumorgenic actions.
 IGFBP 3 may be considered “The Guardian of the Genome”.
o
Kurek R et al. The significance of serum levels of insulin-like growth
factor 1 in patients with prostate cancer. J Clin Endoc Metab, 2000
Jan;85(1):125-9.
 No association between IGF-1, GH and prostate cancer risk.
 Androgen decline or withdrawal did not change IGF-1.
o
Baffa R et al. Low serum insulin-like growth factor 1 : a significant
association with prostate cancer. J Urology, 2000 Sep;6(3):236-239.
 Low IGF-1 Associated with Prostate Cancer
 IGF-1 considerably lower in Prostate CA patients than control.



o
No association of IGF-1, GH levels and PSA increase.
IGF-1 decresed with age
Prostate cancer risk increased with age
.
Finne P et Al IGf-1 Tumor Marker for cancer prostate ? . Can
Research 2004 15;63(14)3991-496 Mar 28;334(13): 800-14
 Declínio IGF-1 diretamente correlacionado com aumento do
risco de câncer de próstata
 Queda 55% de IGF-1, representa aumento de 48% no
risco de ca próstata
Câncer: Efeito Protetor da Reposição de Melatonina
177. Mills E, Wu P, Seely D, Guyatt G. Melatonin in the treatment of cancer: a
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Archili C, De Toma D, Pipino G, et al. Randomized study with the pineal
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Lett. 2001;22(1):45-7
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Cancer Res. 1998 Oct 1;58(19):4383-90
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Melatonin and colon carcinogenesis. IV. Effect of melatonin on proliferative
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Swiss mice. Med Sci Monit. 2000 May-Jun;6(3):471-5
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Conti A, Maestroni GJ. A randomized study of chemotherapy with cisplatin plus
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Câncer: A Associação Com Baixos Niveis do Hormônio do Crescimento
1- Woodson K, Tangrea JA, Pollak M, Copeland TD, Taylor PR, Virtamo J,
Albanes D. Serum IGF-1: tumor marker or etiologic factor? A prospective
study of prostate cancer among Finnish men. Cancer Res. 2003 Jul
15;63(14):3991-4
2- Chokkalingam AP, Pollak M, Fillmore CM, Gao YT, Stanczyk FZ, Deng J,
Sesterhenn IA, Mostofi FK, Fears TR, Madigan MP, Ziegler RG, Fraumeni JF
Jr, Hsing AW. Insulin-like growth factors and prostate cancer: a populationbased case-control study in China. Cancer Epidemiol Biomarkers Prev. 2001
May;10(5):421-7
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Hauck WW, Baserga R, Gomella LG. Low serum insulin-like growth factor 1
(IGF-1): a significant association with prostate cancer. Tech Urol. 2000
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Tammela T, Seppala M, Hakama M, Stenman UH. Insulin-like growth factor I
is not a useful marker of prostate cancer in men with elevated levels of
prostate-specific antigen. J Clin Endocrinol Metab. 2000 Aug;85(8):2744-7
5- Colombo F, Iannotta F, Fachinetti A, Giuliani F, Cornaggia M, Finzi G,
Mantero G, Fraschini F, Malesci A, .Bersani M, et al. Changes in hormonal
and biochemical parameters in gastric adenocarcinoma. Minerva Endocrinol.
1991 Jul-Sep;16(3):127-39
Estudos em Humanos Relacionando Baixos Níveis de GH/IGF-1 em Pacientes
Com Câncer
Baixos Níveis de IGF-1 no Glioma
1.
Lönn S, Inskip PD, Pollak MN, Weinstein SJ, Virtamo J, Albanes D. Glioma risk
in relation to serum levels of insulin-like growth factors. Cancer Epidemiol
Biomarkers Prev. 2007 Apr;16(4):844-6
Baixos Níveis de IGF-1 no Câncer de Próstata
1- Agurs-Collins T, Adams-Campbell LL, Kim KS, Cullen KJ.Ins ulin-like growth
factor-1 and breast cancer risk in postmenopausal African-American women.
