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)

Historically, the leading cause of death among persons with haemophilia and other congenital coagulation disorders was uncontrolled bleeding. Mortality was associated with severe deficiency of coagulation factors VIII or IX and especially with high-titre antifactor neutralizing antibodies (inhibitors). The catastrophic contamination of plasma donor pools with human immunodeficiency virus (HIV) resulted in acquired immunodeficiency syndrome replacing haemorrhage as the leading cause of death among persons with haemophilia. Rather little has been written, however, about mortality among those not infected with HIV. The objective of this study was to identify conditions associated with all-cause mortality among HIV-uninfected patients who were followed for a mean of 8.8 years in the Multicentre Hemophilia Cohort Study. Among the 364 children (mean age 8 years), there were four deaths; two related to cancer, one to trauma, and the fourth to haemorrhage, end-stage liver disease and sepsis. Among the 387 HIV-uninfected adults (mean age 35 years) there were 29 deaths, with haemorrhage the leading cause of death, followed by hepatic, stroke and cancer deaths. Prognostic factors for all-cause mortality among the adults included haemophilia Type A with neutralizing antibodies [age-adjusted relative rate (RR) 3.1, 95% confidence interval (CI) 1.4-6.9] and serologic evidence of both hepatitis B and C virus (RR 4.1, 95% CI 0.97-17.6). Although hepatitis C viral load was slightly lower in patients with hepatitis B virus surface antigenaemia, it was unrelated to vital status. We conclude that causes of death and prognostic factors for current HIV-uninfected haemophilia patients are similar to those noted before the HIV epidemic. Better understanding, prevention and control of neutralizing antibodies and hepatitis infections may substantially improve longevity for people with haemophilia.
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PMID:Factors predictive of death among HIV-uninfected persons with haemophilia and other congenital coagulation disorders. 1219 76

Outlined is a protocol for the administration of emergency contraceptive pills. The indication for such treatment is unprotected intercourse within the past 72 hours. Absolute contraindications include the possibility of an existing pregnancy and a family history of stroke, heart attack, thrombophlebitis, breast or endometrial cancer, or liver tumor. Possibly excluded, depending on evaluation by a physician, are women with abnormal vaginal bleeding, active hepatitis, active gallbladder disease, high blood pressure, acute focal migraine, breastfeeding women, and those unable to understand instructions. The recommended regimen consists of six tablets of Ovral (two taken immediately, two more in 12 hours) or 12 tablets of Lo/Ovral, Nordette, or Levlen (four taken immediately, repeat dosage in 12 hours). The extra pills are to be used in cases of vomiting within three hours of pill ingestion. Women with a history of oral contraceptive-related nausea and vomiting should be provided with Compazine. Women should be informed that this method is effective in only about 92% of cases. All women who receive emergency contraception should be counseled that this is strictly a back-up method and helped to formulate a long-term birth control strategy.
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PMID:Emergency contraceptive pills (ECP) protocol. 1228 80

Drug-induced hypersensitivity syndrome is an uncommon but potentially life-threatening idiosyncratic drug reaction. In the literature, about five cases have been reported concerning hypersensitivity syndrome with lamotrigine. Most cases concern aromatic anticonvulsants but we report a case induced by lamotrigine which is a non aromatic anticonvulsant. A 73-year-old man was treated with lamotrigine for epilepsy due to a cerebrovascular stroke for 5 weeks. After 2 weeks with a single oral dose of 50 mg lamotrigine, the patient received 100 mg. Quickly thereafter fever, erythema and edema involving the periorbital area appeared. He was then admitted to hospital and lamotrigine was immediately discontinued. He developed acute hepatic and renal failure. During his hospital stay, he was treated with systemic and topical corticosteroids. After slow improvement, he was discharged 4 weeks later. Concerning this typical case, we review the characteristics of hypersensitivity syndrome and the different etiopathogenesis. The hypersensitivity syndrome typically develops two to six weeks after a drug is first administered, later than most other serious skin reactions. This syndrome manifests as rash, fever, tender lymphadenopathy, hepatitis and eosinophilia. The mechanism of hypersensitivity syndrome is unknown. Several theories have been proposed. The reaction is secondary to circulating antibodies or concerns toxic metabolities. On the other hand, association of human herpes virus 6 infection may play a role in the development of hypersensitivity syndrome. Hypersensitivity reactions to the aromatic antiepileptic drugs appear to have an immune etiology much like lamotrigine: bioactivation, detoxification, covalent adduct formation, processing and presentation of antigen to the immune system, and consequent formation of antibody and T-cell immune effectors. Another theory involves toxic metabolites; the aromatic antiepileptic agents are metabolised by cytochrome P-450 to an arene oxide metabolite. This is normally detoxified by epoxide hydrolase. This enzyme may be lacking or mutated in persons that develop the syndrome, and this is genetically determined. Lamotrigine is mainly metabolised by hepatic glucuronidation, but hypersensitivity may involve similar processes such aromatic antiepileptic drugs, except that the toxic metabolite has not yet been found. Because of slow evolution and clinical similarity to many infectious illnesses, the diagnosis of hypersensitivity syndrome may be delayed. Prompt recognition and withdrawal of the suspected drug is essential. The goal of research is to describe a "susceptibility profile" identifying individuals at risk for these forms of drug toxicity.
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PMID:[Characteristics of hypersensitivity syndrome to lamotrigine: review of one case reported in the Regional Center of Pharmacovigilance of Nantes]. 1242 44

