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)

Guillain-Barre syndrome is known as one of the autoimmune disease, but the etiology, pathophysiology relating immune reaction, as well as the treatment are not established. It still causes physical handicap although its rate is low. The causes, clinical symptoms and outcome of 132 cases of Guillain-Barre syndrome have been analyzed. The patients' ages ranged from 4 months to 15 years. The antecedent events for 56.1% of the patients were known. These were upper respiratory tract infection, unexplained fever, vomiting, diarrhea, vaccination, measles, german measles, shigellosis, mumps, hepatitis, pertussis and surgery in order of frequency. The CSF protein level reached a maximum at 12.3 +/- 9.5 days. Steroids did not influence the outcome of this disease. More studies are necessary to conquer the disease.
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PMID:Guillain-Barre syndrome in Korean children. 274 76

Three patients with an histological, clinical and immunological diagnosis of chronic autoimmune (lupoid) hepatitis (CAH) and negative hepatitis B virus (HBV) markers were evaluated. The hepatic tissue of these patients, which was obtained through transjugular hepatic biopsy, was investigated with radioactive DNA probes of the previously cloned HBV and hybridized with the DNA from the mentioned tissues. In two of the three samples, viral nucleotide sequences were detected in the nuclei of the hepatocytes. Their appearance was consistent either with a free state or with the presence of integrated concatomeres. Although these findings require further evaluation in larger series, they suggest the possibility that certain proteins encoded or modified by the HBV DNA might represent a hidden antigenic stimulus in an autoimmune disease such as CAH, even in the absence of serological markers of HBV infection.
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PMID:[Unexpected presence of hepatitis B virus DNA in hepatocytes of patients with chronic autoimmune (lupoid) hepatitis]. 275 37

Common variable immunodeficiency (CVI) or hypogammaglobulinemia is a heterogeneous primary immunodeficiency disease in which B cells produce little or no antibody. Since the disease is relatively rare and the spectrum of associated illnesses is broad, patients are given care by a variety of specialists. Thus it has been difficult to determine the incidence of specific complications. In these studies we analyzed 103 consecutively referred CVI patients of age range 3-71 years (average, 29 years) who were followed for a period of 1-13 years (total of 750 patient years). The average serum IgG was 174.4 mg/dl for untreated patients and 301 mg/dl for patients treated with intramuscular immunoglobulin at the time of the first visit. The average IgA was 14.5, and the average IgM was 80.7, with no difference between or after immunoglobulin treatment. About one-half of the patients had T-cell dysfunction, but lymphocyte stimulation responses were inversely related to age, which implies worsened T-cell immunity with age. Serum IgG and IgA levels were found to be statistically associated (P = 0.008), and serum IgG was related to lymphocyte stimulation with concanavalin A (P = 0.01). By 1986, 79 patients were alive, 23 had died, and 1 could not be located. Recurrent bacterial illnesses were common to all patients, and 22% had developed chronic lung disease, 22% autoimmune disease, 15% cancer, 13% hepatitis, and 9% malabsorption. Autoimmune disease was more common in females, and cancer was more likely to develop in the fifth and sixth decades. In 11% of the group, other family members were found to be immunodeficient (hypogammaglobulinemic or IgA deficient). Nine patients died of respiratory insufficiency (with or without other complications), and seven patients died of cancer. These data provide valuable information about the immunologic abnormalities and the spectrum and frequency of illnesses associated with hypogammaglobulinemia.
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PMID:Clinical and immunologic analyses of 103 patients with common variable immunodeficiency. 278 95

We report a male patient with lupoid hepatitis who developed primary liver cell cancer 8 years after the onset of lupoid hepatitis. Primary liver cell cancer is thought to be a rare complication of lupoid hepatitis. To our knowledge, this complication has been previously reported in only 6 patients. The etiology of chronic active hepatitis is not known, but is strongly suspected to be associated with an autoimmune mechanism. There is evidence of an increased incidence of malignancy in other forms of autoimmune disease, and this may represent a further contributing factor to the development of primary liver cell cancer in cases of chronic active hepatitis.
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PMID:A case of primary liver cell cancer complicating lupoid hepatitis. 283 32

Chronic hepatitis in children should be suspected if clinical features and abnormal liver function tests persist for over one month following an episode of acute hepatitis, in children who present with relapsing hepatitis, or those presenting coincidentally with features of chronic liver disease. Specific investigation must be undertaken to define aetiology. For example, hepatitis B, Wilson's disease and alpha 1-antitrypsin deficiency must be excluded. Early histological diagnosis by an experienced histopathologist is mandatory. Chronic persistent hepatitis requires no therapy, but careful follow-up is desirable, especially for hepatitis B-positive cases. If the histological appearances are those of chronic active hepatitis, distinction between HBV-associated and autoimmune varieties is necessary. Autoimmune CAH in children differs from that in adults in that the onset is often acute, response to immunosuppressants usually favourable, and withdrawal of therapy may be successful, especially if diagnosis is established early before serious liver damage occurs. Evidence is presented to suggest that autoimmune CAH is associated with a genetic predisposition to autoimmune disease, characterized by both antigen-specific and antigen-independent T suppressor cell defects. An antibody-dependent non-T cell cytotoxicity operates against liver cell surface antigens. HBV CAH, on the other hand, may respond poorly to immunosuppressants and appropriate therapeutic regimens are not defined. There is some evidence to suggest that early diagnosis and institution of therapy in autoimmune CAH may lessen the incidence of cirrhosis on follow-up. Further studies to understand the interaction between hepatocytes, inflammatory cells and non-parenchymal cells in the process of hepatic fibrosis may provide the means of active intervention in this area in the future.
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PMID:Chronic active hepatitis and related disorders. 308 42