Cancer Detect Prev. 2000;24(3):199-206
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Nomura A, Heilbrun LK, Stemmermann GN, Judd HL. Prediagnostic serum
hormones and the risk of prostate cancer. Cancer Res 1988 Jun
15;48(12):3515-7
Hoffman MA, DeWolf WC, Morgentaler A.Is low serum free testosterone a
marker for high grade prostate cancer? J Urol 2000 Mar;163(3):824-7
Wynder EL, Laakso K, Sotarauta M, Rose DP. Metabolic epidemiology of
prostatic cancer. Prostate 1984;5(1):47-53
Mortalidade Aumentada em Homens Com Câncer de Próstata e Baixos Níveis
de Testosterona
1-
2-
3-
4-
Carrero JJ, Qureshi AR, Parini P, Arver S, Lindholm B, Bárány P, Heimbürger
O, Stenvinkel P. Low serum testosterone increases mortality risk among
male dialysis patients. J Am Soc Nephrol. 2009 Mar;20(3):613-20
Tivesten A, Vandenput L, Labrie F, Karlsson MK, Ljunggren O, Mellström D,
Ohlsson C. Low serum testosterone and estradiol predict mortality in elderly
men. . J Clin Endocrinol Metab. 2009 Jul;94(7):2482-8
Khaw KT, Dowsett M, Folkerd E, Bingham S, Wareham N, Luben R, Welch A,
Day N. Endogenous testosterone and mortality due to all causes,
cardiovascular disease, and cancer in men: European prospective
investigation into cancer in Norfolk (EPIC-Norfolk) Prospective Population
Study. Circulation. 2007 Dec 4;116(23):2694-701
Laughlin GA, Barrett-Connor E, Bergstrom J. Low serum testosterone and
mortality in older men. . J Clin Endocrinol Metab. 2008 Jan;93(1):68-75
5-
6-
7-
8-
Shores MM, Matsumoto AM, Sloan KL, Kivlahan DR. Low serum testosterone
and mortality in male veterans. Arch Intern Med. 2006 Aug 1428;166(15):1660-5
Ribeiro M, Ruff P, Falkson G. Low serum testosterone and a younger age
predict for a poor outcome in metastatic prostate cancer. Am J Clin Oncol.
1997 Dec;20(6):605-8
Iversen P, Rasmussen F, Christensen IJ. Serum testosterone as a prognostic
factor in patients with advanced prostatic carcinoma. Scand J Urol Nephrol
Suppl. 1994; 157: 41-7
Haapiainen R, Rannikko S, Alfthan O, Adlercreutz H. Pretreatment plasma
levels of testosterone and sex hormone binding globulin binding capacity in
relation to clinical staging and survival in prostatic cancer patients. Prostate.
1988;12(4):325-32
Câncer em Homens: Possível Proteção Com a Reposição de Testosterona
1- Dimitrakakis C, Jones RA, Liu A, Bondy CA. Breast cancer incidence in
postmenopausal women using testosterone in addition to usual hormone
therapy. Menopause. 2004 Sep-Oct;11(5):531-535
2- Morales A, Connolly JG, Bruce AW. Androgen therapy in advanced
carcinoma of the prostate. Can Med Assoc J. 1971;105(1):71-2
3- Prout GR Jr, Brewer WR. Response of men with advanced prostatic
carcinoma to exogenous administration of testosterone. Cancer. 1967
Nov;20(11):1871-8
4- Joly-Pharaboz MO, Soave MC, Nicolas B, Mebarki F, Renaud M, Foury O,
Morel Y, Andre JG. Androgens inhibit the proliferation of a variant of the
human prostate cancer cell line LNCaP. J Steroid Biochem Mol Biol 1995
Oct;55(1):67-76
5- Wolf DA, Schulz P, Fittler F. Synthetic androgens suppress the trans- formed
phenotype in human prostate carcinoma cell line LNCaP. Br J Cancer. 1991
Jul; 64 (1): 47-53
6- Andrews P, Krygier S, Djakiew D. Dihydrotestosterone (DHT) modulates the
ability of NSAIDs to induce apoptosis of prostate cancer cells. Cancer
Chemother Pharmacol 2002 Mar;49(3):179-86
Estudos Aonde a Reposição Com Testosterona Parece Conferir Proteção
Contra o Câncer de Próstata
1.
2.
