GALLSTONE CIRRHOSIS: ARE WE ONLY SEEING THE TIP OF THE ICEBERG?

Gallstones are common and their incidence increases with age.¹ Fifty per cent of these stones are in the common bile duct (CBD) in the elderly.² Most of them are silent but with time there is an increasing chance of developing symptoms which are more likely to be serious in the elderly.³ Failure to relieve mechanical obstruction of bile flow may lead to secondary biliary cirrhosis.⁴ It has been estimated that on average secondary biliary cirrhosis develops some seven years after the onset of obstruction from a stricture, four and half years after gallstone obstruction and 10 months after the onset of malignant stricture.⁵ The characteristic features are the pathological findings of portal-portal linkages, with a pattern of monolobular cirrhosis and the preservation of normal vascular relationships.⁶ Secondary biliary cirrhosis may lead to hepatic insufficiency and portal hypertension with the resultant complications, such as bleeding oesophageal varices, hypersplenism with pancytopenia, ascites and encephalopathy. We describe a patient in whom the diagnosis was not suspected until laparotomy and confirmed only at autopsy.     

Expression of alpha-melanocyte stimulating hormone and the invasive ability of the B16 murine melanoma.

The expression of alpha melanocyte stimulating hormone (MSH) has been investigated in two variants of the B16 murine melanoma. The presence of MSH was demonstrated by immunohistochemical methods using anti-MSH antibodies. The low metastasis variant B16-F1, which grows as an encapsulated non-invasive tumour, showed no alpha-MSH immunoreactivity. In contrast, the high metastasis variant BL6 was found to be alpha-MSH positive and the immunoreactivity was found predominantly in the peripheral invading zones of the tumour.     

Staph. Epi. Peritonitis in CAPD

Staphylococcus epidermidis is frequently resistant to first-generation cephalosporins. Although I have generally changed the therapy of S. epidermidis CAPD peritonitis to vancomycin when laboratory reports indicate cephalosporin resistance, it frequently appeared that improvement from the cephalosporin was taking place at the time of antibiotic conversion. Should the antibiotics be changed in this setting?     

Effect of nitric oxide on mitogenesis and proliferation of cerebellar glial cells

In the brain, nitric oxide (NO) has been identified as a messenger molecule and a mediator of excitatory amino acid-induced neurotoxicity. In this study, the effects of NO on serum-induced mitogenesis and cell proliferation of the cerebellar glial cells were assessed. NO-generating agent, S-nitroso-N-acetylpenicillamine (SNAP) increased intracellular cyclic guanosine monophosphate (cGMP) levels. Furthermore, 2 chemically dissimilar NO-generating agents, SNAP and sodium nitroprusside (SNP) inhibited serum-induced thymidine incorporation and cell proliferation. The antimitogenic effect of NO was mimicked by 8-bromo-cGMP and blocked by hemoglobin, a known inhibitor of NO. The effect of NO was not cytotoxic, since the cells were not stained with Trypan blue and did not show increased release of lactate dehydrogenase in the culture supernatants. However, NO-treated cells showed decreased conversion of tetrazolium to blue formazan suggesting that NO inhibited mitochondrial activity in the glial cells. These results demonstrate that NO inhibits serum-induced mitogenesis and cell proliferation of cultured rat cerebellar glial cells.     

Splenic abscess and peritonitis in a continuous ambulatory peritoneal dialysis (CAPD) patient

A 26-year-old female was on continuous ambulatory peritoneal dialysis (CAPD) because of diabetic end-stage renal failure. She developed an acute peritonitis that relapsed repeatedly despite appropriate antibiotic treatment. Investigations showed the presence of a splenic abscess, and splenectomy and peritoneal cannula removal were required. The patient died of myocardial infarction two weeks postoperatively. This is the first recorded case of peritonitis secondary to splenic abscess in a CAPD patient. Autopsy findings suggest that the abscess developed from infection of a splenic infarct.