Hemoperitoneum secondary to rupture of cystic artery pseudoaneurysm

BACKGROUND:Spontaneous hemoperitoneum of hepato- biliary origin is commonly due to hemorrhage from a liver tumor.It is rarely caused by spontaneous rupture of aneurysm in visceral arteries. METHODS:We report an unusual case of hemoperitoneum caused by rupture of cystic artery pseudoaneurysm,and also outline the approach to its management through surgical and radiological methods. RESULTS:In our patient,the pseudoanurysm was initially treated with percutaneous thrombin injection.However this method of treatment failed after initial success.The pseudoanurysm was finally obliterated successfully using microcoil embolization. CONCLUSIONS:The mainstay of treatment of cystic artery pseudoaneurysm is cholecystectomy and ligation of the aneurysm.Recent publications showed success in using microcoil embolisation.In this case we also outline the use of percutaneous thrombin injection as a definitive treatment method and discuss its success or failure as a new method of treatment.     

A cocaine analog and a GBR analog label the same protein in rat striatal membranes.

Because some evidence suggests that cocaine and GBR12935 bind to different sites, we utilized photoaffinity probes from both classes of compounds to see if they label the same protein. [125I]RTI-82 a cocaine analog, and [125I]DEEP, a GBR analog, labeled protein(s) showing the same molecular weight, a similar pharmacological profile and a similar sensitivity to neuraminidase.     

Comparison of the potential therapeutic effects of interleukin 2 or interleukin 4 secretion by a single tumour.

Engineering of a variety of rodent tumour cells to secrete either interleukin 2 (IL-2), or interleukin 4 (IL-4), has been demonstrated to reduce their tumorigenicity. However the mechanisms of action of secreted IL-2 and IL-4 have not been compared in a single rodent tumour. Here we demonstrate that the weakly immunogenic murine fibrosarcoma FS29 had reduced growth rate and in some cases was rejected by syngeneic animals, when modified to secrete either IL-2 or IL-4, but not IL-5. Immunohistochemical analysis of tumour nodules undergoing regression showed stimulation of a largely lymphocytic infiltrate by IL-2 and a macrophage and granulocyte infiltrate, with a small number of lymphocytes by IL-4. Indeed, secretion of low levels of IL-2 and IL-4 in combination resulted in optimal rejection, suggesting that the two cytokines might mobilise different and complementary effector cell mechanisms. Both IL-2 and IL-4-secreting cells failed to induce the rejection of admixed, unmodified FS29 cells. The loss of cytokine secreting cells from such admixtures occurred more rapidly for IL-2-secreting cells. Injection of IL-4-secreting, but not IL-2-secreting FS29 cells could protect mice from a delayed challenge with unmodified FS29 cells. These data suggest that IL-4 secretion stimulates the better long-term host anti-tumour response.     

Hematologic changes during and after cardiopulmonary bypass and their relationship to the bleeding time and nonsurgical blood loss.

The hemostatic dysfunction induced by cardiopulmonary bypass is due, in part, to a platelet dysfunction evidenced by a postoperative extension of the bleeding time; it leads to increased postoperative blood loss and morbidity. This study, which was conducted in 85 patients undergoing cardiopulmonary bypass, was designed to characterize the hematologic changes during and after cardiopulmonary bypass and to elucidate the relationships between these changes, the extension of the bleeding time, and the magnitude of the postoperative nonsurgical blood loss. Variables were measured before, during, and 2, 24, 48, and 72 hours after cardiopulmonary bypass. Univariate and multivariate analyses were performed with either the 2-hour postbypass bleeding time or the 4-hour postbypass blood loss as the dependent variables. The reversal of the extension of the bleeding time in the postoperative period was accompanied by a significant increase in the mean platelet volume and by a significant increase in the level of thromboxane B2 measured in the blood shed from the site of the bleeding time determination. The postoperative bleeding time correlated with the postoperative blood loss, and both parameters were dependent on the duration of cardiopulmonary bypass. In addition, the postoperative bleeding time correlated with the skin temperature and the plasma level of D-dimer, while the postoperative blood loss also correlated with temperature and the plasma levels of C3. These data establish a direct relationship between the postoperative bleeding time, the postoperative blood loss, and temperature. They indicate that the reversal of the postoperative extension of the bleeding time is due in part to rewarming and to the release of larger platelets into the circulation, and they suggest that hyperfibrinolysis and complement activation may play an important role in the cardiopulmonary bypass-induced platelet dysfunction.     

Fatal self-induced hyperinsulinaemia: a delayed post-mortem analytical detection.

The inconspicuous number of cases of self-induced hyperinsulinaemia reported in the literature may suggest that many are obscure enough to escape their detection. A case of fatal suicidal hyperinsulinaemia in a non-diabetic is reported here, and in whom only a retrospective biochemical analysis provided an explanatory cause of death. A quantitative radioimmuno assay (RIA) estimation of the refrigerated postmortem blood sample stored at 4 degrees C for three weeks gave a positive insulin yield. It reiterates the need, in forensic cases, for a very low threshold of suspicion and a good back-up for the appropriate body fluid analysis or tissue microexamination, especially when full details of the circumstances surrounding the death are not available at the autopsy. A brief résumé on insulin is presented as a background to the current forensic interest in the apparent increase in sudden deaths in young diabetics amidst the controversy about the bio-designed 'human' insulin and subjective unawareness of severe hypoglycaemia.