Morales A, Connolly JG, Bruce AW. Androgen therapy in advanced carcinoma
of the prostate. Can Med Assoc J. 1971;105(1):71-2
Prout GR Jr, Brewer WR. Response of men with advanced prostatic carcinoma
to exogenous administration of testosterone. Cancer. 1967 Nov;20(11):1871-8
Estudos Aonde a Reposição Com Testosterona Promove Inibição da
Proliferação do Câncer de Próstata ou Induz a Sua Apoptose
1-
Joly-Pharaboz MO, Soave MC, Nicolas B, Mebarki F, Renaud M, Foury O,
Morel Y, Andre JG. Androgens inhibit the proliferation of a variant of the
2-
3-
human prostate cancer cell line LNCaP. J Steroid Biochem Mol Biol 1995
Oct;55(1):67-76
Wolf DA, Schulz P, Fittler F. Synthetic androgens suppress the transformed
phenotype in human prostate carcinoma cell line LNCaP. Br J Cancer. 1991
Jul; 64 (1): 47-53
Andrews P, Krygier S, Djakiew D. Dihydrotestosterone (DHT) modulates the
ability of NSAIDs to induce apoptosis of prostate cancer cells. Cancer
Chemother Pharmacol. 2002 Mar;49(3):179-86
Estudos Onde a Reposição de Testosterona Reduz Queixas Prostáticas Como
Disúria e Nictúria
1-
2-
34567-
8-
Flamm J, Kiesswetter H, Englisch M. An urodynamic study of patients with
benign prostatic hypertrophy treated conservatively with phytotherapy or
testosterone. Wien Klin Wochenschr 1979 Sep 28;91(18):622-7
Kearns WM. Testosterone in the treatment of testicular deficiency and prostatic
enlargement. Wisconsin Med J. 1941; 40:927 (testosterone proprionate
therapy did not reduce the size of the prostate, but reduced the dysuria)
Meltzer M. Male hormone therapy of prostatic hypertrophy. Lancet. 1939; 59:
279
Trasoff A. The treatment of benign prostatic hypertrophy with testosterone
propionate. J Lab Clin Med. 1940; 25: 377
Markham MJ. The clinical use of peroral methyltestosterone in benign prostatic
hypertrophy. Urol Cutan Rev. 1942; 46: 225
Markham MJ. The clinical use of testosterone propionate in benign prostatic
hypertrophy. Urol Cutan Rev. 1941; 45: 35
Laqueur E. Behandlung der Prostathypertropie mit männlichen Hormone
(Hombreol) une experimentell Begründung dieser Therapie. Schweiz Med
Wochenschr. 1934; 64: 1116
South Med J, 1939, 32: 154
Estudos Onde a Reposição de Testosterona Reduziu o Volume da Próstata e
as Queixas Prostáticas
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4-
South Med J, 1939, 32: 154
de Lignieres B. Transdermal dihydrotestosterone treatment of 'andropause.
Ann Med 1993 Jun;25(3):235-41
Swerdloff RS, Wang C. Dihydrotestosterone: a rationale for its use as a nonaromatizable androgen replacement therapeutic agent. Baillieres Clin
Endocrinol Metab. 1998 Oct;12(3):501-6
Sitruk-Ware R. Contraception, 1989, 39: 1-191
Estudos de Revisão Onde os Autores Não Acharam Associação Entre Os
Níveis de Testosterona e o Risco de Câncer de Próstata e Demonstram
Claramente Que Não Existem Dados ou Evidências Que Dêem Suporte a Visão
de Que a Reposição de Testosterona Esteja Correlacionada Com o Risco de
Câncer
1-
2-
3-
4-
567-
Rhoden NEJM 2004 (“No compelling evidence at present to suggest that men
with higher testosterone levels are at greater risk of prostate cancer or that
treating men who have hypogonadism with exogenous androgens
increases this risk. In fact, it should be recognized that prostate cancer
becomes more prevalent exactly at the time of a man's life when
testosterone levels decline.“)
Morales A. Androgen replacement therapy and prostate safety. Eur Urol 2002
Feb;41(2):113-20 (“To date there is no evidence that exogenous androgens
promote development of prostate cancer”)
Basaria S, Wahlstrom JT, Dobs AS. Anabolic-Androgenic Steroid Therapy in
the Treatment of Chronic Diseases. J Clin Endocrinol Metab. 2001
Nov;86(11):5108-17(“..recent reviews suggest that the incidence of prostate
cancer is not increased by testosterone administration”)
Morley JE. Testosterone replacement and the physiologic aspects of aging in
men. Mayo Clin Proc. 2000 Jan;75 Suppl:S83-7 (“There is no clinical
evidence that the risk of either prostate cancer or benign prostate
hypertrophy increases with testosterone treatment”)
Wirth MP, Hakenberg OW Testosterone and the prostate. Urologe A 2000
Sep;39(5):418-20
Rolf C, Nieschlag E. Potential adverse effects of long-term testosterone
therapy. Baillieres Clin Endocrinol Metab. 1998 Oct;12(3):521-34.