Monoclonal antibodies (MoAb) to L3T4 have been used successfully to suppress autoimmunity in murine models for several human autoimmune diseases. To clarify the immunologic and clinical consequences of treatment with anti-L3T4, we examined the effects of chronic administration of anti-L3T4 on the composition of lymphoid organs, the function of lymphocytes, and the histopathology of autoimmune disease in lupus-prone NZB/NZW F1 (B/W) mice. Weekly treatment with anti-L3T4 (2 mg/mouse) from age 5 to 8 months depleted L3T4+ cells from the spleen and lymph nodes, and prevented the development of splenomegaly and lymphadenopathy. The MoAb bound to target cells in the thymus and modulated their expression of the L3T4 antigen but, in contrast to its effect in extrathymic sites, anti-L3T4 did not deplete the target population from the thymus. In fact, after 3 months of therapy, mice that had been treated with anti-L3T4 had much larger thymuses than control mice that had been treated with saline, suggesting that treatment with anti-L3T4 prevented the thymic atrophy that occurs spontaneously in murine lupus. Despite depleting L3T4+ cells from the spleen, treatment with anti-L3T4 did not diminish the response of splenic lymphocytes to T and B cell mitogens, and it augmented splenic natural killer (NK) cell activity. Finally, treatment with anti-L3T4 decreased the diverse histopathologic manifestations of murine lupus. It dramatically reduced glomerular immunoglobulin and complement deposition and diminished lymphocytic infiltration and vasculitis in the kidneys. Treatment also reduced extrarenal immunopathology, including focal hepatitis and salivary gland infiltration. These observations have implications regarding the use of CD4 MoAb in people with autoimmune diseases.
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PMID:Treatment of murine lupus with monoclonal antibody to L3T4. I. Effects on the distribution and function of lymphocyte subsets and on the histopathology of autoimmune disease. 326 85

In 11 patients, sera displaying a ringlike nuclear immunofluorescent staining on sections of rat liver tissue were shown by Western blotting to contain antibodies to lamins. Sera from 8 patients contained autoantibodies reacting with lamin B, whereas sera from the other 3 patients reacted with lamins A and C. All patients (9 women and 2 men) had a chronic autoimmune disorder, which rarely fulfilled the usual criteria for a diagnosis of systemic lupus erythematosus. The disorder was characterized by acute or chronic (active or granulomatous) hepatitis; steroid-responsive blood cytopenia, often associated with a circulating anticoagulant, or anticardiolipin antibodies, or both; and cutaneous leukocytoclastic angiitis or probable brain vasculitis. Eight patients had at least two of these three conditions. Antilamin autoantibodies may thus be a marker for an unusual subset of autoimmune diseases.
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PMID:Antinuclear autoantibodies specific for lamins. Characterization and clinical significance. 328 45

The hepatitis B virus or Dane particle has been linked to hepatocellular carcinoma and is a major cause of chronic liver disease. Hepatitis B virus is found in blood and many body fluids including human tears. A 31-year-old White male was inadvertently discovered to have chronic active hepatitis secondary to a hepatitis B infection, during an autoimmune disorder work-up for recurrent episcleritis. It was also discovered that two of the patient's family members had developed chronic disease from the virus. Optometrists should be aware of the serious implications of this disease and take the proper precautions when examining hepatitis patients so that the possible risk of contracting infection through contaminated tears will be reduced.
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PMID:Hepatitis B virus in human tears: ocular examination of an asymptomatic carrier. 334 82

The morphologic characterization of portal and lobular infiltrates of chronic active hepatitis (CAH) was performed on liver biopsy sections from 18 patients: 6 HBsAg-positive/anti-delta-negative with tissue signs of hepatitis B virus (HBV) replication, 6 HBsAg-positive/anti-delta-positive with tissue signs of hepatitis delta virus (HDV) replication, and 6 HBsAg-negative without clinical or serologic evidence of autoimmune disease. No statistically significant differences were found among all the three groups of patients studied. Results from the 6 HBsAg-negative cases with T4/T8 ratio greater than 1 confirm the differences reported between this type and autoimmune forms of CAH. The lack of statistically significant differences among patients with CAH of different etiology suggests that etiologic factors play a minor role in determining the characteristics of the inflammatory liver infiltrates.
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PMID:Phenotypic characterization of mononuclear cell infiltrate in chronic active hepatitis (CAH) of different etiology. 349 52

Persistent viral infections have been postulated to be trigger factors for the development of autoimmune disease. We report the development of vitiligo in four patients with human immunodeficiency virus (HIV)-related conditions and in one patient with hepatitis who later developed both psoriasis and acquired immunodeficiency syndrome (AIDS). Other common features were hepatitis and multiple other viral infections. Ribavirin was associated with repigmentation in one patient. Vitiligo may be an example of an autoimmune disease triggered by viral infection in a genetically predisposed host.
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PMID:Human immunodeficiency virus-associated vitiligo: expression of autoimmunity with immunodeficiency? 366 11


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