Hyperreactive malarial splenomegaly (HMS) is found in geographical association with B cell lymphoproliferative disorders such as 'African' chronic lymphocytic leukaemia (CLL) and splenic lymphoma with villous lymphocytes (SLVL). It is sometimes not easy to make a differential clinical diagnosis between these conditions. We have previously used Southern blotting as a definitive method for the diagnosis of monoclonal lymphoproliferation in these disorders, but this is expensive, lengthy and technically difficult. In the present paper we have compared Southern blotting with polymerase chain reaction (PCR) amplification of the immunoglobulin heavy chain gene. We found an excellent correlation between the 2 methods in demonstrating monoclonal populations of lymphocytes in patients with a clinical diagnosis of CLL or SLVL. We have further demonstrated monoclonality in a patient who could not be classified as CLL or SLVL on clinical criteria alone. In contrast, patients with well defined HMS or with non-B cell proliferations all showed polyclonal rearrangements. We propose that the immunoglobulin gene PCR is a useful tool for the investigation of tropical splenomegaly of uncertain origin.

Gastric and plasma alpha amylase and proteins concentrations were evaluated in male and female albino rats fed with Lipton tea and coffee induced gastric ulcer. A total of ninety-six male and female albino rats were studied for 28 days. There was no significant difference (p>0.5) in gastric alpha amylase concentrations between the two beverages and the male and female rats. Also there was no significant difference in plasma alpha amylase between Lipton tea and coffee, (P>0.05) and between sexes, (p>0.05). However, the plasma alpha amylase values were very low as compared to control rats without gastric ulcer. There was significant difference in plasma protein concentrations between rats fed with coffee and Lipton tea, (p<0.05) as more proteins concentrations were recorded in coffee feeding than in Lipton tea. Also there was significant difference in plasma protein concentrations in the weekly studies of 7, 14, 21, 28 days (p>0.05). And no significant differences (p>0.05) between the sexes and rats fed with caffeinated and decaffeinated coffee. Cumulatively, both gastric and plasma proteins showed no significant difference, (p>0.5) in their concentrations in Lipton tea and coffee. But there was significant difference (p<0.05) in gastric protein between caffeinated and decaffeinated coffee. Significant differences, (p<0.05) also existed in gastric protein concentrations between 7, 14, 21 and 28 days. Both Lipton tea and coffee induced gastric ulcer, reduced amylase and increased protein concentrations and such may be associated with panccreatitis, kidney disease, multiple myeloma, bone marrow disorder, chronic inflammatory conditions and amyloidosis.

Objectives: Foetal hepatorenal toxicity and foetal morphology were evaluated following artemether administration to pregnant Wistar albino rats. Methods: Twenty pregnant Wistar rats weighing between 180-200 g were divided into four groups (n=5, each) with Group 1 serving as the control. Groups 2, 3 and 4 received 1.1 mg, 2.2 mg and 3.3 mg per kilogram body weight artemether, respectively orally, twice daily for three days on day 7, 8 and 9 of pregnancy. The animals were sacrificed on day 20 of pregnancy and foetuses were harvested and evaluated for morphological changes. Foetal body weight and crown-rump length (CRL) were measured; alpha-fetoprotein (AFP) was assayed using amniotic fluid, and foetal kidney and liver were evaluated histologically for toxicity. Results: There was a significant decrease in body weight, CRL and AFP of the treated groups compared to the control. The foetal liver of the treated groups revealed distorted cytoarchitecture, marked hepatocyte inflammation and hepatic necrosis. The foetal kidney of artemether-treated groups also showed disorganised renal structure, atrophic and degenerated glomeruli with acute tubular necrosis. Conclusion: Artemether administration to pregnant albino rats causes intrauterine growth retardation or stunted growth, as well as foetal hepatorenal toxicity.

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