Prehn RT. On the prevention and therapy of prostate cancer by androgen
administration. Cancer Res. 1999 Sep 1;59(17):4161-4 (“… contrary to
prevalent opinion, declining rather than high levels of androgens probably
contribute more to human prostate carcinogenesis and ;.. androgen
supplementation would probably lower the incidence of the disease. …
consider the possibility that the growth of androgen-independent prostate
cancers might be reduced by the administration of androgens”)
Estudos Onde a Reposição de Testosterona em Homens Com Câncer de
Próstata Não Exerce Qualquer Efeito Adverso na Progressão ou Recorrência
do Câncer e, Ao Mesmo Tempo, Melhora a Qualidade de Vida e Os Parâmetros
Gerais de Saúde
1- Morales A, Black AM, Emerson LE. Testosterone administration to men with
testosterone deficiency syndrome after external beam radiotherapy for
localized prostate cancer: preliminary observations. BJU Int. 2009
Jan;103(1):62-4 (n = 5; “Men with testosterone deficiency syndrome after
external beam radiotherapy for localised prostate cancer are candidates for
testosterone
therapy
..no
adverse
effects
from
testosterone
supplementation”)
2- Sarosdy MF. Testosterone replacement for hypogonadism after treatment of
early prostate cancer with brachytherapy. Cancer. 2007 Feb 1;109(3):536-41
( (n = 31; For patients with low serum testosterone levels and symptoms of
hypogonadism, testosterone therapy may be used with caution and close
follow-up after prostate brachytherapy)
3- Agarwal PK, Oefelein MG. Testosterone replacement therapy after primary
treatment for prostate cancer. J Urol. 2005 Feb;173(2):533-6 (n = 10
hypogonadal men treated with radical retropubic prostatectomy for organ
confined prostate cancer; testosterone replacement therapy can be
administered carefully and with benefit to hypogonadal patients with prostate
cancer)
Estudos Onde a Reposição de Testosterona Não Demonstra Efeitos Adversos
No Risco de Câncer de Próstata
1- Prout GRJ, Brewer WR. Response of men with advanced prostatic carcinoma
to exogenous administration of testosterone. Cancer (Phila.). 1967;20:1871-8
2- Trunnell JD, Duffy BJ Jr. The influence of certain steroids on the behavior of
human prostate cancer. Trans. NY Acad Sci. 1950;II:12:238-41
3- Brendler H, Lowry O, Brock M. Further investigation of hormonal
relationships. Arch Surg. 1950,61:433-40
4- Pearson OH. Discussion of Dr. Huggins’ paper: “Control of cancers of man by
endocrinological methods." Cancer Res. 1957:17:473-9
5- Morales A, Connolly J, Burr R, Bruce A. The use of radioactive phosphorus to
treat bone pain in metastatic carcinoma of the prostate. Can Med Assoc J.
1970;103: 372-3
Estudos Onde a Reposição de Testosterona Não Demonstra Quaisquer Efeitos
Nos Níveis de PSA ou do Volume da Próstata
3.
4.
5.
6.
7.
8.
9.
10.
11.
Rhoden EL, Morgentaler A. Influence of demographic factors and biochemical
characteristics on the prostate-specific antigen (PSA) response to testosterone
replacement therapy. Int J Impot Res. 2005 Sep 22 (No statistical increase:
average = 0.31 ng/ml after 1 year of treatment of hypogonadal men)
Shibasaki T, Sasagawa I, Suzuki Y, Yazawa H, Ichiyanagi O, Matsuki S, Miura
M, Nakada T. Effect of testosterone replacement therapy on serum PSA in
patients with Klinefelter syndrome. Arch Androl. 2001 Nov-Dec;47(3):173-6
Cooper CS, Perry PJ, Sparks AE, MacIndoe JH, Yates WR, Williams RD. Effect
of exogenous testosterone on prostate volume, serum and semen prostate
specific antigen levels in healthy young men. J Urol. 1998 Feb;159(2):441-3
Cooper CS, MacIndoe JH, Perry PJ, Yates WR, Williams RD. The effect of
exogenous testosterone on total and free prostate specific antigen levels in
healthy young men. J Urol. 1996 Aug;156(2 Pt 1):438-41
Behre HM, Bohmeyer J, Nieschlag E. Prostate volume in testosterone-treated
and untreated hypogonadal men in comparison to age-matched normal
controls. Clin Endocrinol (Oxf). 1994 Mar;40(3):341-9
Douglas TH, Connelly RR, McLeod DG, Erickson SJ, Barren R 3rd, Murphy
GP. Effect of exogenous testosterone replacement on prostate-specific antigen
and prostate-specific membrane antigen levels in hypogonadal men. J Surg
Oncol. 1995 Aug;59(4):246-50
Sih R, Morley JE, Kaiser FE, Perry HM 3rd, Patrick P, Ross C. Testosterone
replacement in older hypogonadal men: a 12-month randomized controlled trial.
