Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alcohol has an porphyrinogenic action and can cause a disturbance of porphyrin metabolism in healthy people as well as lead to a biochemical and clinical manifestation of acute and chronic hepatic porphyrias, especially acute intermittent porphyria and porphyria cutanea tarda. After excessive consumption of alcohol a temporary, clinically asymptomatic secondary hepatic coproporphyrinuria in man can be observed, which can become persistent in cases of alcohol-induced liver damage. Nowadays alcohol-liver-porphyrinuria syndrome is the first to be mentioned in secondary hepatic disturbances of porphyrin metabolism. In people with a genetic lack of uroporphyrinogen-decarboxylase alcohol is able to transform an asymptomatic coproporphyrinuria into a chronic hepatic porphyria or porphyria cutanea tarda. From experimental and clinical studies the conclusion can be drawn that alcohol inhibits the enzymes delta-aminolevulinic-acid-dehydratase (synonym: porphobilinogen-synthase), uroporphyrinogen-decarboxylase and coproporphyrinogen-oxidase and induces delta-aminolevulinic-acid-synthase in the liver. Abstinence of alcohol is a therapeutically and prophylactically important measurement in all types of hepatic porphyrias. For clinical experience follows that in cases with chronic consumption of alcohol, fatty liver, alcohol induced hepatitis and liver cirrhosis porphyrin studies in urine should be made to notice a hepatic porphyria in the latent phase very early. When dealing with abdominal and cutaneous symptoms in clinical context with consumption of alcohol one has to exclude hepatic porphyria differential diagnostically.
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PMID:[Hepatic porphyrias and alcohol]. 1042 Jul 23

Hepatic disorders severely affected by pregnancy include choledochal cysts that can be compressed by the gravid uterus and potentially rupture; hepatic adenomas that exhibit accelerated growth because of hyperestrogenemia during pregnancy; acute intermittent porphyria that is exacerbated by increased female sex hormones during pregnancy; splenic artery aneurysms that can rupture during pregnancy because of compression by the gravid uterus; Budd-Chiari syndrome that is promoted by hyperestrogenemia; and hepatitis E and herpes simplex hepatitis that are particularly severe during pregnancy. Hepatic disorders unique to pregnancy include intrahepatic cholestasis of pregnancy; acute fatty liver of pregnancy; preeclampsia and eclampsia; and hemolysis, elevated liver function tests, and low platelet count (HELLP) syndrome. Most disorders uniquely related to pregnancy are treated by prompt fetal delivery as soon as the fetus is sufficiently mature.
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PMID:Hepatic disorders severely affected by pregnancy: medical and obstetric management. 1857 Sep 41

Most seizures during pregnancy occur in women who already have epilepsy. During pregnancy most women will continue their previous level of seizure control, although 15-30% may experience an increase in seizures. Pregnancy-induced changes in antiepileptic drug pharmacokinetics are a major factor affecting changes in seizure control during pregnancy, although compliance is also a significant factor. Status epilepticus occurs in only 1-2% of pregnancies, and if treated appropriately and aggressively carries a fairly low risk of morbidity and mortality. Structural and metabolic changes may precipitate new-onset seizures during pregnancy. The structural causes include intracranial hemorrhage of multiple types, cerebral venous sinus thrombosis, and ischemic stroke. Metabolic causes include hyperemesis gravidarum; acute hepatitis (due to fatty liver of pregnancy or viral hepatitis); metabolic diseases, such as acute intermittent porphyria; infections, such as malaria; and eclampsia.
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PMID:Seizures in pregnancy: diagnosis and management. 1892 87