Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten patients with non-alcoholic cirrhosis and ten control subjects were studied in basal conditions and after ingestion of a standard mixed test meal. Plasma somatostatin, blood glucose, plasma insulin, C-peptide and glucagon were determined before and 15, 30, 45, 60, 90, 120 and 180 min after the start of the meal. Basal somatostatin levels in patients (31.9 +/- 1.8 ng/l) were significantly higher (p less than 0.01) than in controls (12.5 +/- 0.9 ng/l). The time-course of the somatostatin secretory response after the meal was similar in the two groups, but the increase, evaluated as incremental area above baseline, was significantly smaller (p less than 0.01) in cirrhotics (804 +/- 134 ng/l per min) than in controls (1482 +/- 149 ng/l per min). Data indicate that elevated basal plasma somatostatin concentrations in cirrhosis may be consequent to elevated gastrointestinal and/or pancreatic secretion, whereas the blunted somatostatin response to the mixed test meal may derive from the hyperinsulinemia which occurs in the postprandial period.
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PMID:Plasma somatostatin response to an oral mixed test meal in cirrhotic patients. 167 40

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

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

The oesophageal pH was recorded for 3 h after a test-meal in 27 healthy control subjects (group I), 40 patients with alcoholic cirrhosis (group II), and 22 patients with a normal liver and symptoms of gastro-oesophageal reflux (control refluxers). Gastro-oesophageal reflux was observed in 10 of the cirrhotic patients. Marked reflux episodes lasted longer in cirrhotic refluxers than in control refluxers (P less than 0.05). The frequency of ascites, bleeding from ruptured oesophageal varices, peripheral neuropathy and hepatic encephalopathy were not significantly different according to presence or absence of reflux. Plasma concentrations of gastrin, somatostatin, motilin and vasoactive intestinal peptide (VIP) were measured in groups I and II. Fasting plasma motilin levels, and the release of motilin and of VIP after the meal were higher in group II than in group I. Basal levels and post-prandial profiles of the four peptides tested did not differ between cirrhotics with or without gastro-oesophageal reflux. We conclude that in patients with alcoholic cirrhosis: gastro-oesophageal reflux is frequent (25%) and characterized by prolonged reflux episodes; reflux is not correlated with the degree of liver failure and plays no significant role in the rupture of oesophageal varices; and raised plasma motilin and VIP levels cannot account for the high incidence of reflux in cirrhotics.
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PMID:Gastro-oesophageal reflux and alcoholic cirrhosis. A reappraisal. 288 50

Continued haemorrhage from oesophageal varices despite adequate injection sclerotherapy and tamponade has a high mortality rate. Such patients are usually referred for surgery. Over a 10-year period, 30 patients (21 men and nine women of median age 52 (range 21-70) years) with acute variceal haemorrhage uncontrolled by initial treatment underwent early emergency oesophageal transection. Portal hypertension was caused by alcoholic cirrhosis in 22 patients; other forms of cirrhosis were present in seven and portal vein thrombosis in one. Hepatic function immediately before operation was Pugh grade A in two patients, B in six and C in 22. Deterioration between admission and transection from grade A to B occurred in one patient and from B to C in five. Oesophageal transection stopped variceal haemorrhage in 29 of the 30 patients. Rebleeding from gastric varices within 35 days of surgery occurred in five patients. Postoperative haemorrhage also occurred from perioesophageal vessels (two patients), a gastrotomy (one) and oesophageal ulceration (two). Hepatic failure developed in seven patients, renal failure in five and both hepatic and renal failure in four. Mortality at 30 days occurred in neither of the two patients with liver function of grade A, in one of six of grade B and in 18 of 22 of grade C. The overall 30-day mortality rate was thus 63 per cent. Mortality was related to the preoperative Pugh grade (hazard ratio 3.95 per grade; P = 0.013) and preoperative blood transfusion (hazard ratio 1.37 per unit; P = 0.035). Four of six patients with grade B liver function died within 3 months and 21 of 22 with grade C disease within 1 year. Oesophageal transection is effective at stopping variceal bleeding but does not modify the underlying disease. Caution is urged for patients with grade C hepatocellular impairment proceeding to acute oesophageal transection after initial sclerotherapy. Such patients may benefit more from treatment with somatostatin or an intrahepatic porta-systemic stent shunt while awaiting definitive therapy.
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PMID:Emergency oesophageal transection for uncontrolled variceal haemorrhage. 792 95