Physical exercise does not have harmful effects on liver, yet it can be an occasional cause of heat stroke in long-distance runners if they do not drink enough. Practicing sports does not have harmful liver effects as long as some risk behaviors are avoided such as consumption of anabolizers, sharing syringes or traveling to hepatitis endemic countries without being vaccinated. In patients with acute or chronic liver diseases, physical activity or practicing sports can be allowed as long as these do not lead to an excessive fatigue.
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PMID:[Liver and sports]. 1474 2

Although highly selective cyclooxygenase (COX)-2 inhibitors have been shown to be less toxic to the gastrointestinal tract than conventional non-steroidal anti-inflammatory drugs (NSAIDs), their overall safety profile is questioned. Since different selective COX-2 inhibitors were found to be associated with increased cardiovascular thrombotic events, the thrombotic hazard may be a class effect. Furthermore, warnings have been issued regarding serious skin and hypersensitivity reactions associated with valdecoxib. Lumiracoxib is a novel COX-2 selective inhibitor (coxib) with improved biochemical selectivity over that of currently available coxibs. It is structurally distinct from other drugs in the class and has weakly acidic properties. Clinical studies support a once-daily dosing regimen, despite its relatively short plasma elimination half-life (3 - 6 h). In randomised, controlled clinical trials, lumiracoxib 100 - 200 mg/day has been shown to be superior to placebo in patients with symptomatic osteoarthritis, with clinical efficacy similar to diclofenac 150 mg/day, celecoxib 200 mg/day or rofecoxib 25 mg/day. Furthermore, lumiracoxib 200 - 400 mg/day appeared to be effective in patients with rheumatoid arthritis. In patients with acute pain related to primary dysmenorrhoea, dental or orthopaedic surgery, lumiracoxib 400 mg/day was found to be at least as effective as standard doses of traditional NSAIDs and other coxibs. Endoscopic studies have indicated that lumiracoxib is associated with a rate of gastroduodenal ulcer formation that is significantly lower than with ibuprofen and does not differ from celecoxib. In the Therapeutic Arthritis Research and Gastrointestinal Trial, which enrolled 18,325 patients with osteoarthritis, the cumulative 1-year incidence of ulcer complications (primary end point) was significantly reduced by approximately threefold on lumiracoxib 400 mg/day compared with naproxen 1000 mg/day or ibuprofen 2400 mg/day (0.32 versus 0.91%). Reduction in ulcer complications was more pronounced in the population not taking low-dose aspirin (0.2 versus 0.92%, respectively). Conversely, the gastrointestinal advantage of lumiracoxib was abrogated in patients receiving low-dose aspirin (0.69 versus 0.88%, respectively, p = 0.49). Regarding cardiovascular events contributing to the trialists' composite end point (myocardial infarction, stroke or cardiovascular death), there was no significant difference between lumiracoxib (0.65%) versus combined comparator NSAIDs (0.55%). Similarly, no significant difference was recorded in rates of myocardial infarction (clinical and silent) between the lumiracoxib (0.25%) and the combined NSAID (0.19%) treatment groups. Liver function test abnormalities were more frequent with lumiracoxib (2.57%) than with the comparator NSAIDs (0.63%). Whether or not this would result in an increased risk of clinical hepatitis in the real world setting is unforeseeable.
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PMID:Clinical pharmacology of lumiracoxib, a second-generation cyclooxygenase 2 selective inhibitor. 1588 25

Inhibitors of HIV protease have been shown to have antiapoptotic effects in vitro, yet whether these effects are seen in vivo remains controversial. In this study, we have evaluated the impact of the HIV protease inhibitor (PI) nelfinavir, boosted with ritonavir, in models of nonviral disease associated with excessive apoptosis. In mice with Fas-induced fatal hepatitis, Staphylococcal enterotoxin B-induced shock, and middle cerebral artery occlusion-induced stroke, we demonstrate that PIs significantly reduce apoptosis and improve histology, function, and/or behavioral recovery in each of these models. Further, we demonstrate that both in vitro and in vivo, PIs block apoptosis through the preservation of mitochondrial integrity and that in vitro PIs act to prevent pore function of the adenine nucleotide translocator (ANT) subunit of the mitochondrial permeability transition pore complex.
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PMID:Inhibition of adenine nucleotide translocator pore function and protection against apoptosis in vivo by an HIV protease inhibitor. 1593 50

