Tópico: Omeprazol pode causar demência

[Leotelles]

O alarme foi lançado numa das cinco publicações médicas mais prestigiosas do mundo, “JAMA”, que não é a “bíblia” da medicina, mas é parte de seus livros sagrados. Pois isto nada duvida da autenticidade da publicação. A toma continuada, durante mais de dois anos, de omeprazol, o segundo medicamento mais consumido do mundo depois do paracetamol e uso mais comum para problemas gástricos, favorece a aparição de demência, danos neurológicos e também pode causar anemia. A notícia não surpreendeu os médicos que “desde há cinco anos, talvez mais” que vinham ouvindo falar da existência de todos estes efeitos secundários. mas torna-se dificil a sensibilização tanto dos profissionais de saúde como dos seus pacientes, a fazer ” um uso mais racional deste fármaco”, diz o presidente da Seção de Medicina de Família e Comunidade da Academia de Ciências Médicas de Bilbao, José Antonio Estévez.

O aparecimento de omeprazol, diz o especialista, foi uma autêntica revolução no tratamento de úlceras gástricas e na hérnia de hiato, que são as principais indicações. Para os primeiros, porque as lesões no estômago provocavam dor e mau estar condicionando a qualidade de vida. O maior avanço supõem-se, sem dúvida, no tratamento da hérnia hiatal, cuja principal terapia era a cirurgia que dava muitoa maus resultados.. “Eu tenho visto muitas pessoas, incluindo os jovens, morrerem na sala de cirurgia, porque é um procedimento muito invasivo”, lembra Estevez.

Os resultados obtidos com o fármaco devem ter sido “tão bons em todos esses anos” que os médicos “começaram a receitá-lo de forma abusiva  como prevenção”, não só para estas doenças como também para outras, como a acidez estomacal. e os pacientes a consumir de igual modo. A organização Kaiser Permanente provedora de serviços nos Estados Unidos e referência mundial no manejo sanitário decidiu avaliar os riscos para a saúde do consumo a longo prazo deste fármaco; e os resultados do estudo foi publicado na revista da Associação Médica Americana, “JAMA”.
Os investigadores queriam comprovar se a ingestão prolongada de omeprazol provocava falta de vitamina B12 (chamada de cobalamina), que é essencial para o crescimento da pessoa e essencial para o desenvolvimento normal do sistema nervoso.

É sabido que muitas pessoas de idade têm deficiência de vitamina B12, que se manifesta pelo aparecimento de fadiga, cansaço, diarreia ou feridas na boca, “sintomas tão comuns que podem induzir em erro o médico.”

link: http://profdrjfonseca.pt/2014/09/23/a-utilizacao-de-omeprazol-durante-de-dois-anos-provoca-demencia/


Eu utilizo omeprazol há alguns meses devido a gastrite, queria saber se alguém mais ouviu sobre esta pesquisa.

[Buckaroo Banzai]

Eu pesquisei agora e vi outras notícias sobre isso.

Uma das notícias falava que é facilmente resolvido com suplementos, sem atribuir a afirmação a nenhum pesquisador. Outra, mais extensa, colocava que nem se sabe sobre a relação causal na associação.

O estudo em si:

http://jama.jamanetwork.com/article.aspx?articleid=1788456

[Gigaview]

Entendi que o omeprazol interfere na absorção da V B12, isto é, um efeito colateral contornável, não que o sal faça um dano neurológico direto. É isso?

[Gigaview]

Alcohol (ethanol): Excessive alcohol intake lasting longer than two weeks can decrease vitamin B12 absorption from the gastrointestinal tract.[citation needed]

Aminosalicylic acid (para-aminosalicylic acid, PAS, Paser): Aminosalicylic acid can reduce oral vitamin B12 absorption, possibly by as much as 55%, as part of a general malabsorption syndrome.

Megaloblastic changes, and occasional cases of symptomatic anemia have occurred, usually after doses of 8 to 12 g/day for several months. Vitamin B12 levels should be monitored in people taking aminosalicylic acid for more than one month.

