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)

Haemorrhagic fever with renal syndrome (HFRS) is caused by a group of RNA viruses within the family of Bunyaviridae known as hantaviruses. The classical, severe form of HFRS is characterized by fever, headache, abdominal and lumbar pain, proteinuria, haemorrhagic phenomena, shock and renal failure. The disease is associated with the prototype Hantaan virus and occurs in rural areas of Korea and China with Apodemus mice as reservoir hosts. A clinically less severe form of HFRS, which is caused by Seoul virus, occurs in urban areas with the house rat Rattus novegicus as the main reservoir host. The disease in nonendemic areas may be atypical and patients with symptoms the hepatitis and minimal renal involvement have been observed in Malaysia. Outbreaks of HFRS in humans involving infected laboratory rat colonies have occurred in several medical centres in various countries. Hantaviruses cause a chronic, asymptomatic infection in rodents which excrete the virus in their lungs, saliva and urine. Man becomes infected mainly by inhalation of infected droplets from healthy rodent carriers. Seroepidemiological studies using mainly the indirect immunoflourescent antibody test of sera from humans and rats showed that hantaviruses have a worldwide distribution.
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PMID:Haemorrhagic fever with renal syndrome: clinical, virological and epidemiological perspectives. 289 3

Recombinant human gamma interferon (Biogen) and vinblastine were administered in a phase I study. Side effects included fever and chills, nausea and vomiting, acute symptomatic hyponatremia, reversible myelosuppression, hepatitis, transient hypotension, congestive heart failure, renal insufficiency, and nonselective proteinuria. In most patients, additional host factors contributed to these toxic effects. Side effects occurred despite dose reduction; therefore, protocol accrual was prematurely closed. No correlation between serum concentrations and toxicity was noted. Median serum vinblastine concentration was 1.04 ng/ml; median serum interferon concentration was 17.3 IU/ml.
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PMID:Hyponatremia and other toxic effects during a phase I trial of recombinant human gamma interferon and vinblastine. 309 Dec 46

Using enzyme-linked immunosorbent assay technique (Boehring Institute Laboratory), eighty-one adult patients were studied for hepatitis Bs antigenaemia. Nine of the patients had asymptomatic persistent proteinuria, thirty-nine, nephrotic syndrome, and thirty-three had profuse proteinuria, azotoaemia and hypertension. The histopathology obtained in forty showed twenty-two with MCGN, four with focal glomerulosclerosis, three with proliferative glomerulonephritis, one with minimal change glomerulonephritis and ten with end-stage kidney disease. None of the patients had apparent clinical evidence of liver disease nor a past history of jaundice. One hundred and eighty apparently normal adults served as controls; 33.3% of the patients had positive hepatitis Bs antigenaemia, in contrast to 6% (P less than 0.001) in the normal controls. Hepatitis Bs antigenaemia was more prevalent in the groups with nephrotic syndrome and persistent asymptomatic proteinuria than in the group with advanced renal failure. Hepatitis Bs antigenaemia was detected in all histopathologic forms but was most prevalent in the MCGN (P less than 0.001) which is also the more commonly encountered lesion. The implications of these findings are discussed.
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PMID:Role of hepatitis Bs antigen in chronic glomerulonephritides in Nigerians. 608 37

A phase I-II study of KW2083, an analog of mitomycin C (MMC) was performed in a total of 22 patients. KW2083 was escalated by single intravenous administration of 40, 50, 60, 70, and 80 mg/m2 doses. Treatments were repeated every 4-6 weeks unless unacceptable toxicities occurred. The median times taken to reach nadir for each dose level were 9-12 days for leukocytes and 7-13 days for platelets respectively. The median times taken for recovery were 8-22 days for leukopenia and 10-37 days for thrombocytopenia. Variable and non-predictable hematological toxicity was observed in some cases. Biphasic hematological toxicity was observed in 4 courses. Acute toxicity occurred in 17 courses for 11 patients and consisted of nausea (44%), vomiting (13%), diarrhea (2.7%) and stomatitis (2.7%). Nephrotoxicity (elevation of BUN, 8.1% and proteinuria, 5.4%) occurred in 3 patients who had no previous impairment of renal function. Alopecia (8.1%) was also observed. Marked elevations of hepatic enzymes were noted in one patient who developed acute fulminant hepatitis with the second dose of KW2083. Objective response was observed in one of 20 evaluable patients. From this preliminary study, the maximum tolerable dose is 70 mg/m2 and the optimal dose of KW2083 was determined to be 50 mg/m2 at 6-week intervals. KW2083 has been introduced as an MMC analog of potential interest. However, hematological and non of hematological toxicities are very similar to those of MMC and does not appear that KW2083 will supersede MMC.
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PMID:[Phase I-II study of 7-N-(P-hydroxyphenyl)-mitomycin C (KW2083, M83)]. 647 44

