ABSTRACT
A 73-year-old man presented with haemorrhagic pleural effusion, having been diagnosed with chronic lymphocytic leukaemia (CLL). The differential diagnosis of haemorrhagic pleural effusion is considered. Tuberculosis and pleural infiltration of CLL are considered most likely. Pleural biopsy confirms the diagnosis of pleural involvement of CLL in this case. Although pleural involvement of CLL has been reported several times the presentation of pleural effusion as the first symptom of CLL has not previously been described.
Subject(s)
Hemothorax/etiology , Leukemia, Lymphocytic, Chronic, B-Cell/complications , Pleural Effusion, Malignant/diagnosis , Pleural Effusion/etiology , Tuberculosis, Pleural/diagnosis , Aged , Diagnosis, Differential , Humans , Leukemia, Lymphocytic, Chronic, B-Cell/diagnosis , Lymphocytosis/etiology , MaleABSTRACT
The effects of a long-acting somatostatin analog (SMS 201-995) were studied in an established model of acute necrotizing pancreatitis in rats. SMS 201-995, when given prior to induction of pancreatitis, decreased the mortality rate from 100% to 40% (P = 0.0001). When treatment was given after induction of pancreatitis, the mortality rate was 75% (P = 0.2). Administration of SMS 201-995 did not influence the serum concentrations of amylase markedly, but the lipase levels were significantly lowered (P less than 0.05). The low levels of serum insulin and the glucose level in whole blood were not influenced. The volume of ascitic fluid was reduced (P less than 0.01). Moreover, less peritoneal fat necrosis was seen, suggesting a reduction in toxic factors in the ascitic fluid. Treatment with SMS 201-995 prior to induction of pancreatitis caused a significant increase in the levels of circulating 6-keto-PGF1 alpha, the stable metabolite of prostaglandin I2 (P less than 0.01). The levels of thromboxane B2 and prostaglandin E2 did not change significantly. The present data support the hypothesis that SMS 201-995 is an activator of prostaglandin I2, thereby modifying the course of the disease.
Subject(s)
Eicosanoids/biosynthesis , Octreotide/therapeutic use , Pancreatitis/metabolism , 6-Ketoprostaglandin F1 alpha/biosynthesis , Acute Disease , Amylases/blood , Animals , Dinoprostone/biosynthesis , Lipase/blood , Male , Necrosis , Pancreas/pathology , Pancreatitis/drug therapy , Pancreatitis/pathology , Rats , Rats, Inbred Strains , Thromboxane B2/biosynthesisABSTRACT
Plasma thromboxane concentrations were found to be significantly elevated in acute necrotizing pancreatitis in rats, whereas prostaglandin I2 levels were not. The significance of these alterations was investigated. Pancreatitis was induced by injecting 5% sodium taurocholate into the pancreatic duct. Iloprost (ZK 36374, a stable analog of prostaglandin I2, 25 ng/kg body weight) decreased the mortality rate from 100% to 50%. When treatment with iloprost was combined with simultaneous administration of either Sibelium (flunarizine R 14,950, 0.2 mg/kg body weight) or dazmegrel (UK 38,485, 50 mg/kg body weight) an additional decrease in the mortality rate was recorded. Dazmegrel is a selective thromboxane A2 synthetase inhibitor and flunarizine (a calcium entry blocker) also inhibits the effects of elevated thromboxane A2 levels. With flunarizine and iloprost the mortality rate was 40% (P less than 0.05); with dazmegrel and iloprost it was 10% (P less than 0.01). The results of the present study suggest that thromboxane A2 and prostaglandin I2 play a role in the course of acute necrotizing pancreatitis.
Subject(s)
Epoprostenol/physiology , Epoprostenol/therapeutic use , Pancreatitis/drug therapy , Thromboxane A2/physiology , Vasodilator Agents/therapeutic use , Acute Disease , Animals , Epoprostenol/blood , Flunarizine/therapeutic use , Iloprost , Imidazoles/therapeutic use , Male , Necrosis , Pancreas/pathology , Pancreatitis/blood , Rats , Rats, Inbred Strains , Thromboxane A2/bloodABSTRACT
Acute necrotising pancreatitis in rats was induced by injecting 5% sodium taurocholate into the pancreatic duct. Prostaglandin E2 (100 micrograms/kg subcutaneously twice) decreased the mortality rate from 100% to 60% (NS). When treatment with prostaglandin E2 was combined with simultaneous administration of either dazmegrel (UK 38,485, 50 mg/kg bodyweight) or Sibelium (Flunarizine R 14,950, 0.2 mg/kg body weight) a significant decrease in the mortality rate (p less than 0.05) was recorded. Dazmegrel is a selective thromboxane A2 synthetase inhibitor and prevents the formation of thromboxane A2. Flunarizine (a calcium entry blocker) decreases thromboxane A2 formation and also inhibits the effects of raised thromboxane A2 concentrations. As plasma thromboxane B2 (the stable metabolite of thromboxane A2) concentrations increase and the plasma prostaglandin E2 concentrations decrease in acute necrotising pancreatitis in rats, the results of the present study indicate that these prostaglandins play a role in the pathophysiology of the disease. It is suggested that restoration of the balance in prostanoid concentrations will have a beneficial effect on the course of acute necrotising pancreatitis.
Subject(s)
Dinoprostone/therapeutic use , Pancreatitis/drug therapy , Acute Disease , Animals , Drug Therapy, Combination , Flunarizine/therapeutic use , Imidazoles/therapeutic use , Male , Necrosis , Pancreas/pathology , Pancreatitis/pathology , Rats , Thromboxane-A Synthase/antagonists & inhibitorsABSTRACT
A 67-yr-old Indonesian patient with disseminated histoplasmosis is described. He had general malaise and fever for 6 months; an oral ulcer, bilateral adrenal gland enlargement and partial adrenal insufficiency were found. An adrenal aspirate contained Histoplasma capsulatum. The literature on adrenal involvement in disseminated histoplasmosis is reviewed and it is concluded that bilateral enlargement, demonstrated by sonography or computed tomography, in a patient with general malaise is an important clue to the diagnosis.
