Analgesic abuse,ureteric obstruction,and retroperitoneal fibrosis.

We report two cases of unusual ureteric obstruction in patients with an excessive consumption of analgesics. In a retrospective survey of seven cases of non-malignant retroperitoneal fibrosis seen in the last 15 years it was found that four had taken excessive amounts of analgesics. A careful drug history should be taken in all patients with restroperitoneal fibrosis and ureteric obstruction.     

Pleural Effusion and Fibrosis during Treatment with Methysergide

Two patients being treated for migraine with methysergide developed extensive pleural fibrosis, and in addition one of them had bilateral pleural effusions, After treatment was stopped these complications, which are thought to have been due to the drug, cleared in the next few months.     

Robotic ureterolysis, retroperitoneal biopsy, and omental wrap for the treatment of ureteral obstruction due to idiopathic retroperitoneal fibrosis

Retroperitoneal fibrosis (RPF) is a rare disorder of unclear etiology characterized by chronic inflammation of the retroperitoneum, which can involve any of the retroperitoneal structures, most notably the ureters, aorta, and vena cava. Historically, open biopsy, ureterolysis, and transpositioning or omental wrapping of the involved ureter(s) have been the preferred surgical treatments of RPF, with success rates greater than 90%. More recently, successful laparoscopic biopsy, ureterolysis, and ureteral omental wrapping and intraperi-tonealization have been described. We report the first case in the literature of idiopathic RPF managed with robotic ureterolysis and laparoscopic omental ureteral wrapping.     

Methysergide reduces nonnutritive blood flow in normal and scalded skin

Methysergide is a serotonin antagonist and has been demonstrated to reduce wound blood flow and edema formation. We have determined the effect of methysergide on protein kinetics in normal and scalded skin of anesthetized rabbits. L-[ring-(13)C(6)]- or L-[ring-(2)H(5)]phenylalanine was used to reflect skin protein kinetics by use of an ear model, and L-[1-(13)C]leucine was used to reflect whole body protein kinetics. The results were that infusion of methysergide (2-3 mg. kg(-1). h(-1)) reduced the blood flow rate in normal skin by 50% without changing skin or whole body protein kinetics. After scald injury on the ear, administration of methysergide for 48 h reduced the weight of scalded ears (43 +/- 4 vs. 30 +/- 5 g, P < 0.01) and ear blood flow rate (42.6 +/- 4.9 vs. 5.8 +/- 1.0 ml. 100 g(-1). min(-1), P < 0.0001) and did not change wound protein kinetics. Methysergide reduced arteriovenous shunting and maintained inward phenylalanine transport from the blood to the skin pool. Using the microsphere technique, we found that the infusion of methysergide decreased blood perfusion by 33-36% in both normal and scalded ear skin. We conclude that methysergide administration reduces nonnutritive, as opposed to nutritive, blood flow in normal and scalded skin.     

Mitral Regurgitation Occurring During Methysergide (Sansert) Therapy

The case history of a young woman who developed severe mitral regurgitation after four years of methysergide therapy is reported. Replacement of the mitral valve was required. A brief review of the toxic effects of methysergide is given and special reference is made to lesions of the heart valves that have occurred during methysergide therapy.