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 measured thyrotropin receptor antibodies in serum obtained from 2 groups of patients participating in clinical trials of recombinant interferon-alpha 2b for viral hepatitis. Group I: Patients with hepatitis B (N = 8), received interferon 5 x 10(6) units thrice weekly for 4 months. Group II: Patients with non-A, non-B hepatitis (N = 16) were randomized to receive interferon in a dose of either 0.25 x 10(6) or 3 x 10(6) U thrice weekly for 6 months and then crossed over to receive the other dosage schedule for a further 6 months. None of the patients developed thyrotoxicosis. Thyrotropin receptor antibody activity was detectable within the "normal range" (less than 10 U/l) in 6 patients prior to treatment. In Group I, thyrotropin receptor antibodies became detectable in 6 patients on treatment, in 4 of whom it was 10 U/l. In Group II, thyrotropin receptor antibody activity was unchanged on low-dose interferon, but on the higher dose became detectable in 9 patients, in 7 of whom it was greater than 10 U/l. We conclude that treatment with interferon is associated with the development of thyrotropin receptor antibodies in a large proportion of patients. It is possible that in some patients treated with higher doses of interferon the increase in thyrotropin receptor antibody activity may be sufficient to induce hyperthyroidism.
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PMID:Thyrotropin receptor antibodies following treatment with recombinant alpha-interferon in patients with hepatitis. 175 38

To determine whether thyroid hormone-binding proteins in serum, particularly albumin, facilitate the transfer of T4 into human tissues, we studied cellular T4 uptake (CT4) by human liver (Hep G2) cells from medium containing serum from subjects with familial dysalbuminemic hyperthyroxinemia (FDH) and acquired and familial T4-binding globulin (TBG) excess and patients with normal T4-binding to albumin and normal TBG concentrations. Serum from nine subjects with FDH whose mean serum total T4 (TT4) concentration was 203 +/- 27 nmol/L were matched for TT4 concentrations with serum from nine subjects with acquired TBG excess (TT4, 201 +/- 23 nmol/L) and nine subjects with thyrotoxicosis and normal TBG concentrations (TT4, 205 +/- 28 nmol/L). The subjects' CT4 results were compared to their serum free T4 concentration, measured by equilibrium dialysis (DT4), and their serum free T4 index (FT4I) value. The mean serum DT4 value for the subjects with FDH (23 +/- 5 fmol/L) and those with TBG excess (23 +/- 3 fmol/L) were normal, whereas it was elevated (44 +/- 9 fmol/L; P less than 0.001) for the thyrotoxic patients with normal TBG concentrations. The mean CT4 value also was normal for the subjects with FDH (37.7 +/- 4.9 fmol/plate) and those with TBG excess (36.6 +/- 4.6 fmol/plate), but was elevated for the thyrotoxic patients (62.3 +/- 11.2 fmol/plate; P less than 0.001). In all three groups studied, the relationship between individual CT4 and DT4 values was similar to that previously found in subjects with no T4-binding protein abnormalities. The mean serum FT4I value was lower for the subjects with acquired TBG excess (111 +/- 22) than for the subjects with FDH (133 +/- 22; P less than 0.05), and it was much higher for the subjects with thyrotoxicosis (221 +/- 31; P less than 0.001). In the subjects with FDH and those with thyrotoxicosis the normal relationship between CT4 and FT4I was maintained, while in the subjects with acquired TBG excess, FT4I values were lower than expected. In seven of the nine subjects with TBG excess, the abnormality was associated with conditions known to increase its sialic acid content: hepatitis (one subject), pregnancy (four subjects), and estrogen therapy (two subjects). The CT4 values were similar in nine subjects with acquired TBG excess (seven pregnant women and two subjects with chronic active hepatitis) and five subjects with familial TBG excess (34.8 +/- 4.3 vs. 34.0 +/- 8.6 fmol/plate, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Normal cellular uptake of thyroxine from serum of patients with familial dysalbuminemic hyperthyroxinemia or elevated thyroxine-binding globulin. 314 12

