Dietary fish oil supplementation alters LTB4:LTB5 ratios but does not affect the expression of acute graft versus host disease in mice.

One of the mechanisms by which corticosteroids may modify acute graft vs host disease (GvHD) is via inhibition of arachidonic acid (AA) metabolism. Leukotriene B4 (LTB4) is a product of that pathway which may take part in the pathogenesis of GvHD through the stimulation of T-lymphopoiesis and T-lymphocyte activation. LTB4 is a metabolite of AA (20:4n-6). Alternate dietary sources of polyunsaturated fatty acids (PUFA), specifically eicosapenteinoic acid (20:5n-3) (EPA) and docosahexaenoic acid (22:6n-3) (DHA), shift the LTs formed with a decrease in LTB4 an increase in LTB5. LTB5 is a less potent agonist than LTB4 and this results in a theoretical decrease of LTB4 mediated events. Supplementation of in vitro bone marrow cultures with EPA or DHA had no detrimental effect on myeloid colony formation. Dietary EPA/DHA supplementation in mice with induced GvHD appeared to be safe and well tolerated. The LTB4:LTB5 ratio shifted from 7.65 +/- 1.75 in control-fed animals to 1.03 +/- 0.18. Fish-oil-supplementation did not compromise engraftment or stem cell content. Alone, this therapy was unable to modify GvHD.

Esophageal perforations masked by steroids.

Esophageal perforation is usually an acute, life-threatening event, and its diagnosis can be established on the basis of obvious clinical and radiographic findings. This article describes two cases whereby symptoms of esophageal perforations were masked by concomitant administration of steroids, thus causing marked delay in diagnosis and treatment. Esophageal rupture should be considered when patients receiving steroids develop unexplained fever with pleural effusion or pneumomediastinum, particularly following instrumentation or forceful retching.

Plasma thrombospondin as an indicator of intravascular platelet activation in patients with vasculitis.

The use of plasma thrombospondin (TSP) concentration was investigated as an indicator of intravascular platelet activation. Patients (n = 20) with diseases that have known vasculitis were included in the study. The range and the mean of plasma TSP concentrations of patients with vasculitis were 117 ng/ml to 6500 ng/ml and 791 +/- 1412 ng/ml (mean +/- SD); the range and the mean of plasma TSP concentrations of control individuals (n = 33) were 13 ng/ml to 137 ng/ml and 59 +/- 29 ng/ml. When plasma TSP concentrations were correlated with plasma concentrations of another platelet activation marker, beta-thromboglobulin (beta-TG), it was found that the TSP concentration increased exponentially as the plasma beta-TG level rose. A positive correlation between plasma levels of plasma TSP and serum fibrin degradation products was also observed. The results suggest that platelets are the primary source of plasma TSP in patients with various vasculitis and that plasma TSP can be a better indicator than beta-TG to assess intravascular platelet activation due to its longer circulation half life.