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)

A patient developed disseminated intravascular coagulation with purpura fulminans 1 month after starting Dilantin therapy for a seizure disorder. In addition, the patient developed exfoliative dermatitis, hepatitis, cutaneous vasculitis, and microangiopathic hemolytic anemia. She was successfully treated with adrenal steroids and heparin for her purpura fulminans. The hepatitic dermatologic, along with hemorrhagic, complications of Dilantin are reviewed, and the possible origin of the vasculitis and disseminated intravascular coagulation is discussed.
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PMID:Dilantin-induced disseminated intravascular coagulation with purpura fulminans. A case report. 114 59

Diphenylhydantoin-induced hepatitis and mononucleosis are uncommon in children. The occurrence of these two diseases in the same individual, with progression to hepatic failure is rare and has not been reported in infants. This report represents a 6-month-old male infant who developed an infectious mononucleosis-like syndrome and hepatic failure 16 days after diphenylhydantoin administration. He took this anticonvulsant for controlling seizures after a head injury. Fever, skin rash, hepatosplenomegaly, lymphadenopathy, and atypical lymphocytosis led to the initial diagnosis of infectious mononucleosis. However, negative heterophil antibody did not support the diagnosis. Jaundice ensued in the following course and became more and more profound. Meanwhile, physical examination showed shrinking in liver size. Negative virology studies, including Epstein-Barr virus, cytomegalovirus, and hepatitis B virus, excluded them as causative agents. The patient lapsed into a stage I hepatic coma, but gradually recovered clinically and biochemically after eight successive exchange transfusions and supportive care. Two liver biopsies were performed 20 and 50 days after the onset of disease, respectively. Remarkable hepatic parenchymal loss, cholestasis, and fatty change were found on histologic examination of the first biopsy specimen, and portal fibrosis was noted on the second.
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PMID:Mononucleosis and hepatic failure associated with diphenylhydantoin treatment in an infant. 167 17

Peripheral blood mononuclear (PBM) cells from patients with halothane hepatitis are unusually susceptible to damage from phenytoin metabolites generated by an in vitro drug metabolising system. In order to provide more information about the nature of this susceptibility factor, the effect of removing calcium ions (Ca2+) from the incubation medium of the test system was examined. Phenytoin metabolites were generated by incubating phenytoin with beta-naphthoflavone-induced rat liver microsomes in the presence of 1,1,1-trichloropropene oxide (TCPO), an epoxide hydrase inhibitor. When PBM cells from patients who had recovered from halothane hepatitis were incubated in this system and then maintained in Ca(2+)-containing tissue culture medium (without alpha-tocopherol) for 16 h, cell death, as measured by trypan blue exclusion, was greatly increased (53% and 78% at 0.06 mmol/l and 0.12 mmol/l phenytoin, respectively) compared with control incubations (TCPO omitted). Removal of Ca2+ from the tissue culture medium effectively abolished reactive metabolite-induced cell death. Resting cytosolic free Ca2+ concentration in PBM cells was also measured using the quin-2 fluorescence method and total Ca2+ content was measured by atomic absorption spectrometry. Although variability appeared greater among patients, mean values for these parameters among 12 patients with halothane hepatitis did not differ from controls. It is concluded that enhanced permeability of PBM cells to extracellular Ca2+ may be an important factor in the pathogenesis of drug metabolite-induced cell death in patients susceptible to halothane hepatitis. Such permeability to Ca2+ is not evident in resting cells and presumably results from an interaction between electrophilic metabolites and the pumps which regulate cell calcium homeostasis.
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PMID:Halothane hepatitis: damage to peripheral blood mononuclear cells produced by electrophilic drug metabolites is Ca(2+)-dependent. 249 Sep 33

A case of phenytoin-induced hepatitis with mononucleosis is reported, and syndromes associated with phenytoin hypersensitivity reactions are discussed. A 23-year-old black woman with a two-month history of seizure disorder was admitted to a hospital with nausea, vomiting, fever, lymphadenopathy, diffuse maculopapular rash, left-upper-quadrant tenderness, and hepatomegaly. She was receiving phenytoin sodium 300 mg/day; carbamazepine 200 mg four times daily had been discontinued four days before admission because of leukopenia. Phenytoin was discontinued after admission; however, phenytoin 1 g i.v. was given for a tonic-clonic seizure two days after admission, after which swelling of the face and legs and pruritus developed. Over the next few days, signs and symptoms of hepatotoxicity progressed, and she became comatose. Seizures were treated with diazepam. She began to recover after 10 days of supportive therapy and was discharged several weeks later on primidone therapy. Serious phenytoin hypersensitivity reactions may appear as dermatologic, lymphoid, or hepatic syndromes. Fever, rash, and lymphadenopathy often accompany hepatic injury. Encephalopathy and death may occur. Proposed mechanisms for phenytoin hypersensitivity include antigen-antibody reactions, alteration of lymphocyte function, and an enzyme abnormality causing the production of toxic metabolites. Treatment is supportive; phenobarbital and carbamazepine may be used with caution as alternate anticonvulsant therapy. The possibility of phenytoin hypersensitivity reactions should be considered when patients receiving phenytoin have unusual symptoms, particularly fever, rash, and lymphadenopathy.
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PMID:Phenytoin-induced hypersensitivity reactions. 367 71

