Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatostatin, originally detected by Krulich and ultimately isolated by Brazeau, was initially described as a growth hormone release-inhibiting factor. Subsequent investigation into the use of native somatostatin and the development of long-acting somatostatin analogues, especially octreotide acetate, have fostered increasing uses of these compounds. Though the clinical and investigational uses of somatostatin and its analogues are varied, one central theme remains constant: the ability of these agents to suppress circulating peptide levels. This article, a review of the current non-endocrine applications of somatostatin and its analogues, covers a wide range of potential applications for somatostatin-like compounds. These include use in cirrhosis and variceal bleeding, peptic ulcer disease, pancreatic fistulas, acute and chronic pancreatitis, dumping syndrome, cancer therapy, small bowel fistulas, psoriasis, pain control, and autonomic hypotension. Somatostatin may also play a role in the development and potential treatment of neurologic disease and may have profound found influence on behavior.
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PMID:Non-endocrine applications of somatostatin and octreotide acetate: facts and flights of fancy. 168 32

Somatostatin (ST) and vasopressin (VP) infusions were compared in the treatment of actively bleeding esophageal varices. Fifty-four patients with liver cirrhosis were included in the study. Thirty-two were given ST 4.2 micrograms/min, and 22 patients were given VP 0.4 IU/min for 72 h after endoscopic diagnosis. The role of alcoholic cirrhosis was similar in both groups. Initial control of bleeding was achieved significantly more often (p = 0.0281) when ST was used (84.4%) than during VP treatment (57.1%). Rebleeding occurred in 18.8% and 4.8%, respectively. Side effects of treatment were significantly more common when VP was used than during ST treatment (p = 0.0021). Overall mortality was high in both groups, being 34% in the ST group and 36% in the VP group. ST infusion seems to be more effective and safer than VP in the treatment of acute variceal bleeding. However, the high frequency of rebleeding during ST treatment means that, after primary hemostasis with ST infusion, other methods, such as surgery or sclerotherapy, are needed to prevent the serious complications of rebleeding.
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PMID:Comparison of somatostatin and vasopressin in bleeding esophageal varices. 197 91

The value of first step isotopic angiography (FSIA) with 99-TC in the study of altered liver kidney and spleen circulation in patients with liver cirrhosis and alcoholic hepatitis is analyzed. This technique is used to evaluate the effect of a 250 mcg IV bolus of somatostatin on the activity/time curve at the three circulatory levels. The ratio of basal hepatic artery/portal flow in cirrhotics was 59 + 11/41 + 11% and 39 + 6/61 + 4 in alcoholic hepatitis, significantly different from normal controls (p less than 0.001). In cirrhotics the degree of alteration in FSIA correlated with the severity of liver disease. Somatostatin significantly improved the ratio of basel hepatic artery/portal flow and diminished the pressure at the root of suprahepatic veins (18.5 +/- - v.s. 16 +/- mmHg, p greater than 0.001). Neither the slopes nor the time of maximum isotopic activity of renal and splenic activity/time curves were modified. We concluded highlighting the clinical value of FSIA as a non invasive test in the study of chronic liver diseases.
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PMID:[Isotopic radioangiography in hepatic cirrhosis. Changes induced by somatostatin]. 197 54

The changes of humoral substances in the blood of cirrhotic rats were studied together with their effects on portal hemodynamics at different stages during the development of cirrhosis. The profiles of humoral substances and hemodynamics in two different cirrhotic rat models were also investigated. During the development of cirrhosis, glucagon increased markedly in all stages, histamine and vasoactive intestinal polypeptide (VIP) increased in the early stage, serotonin (5-HT) and somatostatin (SS) increased in the middle and late stages. There were different patterns of humoral substances in different cirrhotic models. Glucagon was the main humoral substance elevated in CCL4 induced cirrhosis, but histamine and 5-HT were mainly elevated in the blood in thioacetamide (TAA) induced cirrhosis. The hemodynamics altered differently in different stages during the development of cirrhosis and differently in the two cirrhotic rat models. Exchange transfusions between normal and cirrhotic rats resulted in an elevation of portal flow in normal rats, but no such changes were found after exchange pressure and an increase of portal blood transfusions between normal rats. The relationship between the humoral substances and portal hemodynamics is discussed. The results of this study strongly support the hypothesis of "humoral mechanism" in the pathogenesis of portal hypertension due to cirrhosis.
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PMID:Changes of blood humoral substances in experimental cirrhosis and their effects on portal hemodynamics. 212 49

The change of humoral substances in the blood of cirrhotic rat was studied at different stages of development, together with their effects on the portal hemodynamics. The profiles of humoral substances and hemodynamics in two different cirrhotic rat models, as well as the changes of portal hemodynamics in the normal rats after perfusion with the arterial blood from cirrhotic rats were also investigated. It was found that: during the development of cirrhosis, glucagon increased markedly at all stages, histamine and vasoactive intestinal polypeptide (VIP) increased at early stage only, while serotonin (5-HT) and somatostatin(SS) increased at middle and advanced stages. In the CCl4 induced cirrhosis, glucagon was the main humoral substance, whereas in the thioacetamide (TAA) induced cirrhosis, histamine and 5-HT were mainly elevated. The portal hemodynamics altered differently in different stages during the development of cirrhosis and in the two different cirrhotic rat models. The perfusion with the arterial blood from cirrhotic rats caused an increase of portal venous pressure and portal venous flow in normal rats.
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PMID:[Changes in humoral substances in induced cirrhosis and their effects on portal hemodynamics]. 257 72

