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)

Modern contraceptive methods are discussed, with special emphasis on oral contraceptives, which are regarded as the most effective. They are also regarded as generally safe, although there are contraindications and the drugs should only be prescribed after careful examination. The need for selecting the drug most suitable for the individual patients, mainly on the basis of the characteristics of the menstrual cycle (suggesting a predominance of estrogen or progestin, within safety limits, such as 50 mcg of estrogen), is emphasized. The examinations required include a general clinical, gynecological, and breast examination, cytology tests, evaluation of the menstrual flow pattern, measurements of arterial pressure, weight, glucose, cholesterol and triglyceride levels, and urine tests. They should be repeated at 6-month intervals, or 3-month intervals in the case of high-risk patients (varicose veins, obesity, heavy smokers, high cholesterol and triglyceride levels, history of jaundice, slight heart condition, clinical or potential diabetes, porphyria or predisposition to uterine myoma). Oral contraceptives are contraindicated in cases presenting a history of thromboembolism, phlebitis, cerebral apoplexy; sickle cell anemia, which indicates a predisposition to thromboembolic accidents; serious liver disease or recent hepatitis; serious heart disease; hormone-dependent neoplasia (breast cancer); predisposition to uterine cancer; erythematous lupus; metorrhagia of unknown origin; psychic disorders, especially of a depressive type. They should also be avoided for 3-4 years after puberty, in order to avoid interfering with the development of the hypothalamus and with growth. A carcinogenic effect of the pill and an increase in the risk of giving birth to abnormal children can be ruled out, although the incidence of abortions due to chromosome anomalies after suspending treatment is rather high (due to the previous inhibition of ovulation, a situation similar to repeated pregnancies at short intervals, which involve the same risk).
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PMID:[Current clinical problems of contraception]. 502 53

Serum Clq binding activity (ClqBA) is increased in diabetes mellitus with liver injury, carcinoma of gastrointestinal tract with metastatic liver and chronic liver disease (CLD). Significant elevations of ClqBA level are observed in the order of liver cirrhosis, chronic aggressive hepatitis and chronic persistent hepatitis. In CLD there are significant correlations between ClqBA and gamma-globulin, rheumatoid factor, anti-DNA-antibody, CH50, C3, C4, C3-activator and HBsAg.
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PMID:Studies on circulating immune complexes of the liver disease. 4. Clq binding activity. 615 28

Therapeutic drugs are well-recognized as a cause of the nephrotic syndrome in humans. However, documentation of the renal histopathologic features is lacking or incomplete in many cases. Even when accurate histopathologic information is available, there is little evidence to support a specific pathogenetic mechanism of renal injury in the vast majority of cases. We describe a patient with diabetes who had hepatitis and dermatitis in association with the use of chlorpropamide. In addition to these well-described toxic reactions to this drug, the nephrotic syndrome developed. Renal biopsy revealed the presence of a proliferative glomerulonephritis that was shown to be of an immune complex nature on immunofluorescence and electronmicroscopic study. Serial serum complement levels and circulating immune complex levels were consistent with an immunologically mediated reaction. Repeated renal biopsy documented resolution of the renal changes. Thus, in this patient, a drug-induced nephrotic syndrome was associated with a proliferative glomerulonephritis, probably due to the formation of immune complexes.
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PMID:Nephrotic syndrome and immune complex glomerulonephritis associated with chlorpropamide therapy. 621 54

A 36-year-old man with juvenile-onset diabetes mellitus developed cholestatic hepatitis of unknown cause, possibly drug-induced. He remained jaundiced for four months, until he died unexpectedly. At autopsy, severe and macroscopically identifiable xanthomatous neuropathy was found in the liver; it involved the unmyelinated nerves in the hilus and in all portal tracts examined. Microscopic evidence of minimal extrahepatic involvement of unmyelinated nerves was also found. Somatic nerves were affected by diabetic neuropathy but not by xanthomatous neuropathy. The condition seems to be a rare complication of diseases that are characterized by accumulations of lipids.
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PMID:Xanthomatous neuropathy of liver. 629 15