An association of granulocytopenia, eosinophilia, skin reaction and hepatitis during propylthiouracil (PTU) therapy for thyrotoxicosis in a 47 year old black female is reported. Clinical and biochemical abnormalities disappeared soon after discontinuation of PTU. That the drug was directly responsible for the observed complications is suggested by the clinical course and by in vitro lymphocyte transformation studies. The latter revealed sensitization to PTU during the acute phase of the disease, which was greatly reduced 5 weeks after discontinuation of the drug and was completely absent after 5 months.
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PMID:Multiple complications of propylthiouracil treatment: granulocytopenia, eosinophilia, skin reaction and hepatitis with lymphocyte sensitization. 622 Oct 46

Obstetrician-gynecologists reviewed patient records of women delivering during January 1986-December 1992 to determine the maternal mortality rate and trends and the causes of maternal deaths in the maternity ward at the National University of Singapore. There were 26,173 deliveries and 9 maternal deaths (a maternal mortality rate of 22.9/100,000). The causes of maternal deaths were pulmonary embolism (underlying condition, systemic lupus erythematosus [SLE]), hemorrhage from multiple sites (thrombotic thrombocytopenia), acute exacerbation of SLE with interstitial pneumonitis, pulmonary fibrosis (systemic sclerosis), fulminant hepatitis (prior hepatitis and liver disease), and cerebral embolism (rheumatic heart disease with mitral valve replacement). There were also three incidental maternal deaths bringing the maternal mortality rate up to 34.4/1000. The incidental causes of death included septicemia from perforated peptic ulcer (uncontrolled thyrotoxicosis), multiple metastases from lung cancer, and suicide (family dispute over adoption of newborn). A cesarean section preceded 4 (44%) of the 9 maternal deaths. Two of these deaths were incidental maternal deaths. Cesarean section was related to two of the remaining six (33%) deaths. These findings show that traditional direct causes of maternal death (hemorrhage, sepsis, embolism, or hypertension) were not responsible for the maternal deaths at this tertiary facility. Instead, the women tended to have medical conditions that placed them at high risk of death regardless of pregnancy status.
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PMID:Maternal mortality: evolving trends. 781 Nov 98

In the present paper we described the first case report of silent thyroiditis following alpha-interferon (IFN-alpha) treatment for chronic type C hepatitis in Japan. A 51-year-old woman with chronic type C hepatitis was treated with 6 million units of IFN-alpha three times a week for 24 weeks. Thyroid function was within normal limits and thyroid autoantibodies were negative before IFN therapy. Sixteen weeks after initiation of the treatment, she complained of increasing fatigue, palpitation and losing 7 kg in weight. Thyroid function tests at that time revealed an increase in serum T3, T4, free T3 and free T4 and a markedly suppressed TSH concentration. Both antithyroglobulin antibody (TgAb) and antimicrosomal antibody (McAb) were positive in a dilution of 1: 400. The computed tomographic (CT) scan of the thyroid showed a decrease in the CT number (Hounsfield unit; H.U.) to 58 H.U. (normal, 95-167 H.U.). The 24-h thyroid uptake of 123I was 0.75%. Aspiration biopsy specimens from a nodule in the right lobe and the remaining struma disclosed papillary adenocarcinoma and Hashimoto thyroiditis, respectively. Thyroid function spontaneously returned to normal two months after the onset of thyrotoxicosis through the subclinical hypothyroid stage. After recovery of thyroid function, patient had an operation of papillary cancer without any complications. These clinical features and laboratory findings led to the diagnosis of silent thyroiditis developing in the course of the long-term IFN therapy, which, to our knowledge, has not been reported before in Japan.
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PMID:An episode of silent thyroiditis in a patient with chronic thyroiditis and papillary adenocarcinoma following alpha interferon treatment for hepatitis C. 792 Aug 83