J Clin Endocrinol Metab. 1997 Jun;82(6):1661-7
Hajjar RR, Kaiser FE, Morley JE. Outcomes of long-term testosterone
replacement in older hypogonadal males: a retrospective analysis. J Clin
Endocrinol Metab. 1997 Nov;82(11):3793-6
Monath JR, McCullough DL, Hart LJ, Jarow JP. Physiologic variations of serum
testosterone within the normal range do not affect serum prostate-specific
antigen. Urology. 1995 Jul;46(1):58-61
-
EXPANSÃO DA LONGEVIDE E MELHORA DA
QUALIDADE DE VIDA ATRAVÉS DA MODULAÇÃO
HORMONAL
11
Longevidade em Homens: A Associação Com Baixos Níveis de Testosterona
1-
2-
3-
4-
56-
Khaw KT, Dowsett M, Folkerd E, Bingham S, Wareham N, Luben R, Welch A,
Day N. Endogenous testosterone and mortality due to all causes,
cardiovascular disease, and cancer in men: European prospective
investigation into cancer in Norfolk (EPIC-Norfolk) Prospective Population
Study. Circulation. 2007 Dec 4;116(23):2694-701
Jankowska EA, Biel B, Majda J, Szklarska A, Lopuszanska M, Medras M,
Anker SD, Banasiak W, Poole-Wilson PA, Ponikowski P. Anabolic
deficiency in men with chronic heart failure: prevalence and detrimental
impact on survival. Circulation. 2006 Oct 24;114(17):1829-37
Shores MM, Matsumoto AM, Sloan KL, Kivlahan DR. Low serum testosterone
and mortality in male veterans. Arch Intern Med. 2006 Aug 1428;166(15):1660-5
Shores MM, Moceri VM, Gruenewald DA, Brodkin KI, Matsumoto AM, Kivlahan
DR. Low testosterone is associated with decreased function and increased
mortality risk: a preliminary study of men in a geriatric rehabilitation unit. J
Am Geriatr Soc. 2004 Dec;52(12):2077-81
Suzuki M. Centenarians in Japan. Nakayamshoten Tokyo (Japan), 1995: 64-78
Haapiainen R, Rannikko S, Alfthan O, Adlercreutz H. Pretreatment plasma
levels of testosterone and sex hormone binding globulin binding capacity in
relation to clinical staging and survival in prostatic cancer patients. Prostate.
1988;12(4):325-32
Longevidade em Homens: A Melhora da Sobrevida Com A Reposição de
Testosterona
1- Morales A, Connolly JG, Bruce AW. Androgen therapy in advanced
carcinoma of the prostate. Can Med Assoc J. 1971;105(1):71-2
2- Prout GR Jr, Brewer WR. Response of men with advanced prostatic
carcinoma to exogenous administration of testosterone. Cancer. 1967
Nov;20(11):1871-8
Longevidade em Homens: A Associação Com Baixos Níveis de GH
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Stochholm K, Christiansen J, Laursen T, Gravholt CH. Mortality and reduced
growth hormone secretion. Horm Res. 2007;68 Suppl 5:173-6
Rosen T, Bengtsson BA. Premature mortality due to cardiovascular disease in
hypopituitarism. Lancet. 1990 Aug 4;336(8710):285-8
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4-
Besson A, Salemi S, Gallati S, Jenal A, Horn R, Mullis PS, Mullis PE..