Serological studies were carried out in the time course of insulin-dependent diabetes mellitus in 419 children, among whom paired sera from 66 were studied in the very beginning of diabetes mellitus. By seroconversion in 83% of the children early in the disease, different, frequently mixed virus infections were diagnosed: Coxsackie B2, B3, B4 (46%), rubella (41%), influenza A, B, C (38%), parainfluenza types 1-3 (35%), mumps (23%), adenovirus infection (18%), HB virus infection (4.5%). Acute respiratory diseases preceded or coincided with the onset of diabetes in half of the children with diagnosed acute respiratory and enterovirus infections. No clinical signs of rubella, mumps, or hepatitis immediately before the onset of diabetes or early in the disease were found. A possible role of virus infection diagnosed early in diabetes, in the etiology of chronic insulitis, in provocation of its exacerbation, and manifestation of diabetes mellitus is discussed.
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PMID:[Antibodies to viruses in children with diabetes mellitus]. 631 65

In a survey the present possibilities are outlined to get knowledge about diseases of inner organs with the help of enzyme determinations in the urine. Here it is remarkable that changes of the enzyme excretion appear not only in renal disease with acute renal failure, pyelonephritis, glomerulonephritis, renal infarction and nephroptosis but are also to be observed in primarily extrarenal diseases such as diabetes mellitus, hyperthyroidism, thesaurismoses, myocardial infarction, hypertension, acute pancreatitis, epidemic hepatitis, liver cirrhosis, obstructive jaundice and rheumatoid arthritis. The causes of the changes of enzyme excretions are various. Since enzymes of different origin and localisation behave themselves variably, the simultaneous determination of a brush border marker (e.g. alanine aminopeptidase), a lysosomal enzyme (e.g. beta-glucuronidase or N-acetyl glucosaminidase) and a low molecular enzyme (e.g. lysozyme) is of use for the recognition of renal alterations. By the control of activities of urinary enzymes it is possible to get without risk informations about pathobiochemical processes in the kidney which are not to be gained by means of other methods.
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PMID:[Urinary enzyme excretion in diseases of the internal organs]. 636 87

Severe congestive cardiac failure developed in a few weeks in a 44 year old man who had undergone porto-caval anastamosis for post-hepatitis cirrhosis one year previously and then treated for anaemia by repeated blood transfusion and chronic daily oral iron therapy. Infiltrative, congestive and restrictive cardiomyopathy was diagnosed in the presence of global cardiomegaly, electrocardiographic changes (microvoltage, diffuse ST-T wave changes), echocardiographic appearances (dilatation of the left ventricle, with hypertrophic and hypokinetic walls), and hemodynamic signs of adiastole with equalisation of filling pressures at 15 mmHg and a cardiac index of 1,88 l/min/m2. Cardiac haemochromatosis was confirmed by the laboratory (serum iron: 35 mumol/l; siderophilin saturation: 100 p. 100; serum ferritin: 1854 ng/ml; induced siderouria: 51 mg/24 hours) and histological findings (endomyocardial biopsy showing pigment overload). The absence of a family history, of homozygote A3 antigen, of diabetes, of iron overload on hepatic biopsy one year previously, excluded the diagnosis of familial idiopathic haemochromatosis. A secondary form of the disease was diagnosed on a possible genetic predisposition (heterozygote A3 antigen) and on environmental factors (blood transfusions, iron therapy, cirrhosis, alcoholism and perhaps the porto-caval anastamosis. Cardiac haemochromatosis was cured in this case by iron chelating therapy comprising daily subcutaneous infusions of 2 g of desferrioxamine for 2 months. The cure was confirmed by regression of the signs of clinical cardiac failure and of cardiomegaly, the increase in QRS voltages and the near normalisation of the hemodynamic and laboratory findings.
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PMID:[Adiastole caused by a secondary cardiac hemochromatosis. Successful treatment with an iron chelating agent]. 641 3