Antibiotics: An increased bacterial load can bind significant amounts of vitamin B12 in the gut, preventing its absorption. In people with bacterial overgrowth of the small bowel, antibiotics such as metronidazole (Flagyl) can actually improve vitamin B12 status. The effects of most antibiotics on gastrointestinal bacteria are unlikely to have clinically significant effects on vitamin B12 levels.

Hormonal contraception: The data regarding the effects of oral contraceptives on vitamin B12 serum levels are conflicting. Some studies have found reduced serum levels in oral contraceptive users, but others have found no effect despite use of oral contraceptives for up to 6 months. When oral contraceptive use is stopped, normalization of vitamin B12 levels usually occurs. Lower vitamin B12 serum levels seen with oral contraceptives probably are not clinically significant.

Chloramphenicol (Chloromycetin): Limited case reports suggest that chloramphenicol can delay or interrupt the reticulocyte response to supplemental vitamin B12 in some patients. Blood counts should be monitored closely if this combination cannot be avoided.

Cobalt irradiation: Cobalt irradiation of the small bowel can decrease gastrointestinal (GI) absorption of vitamin B12.

Colchicine: Colchicine in doses of 1.9 to 3.9 mg/day can disrupt normal intestinal mucosal function, leading to malabsorption of several nutrients, including vitamin B12. Lower doses do not seem to have a significant effect on vitamin B12 absorption after 3 years of colchicine therapy. The significance of this interaction is unclear. Vitamin B12 levels should be monitored in people taking large doses of colchicine for prolonged periods.

Colestipol (Colestid), cholestyramine (Questran): These resins used for sequestering bile acids to decrease cholesterol, can decrease gastrointestinal (GI) absorption of vitamin B12. It is unlikely this interaction will deplete body stores of vitamin B12 unless there are other factors contributing to deficiency. In a group of children treated with cholestyramine for up to 2.5 years, there was not any change in serum vitamin B12 levels. Routine supplements are not necessary.

H2-receptor antagonists: include cimetidine (Tagamet), famotidine (Pepcid), nizatidine (Axid), and ranitidine (Zantac). Reduced secretion of gastric acid and pepsin produced by H2 blockers can reduce absorption of protein-bound (dietary) vitamin B12, but not of supplemental vitamin B12. Gastric acid is needed to release vitamin B12 from protein for absorption. Clinically significant vitamin B12 deficiency and megaloblastic anemia are unlikely, unless H2 blocker therapy is prolonged (2 years or more), or the person's diet is poor. It is also more likely if the person is rendered achlorhydric(with complete absence of gastric acid secretion), which occurs more frequently with proton pump inhibitors than H2 blockers. Vitamin B12 levels should be monitored in people taking high doses of H2 blockers for prolonged periods.

Metformin (Glucophage): Metformin may reduce serum folic acid and vitamin B12 levels. Long-term use of metformin substantially increases the risk of B12 deficiency and (in those patients who become deficient) hyperhomocysteinemia, which is "an independent risk factor for cardiovascular disease, especially among individuals with type 2 diabetes."[33] There are also rare reports of megaloblastic anemia in people who have taken metformin for five years or more. Reduced serum levels of vitamin B12 occur in up to 30% of people taking metformin chronically.[34][35] However, clinically significant deficiency is not likely to develop if dietary intake of vitamin B12 is adequate. Deficiency can be corrected with vitamin B12 supplements even if metformin is continued. The metformin-induced malabsorption of vitamin B12 is reversible by oral calcium supplementation.[36] The general clinical significance of metformin upon B12 levels is as yet unknown.[37]

Neomycin: Absorption of vitamin B12 can be reduced by neomycin, but prolonged use of large doses is needed to induce pernicious anemia. Supplements are not usually needed with normal doses.
Nicotine: Nicotine can reduce serum vitamin B12 levels. The need for vitamin B12 supplementation in smokers has not been adequately studied.

