Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty cases of diseased kidneys at end-stage were studied by fluorescent antibody technique in search for viral etiology of glomerulonephritis and other renal diseases. Among these 40 cases, 12 (30%) were ascribed to immune complex disease because of detection of immunoglobulins and complement in glomeruli of the same kidney specimen. In 8 cases (20%) only complement was detected in glomeruli. In the remaining 50% neither complement nor immunoglobulin deposit was found in glomeruli. The etiologies of the latter cases remain unknown. Of 12 cases of kidney disease of immune complex origin, hepatitis virus type B surface antigen was detected in 2 cases. In these 2 cases the magnitude of immune complex deposits with complement was greater than that of other cases. Other than hepatitis B virus antigen, no other viruses including Coxsackieviruses, ECHO viruses, and HSV-1 could be detected by indirect fluorescent antibody techniques. The proportion of complement deposit to the deposition of complement with immune complex in the diseased kidneys at end-stage was calculated and statistically analyzed.
 ...
PMID:Fluorescent antibody study of diseased, end-stage human kidneys. 35

The epidemiologic, clinical and laboratory features of 40 adults with acute viral hepatitis type B were compared with those of 40 adults with hepatitis non-B. Overall, the clinical presentations were remarkably similar and the etiology could not be determined in individual cases. An exception to this was that all post-transfusion cases in this series were affected by hepatitis B. Men predominated in both the hepatitis B and non-B groups. There was a tendency to seasonal clustering in summer/autumn in both groups. Hepatitis B patients were significantly older and 59% of them had a history of possible parenteral exposure during the six months preceding admission. On the other hand 76% of patients with hepatitis non-B had no apparent parenteral exposure. Dental treatment, injections and contact with jaundiced patients were recorded in both groups and were therefore of no value in determining the exact etiology in individual cases. Fever was more common in hepatitis non-B, while the onset of the disease was insidious and afebrile in 80% of patients with hepatitis B. As a group, patients with hepatitis B had more extensive liver injury and a more prolonged clinical course, and the only fatality was in this group. Cholestatic features were rare and extrahepatic immune complex disease was extremely uncommon in both hepatitis B and non-B.
 ...
PMID:A comparative study of hepatitis B and non-B in hospitalized adults in an endemic area. 83 75

Repeated episodes of febrile panniculitis and hepatitis were the main clinical features in two patients with an IgG1 kappa paraproteinemia and severe depletion of the early components of the classical pathway of complement (acquired C1 inhibitor deficiency). They did not have episodes of cutaneous angioedema or evidence of immune complex disease. In the more severely affected patient, the episodes responded to steroids. These features have not been described with acquired C1 inhibitor deficiency and may be related to complement activation.
 ...
PMID:Recurrent febrile panniculitis and hepatitis in two patients with acquired complement deficiency and paraproteinemia. 311 12

Human hypersensitivity angiitis is an immune complex disease in which patients present with palpable purpuric lesions of the skin and may often have multiple organ involvement. The antigen may be derived from an infectious organism such as the hepatitis virus, streptococcus, or a drug, and complexes with antibody. Under circumstances of vascular turbulence or vessel wall dilatation this complex may become fixed, activating the complement sequence with elaboration of chemotactic factors for neutrophils. These cells release lysosomal enzymes resulting in vessel wall destruction. Red blood cells leak into the tissue producing purpura and the inflammatory infiltrate accounts for the palpability. Although many patients have skin lesions only, others may have involvement of joints, gastrointestinal tract, kidneys, and even the lungs. The central question in the pathogenesis of this disease is why the immune complex is so selective in its site of deposition. Part of the reason must be related to the lattice formation of a particular complex, while other reasons are related to host factors of altered vascular permeability, integrity of clearance mechanisms or even a genetically determined defect of the phagocytic system.
 ...
PMID:Human hypersensitivity angiitis, an immune complex disease. 315 5

A sensitive and reproducible procedure for the detection of soluble immune complexes in sera from patients with various immunopathological disorders is reported. Radiolabeled C1q is reacted with sera containing immune complexes. Separation of free from complex bound [(125)I]C1q is achieved by selective precipitation with polyethylene glycol (PEG). The method is based on both the large molecular size and the C1q-binding property characterizing immune complexes. The minimal amount of aggregated immunoglobulins thus detected is about 10 mug and that of soluble human IgG-anti-IgG complexes is about 3 mug of complexed antibody. Some immune complexes formed in large antigen excess (Ag(2)Ab) can still be detected by this radiolabeled C1q binding assay. The specificity of the radiolabeled C1q binding test was documented by the inability of antigen-F(ab')(2) antibody complexes to lead to a precipitation of [(125)I]C1q in PEG. In a second step, this radiolabeled C1q binding assay was applied to an experimental model of immune complex disease and was shown to be efficient for the detection of in vivo formed immune complexes.Finally, the technique could be applied to the study of sera from patients with systemic lupus erythematosus (SLE) or to carriers of the hepatitis B antigen (HB-Ag). Significantly increased [(125)I]-C1q binding values were observed in 52 sera from SLE patients when compared to values obtained with healthy blood donors (P<0.001). Particularly high values were seen in active disease, a finding which was confirmed by follow-up studies performed with four SLE patients. No increased [(125)I]C1q binding was seen in 18 healthy carriers of the HB-Ag; whereas, sera from carriers with hepatitis appear to precipitate increased [(125)I]C1q percentages: 7/24 cases with acute transient and 4/7 cases with chronic persistent hepatitis were found to increasingly bind [(125)I]C1q. The results were also used for a correlative study of [(125)I]C1q binding to IgG levels in the sera but increased [(125)I]C1q binding could not be attributed to high serum IgG levels which are likely to account for gammaglobulin aggregates. These examples suggest the utility of the radiolabeled C1q binding assay for the evaluation of immune complex diseases in human pathology.
 ...
PMID:Circulating immune complexes in the serum in systemic lupus erythematosus and in carriers of hepatitis B antigen. Quantitation by binding to radiolabeled C1q. 484 46

