Intrasphenoidal migration of a premaxillary Kirschner wire.

OBJECTIVE: The use of Kirschner wire for the fixation of premaxilla is a well-known method in bilateral cleft lip surgery. We report a case in which the Kirschner wire of the premaxillary fixation had migrated intrasphenoidally. RESULTS AND CONCLUSIONS: The foreign body was accidentally discovered during a cephalometric analysis and was taken out surgically through an upper lip sulcus incision. Although the wire remained asymptomatic for 10 years, it constituted a potential danger for intracranial migration.     

Selective unresponsiveness of pancreatic beta-cells to acute sulfonylurea stimulation during sulfonylurea therapy in NIDDM

Patients with non-insulin-dependent diabetes mellitus (NIDDM) who have chronic hyperglycemia lose acute incremental insulin responses to glucose but are able to briskly respond to other beta-cell secretagogues. To investigate whether this is a defect specific for glucose or represents a more general phenomenon, we measured the insulin responses to acute intravenous tolbutamide in 10 obese patients with NIDDM both before and during sulfonylurea therapy with tolazamide. Comparable glycemia was achieved with oral dextrose 2 h before intravenous testing. To assess beta-cell responsiveness to a nonsulfonylurea secretagogue, 1 mg glucagon was administered intravenously during tolazamide therapy. In seven patients, the mean peak insulin increment 5 or 10 min after intravenous tolbutamide was 54 +/- 11 microU/ml when not receiving tolazamide (0.14 +/- 1.3 microU/ml) with tolazamide (P less than .001), even though serum insulin responded rapidly to intravenous glucagon. In four patients tested for reversibility of their refractoriness to intravenous tolbutamide during chronic tolazamide therapy, the mean peak insulin increment 1 wk after discontinuing tolazamide was 79 +/- 22 microU/ml. A relatively rapid development of refractoriness was documented in four patients who were tested only 12 h after beginning tolazamide therapy; the mean peak insulin increments 5-10 min after intravenous tolbutamide were undetectable (-0.5 microU/ml), yet responses to intravenous glucagon were evident. In these NIDDM patients, exposure of pancreatic beta-cells to sustained levels of sulfonylureas induces a reversible state of refractoriness to acute stimulation with sufonylureas but not to another secretagogue.(ABSTRACT TRUNCATED AT 250 WORDS)     

N-3-pyridylmethyl-N''-p-nitrophenylurea ocular toxicity in man and rabbits.

Ingestion of the rat poison N-3-pyridylmethyl-N'-p-nitrophenylurea (PNU) produced ocular toxicity in three humans and in an animal model, the Dutch Belted rabbit. The electroretinogram b wave was especially susceptible to the effects of the rodenticide, and the target tissue appeared to be the retinal pigment epithelium. Injection of PNU itself did not produce ocular toxicity. The poison had to be administered orally. Gentamicin administered orally with PNU prevented the ocular toxicity. Presumably this antibiotic killed those gastrointestinal bacteria responsible for PNU's metabolism into an ocular toxin. L-tryptophan, a known antidote for the lethal effects of PNU, was an antidote for the ocular toxicity when administered orally but not when administered parenterally.     

The role of descending venography in the management of patients with chronic venous disease of the lower extremity.

The purpose of this paper is to evaluate the efficacy and clinical information obtained from the authors' first 17 consecutive descending venograms. All 17 patients had chronic venous disease refractory to standard conservative and surgical measures. The standard classification of valvular insufficiency was used in evaluating these venograms. There were no deaths, slight morbidity and minimal patient discomfort. In 16 patients meaningful clinical information was derived from the venograms, with 7 patients having deep venous valvular surgery. Descending venography will demonstrate the site of incompetent valves and estimate the degree of reflux. This test is necessary before anticipated reconstruction of deep vein valves.     