Nitrous oxide: Nitrous oxide inactivates the cobalamin form of vitamin B12 by oxidation. Symptoms of vitamin B12 deficiency, including sensory neuropathy, myelopathy, and encephalopathy, can occur within days or weeks of exposure to nitrous oxide anesthesia in people with subclinical vitamin B12 deficiency. Symptoms are treated with high doses of vitamin B12, but recovery can be slow and incomplete. People with normal vitamin B12 levels have sufficient vitamin B12 stores to make the effects of nitrous oxide insignificant, unless exposure is repeated and prolonged (such as recreational use). Vitamin B12 levels should be checked in people with risk factors for vitamin B12 deficiency prior to using nitrous oxide anesthesia. Chronic nitrous oxide B12 poisoning (usually from use of nitrous oxide as a recreational drug), however, may result in B12 functional deficiency even with normal measured blood levels of B12.[38]

Phenytoin (Dilantin), phenobarbital, primidone (Mysoline): These anticonvulsants have been associated with reduced vitamin B12 absorption, and reduced serum and cerebrospinal fluidlevels in some patients. This may contribute to the megaloblastic anemia, primarily caused by folate deficiency, associated with these drugs. It is also suggested that reduced vitamin B12 levels may contribute to the neuropsychiatric side effects of these drugs. Patients should be encouraged to maintain adequate dietary vitamin B12 intake. Folate and vitamin B12 status should be checked if symptoms of anemia develop.

Proton pump Alcohol (ethanol): Excessive alcohol intake lasting longer than two weeks can decrease vitamin B12 absorption from the gastrointestinal tract.[citation needed]

Aminosalicylic acid (para-aminosalicylic acid, PAS, Paser): Aminosalicylic acid can reduce oral vitamin B12 absorption, possibly by as much as 55%, as part of a general malabsorption syndrome. Megaloblastic changes, and occasional cases of symptomatic anemia have occurred, usually after doses of 8 to 12 g/day for several months. Vitamin B12 levels should be monitored in people taking aminosalicylic acid for more than one month.

Antibiotics: An increased bacterial load can bind significant amounts of vitamin B12 in the gut, preventing its absorption. In people with bacterial overgrowth of the small bowel, antibiotics such as metronidazole (Flagyl) can actually improve vitamin B12 status. The effects of most antibiotics on gastrointestinal bacteria are unlikely to have clinically significant effects on vitamin B12 levels.

Hormonal contraception: The data regarding the effects of oral contraceptives on vitamin B12 serum levels are conflicting. Some studies have found reduced serum levels in oral contraceptive users, but others have found no effect despite use of oral contraceptives for up to 6 months. When oral contraceptive use is stopped, normalization of vitamin B12 levels usually occurs. Lower vitamin B12 serum levels seen with oral contraceptives probably are not clinically significant.

Chloramphenicol (Chloromycetin): Limited case reports suggest that chloramphenicol can delay or interrupt the reticulocyte response to supplemental vitamin B12 in some patients. Blood counts should be monitored closely if this combination cannot be avoided.
Cobalt irradiation: Cobalt irradiation of the small bowel can decrease gastrointestinal (GI) absorption of vitamin B12.

Colchicine: Colchicine in doses of 1.9 to 3.9 mg/day can disrupt normal intestinal mucosal function, leading to malabsorption of several nutrients, including vitamin B12. Lower doses do not seem to have a significant effect on vitamin B12 absorption after 3 years of colchicine therapy. The significance of this interaction is unclear. Vitamin B12 levels should be monitored in people taking large doses of colchicine for prolonged periods.

Colestipol (Colestid), cholestyramine (Questran): These resins used for sequestering bile acids to decrease cholesterol, can decrease gastrointestinal (GI) absorption of vitamin B12. It is unlikely this interaction will deplete body stores of vitamin B12 unless there are other factors contributing to deficiency. In a group of children treated with cholestyramine for up to 2.5 years, there was not any change in serum vitamin B12 levels. Routine supplements are not necessary.

H2-receptor antagonists: include cimetidine (Tagamet), famotidine (Pepcid), nizatidine (Axid), and ranitidine (Zantac). Reduced secretion of gastric acid and pepsin produced by H2 blockers can reduce absorption of protein-bound (dietary) vitamin B12, but not of supplemental vitamin B12. Gastric acid is needed to release vitamin B12 from protein for absorption. Clinically significant vitamin B12 deficiency and megaloblastic anemia are unlikely, unless H2 blocker therapy is prolonged (2 years or more), or the person's diet is poor. It is also more likely if the person is rendered achlorhydric(with complete absence of gastric acid secretion), which occurs more frequently with proton pump inhibitors than H2 blockers. Vitamin B12 levels should be monitored in people taking high doses of H2 blockers for prolonged periods.