The site of impaired glucose uptake in cirrhosis is uncertain. We therefore performed hyperglycemic clamps (glucose 10 mmol/L) in 10 patients with compensated alcoholic cirrhosis and impaired glucose tolerance and in six control subjects. Muscle glucose uptake was estimated in patients and controls with the forearm technique. In the cirrhotic subjects splanchnic glucose uptake was measured with hepatic vein catheterization and primed continuous infusions of indocyanine green and [6-3H]glucose. To assess insulin-independent glucose uptake and the effects of elevated nonesterified fatty acid levels on glucose uptake, we repeated the study with somatostatin to induce insulin deficiency and a nicotinic acid analog, acipimox, to inhibit lipolysis. Substrate disposal was assessed on indirect calorimetry. Despite similar stimulated insulin levels, total glucose utilization was lower in the cirrhotic subjects (3.9 +/- 0.3 vs. 8.8 +/- 1.7 mg/kg/min, p = 0.006). This deficiency was accounted for by lower nonoxidative glucose disposal (1.2 +/- 0.2 vs. 5.8 +/- 1.6 mg/kg/min, p = 0.002). Forearm glucose uptake was lower in the cirrhotic subjects (0.39 +/- 0.06 vs. 1.21 +/- 0.3 mg/100 ml/min, p = 0.001). However, splanchnic glucose uptake at 1.59 +/- 0.14 mg/kg/min was similar to that reported in other studies of normal subjects. Insulin-independent glucose uptake was normal, and acipimox had no effect on total or forearm glucose utilization. Glucose intolerance in cirrhosis is characterized by impaired peripheral insulin-stimulated non-oxidative glucose disposal. The high nonesterified fatty acid levels seen in cirrhosis most likely do not contribute to this defect. Splanchnic glucose uptake is normal in cirrhosis.
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PMID:Normal splanchnic but impaired peripheral insulin-stimulated glucose uptake in cirrhosis. 810 Jul 99

Hyperinsulinemic euglycemic clamps were performed on six patients with compensated alcoholic cirrhosis and on six normal comparison subjects. As in previous studies, glucose uptake in the cirrhotic patients was only 21% of the comparison value. The cirrhotic patients had high growth hormone (GH) and low insulin-like growth factor-I (IGF-I) levels, with low insulin-like growth factor-binding protein (IGFBP)-3 levels, but surprisingly high IGFBP-I levels (26.8 +/- 8.4 microgH vs. 3.2 +/- 0.2 microm/L, P < .001). The log IGFBP-1 level was inversely correlated with the log insulin sensitivity (r = -.95). The clamps were repeated with a somatostatin infusion to suppress GH secretion. IGFBP-1 increased in both groups, especially in the cirrhotic subjects. Insulin sensitivity increased in the normal subjects but was unchanged in the cirrhotic patients. Following GH treatment (0.13 U/kg/d for 5 days), the clamps were repeated. GH, IGF-1, and IGFBP-3 levels were now similar in the two groups; IGFBP-1 levels decreased in the cirrhotic patients but remained fivefold higher than the comparison value (10.6 +/- 3.7 vs. 2.1 +/- 0.4, P < .05). Glucose uptake in the cirrhotic patients remained only 29% of the comparison value, but the change in their insulin sensitivity was inversely correlated with the change in their IGFB-1 levels (r = -.84). These results suggests an important role for IGFBP-1 in modulating insulin sensitivity in cirrhosis.
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PMID:High insulin-like growth factor binding protein 1 levels in cirrhosis: link with insulin resistance. 870 51

In the liver, the autonomic nervous system plays an important role in degenerative and inflammatory changes. The aim of the present study was to investigate the distribution of neuronal fibres containing neuropeptides in livers of 5 patients with cirrhosis by immunocytochemical localization at the light and electron microscopical level of substance P (SP), neuropeptide Y (NPY), somatostatin (SOM), and calcitonin gene-related peptide (CGRP). In patients with alcoholic cirrhosis, a decreased number of neuronal fibres was found in the portal tract and fibrous septa as well as in the sinusoids of regenerative nodules. NPY- and SP-immunoreactive neuronal fibres were more numerous than CGRP-containing fibres. They were located mainly in portal tracts. These findings led to the conclusion that peptidergic innervation plays a role in inflammatory and fibrotic changes in cirrhotic liver.
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PMID:Immunocytochemical study on the liver innervation in patients with cirrhosis. 1114 32

Portal hypertensive colopathy (PHC) is a recently described entity in patients with portal hypertension which can cause even life-threatening lower gastrointestinal bleeding. In contrast to variceal bleed, there is no standardized treatment for the control of bleeding from these lesions. We report a case of alcoholic cirrhosis with portal hypertension, in whom bleeding from colonic angiodysplasia-like lesions was effectively controlled by somatostatin infusion.
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PMID:Severe acute bleeding from portal colopathy controlled by somatostatin: a case report. 1568 64