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)

We report the case of a 32-year-old woman who had pruritic urticarial skin lesions associated with episodes of arthralgia. The first site affected by the eruption was the inside surface of the thighs; the patient also reported the presence of leukorrhea. The woman had previously been treated with H1 antagonist with moderate and transitory results; skin lesions reappeared just after the interruption of the treatment. Her biochemical data showed increased levels of erythrocyte sedimentation rate, blood eosinophilia and hypocomplementemia. Antinuclear antibodies, rheumatoid factor, cryoglobulins and serological diagnosis for hepatitis or mononucleosis viruses resulted negative. Considering the initial site of the cutaneous features and the presence of leukorrhea, we requested a vaginal smear and a culture of the cervical secretion, which revealed the presence of a Trichomonas infection. Furthermore, the SDS-PAGE revealed the presence of a molecular mass of 230,000 Da (230-kDa) in the serum, which indicated a Trichomonas surface protein. The following treatment with oral metronidazole caused the eradication of the Trichomonas infection after 3 weeks and subsequently the resolution of the urticarial clinical features. We wish to underline that in the presence of a case of urticaria vasculitis syndrome which seems to be without cause, it is important to investigate every diagnostic suspicion scrupulously.
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PMID:Urticaria from Trichomonas vaginalis infection. 1035 1

Eosinophilia is a distinctive feature of primary biliary cirrhosis (PBC), especially in its early stages. Intriguingly, treatment with ursodeoxycholic acid (UDCA) ameliorates eosinophilia as well as liver tests in patients with PBC. It remains unknown, however, whether eosinophils in PBC patients are functionally activated and whether UDCA inhibits eosinophil activation. In the present study, we systematically examined eosinophil dynamics in the blood and liver in patients with stage I to II PBC before and after UDCA treatment. We determined serum concentrations of eosinophil granule proteins (major basic protein [MBP] and eosinophil-derived neurotoxin [EDN]) by radioimmunoassay and quantitated eosinophil degranulation using computer-assisted morphometry after MBP immunohistochemistry. Before UDCA treatment, patients with PBC (n = 25) showed significantly higher circulating eosinophil counts (P <. 05) and serum concentrations of MBP (P <.0005) and EDN (P <.02) compared with patients with chronic viral hepatitis (n = 22), autoimmune hepatitis (n = 10), and obstructive jaundice (n = 12). Four-week UDCA treatment significantly reduced blood eosinophil counts (P <.0001) and serum MBP (P <.0001) and EDN (P <.0001) levels in PBC patients. MBP immunohistochemistry and computer-assisted quantitative morphometry showed infiltration and degranulation of eosinophils in the portal tract in patients with PBC and significant reductions in the number of sites and the area occupied by extracellular MBP deposits after UDCA treatment for 2 years (P <.02) but not in placebo-treated patients. Our results suggest that eosinophils in patients with PBC are not only increased in number, but also release granule proteins, and that UDCA treatment inhibits this eosinophil activation/degranulation.
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PMID:Ursodeoxycholic acid inhibits eosinophil degranulation in patients with primary biliary cirrhosis. 1038 76

Drug-induced hypersensitivity syndrome is a multiorgan-system reaction characterized by fever, pleomorphic eruption, lymphadenopathy, eosinophilia, lymphocytosis and hepatitis. We report a drug hypersensitivity syndrome in a 6-year-old Tunisian child treated for epileptic absences with sodium valproate and ethosuximide. Imputability of these 2 drugs is probable because of the chronological and clinical features. Positive rechallenge with ethosuximide confirmed the toxicity of this drug. Sodium valproate was also responsible because patch testing was positive and followed by a generalized eruption. Human herpesvirus 6 (HHV6) antibody titers increased significantly within 15 days. There was a favourable outcome after discontinuation of the drugs and corticosteroid therapy. Our case is interesting because this drug hypersensitivity syndrome occurred with non-aromatic anticonvulsant drugs. It is the 1st case with ethosuximide and the 2nd with sodium valproate. We also observed a reactivation of HHV6 infection that may contribute to the development of this hypersensitivity syndrome.
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PMID:Hypersensitivity syndrome due to 2 anticonvulsant drugs. 1047 12

