Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In March 1989, ultrasonography revealed a hepatic mass in a 40 year old nulliparous woman who was then referred to the University of Southern California--Los Angeles (UCLA) Liver Unit. She exhibited no symptoms of a liver condition. From 19-28 years old, she took the combined oral contraceptive (OC) Ovulen 21 for irregular menses. After a brief period of taking Ortho Novum 1/80, she took Demulen 1/35-24 between ages 28-34. Her physician diagnoses endometriosis at 34. He stopped OC therapy and prescribed the progestin Norlutate. She had no history of hepatitis, toxin exposure, and previous liver disease. Further no one in her family had had liver disease or neoplasms. Computer tomography identified a 6.5 cm x 3.5 cm mass in the right lobe of the liver which matched a cold defect on a liver scan using technetium Tc 99m sulfur colloid. The mass selectively took up gallium. Arteriography revealed the mass to be a vascular tumor, but it did not exhibit a typical vascular pattern of an adenoma or the neovascularity of hepatocellular carcinoma. Physicians at UCLA used peritoneoscopy to take percutaneous needle biopsies of the right lobe which confirmed a hepatic adenoma. they then removed the right lobe of the liver. The remaining part of the liver was normal. Histologic examinations of the removed section showed features of a well differentiated hepatocellular carcinoma. Further tumor cells had invaded normal hepatic parenchyma. The physicians believed that hepatic adenoma was in the process of transforming into hepatocellular carcinoma in this patient. They thought that long term OC use, and possibly long term progestin use, may have contributed to the formation of the liver neoplasms. They emphasized the need for a pilot study to develop guidelines on surveillance ultrasonography of women taking OCs over a long period.
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PMID:Hepatocellular carcinoma coexisting with hepatic adenoma. Incidental discovery after long-term oral contraceptive use. 166 98

A case is reported of a 39-year-old woman who had postoperative pulmonary embolism after taking combined oral contraceptives from 1967 to 1970. Her related history included birth of 2 large infants, phlebitis, and varicosities. Her operation for retroverted uterus and tubal sterilization was followed the next day by a severe pulmonary embolism treated with heparin. This treatment resulted in a pelvic hematoma, abundant metrorrhagia, and anemia requiring 4 transfusions. 4 months later she developed jaundice due to hepatitis virus B, which potentiated the effect of the antiprothrombin treatment and precipitated 2 new pelvic masses, fever, and metrorrhagia. She was given hysterectomy, which revealed bilateral hematosalpinx, probably related to endometriosis. 1 year later she was in good health, but her serum lipids were found high in the alpha- and pre-beta-lipoprotein bands. A delay of 2 months between stopping oral contraceptives and surgery is recommended.
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PMID:[Postoperative thromboembolic accident observed during estro-progestative treatment. Apropos of a case]. 516 37

Endometriosis is a disease observed in women in fertile age, it causes pelvic pain characterized by dysmenorrea and dyspareunia. Moreover, there is an association with infertility. Between the alternative of the medical therapeutics of endometriosis drugs with hipogonadotrofic and hypoestrogenic effects, as the danazol and gestrinona has been used. At present, there are analogies of GnRH factor where leuprolide acetate allow a continue liberation in a monthly administration. This is a case of a woman with extensive endometriosis that has hepatitis due to danazol and subsequently was treated with leuprolide acetate. The effectiveness of leuprolide acetate is analyzed in relation with the relief of pain and the laparoscopic evaluation of the endometriosis focus.
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PMID:[Advanced endometriosis treatment with leuprolide acetate]. 799 63

Serum autoantibodies to the glycolytic enzyme enolase have been reported in a diverse range of inflammatory, degenerative, and psychiatric disorders. Diseases in which these antibodies have been reported in high incidence include autoimmune polyglandular syndrome type 1 (80%, 35 of 44), primary (69%, 60 of 87), and secondary (58%, 14 of 24) membranous nephropathy, cancer-associated retinopathy (68.8%, 11 of 16), autoimmune hepatitis type 1 (60%, 12 of 20), mixed cryoglobulinemia with renal involvement (63.6%, seven of 11), cystoid macular edema (60%, six of 10), and endometriosis (50%, 21 of 41). In autoimmune polyglandular syndrome type 1 patients, all had chronic mucocutaneous candidiasis with demonstrated antibody reactivity to candida enolase, which is suggestive of cross reactivity or epitope mimicry. Formation of autoantibodies to enolase may be a normal process, with reported incidence in apparently healthy subjects ranging from 0% (zero of 91) to 11.7% (seven of 60). Nonetheless, we suggest that excessive production of these autoantibodies, which are generated as a consequence of uptake of enolase by antigen-presenting cells and subsequent B cell activation, can potentially initiate tissue injury as a result of immune complex deposition.
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PMID:Disease association, origin, and clinical relevance of autoantibodies to the glycolytic enzyme enolase. 1128 54

We describe a 47-year-old woman with severe aplastic anemia with genital bleeding who developed acute severe hepatitis after the administration of danazol while she was receiving cyclosporin. She had been diagnosed with severe aplastic anemia 1 year previously and, while hospitalized, had received methyl prednisolone pulse therapy, which was not successful. She was then referred to our hospital. She was treated with antithymocyte globulin, cyclosporin, granulocyte colony-stimulating factor, and methyl prednisolone; a good response was achieved after 3 months of this therapy. Subsequently, oral administration of cyclosporin was continued, but she was readmitted to our hospital when pancytopenia gradually developed and the genital bleeding recurred. Danazol was administered for pancytopenia and endometriosis. Four days after the first administration of danazol, epigastric pain occurred, and the danazol was stopped. Eighteen days after the first danazol administration, very severe hepatic injury occurred abruptly. The patient died of hepatic failure. Postmortem examination revealed centrilobular massive necrosis of the liver. Danazol was implicated as the agent responsible for causing the hepatic failure. Drug interactions between danazol and cyclosporin may cause adverse effects.
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PMID:Fatal acute hepatic failure induced by danazol in a patient with endometriosis and aplastic anemia. 1175 52