The Gay Bowel Syndrome

Our experience in the management of 260 male homosexuals with coloreetal problems is described. The increased incidence of amebiasis, shigellosis and hepatitis, specific and nonspecific protocolitides, venereal disease and anal warts, is emphasized. It is important to recognize homosexual patients and the conditions to which they are predisposed.     

IMMUNOHISTOCHEMICAL ASSAY FOR OESTROGEN RECEPTORS IN PARAFFIN WAX SECTIONS OF BREAST CARCINOMA USING A NEW MONOCLONAL ANTIBODY

The aim of this study was to evaluate the utility of a new monoclonal antibody (AER311) that targets the oestrogen receptor (ER) in an immunohistochemical assay (IHA) applied to breast cancers. Ninety-seven cases of invasive ductal carcinoma were studied by AER311-IHA using a pressure-cooking antigen retrieval technique applied to formaldehyde-fixed, paraffin-embedded tissue sections; immunostaining was assessed by semi-quantitative scoring ( H score). There was 80 per cent concordance between the ER status measured by dextran-coated charcoal (DCC) assay and AER311-IHA, with 63/97 (65 per cent) tumours positive and 15/97 (15 per cent) tumours negative by both assays. Of the 12 DCC-positive cases that were negative by AER311-IHA, 11 were borderline positive (3–8 fmol/mg). Similarly, six of seven DCC-negative cases that scored positive by AER311-IHA had only borderline positive H scores (<50). When AER311-IHA was compared with 1D5-IHA, there was good concordance in ER status (77 per cent) and a significant correlation ( r =0·7, P <0·001) between H scores. Nevertheless, the correlation between ER level determined by AER311-IHA and that measured by DCC ( r =0·53, P <0·001) was higher than that for 1D5-IHA ( r =0·32, P =0·002). AER311-IHA can therefore provide reliable information about the ER status of breast carcinoma on paraffin sections and is an acceptable alternative to other commercially available monoclonal antibodies.     

The Diagnosis of Alcohol and Cannabis Dependence in Cocaine Dependents and Alcohol Dependence in their Families

Genetic research in alcoholism has made major advances in recent decades. Twin, adoption, high-risk and familial studies have demonstrated an inheritance factor in alcoholism. Few studies have demonstrated a genetic predisposition to cocaine and cannabis dependence. Two hundred and sixty-three inpatients were given a structured psychiatric interview retrospectively (180) and prospectively (113) to obtain DSM-III-R diagnosis of cocaine, alcohol and cannabis dependence disorders in the inpatients and of alcohol dependence in family members. Our study reveals a large number of cocaine dependents with a positive family history for alcohol dependence. Approximately 50% of cocaine addicts had at least a first or second degree relative with a diagnosis of alcohol dependence when studied by the family history and study methods. As many as 89% of cocaine dependents diagnosed by DSM-III-R criteria for cocaine dependence qualified for other alcohol and drug dependence diagnoses. Our study finds a high prevalence of alcohol (67% and 89%) and cannabis dependence (51% and 46%) in patients with cocaine dependence. Previous reports regarding alcohol and other drug dependence among cocaine dependents and their families are few and inconclusive. The diagnosis of other drug and alcohol dependence in cocaine dependence and in family members of cocaine dependents has important impact on etiology, prognosis and treatment.     

Alcoholic and Non-alcoholic Liver Disease in Relation to Alcohol Consumption in Scotland, 1978–84.

A common strategy in epidemiological studies linking alcohol consumption in the general population with liver cirrhosis mortality is to use non-specific cirrhosis mortality rates in which alcoholic and non-alcoholic causes of death are not distinguished. Evidence is presented from Scottish mortality data for 1979 to 1984 that the two forms of cirrhosis have quite different epidemiological profiles. Similar findings emerge from morbidity data. The two forms of disease should be distinguished in future studies in which liver cirrhosis is used as a proxy for consumption, despite the manifest shortcomings of currently available data.     

EXCRETION OF BILE ACIDS IN ERYTHROBLASTOSIS FOETALIS

The excretion pattern of intramuscularly injected cholic acid-24–¹⁴C was studied for 4 days after the injection in 10 cases of erythro-blastosis (EB). Seven patients with EB and raised serum conjugated bilirubin excreted 3643% of the injected isotope in the urine, whereas the amounts of isotope in the faeces varied greatly. In 3 cases without raised serum conjugated bilirubin less isotope was recovered in the urine and always more than 10% of injected isotope was recovered in the faeces. Cholic acid-24–¹⁴C was excreted essentially unchanged in all cases but in conjugated form. In all cases of EB the urine was found to contain bile acids, chiefly cholic acid. The infants with EB associated with cholestasis excreted 4.8–132.3 μmol of these acids per day; the corresponding values in the absence of cholestasis being 0.4–0.9 μmol per day. In the infants with physiological jaundice the excretion ranged from less than 0.01 to 0.7 μmol per day; the correspondign values in the 2 patients with hyperbilirubinaemia were about 0.2 μmol per day. The infants with EB associataed with cholestasis were found to excrete as large amounts of bile acids in the urine as the infants with intrahepatic cholestasis. These findings strongly suggest that increased serum conjugated bilirubin, irrespective of the patho-genesis of the liver damage, is associated with an impaired bile acid excretion to the intestine. EB without increased serum conjugated bilirubin did not seem to alter the bile acid metabolism, since the urinary excretion of cholic acid and chenodeoxycholic acid in these cases was practically the same as in jaundiced newborn infants.     