Immunological aspects of 40 northern Nigerian children with nephrotic syndrome of recent onset are reported. Eight our of 30 had hepatitis-associated antigen in their sera. Hypocomplementaemia was rare. Measurement of serum C3, C4, and ASOT was not of diagnostic value. Proteinuria selectivity index was poor in half of the patients, and appeared t o depend on the severity of the kidney lesion. Abnormal immunofluorescence of kidney glomeruli to immunoglobulins, complement, Plasmodium malariae, and Plasmodium falciparum was found in 26 of the 29 children. The pattern of immunofluorescence was chiefly granular and was confined to the glomeruli. IgM was predominant. It was concluded that immunological reaction is involved in the pathogenesis of nephrotic syndrome in northern Nigerian children.
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PMID:Immunological aspects of nephrotic syndrome in northern Nigeria. 701 Dec 14

The nature of circulating immune complexes (CIC) which appear in patients with type B hepatitis was investigated using a method of Raji cell fluorescent immunoassay. CIC were found in seventeen of thirty-five cases (48.6%) with HBs antigen (HBsAg)-positive liver diseases (4/8 cases with acute hepatitis, 9/18 cases with chronic hepatitis, and 4/9 cases with liver cirrhosis), whereas no CIC were detectable in sera of ten asymptomatic, healthy carriers with HB virus. Among the seventeen cases with CIC-positive liver diseases, HBs antigen-antibody immune complexes (HBsIC) were demonstrated in eleven (65%). A high incidence (54%) of proteinuria was observed in patients with CIC-positive liver disease compared to those without them (10%). Moreover, 83% of patients with HBsIC were associated with proteinuria. A case of fulminant type B hepatitis showed high titers of both CIC and HBsIC during the acute phase of the disease; in the recovery stage, the titers decreased to within normal ranges. These results demonstrate that HBsAg is a possible antigen in CIC during type B hepatitis. Determination of serum HBsIC is significant for the clinical evaluation of HB virus-related liver diseases.
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PMID:Significance of circulating HBs antigen-antibody immune complexes in patients with HBs antigen-positive liver disease. 711 81

Fifty-five renal allografts (44 from living-related and 11 from cadaver donors) that have functioned for at least 20 years (mean 22.9 +/- 2.3, range 20.1 to 30.7 years) were evaluated in three groups based on renal function: group I (n = 26), with a GFR of > or = 60 ml/min/1.73 m2 or serum creatinine < or = 1.4 mg/dl and no proteinuria; group II (n = 9), with a GFR of > or = 60 ml/min/1.73 m2 or serum creatinine < or = 1.4 mg/dl but > 150 mg proteinuria/24 hr; and group III (n = 20), with a GFR < 60 ml/min/1.73 m2 and/or serum creatinine > 1.4 mg/dL with or without proteinuria. Allograft factors, including acute rejection (AR) in 62% (34/55) and delayed function (DF) in 55% (6/11) of the cadaver grafts, did not preclude 20-year success and the prospect of continued survival since they were not significantly more frequent in group I, II, or III. However, AR was confined to a limited period within the first three months posttransplant in 18/18 recipients in groups I and II but only in 7/16 of group III (P = 0.0002). In groups I and II AR was treated with IVMP in 14/18 cases and only 6/16 in group III (P = 0.035). Donor age < or = 50 years and recipient age < or = 40 years each occurred in 87% (48/55) of these transplants. One- or two-HLA haplotype matching was present in 98% (43/44) of living related transplants. Major risks to the recipient were coronary artery disease (11 cases and 3 deaths), malignancy (18 cases and 1 death), and severe infection and hepatitis (35 cases and 3 deaths, 2 of whom also had coronary artery disease). Hypertension occurred in 25 recipients and diabetes mellitus in 12. Potential open-end success was compromised by renal dysfunction in groups II and III, but appeared possible in 12 of the 26 patients in group I. There is no apparent "safe-haven" point of time for immunosuppressed renal allograft recipients, who remain at increased risk for eventual renal allograft dysfunction, as well as cardiovascular, neoplastic, infectious, and metabolic diseases. In order to clarify and standardize the words "long-term," a simple classification of long-term allograft survivals is proposed.
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PMID:The fate of renal allografts functioning for a minimum of 20 years (level 5A)--indefinite success or beginning of the end? A proposed classification of long-term allograft survivals. 748 35