Reduced longevity in untreated patients with isolated growth hormone
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Bates AS, Van't Hoff W, Jones PJ , Clayton RN. The effect of hypopituitarism
on life expectancy. J Clin Endocrinol Metab. 1996;81(3):1169-72
Longevidade: A Melhora Com a Reposição de GH
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2-
3-
4-
Li N, Zhou L, Zhang B, Dong P, Lin W, Wang H, Xu R, Ding H. Recombinant
human growth hormone increases albumin and prolongs survival in patients
with chronic liver failure: a pilot open, randomized, and controlled clinical
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Sonntag WE, Carter CS, Ikeno Y, Ekenstedt K, Carlson CS, Loeser RF,
Chakrabarty S, Lee S, Bennett C, Ingram R, Moore T, Ramsey M. Adultonset growth hormone and insulin-like growth factor I deficiency reduces
neoplastic disease, modifies age-related pathology, and increases life span.
Endocrinology. 2005;146(7):2920-32
Khansari DN, Gustad T. Effects of long-term, low-dose growth hormone therapy
on immune function and life expectancy of mice. Mech Ageing Dev. 1991
Jan;57(1):87-100
Bengtsson BA, Koppeschaar HP, Abs R, Bennmarker H, Hernberg-Stahl E,
Westberg B, Wilton P, Monson JP, Feldt-Rasmussen U, Wuster C. Growth
hormone replacement therapy is not associated with any increase in
mortality. KIMS Study Group. J Clin Endocrinol Metab. 1999;84(11):4291-2
Longevidade: A Associação Com Baixos Níveis de IGF-1
1- Guimarães SM, Lima EQ, Cipullo JP, Lobo SM, Burdmann EA. Low insulinlike growth factor-1 and hypocholesterolemia as mortality predictors in acute
kidney injury in the intensive care unit. Crit Care Med. 2008 Dec;36(12):316570
2- Arai Y, Takayama M, Gondo Y, Inagaki H, Yamamura K, Nakazawa S,
Kojima T, Ebihara Y, Shimizu K, Masui Y, Kitagawa K, Takebayashi T, Hirose
N. Adipose endocrine function, insulin-like growth factor-1 axis, and
exceptional survival beyond 100 years of age. J Gerontol A Biol Sci Med Sci.
2008 Nov;63(11):1209-18
3- Brugts MP, van den Beld AW, Hofland LJ, van der Wansem K, van Koetsveld
PM, Frystyk J, Lamberts SW, Janssen JA. Low circulating insulin-like growth
factor I bioactivity in elderly men is associated with increased mortality. J Clin
Endocrinol Metab. 2008 Jul;93(7):2515-22
4- Petretta M, Colao A, Sardu C, Scopacasa F, Marzullo P, Pivonello R,
Fontanella L, de Caterina M, de Simone A, Bonaduce D. NT-proBNP, IGF-I
and survival in patients with chronic heart failure. Growth Horm IGF Res.
2007 Aug;17(4):288-96
5- Jankowska EA, Biel B, Majda J, Szklarska A, Lopuszanska M, Medras M,
Anker SD, Banasiak W, Poole-Wilson PA, Ponikowski P. Anabolic deficiency
in men with chronic heart failure: prevalence and detrimental impact on
survival. Circulation. 2006 Oct 24;114(17):1829-37
6- Rasmuson T, Grankvist K, Jacobsen J, Olsson T, Ljungberg B. Serum
insulin-like growth factor-1 is an independent predictor of prognosis in
patients with renal cell carcinoma. Acta Oncol. 2004;43(8):744-8
7- Denti L, Annoni V, Cattadori E, Salvagnini MA, Visioli S, Merli MF, Corradi F,
Ceresini G, Valenti G, Hoffman AR, Ceda GP. Insulin-like growth factor 1 as a
predictor of ischemic stroke outcome in the elderly. Am J Med. 2004 Sep
1;117(5):312-7
8- Onenli-Mungan N, Yildizdas D, Yapicioglu H, Topaloglu AK, Yüksel B, Ozer
G. Growth hormone and insulin-like growth factor 1 levels and their relation to
survival in children with bacterial sepsis and septic shock. J Paediatr Child
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9- Laughlin GA, Barrett-Connor E, Criqui MH, Kritz-Silverstein D. The
prospective association of serum insulin-like growth factor I (IGF-I) and IGFbinding protein-1 levels with all cause and cardiovascular disease mortality in
older adults: the Rancho Bernardo Study. J Clin Endocrinol Metab. 2004
Jan;89(1):114-20
10- Vasan RS, Sullivan LM, D'Agostino RB, Roubenoff R, Harris T, Sawyer DB,
Levy D, Wilson PW. Serum insulin-like growth factor I and risk for heart failure