The incidence and amount of immunoglobulin (Ig)-bound hepatitis B associated surface antigen (HBs) has been determined in various forms of hepatitis B, using radioimmunological techniques. Both the total concentration of HBs and that of Ig-bound HBs were measured in serum samples from 54 patients with acute hepatitis B, 28 with chronic hepatitis and 28 healthy chronic carriers. The following observations were made: (1) Ig-bound HBs was detected in 79% of patients with acute hepatitis B in one or several samples; the highest level of Ig-bound HBs was observed 60-120 days after the onset of jaundice, while the total amount of HBs was progressively decreasing. (2) Ig-bound HBs was detected in 46% of 28 patients with chronic hepatitis. This frequency was higher in patients with chronic aggressive hepatitis (75%) than in patients with chronic persistent hepatitis (33%). The mean levels of total HBs and Ig-bound HBs are more significantly increased in patients with chronic aggressive hepatitis than in patients with chronic persistent hepatitis or healthy carriers. (3) Ig-bound HBs was detected in 46% of healthy chronic carriers. (4) The persistence of Ig-bound HBs in serum was not related to the antigen sub-type. (5) Extra-hepatic manifestations suggestive of an immune complex disease were observed in only 2 of 31 patients with chronic persistence of Ig-bound HBs. These data suggest that small amounts of HBs-antibody complexes may persist in circulating blood without always being harmful for the host.
 ...
PMID:Quantitation of immunoglobulin-associated HBs antigen in patients with acute and chronic hepatitis, in healthy carriers and in polyarteritis nodosa. 610 64

The case of a 25-year-old patient is reported who suffered from a syndrome similar to immune complex disease following cholera revaccination. The clinical picture included fever, muscle, joint and abdominal pain, vomiting, serositis, hepatitis, suspected myocarditis, anaemia and thrombocytopenia. Clinical symptoms subsided spontaneously within two weeks. This case illustrates a hazard of cholera vaccination so far not reported in the literature.
 ...
PMID:Episode resembling immune complex disease after cholera vaccination. 623 47

Human babesiosis (Nantucket fever) is a rare, tick-borne intraerythrocytic parasitic disease characterized by fever, lymphadenopathy, arthralgias, and hemolytic anemia. A 34-year-old woman, who had previously undergone surgical removal of her spleen, was hospitalized because of presumed hepatitis. The many retinal nerve fiber layer infarcts and serologic abnormalities suggested collagen disease. The diagnosis of babesiosis was established by the demonstration of intraerythrocytic parasites and a greatly elevated titer to Babesia microti. The infection was treated with chloroquine, orally administered quinine, and pyramethamine, and her symptoms resolved within one month. The retinopathy was probably the result of focal vasculitis secondary to immune complex disease caused by chronic infection.
 ...
PMID:Ocular findings in human babesiosis (Nantucket fever). 720 Mar 25

The case of a young female patient with chronic active hepatitis B, vasculitic purpura, edema, and circulating immune complexes due to mixed cryoglobulinemia is described. Serum transaminases were elevated. Serological assays showed hepatitis B surface antigen (HBsAg), antibody to hepatitis B e antigen (anti-HBe), and antibody to hepatitis B core antigen (anti-HBc) antibodies but no antibody to hepatitis C virus (anti-HCV) or antibody to hepatitis delta virus (anti-HDV) antibodies. Using hepatitis B virus-polymerase chain reaction (HBV-PCR) and direct sequencing a precore/core (preC/C) mutant unable to synthesize HBeAg was detected in serum. HBV antigens were demonstrated in the circulating immune complexes. Following 1 month of treatment with interferon-alpha 2b3 miu three times weekly, alanine aminotransferases returned to normal levels while cryoglobulins and immune complexes disappeared from serum. In addition, 2 months after the onset of treatment serum HBV-DNA was no longer detectable by PCR. Prior to treatment the analysis of cellular immune reactions of peripheral blood mononuclear cells showed a major proliferative response to HBcAg, preS1Ag and HBxAg and a minor response to HBeAg and HBsAg. One month after conclusion of treatment a decline in T-cell reactivity against all HBV antigens was observed. During clinical response to the therapy, however, a strong proliferative response of T cells to HBcAg and HBeAg was demonstrated. In conclusion, immune complex disease may complicate chronic hepatitis B in patients expressing HBe-minus HBV mutants. Treatment with interferon-alpha was found to be effective in mixed cryoglobulinemia even in the presence of HBe-minus HBV mutants.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Mixed cryoglobulinemia type II in chronic hepatitis B associated with HBe-minus HBV mutant: cellular immune reactions and response to interferon treatment. 789 64