QJM: An International Journal of Medicine

OZAWA,, TAKESHI;PLUSS,, RICHARD;LACHER,, JOHN;BOEDECKER,, EDWARD;GUGGENHEIM,, STEPHEN;HAMMOND,, WILLIAM;MCINTOSH,, RAWLE

doi: 10.1093/oxfordjournals.qjmed.a067440pmid: N/A

Abstract Three patients with clear cell renal carcinoma and one with another intrarenal malignancy were studied for the presence of glomerular localized immunoglobulins, complement components and tumor specific antigen and antibody by immunofluorescence. To determine the association and elucidate the pathogenic mechanisms involved in the relationship between tumors and glomerular deposits, antibody eluted from tumor tissue and renal glomendi, cryoproteins, serum antibodies and rabbit antisera to tumor tissue were tested for specificity to antigen. The relationship between tumor antigens and the lipoprotein antigen localized in normal proximal tubular brush border (RTE) and the small bowel mucosa, was studied by immunofluorescence, absorption and blocking studies as well as complement fixation. Immunoglobulins and complement components were localized in the glomeruli and tumor membrane of all patients. Sera and glomerular fixed antibody from three patients with renal cell carcinoma localized to normal proximal tubular brush border and jejunal mucosa as well as to tumor membrane and the glomeruli and proximal tubules of all of these three patients. Anti RTE activity was also detected by complement fixation. Immunologic similarity between RTE and renal cell carcinoma antigen was confirmed by absorption studies. Furthermore, cryoprecipitable complexes of tumor antigen and specific antibody were isolated from the serum. The tumor antibody was immunologically similar to RTE. In the other case the rabbit anti-tumor antibody and the patient's serum fixed to the tumor membrane and kidney of the patient but did not show cross reactivity with the renal cell carcinoma or RTE. These studies suggest that the tumor antigen in renal cell carcinoma is similar to RTE and the glomerular deposits represent tumor antigen and antibody complexes. In addition these investigations support the hypothesis that tumor immune complexes are significant in the glomerular lesions, and that the origin of renal cell carcinoma is in the proximal tubule. The investigations also show that tumor antibodies are specific for tumors of the same morphological type but not for other tumors in the same tissue. Moreover, the renal glomerulus appears to be a chosen anatomic site for deposition of tumor antigens and antibodies and studies of the kidney may provide insight into the nature of tumor antigens and antibodies. Cryoprecipitation appears to be a valuable method in isolation of tumor complexes and characterization of tumor specific antigen and antibody. This content is only available as a PDF. © Oxford University Press

DIXON,, K.;EXON, P., D.;MALINS, J., M.

doi: 10.1093/oxfordjournals.qjmed.a067441pmid: N/A

Abstract Seventy-two insulin-treated diabetic patients were classified on the basis of a clinical evaluation of their control of diabetes. There were 39 stable patients, 23 unstable patients and 10 patients of intermediate degree of control. Four insulin resistant patients were also studied. Serum insulin antibodies were measured in each patient and the concept of insulin buffering by its antibody was developed. Most unstable patients had low concentrations of insulin antibody. Twenty-four of the 39 stable patients had a significant concentration of insulin antibody and 15 patients had low levels of antibody. The insulin resistant patients had high levels of antibody. All unstable patients had low antibody buffering and all insulin resistant patients had high antibody buffering. Although many stable patients had buffering antibodies others lacking antibody required a low insulin dose and their stability of diabetic control was attributed to residual pancreatic function. This content is only available as a PDF. © Oxford University Press

SMITH,, R.;FRANCIS, M. J., O.;BAUZE, R., J.

doi: 10.1093/oxfordjournals.qjmed.a067442pmid: N/A

Abstract The clinical features of 62 patients with the diagnosis of oeteogenesis imperfecta, a generalized connective tissue disorder, have been reviewed. The structural polymeric collagen of the skin has been examined by biochemical and histological methods in 21 of these patients and in two further patients with osteogenesis imperfecta who died soon after birth. The results provide evidence of heterogeneity within this group of patients. Three main types of disorder are recognizable: those patients with dominantly inherited mild bone disease, blue sclerae and low amounts of polymeric collagen; those who occur sporadically, with severe bone disease, normal coloured sclerae and polymeric collagen of reduced stability; and occasional infants with severe bone disease who die at birth or soon after and whose polymeric collagen appears to be abnormal. It is speculated that these differences could be due to distinct abnormalities of collagen metabolism. This content is only available as a PDF. © Oxford University Press

PREECE, M., A.;TOMLINSON,, S.;RIBOT, C., A.;PIETREK,, J.;KORN, H., T.;DAVIES, D., M.;FORD, J., A.;DUNNIGAN, M., G.;O'RIORDAN, J. L., H.

doi: 10.1093/oxfordjournals.qjmed.a067443pmid: N/A

Abstract Highly sensitive assays have been developed that enable 25-hydroxycholecalciferol (25-hydroxyvitamin D3) and 25-hydroxyergocalciferol (25-hydroxyvitamin D2) to be measured in the same serum sample. With these assays it has been shown that endogenously produced cholecalciferol (vitamin D3) is important in man; the findings further emphasize the role of vitamin D metabolites as hormones rather than vitamins in the traditional sense. Dietary sources of vitamin D appear to be inadequate and vitamin D deficiency has been shown to be the cause of rickets and osteomalacia in Asian immigrants to Britain. This condition may be readily treated with small doses of vitamin D. In addition, sub-clinical deficiency was found in the Asian community. In the elderly, also, vitamin D deficiency was established as an important cause of osteomalacia and again evidence for the existence of a sub-clinical deficiency state was found. It is therefore suggested that the present prophylactic practices should be reviewed. Secondary hyperparathyroidism (reflected by elevated concentrations of circulating immunoassayable parathyroid hormone) was shown to be the rule rather than the exception in vitamin D deficiency. Some patients, however, had failed to respond to a hypocalcaemic stimulus. In others, there were high concentrations of parathyroid hormone despite normal serum calcium concentrations. Thus the relationship between parathyroid hormone and metabolites of vitamin D may not be mediated through changes in serum calcium alone, and it is postulated that metabolites of vitamin D may directly affect the secretion of parathyroid hormone. This content is only available as a PDF. © Oxford University Press