Metformin (Glucophage): Metformin may reduce serum folic acid and vitamin B12 levels. Long-term use of metformin substantially increases the risk of B12 deficiency and (in those patients who become deficient) hyperhomocysteinemia, which is "an independent risk factor for cardiovascular disease, especially among individuals with type 2 diabetes."[33] There are also rare reports of megaloblastic anemia in people who have taken metformin for five years or more. Reduced serum levels of vitamin B12 occur in up to 30% of people taking metformin chronically.[34][35] However, clinically significant deficiency is not likely to develop if dietary intake of vitamin B12 is adequate. Deficiency can be corrected with vitamin B12 supplements even if metformin is continued. The metformin-induced malabsorption of vitamin B12 is reversible by oral calcium supplementation.[36] The general clinical significance of metformin upon B12 levels is as yet unknown.[37]

Neomycin: Absorption of vitamin B12 can be reduced by neomycin, but prolonged use of large doses is needed to induce pernicious anemia. Supplements are not usually needed with normal doses.

Nicotine: Nicotine can reduce serum vitamin B12 levels. The need for vitamin B12 supplementation in smokers has not been adequately studied.

Nitrous oxide: Nitrous oxide inactivates the cobalamin form of vitamin B12 by oxidation. Symptoms of vitamin B12 deficiency, including sensory neuropathy, myelopathy, and encephalopathy, can occur within days or weeks of exposure to nitrous oxide anesthesia in people with subclinical vitamin B12 deficiency. Symptoms are treated with high doses of vitamin B12, but recovery can be slow and incomplete. People with normal vitamin B12 levels have sufficient vitamin B12 stores to make the effects of nitrous oxide insignificant, unless exposure is repeated and prolonged (such as recreational use). Vitamin B12 levels should be checked in people with risk factors for vitamin B12 deficiency prior to using nitrous oxide anesthesia. Chronic nitrous oxide B12 poisoning (usually from use of nitrous oxide as a recreational drug), however, may result in B12 functional deficiency even with normal measured blood levels of B12.[38]

Phenytoin (Dilantin), phenobarbital, primidone (Mysoline): These anticonvulsants have been associated with reduced vitamin B12 absorption, and reduced serum and cerebrospinal fluidlevels in some patients. This may contribute to the megaloblastic anemia, primarily caused by folate deficiency, associated with these drugs. It is also suggested that reduced vitamin B12 levels may contribute to the neuropsychiatric side effects of these drugs. Patients should be encouraged to maintain adequate dietary vitamin B12 intake. Folate and vitamin B12 status should be checked if symptoms of anemia develop.

Proton pump inhibitors (PPIs): The PPIs include omeprazole (Prilosec, Losec), lansoprazole (Prevacid), rabeprazole (Aciphex), pantoprazole (Protonix, Pantoloc), and esomeprazole (Nexium). The reduced secretion of gastric acid and pepsin produced by PPIs can reduce absorption of protein-bound (dietary) vitamin B12, but not supplemental vitamin B12. Gastric acid is needed to release vitamin B12 from protein for absorption. Reduced vitamin B12 levels may be more common with PPIs than with H2-blockers, because they are more likely to produce achlorhydria (complete absence of gastric acid secretion). However, clinically significant vitamin B12 deficiency is unlikely, unless PPI therapy is prolonged (2 years or more) or dietary vitamin intake is low. Vitamin B12 levels should be monitored in people taking high doses of PPIs for prolonged periods.