Capillaria hepatica is a helminth that may cause an extremely rare condition of parasitic hepatitis. Only 29 cases have been published, 2 of them in Brazil. We report here 3 cases of children in Brazil with massive hepatic capillariasis who presented the characteristic triad of this type of infection, i.e., persistent fever, hepatomegaly, and eosinophilia. The diagnosis was made by liver biopsy. All children responded well after treatment with thiabendazole (case 1), albendazole (case 3), and albendazole in combination with a corticoid (case 2). Case 1 has been followed-up for 24 years, an event not previously reported in the literature.
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PMID:Hepatic capillariasis in children: report of 3 cases in Brazil. 1054 2

We report four cases of the side effects of minocycline seen during the last two years in our department. There was one case of drug-related lupus and three cases of hypersensitivity reactions, including one eosinophilic pneumopathy with pericarditis, one nephropathy and one severe, pseudo-infectious episode of high fever, rash, lympadenopathy, hepatitis and eosinophilia. Minocycline is a tetracycline agent widely used for acne therapy in France and all over the world. During the last few years, there has been an increasing number of reports concerning systemic adverse reactions to minocycline, with on the one hand auto-immune disorders (lupus, autoimmune hepatitis, vascularitis with ANCA), occurring after a prolonged course of therapy and reported recently in the last few years, and on the other hand, hypersensitivity reactions (eosinophilic pneumopathies, hepatitis, nephropathies, myocarditis, serum sickness or pseudo-infectious reactions), occurring precociously in the course of therapy, and potentially severe. Although these side effects are uncommon in the context of the high number of patients who have been prescribed the drug, the first-line antibiotic therapy in acne must probably be reconsidered.
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PMID:[Systemic reaction induced my minocycline treatment: a report of four patients and a review of the literature]. 1057 23

To assess epidemiological and clinical significance of drug hepatotoxicity in the setting of liver diseases consultation, ten thousand and three hundred forty two prospectively designed clinical records from patient cared for in our Liver Unit in the period 1988-1998 were incorporated into the study; 58 out of 10,342 (prevalence = 5.6%) fulfilled at least the first three of the following causality requirements: 1.--Liver injury associated in time to drug exposition; 2.--Negative evaluation of more common other etiologies; (alcohol, viruses, immunologic, metabolic, etc) 3.--Favourable response to drug withdrawal (ALT < 50% of baseline in 8 to 30 days in acute hepatitis type, and alkaline phosphatase and/or total bilirubin < 50% of baseline up to 6 months, in acute cholestasis) 4.--Inadverted or rarely prescribed positive challenge. Acute hepatitis type of injury were considered when serum ALT rise 8 times or more above normal superior level with alkaline phosphatase (APh) below 3 times; "pure" cholestasis when APh rise 3 times or more above normal with ALT below 8 times; mixed acute injury or cholestatic hepatitis when both ALT and APh were elevated above 8 and 3 times respectively, and indeterminate type when both enzymes were below the referred levels. Chronic injury were considered when six or more month of evolution and compatible liver histology happens. Clinical severity were expressed as mild (absence of major clinical complications, serum bilirubin < 5 mg/dl and prothrombin concentration > 75%), moderate (presence of clinical complications, bilirubin > 5 mg/dl and prothrombin concentration between 50-75%), and severe (major clinical complications with bilirubin > 5 mg/dl and prothrombin concentration < 50%). Female/male ratio was 1.4:1, with age average 39 years (R = 15-77) and major concentration of cases above 40. More than 50% of cases received 2 or more drugs. Jaundice was present in 60.4%, and systemic manifestations of hypersensibility (fever, adenomegalies, rush, mononucleosis like syndrome, eosinophilia) in 29.3%. Acute injury represented 91.4% of the cases: 41.4% acute hepatitis, 15.5% "pure" cholestasis, 24.1% cholestatic hepatitis, and 10.3% indeterminate type. Four patients (4.5% of acute injury cases) were presented as severe acute liver failure, leading to liver transplant in one of them, drug association (INH-rifampicin and carbamazepine-phenobarbital) and inadverted challenge (sulphonamides and pemoline) were associated to clinical severity. Chronic injury were found in five patient (8.6%), four of them associated to chronic hepatitis and the other one to a ductopenic syndrome. Six drugs represented 53.4% of our cases; oral contraceptives (7 cases), INH alone or combined with rifampicin (6 cases), sulfonamides and clorpropamida (5 cases each), carbamazepine and amiodarone (4 cases each). Normalization of liver enzymes after drug suppression took 2 to 8 weeks in acute hepatitis type (X = 4 weeks), 4 to 20 in "pure" cholestasis (X = 12 weeks) and 8 to 24 weeks in cholestatic hepatitis or mixed type (X = 16 weeks). Two cases of chronic hepatitis normalize the histological activity index in 20 and 18 month respectively, one case remains as chronic hepatitis at 10 month and the other one progress to cirrhosis; the ductopenic syndrome normalize histology in 19 months receiving urso-deoxicolic acid, 10 mg/k/day.
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PMID:[Clinic-epidemiological significance of drug hepatotoxicity in liver disease consultation]. 1092 31