Since their initial description in 1957, the interferons (IFNs) have been increasingly used to treat a wide array of diseases. Acute adverse effects, i.e. 'flu-like' syndromes, hypo- or hypertension, tachycardia, headache, myalgias and gastrointestinal disorders, occur within the first hour or day after starting treatment. They are seldom treatment-limiting and are easily manageable. Sub-acute and chronic effects develop after several days, usually within 2 and 4 weeks of therapy. The most typical is neurological toxicity, including fatigue/asthenia, and behavioural and cognitive changes. Such symptoms may seriously impair quality of life and result in treatment discontinuation. Seizures have seldom been described. Other infrequent central nervous system adverse effects include vertigo, cramp and oculomotor nerve paralysis. Distal paraesthesias and peripheral neuropathy have been reported. IFN-associated autoimmunity is quite rare but a matter of concern. Biological or clinical manifestations usually require several months to become apparent. Autoantibodies have been shown to develop in most patients but have been inconsistently associated with clinical symptoms of systemic lupus erythematosus, rheumatoid-like arthritis and thyroiditis. Both hypo- and hyperthyroidism have been described but are usually reversible. Other infrequent autoimmune reactions include diabetes, pemphigus and worsening of multiple sclerosis. Although several patients present with a pre-existing autoimmune disorder, no predisposing factor has been clearly established. While hypotension and tachycardia are the most frequent acute cardiovascular complications, a few additional cases of cardiac arrhythmias and myocardial ischaemia have been reported after a short course or several weeks of treatment. These latter complications do not appear to be dose-dependent or age-related. Isolated cases of congestive heart failure have also been described. Mild proteinuria has been observed in 15 to 25% of patients, but acute renal toxicity is uncommon. A transient rise in serum aminotransferase levels is frequently noted during the first stage of therapy, especially in patients receiving the highest dosages. Direct hepatotoxicity is extremely rare. Autoimmune hepatitis, which is ill-diagnosed as chronic viral hepatitis, and de novo induction of autoimmune hepatitis, account for the majority of liver diseases. Haematotoxicity is relatively common but mild to moderate, and develops gradually during the first weeks of treatment. Neutropenia is the most common haematological toxicity, but is usually not dose-limiting and resolves rapidly upon drug discontinuation. Myelosuppression, autoimmune and immune allergic haemolytic anaemias and thrombocytopenias have seldom been described. Cutaneous adverse effects comprised nonspecific erythema and hair loss and, less frequently, vasculitis, local ulcerations at the site of injection and exacerbation of psoriasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical toxicity of the interferons. 751 63

Hepatitis C virus (HCV) infection is one of the important causes of chronic and severe hepatitis in China. In an attempt to understand if there is any relationship between HCV infection and glomerulonephritis (GN), serum samples from 570 GN patients and 100 normal volunteers were screened for anti-HCV antibody (HCV-Ab) with ELISA method. Among the cases with positive HCV-Ab, serum HCV-RNA was tested with nested RT-PCR method. The incidence of serum HCV-Ab was 2 in 100 normal volunteers (2%) and 34 in 570 GN patients (6%). The incidence of positive serum HCV-RNA was 0 in normal volunteers whereas 21 in GN patients. The main clinical manifestation of GN patients with serum positive HCV-Ab was an unique proteinuria with/without nephrotic syndrome or renal failure, whereas the pathologic lesions in GN patients with serum positive HCV-Ab or HCV-RNA consisted of different disease entities. There was no close link between MPGN and active HCV infection. From the data observed, it seems that there is a coincidence between glomerular diseases and HCV infection rather than a matter of cause and consequence.
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PMID:[Is there hepatitis C virus associated glomerulonephritis?]. 753 65

Hepatitis C virus (HCV) is the leading cause of non-A, non-B hepatitis among renal allograft recipients. We sought to identify and describe a proteinuric renal disease occurring in our HCV-infected renal transplant patients. Patients with proteinuria exceeding 1 g/day were identified from a cohort of 98 HCV-infected kidney recipients. Qualitative and quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and restriction fragment-length polymorphism of the amplified RT-PCR product was performed to detect circulating HCV RNA, viral titer, and strain type, respectively. An immune complex nephritis (ICN) of the membranoproliferative pattern (MPGN) was found on five of eight biopsies. Two patients infected with the Hutch strain-type developed nephrotic-range proteinuria within three months posttransplant while the remaining three MPGN patients had been transplanted greater than 5 years prior to the onset of proteinuria. Testing for rheumatoid factors, cryoglobulins, hypocomplementemia, and circulating immune complexes failed to show a consistent pattern. Sucrose density gradient (SDG) equilibrium centrifugation was used to determine the buoyant-density of HCV virions from control (HCV-infected nonproteinuric recipients; n = 5) and nephrotic patients (n = 5). Whereas HCV virions from the control patients had a low buoyant density on sucrose gradients, a substantial percentage of the circulating HCV RNA from the MPGN patients was present in the high-density fractions in association with IgM and IgG. Treatment of the pooled high-density layers with NP40 followed by recentrifugation resulted in a shift of the HCV RNA to the medium-density layers. In conclusion, MPGN developed in five HCV-infected kidney recipients despite pharmacologic immunosuppression. Both the physicochemical properties of the HCV virions on SDG and their association with IgG and IgM in the high-density layers provide indirect evidence for the presence of circulating complexes of anti-HCV antibody and HCV antigen(s).
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PMID:De novo membranoproliferative glomerulonephritis in hepatitis C virus-infected renal allograft recipients. 754 75


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