Zidovudine (AZT, Combivir, Retrovir): Reduced serum vitamin B12 levels may occur when zidovudine therapy is started. This adds to other factors that cause low vitamin B12 levels in people with HIV, and might contribute to the hematological toxicity associated with zidovudine. However, the data suggest vitamin B12 supplements are not helpful for people taking zidovudine.[citation needed]

Folic acid: Folic acid, particularly in large doses, can mask vitamin B12 deficiency by completely correcting hematological abnormalities. In vitamin B12 deficiency, folic acid can produce complete resolution of the characteristic megaloblastic anemia, while allowing potentially irreversible neurological damage (from continued inactivity of methylmalonyl mutase) to progress. Thus, vitamin B12 status should be determined before folic acid is given as monotherapy.[39]

Potassium: Potassium supplements can reduce absorption of vitamin B12 in some people. This effect has been reported with potassium chloride and, to a lesser extent, with potassium citrate. Potassium might contribute to vitamin B12 deficiency in some people with other risk factors, but routine supplements are not necessary.[40] (PPIs): The PPIs include omeprazole (Prilosec, Losec), lansoprazole (Prevacid), rabeprazole (Aciphex), pantoprazole (Protonix, Pantoloc), and esomeprazole (Nexium). The reduced secretion of gastric acid and pepsin produced by PPIs can reduce absorption of protein-bound (dietary) vitamin B12, but not supplemental vitamin B12. Gastric acid is needed to release vitamin B12 from protein for absorption. Reduced vitamin B12 levels may be more common with PPIs than with H2-blockers, because they are more likely to produce achlorhydria (complete absence of gastric acid secretion). However, clinically significant vitamin B12 deficiency is unlikely, unless PPI therapy is prolonged (2 years or more) or dietary vitamin intake is low. Vitamin B12 levels should be monitored in people taking high doses of PPIs for prolonged periods.

Zidovudine (AZT, Combivir, Retrovir): Reduced serum vitamin B12 levels may occur when zidovudine therapy is started. This adds to other factors that cause low vitamin B12 levels in people with HIV, and might contribute to the hematological toxicity associated with zidovudine. However, the data suggest vitamin B12 supplements are not helpful for people taking zidovudine.[citation needed]
Folic acid: Folic acid, particularly in large doses, can mask vitamin B12 deficiency by completely correcting hematological abnormalities. In vitamin B12 deficiency, folic acid can produce complete resolution of the characteristic megaloblastic anemia, while allowing potentially irreversible neurological damage (from continued inactivity of methylmalonyl mutase) to progress. Thus, vitamin B12 status should be determined before folic acid is given as monotherapy.[39]

Potassium: Potassium supplements can reduce absorption of vitamin B12 in some people. This effect has been reported with potassium chloride and, to a lesser extent, with potassium citrate. Potassium might contribute to vitamin B12 deficiency in some people with other risk factors, but routine supplements are not necessary.[40]

http://en.m.wikipedia.org/wiki/Vitamin_B12

[Sergiomgbr]

Notícia nada boa para gordos nerds com hiato desregulado(ficar sentado muito tempo no computador).

[Gigaview]

...

Ou seja, um estudo relaciona o uso de omeprazol à falta de vitamina B12, outros relacionam a falta de B12 com demência, porém, em medicina as coisas não são simples e diretas assim. Não temos dados para afirmar que uma coisa leva à outra, e no mundo todo, muitas, mas muitas pessoas usam omeprazol por longos períodos e não tem sido constatado aumento da demência neste grupo e nem no geral.

...

http://www.fabioatui.com.br/o-uso-omeprazol-causa-demencia/

Conclusão: sensacionalismo.

[Sergiomgbr]

Eu é que não vou ficar tomando pra saber.

[Osler]

A acidez gástrica é importante não só para correta ação inicial da digestão, mas também serve de prevenção de infecções, pouco microorganismos resistem ao pH gastrico habitual.
Pacientes com hipo ou acloridria secundária ou não ao uso de Omeprazol podem apresentar distúrbio de absorção principalmente de B12 e propenção a determinadas infecções (Tuerculose é um exemplo)
A deficiência de B12 leve a diversos quadro clínicos, inclusive a Síndrome Demencial, porém atualmente ela é facilmente dosada em um exame rotineiro de sangue e pode ser reposta tanto por via oral quanto parenteral.  Eu peço dosagem de B12 para todos os meus pacientes do consultorio como "rotina" laboratorial (lembrando que eu só faço clínica pirvada.
Todo paciente com quadro de Sd demêncial é submetido a uma serie de exames para se determinar a causa, assim há algum tempo dosar vitamina B12 é mandatório nesses casos, até porque é uma causa poterncialmente reversível