EXCRETION OF BILE ACIDS IN EXTRAHEPATIC BILIARY ATRESIA AND INTRAHEPATIC CHOLESTASIS OF INFANCY

This series included 24 infants, 16 boys and 8 girls, who were admitted to hospital with the diagnosis of obstructive jaundice. Five of the infants were subsequently found to have extra-hepatic biliary atresia (BA) and the other 19 infants intrahepatic cholestasis of infancy (IHC). The infants were investigated given special attention to: the quantitative urinary excretion of cholic and chenodeoxycholic acids, the isotope excretion after intramuscular injection of cholic acid-24–¹⁴C, the nature of labelled urinary bile acids, the half-life and the pool size of cholic acid. At the first examination of the infants after admission the urinary excretion of cholic and chenodeoxycholic acids varied greatly between the patients. However, on comparing the values obtained in the two groups, it was found that there was virtually no difference between the mean daily values of cholic and chenodeoxycholic acids in urine, and the ratio cholic to chenodeoxycholic acid between the BA group and the IHC group. After the injection of isotopic cholic acid most of the isotope was recovered in the urine in all cases. In the infants with BA the faecal excretion of the isotope was low, being less than 3 per cent of the injected isotope. Out of the 19 infants with IHC the recovery of the injected isotope in faeces was also less than 3% in 11 infants. In 8 infants with IHC the faecal isotope excretion was significantly high to exclude extrahepatic biliary atresia. The first 24 hour urine specimen contained small amounts of unconjugated labelled cholic acid in all cases whereas in no case did the patients excrete unconjugated labelled cholic acid 48 hours after the injection of the isotope. No transformation of cholic acid was observed. There was no difference between the BA group and IHC group with regard to the percentage labelled glycine conjugates of total excreted urinary conjugates. Neither was there any difference between the two groups with regard to half-life and pool size of cholic acid. There was no difference with respect to the bile acid metabolism between infants with congenital CMV infection, decreased serum concentrations of alfal-antitrypsin and the other patients.     

EFFECTS OF A FEMINIZING TESTICULAR LEYDIG CELL TUMOUR ON NONTUMOROUS TESTICULAR TISSUE: AN ULTRASTRUCTURAL STUDY

The ultrastructural effects of a Leydig cell tumour of the testis on nontumorous testicular tissue have not yet been reported. Described here are the electron microscopic findings in the nonneoplastic testicular tissue of a patient with a feminizing testicular Leydig cell neoplasm. Serial studies were carried out over a period of 3 1/2 years prior to removal of the tumour. The overall general picture was characterized by progressive degeneration of Leydig cells, cells of the germinal series and Sertoli cells. Concomitantly, there was increasing thickening and fibrosis of the tubular walls. Cytoplasmic focal accumulations of glycogen, increasing with the duration of the disease, were conspicuous in many spermatogonia. All of these alterations are nonspecific and are attributable to adverse endocrine effects introduced by the oestrogen-secreting tumour. They were present bilaterally and were more prominent on the tumour-bearing side. Attention is drawn to the role of artifacts, fixation technique and degenerative processes in the production and appearance of certain ultrastructural findings, such as ‘light’ and ‘dark’ cells, myelin figures, membranous whorls and focal glycogen accumulations.     

Bile acid synthesis and excretion following release of total extrahepatic cholestasis by percutaneous transhepatic drainage

Abstract. Urinary, biliary and serum bile acids were studied in three patients before and after percutaneous transhepatic drainage for total bile duct obstruction.
Before drainage high urinary excretion often different bile acids occurred. The percentage distribution was: cholic and chenodeoxycholic acid (66–86%), hyo-cholic (3–16%), 3β 12α-dihydroxy-5-cholenoic (3–6%) and 3β-hydroxy-5-cholenoic acid (2–8%). These acids were regularly found in serum. In addition small amounts (less than 2%) of norcholic, allocholic, 3β, 7α-dihydroxy-5β-cholanoic, 3α, 7α-dihydroxy-5α-cholanoic and lithocholic acid were excreted in urine. Trace amounts of these bile acids were found in serum.
After start of drainage biliary bile acid excretion increased rapidly during the first day, dropped to a minimum during the second or third day and then slowly increased again. In spite of normal volumes of bile produced, the total serum bile acids and the urinary excretion of bile acids remained increased during a drainage period of 19 days. The bile acids were of the same type as observed during cholestasis. In serum the increase was mainly due to high concentrations of chenodeoxycholic and 3β-hydroxy-5-cholenoic acid, as sulphate esters.
Glycine and taurine conjugates of cholic, chenodeoxycholic and hyocholic acid were mainly excreted in bile. Bile acid sulphate esters were only present in trace amounts in bile and were mainly excreted in urine. This, combined with low renal clearance, explains the elevated serum levels of sulphate esters of chenodeoxycholic and 3β-hydroxy-5-cholenoic acid conjugates.