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)

After seven months' continuous treatment for suspected tuberculosis with rifampicin and ethambutol a nine-year-old boy developed polyarthritis, rash and hepatitis in association with anti-native DNA antibodies and positive antinuclear factor. Six weeks after withdrawal of the antituberculosis drugs and conservative management, the boy was clinically well and ten months later he remained well clinically and liver function tests, anti-DNA antibody and antinuclear factor tests were normal.
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PMID:Polyarthritis, hepatitis and anti-native DNA antibodies after treatment with ethambutol and rifampicin. 108 73

The association of arthritis, arthralgia, and various types of skin rashes, as a prodrome to viral hepatitis, although well recognized in adults, has not been well described in children. In an 18-month period, three children presented with this serum sickness-like illness before the onset of evident liver involvement. In one case, the prodromal symptoms occurred four weeks before biochemical or clinical evidence of hepatitis. The SSLI tended to subside with the onset of clinically evident liver disease. Hepatitis B surface antigen (HBsAg, Australia antigen) was detected in the sera of two patients, but free antibody to the antigen was not demonstrable in either one. Serum complement levels were low during the prodromal phase and tended to return to normal value at the onset of extensive liver involvement. The diagnosis of viral hepatitis should be considered in children presenting with polyarthritis, polyarthralgia, and a rash (serum sickness-like illness) of uncertain etiology.
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PMID:Articular and cutaneous prodromal manifestations of viral hepatitis. 118 34

The study included 68 children aged from 1 to 16 years treated for acute leukemias and bone marrow aplasia. Cytomegalovirus antigen (CMV) was detected by immunofluorescence in urinary sediment cells and in cell cultures after their inoculation with CMV. Besides, the activity of IgG and IgM classes of antibodies against CMV was determined. Presence of one or more markers of CMV infection was demonstrated in 31 children, i.e., 45.5%. In eight children (11.7%) clinical manifestation of CMV infection were demonstrable with fever, hepatitis, pneumonia, rash. In all the children who completed the treatment with hyperimmune globulin, regression of clinical symptoms and signs of CMV infection with the elimination of virus antigen from urine was achieved.
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PMID:Cytomegalovirus infection in children with blood diseases. 128 81

Sulfasalazine is an important therapeutic agent in the management of chronic inflammatory bowel disease (CIBD). Unfortunately, adverse reactions to this drug have been reported in 5-55% of treated patients. These include dose-related side effects like nausea, malaise, and headache or hypersensitivity reactions such as rash, fever, hives, arthralgia, hepatitis, etc. Studies in adults with successful reintroduction of sulfasalazine after a desensitization program have been reported; however, with regard to children, no such data are available. Fourteen children and adolescents (5-16 yr old) diagnosed to have CIBD manifested hypersensitivity to sulfasalazine within 2 months of onset of treatment. All had pancolitis--secondary to Crohn's disease (CD) in four and to ulcerative colitis (UC) in 10. All of them were on steroids. Sulfasalazine was discontinued in all after symptoms of hypersensitivity developed. Three patients with severe reaction were diagnosed prior to desensitization experience. Desensitization, beginning with 5-50 mg of sulfasalazine/day, was attempted in the other 11 children. The dose was gradually increased by 5-50 mg increments every 3 days. Desensitization was successful in only five children, who were ultimately able to tolerate 1.5-3.0 g of sulfasalazine daily again. In the rest (six of 11 patients), oral 5-ASA (Asacol) was administered, and three could not tolerate it. One of these three with intolerance to Asacol required colectomy. One did not tolerate Asacol or Dipentum. Our findings suggest that sulfasalazine desensitization should be attempted in all patients developing hypersensitivity reactions before trying alternative therapy.
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PMID:Sulfasalazine desensitization in children and adolescents with chronic inflammatory bowel disease. 809 41