in elderly individuals without a previous myocardial infarction: the
Framingham Heart Study. Ann Intern Med. 2003 Oct 21;139(8):642-8
11- Roubenoff R, Parise H, Payette HA, Abad LW, D'Agostino R, Jacques PF,
Wilson PW, Dinarello CA, Harris TB. Cytokines, insulin-like growth factor 1,
sarcopenia, and mortality in very old community-dwelling men and women:
the Framingham Heart Study. Am J Med. 2003 Oct 15;115(6):429-35
12- Roubenoff R, Parise H, Payette HA, Abad LW, D'Agostino R, Jacques PF,
Wilson PW, Dinarello CA, Harris TB. Cytokines, insulin-like growth factor 1,
sarcopenia, and mortality in very old community-dwelling men and women:
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13- Ruiz-Torres A, Soares de Melo Kirzner M. Ageing and longevity are related to
growth hormone/insulin-like growth factor-1 secretion. Gerontology. 2002
Nov-Dec;48(6):401-7
14- Fernández-Reyes MJ, Alvarez-Ude F, Sánchez R, Mon C, Iglesias P, Díez
JJ, Vázquez A. Inflammation and malnutrition as predictors of mortality in
patients on hemodialysis. J Nephrol. 2002 Mar-Apr;15(2):136-43
15- Caregaro L, Alberino F, Amodio P, Merkel C, Angeli P, Plebani M, Bolognesi
M, Gatta A. Nutritional and prognostic significance of insulin-like growth factor
1 in patients with liver cirrhosis. Nutrition. 1997 Mar;13(3):185-90.
Longevidade: A Melhora Com a Reposição de IGF-1
1- Serose A, Salmon A, Fiszman MY, Fromes Y. Short-term treatment using
insulin-like growth factor-1 (IGF-1) improves life expectancy of the deltasarcoglycan deficient hamster. J Gene Med. 2006 Aug;8(8):1048-55
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Cappola AR, O'Meara ES, Guo W, Bartz TM, Fried LP, Newman AB.
Trajectories of dehydroepiandrosterone sulfate predict mortality in older adults:
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Enomoto M, Adachi H, Fukami A, Furuki K, Satoh A, Otsuka M, Kumagae S,
Nanjo Y, Shigetoh Y, Imaizumi T. Serum dehydroepiandrosterone sulfate levels
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Glei DA, Goldman N. Dehydroepiandrosterone sulfate (DHEAS) and risk for
mortality among older Taiwanese. Ann Epidemiol. 2006 Jul;16(7):510-5
Jankowska EA, Biel B, Majda J, Szklarska A, Lopuszanska M, Medras M, Anker
SD, Banasiak W, Poole-Wilson PA, Ponikowski P. Anabolic deficiency in men
with chronic heart failure: prevalence and detrimental impact on survival.
Circulation. 2006 Oct 24;114(17):1829-37
Mazat L, Lafont S, Berr C, Debuire B, Tessier JF, Dartigues JF, Baulieu EE.
Prospective measurements of dehydroepiandrosterone sulfate in a cohort of
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Feldman HA, Johannes CB, Araujo AB, Mohr BA, Longcope C, McKinlay JB.
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prospective results from the Massachusetts Male Aging Study. Am J Epidemiol.
2001 Jan 1;153(1):79-89
Longevidade: A Associação Com os Níveis de Progesterona
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Mohr PE, Wang DY, Gregory WM, Richards MA, Fentiman IS. Serum
progesterone and prognosis in operable breast cancer. Br J Cancer.
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Longevidade: A Melhora Com a Reposição de Estradiol
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4-
Petitti DB, Perlman JA, Sidney S. Noncontraceptive estrogens and
mortality: long-term follow-up of women in the Walnut Creek Study.
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therapy before breast cancer diagnosis significantly reduces the
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Wright DW, Kellermann AL, Hertzberg VS, Clark PL, Frankel M,
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da Melatonina em Idosos
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melatonin circadian rhythm a physiological feature associated with healthy
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12PROFILAXIA E TRATAMENTO DA
DEPRESSÃO
ATRAVÉS
DA
MODULAÇÃO HORMONAL:
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