Successful Treatment of Enterocutaneous Fistula in a Hemodialysis Patient with Somatostatin

Although cysticercosis is the most common parasitic disease affecting the central nervous system, spinal cysticercosis is rare. A rare form of spinal cysticercosis involving the whole spinal canal is presented. A 45-year-old Korean male had a history of intracranial cysticercosis and showed progressive paraparesis. Spinal magnetic resonance scan showed multiple cysts compressing the spinal cord from C1 to L1. Three different levels (C1-2, T1-3, and T11-L1) required operation. Histopathological examination confirmed cysticercosis. The patient improved markedly after surgery.

Octreotide-LAR-associated erythema multiforme in an acromegalic subject: case report

Long-acting somatostatin analogs are often used for treating acromegaly, either as adjuvant to surgery or radiotherapy or, more recently, as a primary therapeutic option. These drugs seem to be reasonably safe, but new adverse effects not yet described may occur during the use of the relatively new long-acting formulations. In this case report, we describe a severe cutaneous reaction (erythema multiforme) in a patient treated with long-acting release (LAR) octreotide, and also discuss the need of previous "testing" with short subcutaneous preparation of octreotide.

Análogos da somatostatina de longa duração são freqüentemente usados no tratamento da acromegalia, como adjuvante à cirurgia ou à radioterapia ou, mais recentemente, como opção terapêutica primária. Essas drogas parecem ser razoavelmente seguras, mas podem ocorrer feitos colaterais ainda não descritos com o uso das relativamente novas formulações de ação prolongada. Neste relato de caso, descrevemos uma reação cutânea grave (eritema multiforme) em uma paciente tratada com octreotide de liberação prolongada (LAR) e discutimos a necessidade de submeter os pacientes previamente a um "teste" com a formulação subcutânea do octreotide de ação rápida.

Somatostatina por via epidural em ratos: efeito sobre a transmissao da dor / Effect of epidural somatostatin on pain transmission in rats

Foram avaliados os efeitos da somatostatina-201-995 por via epidural sobre a transmissao da dor em ratos.Os ratos do G-I(10)receberam salina; os do G-II, 10 mcg de SST; os do G-III, 30 mcg de SST. O volume foi de 40mcl. A SST nao alterou a resposta a dor (imersao em agua quente). Houve efeitos colaterais em cinco ratos.

Electrophysiological effects of somatostatin at the supraventricular level of isolated guinea pig hearts

The objective of the present study was to evaluate the electrophysiological effects of the peptide somatostatin (SST) at the supraventricular level in isolated guinea hearts. ECG recording from isolated hearts perfused by the Langendorff method i9ndicating that 1.0 uM SST induced a decrease in heart rate from 174 ñ 15 to 157 ñ 9 bpm (N=6, P<0.05), blocked AV conductio9n (the PR interval increased from 92 ñ 11 ms to 106 ñ 5 ms, N+5, P<0.05) and increased the QTc interval from 210 ñ 0 to 232 ñ 4 ms (N+5, P<0.05). The supraventricular effect of SST, particulary upon the AV conduction , were potentiated by a reduction in calcium concentration from 2.5 to 0.5 mM in the perfusing solution. Thus, 1.0 uM SST induced 2nd degree AV conduction block progressing to AV dissociation in 75% of thye hearts in the low calcium medium instead of the first degree conduction block observed in all hearts in normal calcium medium. His bundle electrogram evidence a complete A-H dissociation withouth significant change in the H-V interval and microelectrode studies showed a complete abolition of the AV node action potential in the presence of 1.0 uM SST. Both results demonstrate that the site of AV conduction block induced by SST is at the AV node. All the supraventricular effects of SST were transitory, subsiding within abouth 10 min of hormone exposition, showing desensitization. The effects of somatostatin here described were not blocked by 10 uM atropine, indicating that they are not mediated by muscarinic receptors. These data provide a direct electrophysiological demonstration of the supraventricular effects of SST, and suggest that this peptide decreases calcium influx during the action potential

inhibition of liver regeneration by somatostatin infusion and its reversal by pancreatic polypeptide and hepatocyte-stimulating substance

Several hepatotrophic hormones are known to be involved in initiating and potentiating the hepatic proliferative response to injury or hepatectomy. Little is known, however, about factors promoting termination of the regenerative response when the liver is restored. Because somatostatin [SRIF], isolated from gastric pancreatic and portal circulation, is an inhibitory hormone, we attempted to evaluate is potential role in regulating liver cell regeneration. We also studied the relationship of SRIF to insulin, glucagon, pancreatic polypeptide, and hepatocyte-stimulating substance on regenerating the liver following extended hepatectomy in rats. Male Sprague-Dawley rats were either sham-operated [n = 6] or subjected to 68% hepatectomy [n = 35]. Subcutaneous infusions of either saline or hormones were started 18-24 h preoperatively and continued until sacrifice 24 h following hepatectomy. At sacrifice, peripheral blood was obtained to determine serum insulin, glucagon, and SRIF levels. Liver regeneration was assayed by measuring the incorporation of radiolabelled thymidine into hepatocyte DNA. Liver regeneration was significantly [P<0.01] inhibited by SRiF Glucagon or glucagon and insulin combined did not reverse this effect. Insulin and glucagon levels were not significantly influenced by SRIF infusion. Pancreatic polypeptide and hepatocyte stimulating substance were both able to reverse the inhibitory effect of SRIF on liver regeneration and at the same time caused serum glucagon levels to increase and serum insulin levels to decrease. Thus SRIF inhibits liver regeneration after hepatectomy either by acting directly on the hepatocytes or via other factors which are not insulin and glucagon. Pancreatic polypeptide and hepatocyte stimulating substance reverse SRIF mediated inhibition of liver regeneration, possibly by changing insulin and glucagon levels, although other mechanisms may be involved