During a 2-yr period 15 patients (17 episodes) with variceal bleeding (VB) and 7 with cirrhosis and acute gastroduodenal haemorrhage (GDH) received intravenous somatostatin (250 mcg per hr after a bolus of 250 mcg). Initial control of bleeding was achieved in 13 (76%) with VB and in all with GDH. Three of the 4 patients with VB and 2 with GDH who rebled during treatment were controlled increasing the infusion to 500 mcg/hr. Patients with VB received somatostatin for 24 hrs, time selected for initiating injection sclerotherapy, and those with GDH for 48-72 hrs. At 24 hrs 71% of patients with VB and all with GDH were free of bleeding. Combining different therapies VB was controlled in 16 of the 17 episodes (94%) with only one death. No complications were observed in any of the 22 patients treated.
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PMID:[Somatostatin in the emergency treatment of upper digestive hemorrhage in patients with portal hypertension]. 257 49

The most common complication of chronic pancreatitis is pain, which in many cases seems related to pancreatic ductal obstruction with ductal hypertension. Longitudinal pancreaticojejunostomy is indicated in patients with a dilated (larger than 7 mm) duct and pain that requires narcotic analgesics for relief. Chronic pseudocysts may be corrected surgically without the usual 6-week wait, and asymptomatic pseudocysts less than 4 cm in diameter may not require surgery at all. The relative efficacy and risks of percutaneous drainage of pseudocysts versus the standard surgical approaches need to be studied. Pancreatic fistulas may be external or internal, where pancreatic ascites or hydrothorax can be the clinical manifestation. The pharmacologic suppression of pancreatic secretion (e.g., with somatostatin) may be useful in their management, but surgery may be required. Pancreatic resection or internal drainage is usually effective. Persistent jaundice should be relieved surgically by choledochoduodenostomy to avoid the development of secondary biliary cirrhosis. Obstruction at various levels of the gastrointestinal tract (duodenum, small bowel, colon) may require bypass (gastrojejunostomy) or resection. Hemorrhage from major arteries is an infrequent but often lethal complication of chronic pancreatitis, especially associated with pseudocysts. Angiography is invaluable for diagnosis and occasionally for treatment (embolization). Surgery is preferred in good-risk patients, with suture ligation (resection) of the bleeding source. Chronic pancreatitis is the most common cause of splenic vein thrombosis. The resultant hemorrhage from gastric varices is managed effectively by splenectomy.
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PMID:Complications of chronic pancreatitis. 265 60

The effect of somatostatin on splanchnic hemodynamics in patients with liver cirrhosis is not clearly defined, as some authors report a decrease in portal pressure and in liver blood flow during intravenous administration of this hormone, while others do not. In 19 subjects with liver cirrhosis and portal hypertension the following parameters were measured before and during intravenous administration of somatostatin (7.5 micrograms/min): porto-hepatic gradient, estimated hepatic blood flow, specific splenic blood flow, cardiac index. Estimated hepatic blood flow decreased significantly during somatostatin infusion (p less than 0.05), averaging a 13% decrease; porto-hepatic gradient, splenic specific blood flow and cardiac index did not vary significantly. These data indicate that somatostatin infused at a dose of 7.5 micrograms/min induces a slight decrease in liver blood flow without affecting portal hypertension.
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PMID:Effect of somatostatin on splanchnic hemodynamics in patients with liver cirrhosis and portal hypertension. 286 99

The effects of a somatostatin analogue, SMS 201-995 on hepatic haemodynamics were studied in rats with dimethylnitrosamine-induced cirrhosis. An intravenous infusion of 1, 2 or 4 micrograms kg-1 body wt h-1 SMS 201-995 produced a rapid and sustained decrease in portal pressure, portal venous flow and liver blood flow without significantly altering arterial blood pressure or pulse. The reductions in portal pressure, portal venous flow and liver blood were accompanied by an increase in splanchnic vascular resistance. Portal venous resistance was not affected. Subcutaneous injection of 2 micrograms kg-1 body wt SMS 201-995 produced a gradual decrease in portal pressure, the maximum reduction occurring 18 min after administration. This reduction in portal pressure was sustained for a further 20 min. The results suggest that SMS 201-995 may be of value in the control of bleeding oesophageal varices. Furthermore, the prolonged duration of action of SMS 201-995 following its subcutaneous administration suggests that the analogue may be useful in the long-term management of portal hypertension in patients with cirrhosis.
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PMID:The effects of a somatostatin analogue SMS 201-995 on hepatic haemodynamics in the cirrhotic rat. 286 12

Bleeding from esophageal varices is a feared complication of liver cirrhosis with high mortality. Pharmacotherapy of the acute bleeding episode with vasopressin has been shown to be effective in controlled studies, but side effects of this therapy are high and therefore replacement of vasopressin with somatostatin is under investigation. Another potential lead is the combination of vasopressin with vasodilators such as nitroglycerin. While acute pharmacotherapy of the patient with esophageal varices is well accepted, chronic or prophylactic pharmacotherapy is still in the investigative stage. Prophylactic therapy with beta-blockers, e.g. propranolol, has been shown to be effective in compensated patients with alcoholic cirrhosis. In patients with more advanced stages of the disease, or with cirrhosis of other etiology, the effectiveness of propranolol has not been proven. The mechanism of propranolol is similar to that of vasopressin, i.e. it lowers portal pressure by reducing portal flow. To maintain function of the affected organ, an alternative approach--namely lowering of portal pressure through reduction of the pathologically elevated resistance--should be actively investigated.
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PMID:[Pharmacological therapy of portal hypertension]. 286 82


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