MONTGOMERY, R., DARRAGH;RICHARDSON, B., P.

doi: 10.1093/oxfordjournals.qjmed.a067444pmid: N/A

Abstract The incidence of gastric carcinoma was studied in a series of 210 patients presenting with apparently benign gastric ulcer. In eight cases (3.9 per cent), carcinoma was diagnosed within 18 months and was almost certainly present from the outset; in 2.4 per cent the diagnosis was delayed for over three months, and the five-year death-rate due to gastric carcinoma was 3.2 per cent. In a mean follow-up period of 5.7 years after first diagnosis of an ulcer (8.2 years after first symptoms), three fresh cases of gastric carcinoma were found, and in two of these the cancer was at a different site from the ulcer. The five-year incidence of fresh gastric carcinoma was 0.6 per cent. Unsuspected superficial spreading carcinoma was detected by histology in 5.4 per cent of gastrectomy specimens. The significance of these findings is discussed in relation to the management of gastric ulcer and the early diagnosis of cancer. This content is only available as a PDF. © Oxford University Press

IBELS, L., S.;SIMONS, L., A.;KING, J., O.;WILLIAMS, P., F.;NEALE, F., C.;STEWART, J., H.

doi: 10.1093/oxfordjournals.qjmed.a067445pmid: N/A

Abstract Fasting serum triglyceride and cholesterol measurements, and lipoprotein characterization by ultracentrifugation, were performed in four groups of patients with chronic renal disease (uraemic, short- and long-term haemodialysis and renal transplant recipients) and the results compared with those obtained from age- and sexmatched control subjects. Basal insulin and growth hormone levels, and serum creatinine and albumin concentrations were measured in, and detailed dietary histories taken from patients in each group. The predominant lipid abnormalities were hypertriglyceridaemia and increased very low density lipoproteins (type IV hyperlipoproteinaemia) in both uraemic and haemodialysis patients. Following renal transplantation, a different pattern of hyperlipidaemia was found. Hypercholesterolaemia was more common and hypertriglyceridaemia less common than in the uraemic and haemodialysis group. The lipoprotein abnormalities were increased low density and/or very low density lipoproteins, with types IIa, IIb and IV hyperlipoproteinaemia occurring equally frequently. In uraemic and haemodialysis patients, the pioportion of carbohydrate in the diet was high, and may have played a role in the genesis of hypertriglyceridaemia. There was a positive correlation between relative body weight and serum triglyceride in the long-term dialysis group. In renal allograft recipients hypertriglyceridaemia could be attributed, at least in part, to obesity, prednisone dosage and the degree of impairment of graft function. The aetiology of hypercholesterolaemia in the transplant recipients was unclear. Neither basal insulin nor growth hormone levels were elevated in any patient group. Uraemic hypertriglyceridaemia is a clearly defined and well documented metabolic abnormality which is not corrected by dialysis. Post-transplantation hyperlipidaemia however, is a condition of variable presentation and multifactorial aetiology. This content is only available as a PDF. © Oxford University Press

GAZZARD, B., G.;PORTMANN,, B.;MUREAY-LYON, IAIN, M.;WILLIAMS,, ROGER

doi: 10.1093/oxfordjournals.qjmed.a067446pmid: N/A

Abstract The clinical course and causes of death in 132 consecutive patients with fulminant hepatic failure and grade III or IV encephalopathy have been reviewed. 105 patients died and in 96 of these an autopsy examination was performed. In 36 patients there was cerebral oedema and the mean age of this group was significantly younger than the other fatal cases. In 28 patients death was attributed to major haemorrhage which originated in the gastrointestinal tract in 25. The prothrombin time ratio was not significantly greater in patients with major bleeding than in those without but they did have a significantly lower platelet count. Sepsis contributed to death in 12 patients. In 25 patients massive hepatic necrosis only was found at autopsy and death was considered to be due solely to hepatic failure. The degree of hepatocyte loss was assessed in 80 fatal cases by a histological morphometric technique on a needle specimen of liver taken immediately postmortem. The proportion of the liver volume occupied by hepatocytes (hepatocyte volume fraction, HVF) was greatly reduced in all patients (normal 85 ± SD 5 per cent) but the mean value was significantly higher in the patients dying with sepsis, cerebral oedema or haemorrhage than in the group in whom death was attributed solely to hepatic failure. There were ten patients in whom liver function was improving at the time of death which was due to cerebral oedema (9) or haemorrhage (1). These observations suggest that many patients presently dying from fulminant hepatic failure may be expected to survive, once more effective therapy is available for the complications of the illness. This content is only available as a PDF. Author notes " 1Present address: Charing Cross Hospital, London W.C.2 © Oxford University Press

doi: 10.1093/oxfordjournals.qjmed.a067447pmid: N/A

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