A 30-year-old incarcerated man was sprayed with the "tear gas" ortho-chlorobenzylidene malononitrile (CS). He was hospitalized 8 days later with erythroderma, wheezing, pneumonitis with hypoxemia, hepatitis with jaundice, and hypereosinophilia. During the subsequent months he continued to suffer from generalized dermatitis, recurrent cough and wheezing consistent with reactive airways dysfunction syndrome, and eosinophilia. These abnormalities responded to brief courses of systemic corticosteroid but recurred off therapy. The dermatitis resolved gradually over 6-7 months, but the patient still had asthma-like symptoms a year following exposure. Patch testing confirmed sensitization to CS. The mechanism of the patient's prolonged reaction is unknown but may involve cell-mediated hypersensitivity, perhaps to adducts of CS (or a metabolite) and tissue proteins. This is the first documented case in which CS apparently caused a severe, multisystem illness by hypersensitivity rather than direct tissue toxicity. Both the ethics and safety of CS use remain controversial, in part because of the difficulty documenting sporadic injuries received in the field, and also because the charged circumstances surrounding CS use may lead to both underreporting and exaggerated claims of medical harm. The medical literature on CS focuses mainly on its immediate irritant effects and on transient dermal and ocular injuries, with only 2 prior case reports of acute lung injury related to CS exposure. Given the paucity of documented lasting effects despite its widespread use for more than 3 decades, CS appears to be safe when deployed (outdoors) in a controlled manner, but it can cause important injuries if misused or if applied to a sensitized individual.
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PMID:Medical hazards of the tear gas CS. A case of persistent, multisystem, hypersensitivity reaction and review of the literature. 1094 52

Hypersensitivity syndrome is defined as a drug-induced complex of symptoms consisting of fever, rash, and internal organ involvement. The hypersensitivity syndrome is well recognized as being caused by anticonvulsants. Olanzapine is an atypical antipsychotic agent whose side effects include sedation, weight gain, and increased creatinine kinase and transaminase levels. To date, there have been no reports of hypersensitivity syndrome related to this drug. A 34-year-old man developed a severe generalized pruritic skin eruption, fever, eosinophilia, and toxic hepatitis 60 days after ingestion of olanzapine. After termination of olanzapine treatment, the fever resolved, the skin rash was reduced, eosinophil count was reduced to normal, and the transaminase levels were markedly reduced. Clinical features and the results of skin and liver biopsies indicated that the patient developed hypersensitivity syndrome caused by olanzapine.
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PMID:A case report of olanzapine-induced hypersensitivity syndrome. 1121 18

Hypersensitivity syndrome is a rare but potentially fatal reaction to some pharmacologic agents, including some antiepileptic drugs. Typically, the syndrome presents with fever, rash, tender lymphadenopathy, hepatitis, and eosinophilia. We report a novel case of clinical hypersensitivity syndrome secondary to gabapentin. A patient developed altered mental status, fever, diffuse macular rash, and an enlarged spleen. This constellation of symptoms and signs began 9 days after gabapentin therapy was begun. Quick resolution was noted after gabapentin was discontinued. To our knowledge, there are no reports of hypersensitivity syndrome to gabapentin.
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PMID:Gabapentin-induced hypersensitivity syndrome. 1130 46

A case of clozapine-induced toxic hepatitis in a 49-year old woman with schizophrenia is described. The daily clozapine dose was clinically titrated to 300 mg. Subsequently, the patient experienced lethargy and anorexia, and fever, eosinophilia, leucocytosis and abnormal liver parameters were found. The serum concentration of clozapine was 8595 nmol/l, and treatment was discontinued. After eight days, the condition stabilised, and low-dose clozapine treatment was successfully reinstituted with serum monitoring (TDM).
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PMID:[Clozapine-induced toxic hepatitis]. 1130 64


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