We report a 53-year-old man with sero-negative rheumatoid arthritis who developed a fever, rash and hepatitis 3 weeks after starting sulphasalazine therapy. This was associated with a T cell lymphocytosis, eosinophilia and evidence of classical complement pathway activation. He responded to high dose corticosteroids. This is a rare but characteristic reaction which is likely to be encountered by rheumatologists more frequently with the increasing use of sulphasalazine. It should be recognized promptly as it may be fatal and can be confused with other systemic diseases.
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PMID:The three week sulphasalazine syndrome. 136 31

This retrospective study evaluated treatment with sulfasalazine (SAS) in a mean dosage of 2.1 g/day in 95 patients with rheumatoid arthritis (RA) who were followed-up for 3 months to 4 years. Mean disease duration was 7 years; 79 patients had previously received at least one disease-modifying drug. Four per cent of patients were lost to follow-up. Mean duration of treatment was 15 months (3 weeks-50 months). Treatment continuation rates were 57% at one year, 40% at two years, and 26% at three years. Reasons for discontinuation of SAS included adverse effects (n = 24), inefficacy (n = 33), and death unrelated to SAS therapy (n = 2). In four patients, SAS was discontinued within three months of the first dose because of a severe adverse effect (diffuse erythematous rash, diffuse bullous rash, hepatitis with jaundice, agranulocytosis). SAS-induced biologic markers for lupus were seen in one patient. Furthermore, 12% of evaluable patients developed antinuclear antibodies during SAS therapy. The SAS treatment continuation rate was higher (p = 0.05) among patients under 40 years of age (n = 18) than among older patients. This difference was due to a correlation between age and tolerance with less SAS-induced side effects in patients under 40 years of age (p = 0.03). The SAS treatment continuation rate was unrelated to the duration of rheumatoid arthritis or number of previous maintenance treatments. This study suggests that rheumatoid arthritis patients under 40 years of age exhibit better tolerance to SAS therapy.
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PMID:[Therapeutic maintenance and tolerance of sulfasalazine in rheumatoid polyarthritis. Retrospective study of 95 patients]. 136

Aromatic anticonvulsants such as phenytoin, phenobarbital and carbamazepine are associated with a hypersensitivity syndrome (fever, rash lymphadenopathy, hepatitis) suggestive of an immune component. We have identified immunoglobulin G antibodies in the sera of nine affected patients which recognize a 53-kD protein which is constitutively expressed and PB inducible in rat liver microsomes. No such reactivity was observed in sera from healthy controls, patients on chronic phenytoin therapy without toxicity or patients with hepatic failure not receiving anticonvulsants. Using highly purified rat hepatic cytochrome P450, P450 3A1 was identified as the major antigenic species, whereas less intense reactivity was noted with P450 2C11. P450 2C6 and 3A2 were minor antigens in some patients. In all patients, the apparent constitutive and phenobarbital-inducible expression of the antigen was a composite effect of antibodies reacting with at least two isozymes, one of which was constitutively expressed and the other PB inducible. In human liver, a 53-kD antigen was expressed to a greater extent in microsomes from a patient with a fatal hepatotoxic reaction to phenytoin compared to microsomes from normal liver or from a sulfonamide hepatitis patient. Western blotting with microsomes prepared from lymphoblastoid cell lines transfected with different human hepatic cytochromes P450 failed to identify P450s 1A1, 1A2, 2A3, 2B6, 2C9, 2D6, 2E1, 3A4 or epoxide hydrolase as the target antigen. Identification of the antigen will be important in understanding the relationship between drug metabolism and the subsequent immune response in the pathogenesis of these rare but severe forms of drug toxicity.
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PMID:Human anti-cytochrome P450 antibodies in aromatic anticonvulsant-induced hypersensitivity reactions. 140 97

