PERINEAL PROCTECTOMY FOR RECTAL PROLAPSE IN ELDERLY AND DEBILITATED PATIENTS

This paper details the indications, operative technique and results of perineal proctectomy in the management of complete rectal prolapse in a high risk, elderly and debilitated group of patients. Eighteen procedures were performed by one surgeon (A.L.P.) on 16 consecutive patients over a 5 year period. Data collection was via: (i) retrospective analysis of hospital and office records; and (ii) response to a postal questionnaire by the patient, a relative or attending nursing staff. There were 14 females and two males with a mean age of 81 years. All patients had significant associated medical conditions. The interval from the time of a surgical procedure until review varied from 3 to 37 months with a mean follow-up period of 16 months. Total hospital stay varied between 6 and 20 days with a mean of 7 days. Eleven procedures were performed under general anaesthesia and seven under spinal anaesthesia. There was no postoperative mortality. One patient suffered an anastomotic haemorrhage that required operative intervention and another patient suffered a rectal stricture that necessitated dilatation. Two patients were re-operated for recurrent symptomatic prolapse at 34 and 36 months after the initial procedure. Continence improved in seven patients, worsened in one and was unchanged in the remaining patients. Fifteen of 16 patients were considered to have had a successful result from the operation with satisfactory control of the symptom of rectal prolapse. Perineal proctectomy is a low risk operative procedure for the elderly and debilitated group of patients in controlling complete rectal prolapse. If the condition recurs, the procedure can be repeated with equally low morbidity.     

Demonstration of a capsule plasmid in Bacillus anthracis

Virulent and certain avirulent strains of Bacillus anthracis harbor a plasmid, designated pXO2, which is involved in the synthesis of capsules. Two classes of rough, noncapsulated (Cap-) variants were isolated from the capsule-producing (Cap+) Pasteur vaccine strains ATCC 6602 and ATCC 4229. One class was cured of pXO2, and the other class still carried it. Reversion to Cap+ was demonstrable only in rough variants which had retained pXO2. Proof that pXO2 is involved in capsule synthesis came from experiments in which the plasmid was transferred by CP-51-mediated transduction and by a mating system in which plasmid transfer is mediated by a Bacillus thuringiensis fertility plasmid, pXO12. Cells of Bacillus cereus and a previously noncapsulated (pXO2-) strain of B. anthracis produced capsules after the acquisition of pXO2.     

Small vessel vasculitis caused by hepatitis B virus immune complexes: Small vessel vasculitis and HBsAg

In a comprehensive study of 80 patients with vasculitis, 4 had concurrent hepatitis B virus (HBV) infection. Polyarteritis nodosa was present in 2 and in the other 2, cutaneous vasculitis, presenting clinically as palpable or Henoch-Schönlein purpura. In one of these patients skin biopsies demonstrated granular deposits of IgM, C3, C4, and the hepatitis B surface antigen (HBsAg) and electron-dense deposits of aggregated 20-nm particles resembling HBsAg in postcapillary venules. Evidence for circulating HBsAg-immune complexes included increased serum C1q binding activity, decreased serum complement, and a cryoprecipitate containing both HBsAg and IgM anti-HBs. Aggregated 20-nm particles resembling intact HBsAg were also seen by negative staining electron microscopy of the serum cryoprecipitate. This patient fulfills all the criteria for a specific immune complex vasculitis caused by his immune response to a chronic HBV infection. These findings emphasize that HBV infection may be associated with small vessel vasculitis as well as polyarteritis nodosa, mixed cryoglobulinemia, and glomerulonephritis. A similar immune response to other viral infections may be expressed as palpable (Henoch-Schönlein) purpura also.     

Eosinophil-activating factor (EAF) production by a human cell line (ESH 98) stimulated with tumour necrosis factor.

A new cell line has been produced by fusing human cervical keratinocytes with HeLa cells. This cell line secretes eosinophil-activating activity upon stimulation with tumour necrosis factor (TNF). About one-third of the eosinophil-activating activity co-purifies with eosinophil-activating factor (EAF) from mononuclear cell supernatants. The purification procedure indicates that it resembles EAF in molecular weight and acidity. It also resembles EAF in its effect on eosinophils. Not only does it enhance the cytotoxic activity of eosinophils to antibody-coated schistosomula of Schistosoma mansoni, but it also increases the oxidative activity of eosinophils, as measured by reduction of nitroblue tetrazolium, and changes the morphology of eosinophils, affecting the distribution of F-actin in the cell.