The aim of this study was to examine whether or not membrane fluidity directly influences infection by enveloped viruses, and, more precisely here, the susceptibility of A/J mouse hepatocytes to Mouse Hepatitis Virus type 3 (MHV3). We therefore studied, in parallel, the effects on hepatocyte membrane fluidity and on intracellular viral titre of two treatments, i) a hypercholesterolaemic diet to increase the hepatocyte membrane cholesterol content, ii) direct phosphatidylserine incorporation into hepatocyte membrane. Membrane fluidity was monitored on isolated hepatocytes by fluorescence anisotropy with TMA-DPH, and the viral titre was determined by plaque assay. The results clearly demonstrate that membrane fluidity is not directly involved in viral infection mechanisms.
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PMID:Contrary results on mouse hepatitis virus type 3 susceptibility in A/J mouse hepatocytes of phosphatidylserine treatment and of a hypercholesterolaemic diet: no correlation with membrane fluidity levels. 798 Jun 8

Dilantin hypersensitivity syndrome is characterized by fever, rash, lymphadenopathy, facial edema, and hepatitis. Anemia, pharyngitis, diarrhea, and nephritis may also be present. The eruption may present as the classic erythematous follicular papules and pustules; or it may be pleomorphic, presenting as a morbilliform eruption, erythroderma, or toxic epidermal necrolysis. Early recognition and discontinuation of the medication are necessary to prevent a potentially fatal outcome. A case is presented and the literature reviewed.
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PMID:Dilantin hypersensitivity reaction. 872 70

We determined the diseases associated with extremely high levels of alkaline phosphatase in hospitalized patients. Computerized laboratory records of the Hospital of Saint Raphael identified all inpatients who had elevations of alkaline phosphatase above 1,000 U/l from April 1994 to September 1995. Thirty-seven inpatients with alkaline phosphatase levels above 1,000 U/l were identified. Six had bone involvement from malignancy or Paget's disease and were eliminated from further analysis, and 31 patients were included in the study. Levels of alkaline phosphatase ranged from 1,014 to 3,360 U/l. Ten patients had sepsis as the cause of the elevated alkaline phosphatase. These included gram-negative organisms, gram-positive organisms, and two patients with fungal sepsis. Seven of 10 patients with sepsis had an extremely high alkaline phosphatase level and a normal bilirubin, 3 of 10 patients with sepsis also had acquired immunodeficiency syndrome (AIDS). Eight patients had biliary obstruction, 7 with malignant obstruction and 1 with a common bile duct stone. Nine patients had AIDS. The cause of the elevated alkaline phosphatase in these included three with sepsis, three with mycobacterium avium intracellulare (MAI) infection, two with cytomegalovirus infection, and one with Dilantin toxicity. Three patients had diffuse liver metastases. Finally, four patients had benign intrahepatic disease, including one patient with liver hemangiomas, one patient with sarcoid hepatitis, one patient with lead toxicity, and one patient with drug-induced cholestasis. Extremely high elevations of alkaline phosphatase are most frequently seen in patients with sepsis, malignant obstruction, and AIDS. Patients with sepsis can have an extremely high alkaline phosphatase level and a normal bilirubin. A variety of other causes were also noted.
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PMID:Extremely high levels of alkaline phosphatase in hospitalized patients. 985 66

Phenytoin hypersensitivity syndrome (PHS) is a rare, and important entity characterized by rash, fever, lymphadenopathy, leukocytosis with atypical lymphocytes, eosinophilia and associated hepatitis. In this article, we present the clinical, laboratory and histopathologic results of 5 cases of PHS. In therapy, pheyntoin was stopped and sodium valproate (10-20 mg/kg day) was started. Additionally, prednisolone was given in two patients who had not resolved eruption with conservative therapy.
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PMID:Phenytoin hypersensitivity syndrome. 1173 81

Phenytoin is a highly effective and widely prescribed anticonvulsant agent, but it can be associated with dose-related side effects and hypersensitivity reactions. We present a case of phenytoin-induced cholestatic hepatotoxicity in a 47-year-old woman who had exfoliative dermatitis, an increase in liver enzymes with a cholestatic pattern, and eosinophilia after 25 days of phenytoin therapy. The diagnostic workup showed no other possible causes, and the results of a percutaneous liver biopsy were consistent with drug-induced toxic hepatitis. Within 3 weeks after discontinuing phenytoin therapy, her liver function tests returned to normal values.
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PMID:Phenytoin-induced toxic cholestatic hepatitis in a patient with skin lesions: case report. 1263 Jun 49

Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome is an adverse drug reaction most commonly associated with aromatic antiepileptic agents. It is characterized by the triad of skin eruption, fever, and systemic involvement, with the latter usually manifesting as hepatitis and lymphadenopathy. Mortality is primarily due to hepatic failure and can be as high as 10%. Formerly referred to by names such as Dilantin hypersensitivity syndrome and anticonvulsant hypersensitivity syndrome, DRESS syndrome is a more precise term since this reaction pattern can be seen with other agents. DRESS syndrome has also been reported in association with sulfonamides, allopurinol, terbinafine, minocycline, azathioprine, and dapsone as well as with several antiretroviral agents such as abacavir and nevirapine. We describe a patient with HIV who developed nevirapine hypersensitivity syndrome who was successfully treated with intravenous immune globulin (IVIG).
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PMID:Case reports: treatment of nevirapine-associated dress syndrome with intravenous immune globulin (IVIG). 1600 28


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