Bilateral symmetrical polyarthritis occurred in three patients (2 males and 1 female), with no previous history of inflammatory rheumatologic disease, given alpha-interferon for 1 1/2, 7, and 10 months as treatment of chronic non A-non B hepatitis, myelofibrosis, and thrombocytopenia with myeloproliferative disorder, respectively. Joint manifestations developed 1 1/2, 3, and 10 months after initiation of alpha-interferon in a dosage of 3.10(6) U three times a week, 4.5.10(6) U per day, and 8.10(6) U three times a week. Polyarthritis persisted following withdrawal of alpha-interferon in the two last patients of whom one had rheumatoid nodules and positive rheumatoid serology and the other had scleritis, exanthema, and negative rheumatoid serology. Erosive rheumatoid arthritis was diagnosed after 28 months and 12 months, respectively, in two patients who required systemic corticosteroids with antimalarials (1 case) or azathioprine after failure of methotrexate (one case). Follow-up in the third case (12 months) is too short to allow differentiation of systemic lupus erythematosus (ANA: 1/1500 H with anti-DNA antibodies 58 U/ml) and chronic autoimmune hepatitis. Reports of chronic inflammatory rheumatologic disease during alpha interferon therapy are exceedingly few in number. In the cases reported herein, alpha-interferon may have either triggered or revealed the joint disease. To prevent occurrence of this complication, exclusion from alpha-interferon therapy of patients with autoantibodies or a positive history for clinical evidence of immune dysfunction may be considered.
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PMID:[3 cases of polyarthritis treated with recombinant alfa interferon]. 141 Nov 90

Viral A hepatitis is a self-limited infection occurring predominantly among children usually as an anicteric often subclinical illness. Adults afflicted with this virus are more likely to develop icteric hepatitis. This is exemplified in developed countries when a common source outbreak occurs among non-immune adults. Fulminant hepatitis is uncommon in the USA and hepatitis A has never been documented to evolve into chronic hepatitis. However, prolonged cholestasis and relapsing hepatitis are well described. The usual features of cholestatic viral hepatitis A are pruritus, fever, diarrhoea, and weight loss. Serum bilirubin levels are > 10 mg/dl and the clinical course lasts at least 12 weeks. Cholestasis will spontaneously resolve, although corticosteroids will hasten the resolution but may predispose the patient to develop a relapse of the hepatitis. A biphasic or relapsing form of viral hepatitis A occurs in 6 to 10% of cases. The initial episode lasts 3 to 5 weeks and is followed by a period of remission characterized by normal liver chemistries lasting 4 to 5 weeks. Relapse may mimic the initial episode of the acute hepatitis. The full duration of the illness ranges from 16 to 40 weeks from the onset and immunoglobulin M antibody to hepatitis A virus persists throughout the clinical course. Hepatitis A virus has been recovered from stools during the relapse. Extrahepatic manifestations of hepatitis A include evanescent skin rash and transient arthralgias. Documented cases of arthritis and cutaneous vasculitis have been associated with cryoglobulinaemia and are rare.
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PMID:Atypical clinical manifestations of hepatitis A. 147 99

The emergence of the acquired immunodeficiency syndrome (AIDS) has fueled concerns of both physicians and their patients about safety of blood transfusions. Although AIDS has generated the most fear, the risk today is extremely remote (1/60.000 units of blood). The risk of transmitting infectious disease by homologous transfusion is decreasing, as more donor screening and testing measures are implemented. The blood supply is safer that at any time, but small transfusion risks exist. The most common problems associated with transfusions are temporary: one in 100-300 recipients will experience fever or rash. The biggest problem is a mismatch of the well-known ABO blood groups and once in every 100-400.000 transfusions the hemolytic reaction is fatal. Viral hepatitis is another serious and important risk. At present hepatitis seems to strike between 1 and 3 percent of transfusion recipients. Most, if not all, of transfusion-associated hepatitis cases are caused by hepatitis C virus. Cytomegalovirus can cause primary infection, reactivation or reinfection by transfusion. Immunosuppressed patients are more likely to develop more severe disease. Epstein-Barr virus does not seem to cause significant post-transfusion disease. Bacterial or protozoal infections are an infrequently encountered adverse effect of transfusion. However, some clinical cases document the potential hazard of blood components as a vector for bacteria or protozoa. Homologous blood transfusion down-regulates some immune functions. Host defences against malignancy and infection may in some instances be severely compromised by transfusions of homologous blood.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Transfusion risks and alternatives to transfusion]. 149 80


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