The haemodialysis patient with night sweats, ascites, and increased CA 125.
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Ascites↗
Biomedical subjects
G Hasche
Publications and source records attributed to G Hasche.
[Hypocomplementemic urticarial vasculitis syndrome].
HISTORY AND ADMISSION FINDINGS: A 40-year-old woman was admitted with recurrent membranoproliferative glomerulonephritis. For many years she had been suffering from joint pains and attacks of angio-oedema of the upper and lower lip. Physical examination was unremarkable except for marked oedema and urticaria of the trunk and limbs. INVESTIGATIONS: Skin biopsy revealed urticaria with vasculitis. Complement fractions C3, C4 and C1q were reduced, and C1q antibodies were demonstrated. DIAGNOSIS, TREATMENT AND COURSE: The findings of urticaria with vasculitis and reduced complement levels as cardinal symptoms together with joint pains, glomerulonephritis and C1q antibodies as minor symptoms were diagnostic of hypocomplementaemic vasculitic urticaria syndrome. The urticaria disappeared immediately when immunosuppressive treatment with prednisolone and cyclophosphamide was started, and the nephritic signs regressed. CONCLUSION: Differentiation of a vasculitic and a non-vasculitic form of chronic urticaria provides an initial step in delineating the underlying disease. Severe systemic disease such as collagen disease or vasculitis is not rare in vasculitic urticaria and requires long-term immunosuppression.
Adult↗
A randomized multicenter trial of the anti-ICAM-1 monoclonal antibody (enlimomab) for the prevention of acute rejection and delayed onset of graft function in cadaveric renal transplantation: a report of the European Anti-ICAM-1 Renal Transplant Study Group.
BACKGROUND: T-cell activation through T-cell receptor engagement requires co-stimulatory molecules and also adhesion molecules such as ICAM-1. Moreover ICAM-1 mediates leukocyte invasion from the blood into tissue during inflammatory processes. In animal studies using mouse monoclonal antibodies against ICAM-1 (enlimomab), renal allograft survival has been improved and reperfusion damage from ischemia reduced. The European Anti-ICAM-1 Renal Transplant Study (EARTS) was a randomized, double-blind, parallel-group, placebo-controlled study lastingl year and performed in 10 transplant centers in Europe. METHODS: A total of 262 recipients of cadaveric kidneys were given either enlimomab or a placebo for 6 days and were given triple immunosuppressive therapy of cyclosporine, azathioprine, and prednisolone. The primary efficacy endpoint was the incidence of the first acute rejection within 3 months, and each event was assessed by a committee including investigators and independent pathologists. RESULTS: There was no significant difference in the incidences of first acute rejection at 3 months between the placebo and enlimomab groups (39% vs. 45%), and enlimomab did not reduce the risk of delayed onset of graft function (DGF) (26% vs. 31%). Neither was there a difference in patient survival (95% vs. 91%) or graft survival (89% vs. 84%) at 1 year. Fatal events occurred in 19 (7%) patients (7 placebo, 12 enlimomab). Clinically, the most important non-fatal adverse events were infections; however, there was no statistically significant difference between the incidences in the two groups (70% vs. 79%). CONCLUSION: Short term enlimomab induction therapy after renal transplantation did not reduce the rate of acute rejection or DGF.
Acute Disease↗
[Anti-HBc IgM in acute and chronic hepatitis B virus infection].
Hepatitis B core antigen (HBcAg) synthesized in E. coli was used for determination of immunoglobulin M class-specific antibodies against HBcAg. It was found that 98% of cases with acute hepatitis B surface antigen (HBsAg) positive hepatitis type B were anti-HBc immunoglobulin M (IgM) positive. Atypical hepatitis B was detected in 33% of anti-HBc-positive HBsAg-negative cases with acute hepatitis. Anti-HBc IgM was positive for 6 months in acute resolving hepatitis type B, whereas cases resulting in chronic hepatitis B remained anti-HBc IgM-positive for up to 900 days. Chronic HBsAg carriers with severe liver disease had anti-HBc IgM more often than individuals with minor liver damage; 83% of HBsAg-positive liver cirrhoses, 63% of chronic aggressive hepatitis, 50% of HBsAg-positive liver carcinoma, but only 17% of chronic persistent hepatitis or 7% of healthy blood donors were anti-HBc IgM-positive. Determination of anti-HBc IgM is useful in detecting atypical hepatitis B virus infections without HBsAg in serum and, with some restrictions, in discriminating acute and chronic hepatitis type B.
Acute Disease↗
Use of hepatitis B core antigen produced in Escherichia coli to detect immunoglobulin M specific antibodies in an enzyme-linked immunosorbent assay.
The antigenic activity of HBcAg produced in Escherichia coli and HBcAg from human liver was compared in a mu-specific solid-phase antibody-capture assay for detection of anti-HBc-IgM. HBcAg from liver could be detected in dilutions up to 1:3, HBcAg from Escherichia coli in dilutions up to 1:10,000. Using HBcAg from Escherichia coli, sera from five patients with acute resolving hepatitis B and sera from four patients with acute hepatitis B who had developed chronic liver disease were tested for anti-HBc-IgM in ELISA. IgM fractions separated out of the same sera by immunoaffinity chromatography were tested for anti-HBc-IgM using a commercially available test. The results were in good agreement with those obtained by ELISA. Anti-HBc-IgM could be detected up to 900 days after onset of disease. Different groups of patients were tested for presence of anti-HBc-IgM in ELISA. Fifty-nine of 60 patients with acute hepatitis B were positive for anti-HBc-IgM at onset of illness. Ten of 16 patients with chronic aggressive hepatitis and seven of 23 HBsAg positive dialysis patients were also positive for anti-HBc-IgM, whereas only two of 12 patients with chronic persistent hepatitis and one of 15 HBsAg positive blood donors ("healthy" carriers of HBsAg) had detectable anti-HBc-IgM.
Enzyme-Linked Immunosorbent Assay↗
HBV-DNA in sera of patients with HBsAg-positive primary liver cell carcinoma.
Sera of ten patients with HBsAg-positive primary liver carcinoma were tested for anti-HBc-IgM and HBV-DNA. Five patients were positive for anti-HBc-IgM and six for HBV-DNA. There was no correlation between the presence of anti-HBc-IgM and HBV-DNA. Our study suggests that complete viral replication exists in some HBsAg-positive primary liver carcinomas.
Aged↗