Biomedical subjects
Publications and source records attributed to B Dubin.
Yet another application of suction lipectomy equipment is presented to remove the pathologic tissue in cherubism. Owing to the variations of consistency of the material in this condition, this technique may not be successful in all patients, but it is certainly recommended when indicated.
It is necessary that the treatment of arteriovenous malformations in general be undertaken by a team that consists of a radiologist who is experienced in angiography and embolization and a plastic surgeon. The latter should be well versed in angiographic techniques and should be able to comprehend the dynamics of these malformations. In this report, three patients with high-flow, high-shunt arteriovenous intraosseous malformations of the head are presented. Two of these presented as emergencies with almost uncontrollable bleeding and were initially treated with embolization and then mandibular resection and reconstruction within the first 48 hours. In one patient, a further reconstructive procedure using free vascularized tissue was carried out. A third patient with involvement of the maxilla, again presenting with bleeding, was treated with embolization and, because of the deformity that would be created by resection, was simply observed. However, this patient is to be reassessed in the future and may well come to maxillectomy. It is emphasized that the treatment of these patients requires careful assessment, embolization, and resection as indicated after discussion between radiologist and surgeon.
Tetracosactrin (Synacthen) tests were performed on 19 elderly women who had leucocyte ascorbic acid (LAA) levels of less than 15 microgram/108 WBC. 9 were then given a daily dose of 200 mg ascorbic acid orally for 2 weeks while the other 10 were left untreated. Following this, tetracosactrin tests were repeated in both groups. All initial plasm cortisol responses to tetracosactrin were within normal limits. Treatment with ascorbic acid produced no changes in these. This suggests that the low LAA levels often found in old people do not result in adrenal insufficiency.
Fifteen patients with non-ketotic hyperosmolar diabetic coma were investigated and compared with ketoacidotic patients. Basal plasma insulin levels were low in all patients (14.8 +/- 1.0 micronU/ml in hyperosmolar coma, 11.0 +/- 1.3 in keto-acidosis), but insulin level increased after intravenous tolbutamide (between 30 and 105 micronU/ml) in eight hyperosmolar comas. Insulin showed no increase in seven hyperosmolar comas and in none of the ketoacidotic patients. In hyperosmolar coma plasma free fatty acids (1710 +/- 197 micronEq/1), triglycerides (3,4 +/- 0,4 g/1) and cortisol levels (49,7 +/- 9,0 microgram/100 ml) were increased, must as in keto-acidosis. Growth hormone (1,7 +/- 0,1 ng/ml) was normal, unlike the case in keto-acidosis. Plasma lactate concentrations were elevated and account for the frequent mild acidosis found in hyperosmolar coma. In spite of the low peripheral "insulin/glycemia ratio", the positive response to tolbutamide in half of the hyperosmolar cases suggests a less complete pancreatic deficiency than in keto-acidosis. The plasma high free fatty acid and triglyceride levels suggest that the lack of ketosis is not due to inhibition of lipolysis but could be a consequence of inhibition of hepatic ketogenesis.