Late Ureteral Stenosis Following Renal Transplantation: Risk Factors and Impact on Patient and Graft Survival

The aim of this retrospective study of a cohort of 1787 consecutive kidney transplantations was to analyze the risk factors associated with the occurrence of ureteral stenosis and the impact of ureteral stenosis on graft and patient survival. Between January 1990 and December 2002, 1787 renal transplantations were performed at our center. Only stenosis observed after the first month, were considered. Among the parameters studied were: donor age and serum creatinine before procurement; recipient age, cold ischemia time, delayed graft function (DGF), number of arteries and the presence of a double J stent. The follow-up parameters were the number and timing of acute rejection episodes, cytomegalovirus (CMV) infection, acute pyelonephritis, renal function and death. Ureteral stenosis occurred in 4.1% of patients and was correlated with donor age > 65 years (p = 0.001), kidneys with more than 2 arteries (p = 0.009) and DGF (p = 0.016). Ureteral stenosis did not affect 10-year patient and graft survival rates, which were respectively 90% and 64% for the stenosis group, 86% and 63% for the no-stenosis group (p = NS). These data suggest an important role for donor age, number of renal arteries and DGF for the occurrence of ureteral stenosis following renal transplantation.     

Mechanisms of L-NG nitroarginine/indomethacin-resistant relaxation in bovine and porcine coronary arteries.

1. Coronary arteries from bovines (BCA) and pigs (PCA) were used for measuring endothelium-dependent relaxation in the presence of L-NG nitroarginine and indomethacin. As some compounds tested have been found to have an inhibitory effect on autacoid-activated endothelial Ca2+ signalling, endothelium-dependent relaxation was initiated with the Ca2+ ionophore A23187. 2. The common compounds for modulating arachidonic acid release/pathway, mepacrine and econazole only inhibited L-NG nitroarginine-resistant relaxation in BCA not in PCA. In contrast, proadifen (SKF 525A) diminished relaxation in BCA and PCA. Mepacrine and proadifen inhibited Hoe-234-initiated relaxation in BCA and PCA, while econazole only inhibited Hoe 234-induced relaxation in PCA. Due to the multiple effects of these compounds, caution is necessary in the interpretation of results obtained with these compounds. 3. The inhibitor of Ca(2+)-activated K+ channels, apamin, strongly attenuated A23187-induced L-NG nitroarginine-resistant relaxation in BCA while apamin did not affect L-NG nitroarginine-resistant relaxation in PCA. 4. Pertussis toxin blunted L-NG nitroarginine-resistant relaxation in BCA, while relaxation of PCA was not affected by pertussis toxin. 5. Thiopentone sodium inhibited endothelial cytochrome P450 epoxygenase (EPO) in PCA but not in BCA, while L-NG nitroarginine-resistant relaxation of BCA and PCA were unchanged. Protoporphyrine IX inhibited EPO in BCA and PCA and abolished L-NG nitroarginine-resistant relaxation of BCA not PCA. 6. An EPO-derived compound, 11,12-epoxy-eicosatrienoic acid (11,12-EET) yielded significant relaxation in BCA and PCA in three out of six experiments. 7. These findings suggest that L-NG nitroarginine-resistant relaxation in BCA and PCA constitutes two distinct pathways. In BCA, activation of Ca(2+)-activated K+ channels via a pertussis-toxin-sensitive G protein and EPO-derived compounds might be involved. In PCA, no selective inhibition of L-NG nitroarginine-resistant relaxation was found.     

Right hemothorax: an unusual presentation of ruptured infrarenal abdominal aortic aneurysm

The authors describe what they believe is the first reported case of rupture of an infrarenal abdominal aortic aneurysm into the right pleural cavity. A 75-year-old woman presented simultaneously with two common causes of severe abdominal pain and hypotension: perforated duodenal ulcer and ruptured abdominal aortic aneurysm. The absence of an infrarenal retroperitoneal hematoma delayed the diagnosis of rupture of the abdominal aortic aneurysm and the terminal event was exsanguination into the right pleural cavity through an erosion in the right hemidiaphragm.