Hepatitis virus C (HCV) is worldwide a health problem, which may lead to serious complications. The aim of this study was to correlate the onset of the cerebral ischemic attack accompanied by mixed cryoglobulinemia, with the chronic hepatitis C virus infection. These studies were carried out in 12 patients with serologic/virusologic confirmed chronic HCV infection associated with ischemic stroke. Ischemic stroke occurred in equal proportion in women and men. The patients did not know of HCV infection diagnosis at that moment. All patients had type II mixed monoclonal cryoglobulinemia, hypergammaglobulinemia with polyclonal IgG and monoclonal IgM, blood hyperviscosity, high level of cryocrit, positive rheumatoid factor, normal levels of serum transaminases, negative serum hepatitis B surface antigen (HBs Ag), negative anti HBc antibodies, positive HCV antibodies, positive serum RNA HCV, decreased serum C3 and C4 levels, antinuclear antibodies-false positive. Immunological tests for autoantibodies, namely, anti-Sm antibody, anti-RNP antibody, anti-SS-A and -B antibodies, and anti-Scl antibody were not detectable due to high level serum cryoglobulin. Cryoglobulin was washed several times with an isotonic chloride solution for purification, then subject to immunological analyses. The purified cryoglobulin contained monoclonal IgM-kappa, polyclonal IgG. Cryoglobulinemia is a risk factor for ischemic stroke, as it causes arterial thrombosis.
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PMID:Cerebral ischemic attack secondary to hepatitis C virus infection. 1681 84

HIV protease inhibitors are an integral part of effective anti-HIV therapy. The drugs block HIV protease, prevent proper packaging of HIV virions, and decrease the HIV viral burden in the peripheral blood of infected individuals. In addition to direct anti-viral effects, the HIV protease inhibitors also modulate apoptosis. A growing body of work demonstrates the anti-apoptotic effects of HIV protease inhibitors on CD4+ and CD8+ T cells during HIV infection. The mechanism of this apoptosis inhibition is supported by several proposed hypotheses for how they alter the fate of the cell, including preventing adenine nucleotide translocator pore function, which consequently prevents loss of mitochondrial transmembrane potential. More recently, the anti-apoptotic effects of the HIV protease inhibitors have been tested in non-HIV, non-immune cell, whereby protease inhibitors prevent apoptosis, and disease in animal models of sepsis, hepatitis, pancreatitis and stroke. Interestingly, when HIV protease inhibitors are used at supra-therapeutic concentrations, they exert pro-apoptotic effects. This has been demonstrated in a number of tumor models. Although it is unclear how HIV protease inhibitors can induce apoptosis at increased concentrations, future research will define the targets of the immunomodulation and reveal the full clinical potential of this intriguing class of drugs.
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PMID:HIV protease inhibitors modulate apoptosis signaling in vitro and in vivo. 1745 62

HIV protease inhibitors are the backbone of HIV therapy. In addition to blocking intracellular HIV protease and dramatically decreasing viral burden, the protease inhibitors also regulate apoptosis. A growing body of data has confirmed the immunomodulatory effects of HIV protease inhibitors which block CD4+ and CD8+ T cell death in models of HIV infection. The mechanism of this apoptosis inhibition is still under active investigation and supported by several proposed hypothesis for how they alter the fate of the cell. More recently, the anti-apoptotic effects of the HIV protease inhibitors has been extended to the non-HIV, non-immune cell, whereby protease inhibitors prevent apoptosis, and disease, in animal models of sepsis, hepatitis and stroke. Interestingly, when HIV protease inhibitors are used at supra-therapeutic concentrations, they exert pro-apoptotic effects. This has been demonstrated in a number of tumor models. Although it is unclear how HIV protease inhibitors can induce apoptosis at increased concentrations, future research will define the targets of the immunomodulation and reveal the full clinical potential of this intriguing class of drugs.
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PMID:HIV protease inhibitors impact on apoptosis. 1822 Sep 72

Chickenpox is one of the most common infectious diseases in children. In most of the cases the disease is mild and no complications of it are being observed. However, in some of the paediatric patients, the disease may have a serious course with different complications. Most of them are not life-threatening, but some of them, like myocarditis, hepatitis or thrombocytopenia, may be dangerous. Neurological complications of Varicella-zoster virus infection, like encephalitis, meningitis, transverse myelitis, cerebellitis, polyneuropathy or an ischemic stroke, are relatively rare. The authors present 5 children with different neurological complications of chickenpox. The neurological complications of chickenpox did not result in permanent sequel but the cost of hospitalization and the exclusion of the child from everyday activity seem to justify the idea of the routine vaccination.
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PMID:[Chickenpox--neurological complications in children]. 1835 Jul 25


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