A middle-aged diabetic woman after four weeks of chlorpropamide treatment developed cholestatic hepatitis with systemic manifestations of idiosyncratic reaction. After recovery, unintended rechallenge with the same drug induced a brisk exacerbation of the symptoms and signs that reversed completely following chlorpropamide withdrawal. Tolbutamide medication was subsequently well tolerated for several weeks, followed by another flare of cholestatic liver lesion and cutaneous eruption with eosinophilia (after each reaction the patient was treated with insulin). Eventually glibenclamide (glyburide) was instituted resulting in very satisfactory control of diabetes, with no untoward reaction.
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PMID:Favorable effects of glibenclamide in a patient exhibiting idiosyncratic hepatotoxic reactions to both chlorpropamide and tolbutamide. 644 88

Most immunologically-mediated diseases are inflammatory in nature, as assessed by cellular infiltrates at the lesion site. Recent immunohistological studies using monoclonal antibodies on tissue sections and synovial or cerebrospinal fluid reveal that B- and T-lymphocytes (predominantly T) participate in this reaction, together with monocytes and macrophages. The etiopathogenesis of inflammatory diseases of immunological origin can be discussed at two levels. (1) Lesions may be secondary to the cytopathic effect of antibodies, either by direct cytolysis or by opsonization, antigenic modulation, or blockage of functionally-relevant molecules. Immune complexes formed in the circulation or locally at the lesion site may intervene. Direct cellular mechanisms are probably involved, as suggested by evidence in hepatitis (indirect) and in juvenile insulin-dependent diabetes (direct). K-cells may act by antibody-dependent cytotoxicity, particularly in autoimmune diabetes and thyroiditis where lymphocyte-dependent antibodies are demonstrated. Unfortunately, the absence of adequate markers does not permit adequate detection of K-cells in inflammatory reaction sites. (2) Etiological factors are multiple in a given disease and even in a single patient. Deficiency of suppressor T-cells, assessed using monoclonal anti T-cell antibodies, represents a major predisposing factor, although suppressor cell deficit may be restricted to some antigens (EBV) in certain patients. The deficiency of interleukin-2 production in lupus and rheumatoid arthritis is intriguing but the mechanism and its relationship to disease etiology are unknown. Other immunological factors include intrinsic B-cell hyperactivity, anti-T-cell auto-antibodies, and complement deficiencies, whereas non-immunological factors such as viruses, drugs or sex hormones are important but ill-defined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The immunological basis of inflammatory diseases. 648 71

6 girls, aged 4-16 years, with acanthosis nigricans and hirsutism were studied. Fasting and postglucose hyperinsulinism was present in the 5 older girls. In the youngest, a transitory diabetes with hyperinsulinism was induced by a cortisone therapy for hepatitis. Insulin resistance, suggested by the failure to significantly decrease blood glucose after insulin injection (0.1 U/kg), was demonstrated in three steps: (1) Patient plasma failed to bind 125I-insulin after a 5-day incubation followed by precipitation by antihuman globulin serum. (2) Specific 125I-insulin binding to rat liver membranes was identical in the presence of patient plasma and control plasma. (3) Specific 125I-insulin binding to the erythrocytes of the 6 patients (3.5-7.0%) was significantly lower (p less than 0.01) than in controls (4.5-19.5%). Moreover, the significant correlation present in controls between total binding and reticulocyte counts (r = 0.824, p less than 0.001) was absent in the patients. These data demonstrate further that, in the juvenile type of acanthosis nigricans, insulin resistance which may precede hyperinsulinism is not related to anti-insulin antibodies nor to antireceptor antibodies, but results from a primary defect of insulin receptors.
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PMID:Insulin-specific binding to erythrocytes in 6 girls with acanthosis nigricans. 648 30


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