Antibody seronegative human T-lymphotropic virus type III (HTLV-III)- infected patients with acquired immunodeficiency syndrome or related disorders

The human T-lymphotropic virus type III (HTLV-III) is the primary cause of the acquired immunodeficiency syndrome (AIDS) and related disorders (ARC). Prior studies have reported that nearly all symptomatic patients with AIDS or ARC manifest antibody to HTLV-III. This observation has engendered efforts to screen for HTLV-III, especially prior to blood donation, with assays for antibody to HTLV-III. We report the first two cases, one with AIDS and one with ARC, that are HTLV-III virus positive but antibody negative. Accurate diagnosis of HTLV-III infection in some cases may require direct virus culture or tests for antigen. In addition, lack of HTLV-III antibody may indicate an atypical clinical course of AIDS.     

The double contrast barium enema: a retrospective single centre audit of the detection of colorectal carcinomas.

AIM: To determine retrospectively the sensitivity and specificity of the double contrast barium enema (DCBE) as performed in one institution for the detection of colorectal carcinoma. SUBJECTS AND METHODS: Eight hundred and eighty barium enema reports were reviewed of consecutive adult patients who underwent DCBE and also had hospital case notes with a minimum follow up of two years, a later diagnostic colonoscopy, or operative and histological findings. RESULTS: Seventy-four true positive cases of colorectal carcinoma diagnosed at DCBE were confirmed at surgery and histological examination. There were four false positive diagnoses of carcinoma at DCBE. Eight false negative cases at DCBE were demonstrated within a two-year follow-up period. The sensitivity of the DCBE for detecting colorectal carcinoma was therefore 90.2% and the specificity was 99.5%. CONCLUSION: DCBE is a sensitive and highly specific investigation for the detection of colorectal carcinoma.     

Acute Polymyositis Following Renal Transplantation

Myositis is a rare complication following renal transplantation and is most commonly the result of drug-mediated myotoxicity. Other causative disorders include viral infection, electrolyte imbalance and myositis of autoimmune origin. We describe a 60-year-old patient who developed acute polymyositis 4 weeks after a 000 human leukocyte antigen (HLA) mismatch cadaveric renal transplant. Following an uncomplicated transplant course with maintenance triple immunosuppression (prednisolone, mycophenolate mofetil and cyclosporine), the patient presented with severe symmetrical proximal muscle weakness associated with a rise in serum creatine kinase to 46800 U/L. Electromyography confirmed myopathic changes and muscle biopsy demonstrated extensive muscle-fiber necrosis with an inflammatory infiltrate. There were no obviously culpable drugs and viral studies were negative. Prompt initiation of high-dose steroid therapy led to clinical and biochemical recovery. Acute polymyositis may occur following renal transplantation. Potential mechanisms include viral antigen transmission or a localized form of graft vs. host disease.