We report two cases of autoimmune thyroid disorders which appeared after 6 months of recombinant alpha interferon therapy given for chronic non-A, non-B hepatitis. There was no family or personal history of thyroid disease, or had the patients taken any hepatic or thyroid toxic drugs. The other causes of hepatic and thyroid diseases were ruled out. The first case concerned a 33-year-old woman with sporadic hepatitis C. Therapy was complicated by the appearance of antimicrosomal thyroid antibodies and hypothyroidism. At 22 months, substitutive therapy was still necessary in one case. The second case involved a 37-year-old woman with post-transfusional non-A, non-B hepatitis which was complicated by transient hypothyroidism preceding thyrotoxicosis (with TSH-receptor antibodies). We observed a return to euthyroidism and loss of associated antibodies after withdrawal of interferon and institution of hormonal therapy.
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PMID:[Autoimmune dysthyroidism induced by alpha interferon in two female patients with chronic non-A, non-B hepatitis]. 825 18

A 22-year-old Chinese man, a HBsAg carrier, presented with relapse of thyrotoxic Graves' disease complicated by thrombocytopenia and hepatitis. Platelet count and liver enzymes gradually improved following successful treatment of the thyrotoxicosis with radioactive iodine. Possible pathogenetic links and therapeutic implications are discussed.
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PMID:A patient with Graves' disease, thrombocytopenia and chronic hepatitis B. 903 9

The appearance of moderate jaundice with mildly raised levels of plasma bilirubin is an uncommon complication of thyrotoxicosis and is usually accompanied by signs of right heart failure. Some described cases were actually related, at least in part, to autoimmune chronic hepatitis. In this paper we describe a case of thyrotoxicosis accompanied by deep jaundice with very high levels of bilirubin occuring in the absence of cardiac failure and with no signs of hepatitis. Jaundice disappeared shortly after the start of thyrostatic drug treatment, supporting a possible detrimental effect of hyperthyroidism on the hepatic bilirubin metabolism.
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PMID:Appearance of severe jaundice after radiometabolical treatment of thyrotoxicosis. 1021 89

Abnormal liver function in thyroid disorders may be secondary to thyrotoxicosis or to autoimmune injury to the liver. We report the case of a 36-year-old female who developed jaundice and pruritus with mild cholestasis and moderately elevated transaminase levels. The diagnosis of Graves' disease was made shortly thereafter. Laboratory findings were: alanine and aspartate aminotransferase 219 (IU/I (N: 9-50) and 102 IU/I (N: 10-15) respectively, alkaline phosphatase 336 IU/I (N: 40-135), bilirubin 24 micromol/I (N: 2-23), and gamma-glutamyl transpeptidase 232 IU/I (N: 9-43). Abdominal ultrasonography showed normal bile ducts; echocardiography ruled out heart failure; viral and autoimmune markers for hepatitis and cirrhosis were negative. Percutaneous liver biopsy showed moderate intrahepatic steatosis, anisokaryosis, lymphocyte infiltration in the portal areas, and Kupffer cell hyperplasia. Outcome was favorable after seven months of iodine therapy, confirming the diagnosis of thyrotoxicosis hepatitis.
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PMID:[Thyrotoxicosis hepatitis: a case report]. 1145 76

Complete clinical examination covered 37 patients in various stages after acute occupational poisonings with pesticides (8 examinees), with explosive gases (9 subjects), with carbon oxide (3 examinees), with cadmium oxides (1 examinee), with nitrogen compounds (4 ones), with sulfurous gases (2 examinees), with organic solvents (10 subjects) including chlorinated hydrocarbons (2 subjects). Post-intoxication period appeared to include syndromes characteristic for each poison and corresponding to severity of acute state (from cephalgia to parkinsonism and thyrotoxicosis after acute poisoning with carbon oxide, organic neurologic signs and toxic hepatitis after acute poisoning with phosphorus organic compounds, cerebral asthenia after acute exposure to organic solvents, severe encephalopathy and toxic auditory and optic neuropathy after hydrogen sulfide). Inadequate medical rehabilitation and continuous occupational exposure induced deterioration in clinical signs and advanced post-intoxication syndromes.
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PMID:[Diagnostic problems of post-intoxication states]. 1150 30


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