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)

Aim of this study was to investigate whether octreotide, a synthetic somatostatin analogue that inhibits growth hormone, insulin and glucagon secretion and improves glycaemic control in insulin dependent diabetic patients was able to exert similar effects in insulin treated type 2 diabetic patients with chronic renal failure who have high plasma glucagon levels. For this purpose saline or octreotide was randomly administered by continuous subcutaneous infusion (100 mcg/daily) in addition to usual insulin treatment for 5 days to six type 2 insulin treated diabetic patients with chronic renal failure and to six type 2 patients with normal renal function, as a control group. At day 3 of insulin plus saline or insulin plus octreotide treatment, total glucose uptake and hepatic glucose production (HGP) were investigated during an euglycemic clamp; at day 5 GH, glucagon and C-peptide plasma levels were evaluated. Octreotide treatment lowered endogenous insulin secretion (evaluated by C-Peptide levels assay), GH and glucagon in all patients, but caused a significant reduction of daily insulin requirement (32 +/- 14 I.U. vs 41 +/- 19 I.U., P<0.02) only in patients with renal failure. HGP was significantly (P<0.05) lowered in patients with renal failure but glucose uptake remained unchanged. The lowering effect of octreotide on insulin requirement in diabetic patients with renal failure in spite of the contemporaneous inhibition on insulin secretion could be explained on the basis of the greater reduction of glucagon levels which are very elevated in these patients as compared to patients with normal renal function. The lowering of glucagon could decrease HGP and, consequently, insulin requirement.
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PMID:Effect of octreotide on insulin requirement, hepatic glucose production, growth hormone, glucagon and c-peptide levels in type 2 diabetic patients with chronic renal failure or normal renal function. 1113 81

The chelator somatostatin analogue dota-D-phe(1)-tyr(3)-octreotide (DOTATOC), which is stably labeled with the beta-emitting radioisotope yttrium 90 ((90)Y), is used as internal radiotherapy for the treatment of patients with advanced neuroendocrine tumors. We report 5 patients who developed chronic renal failure, caused in 3 patients by biopsy-proven thrombotic microangiopathy (TMA). Twenty-nine patients (14 men, 15 women) with normal renal function before therapy were treated with divided intravenous doses of (90)Y-DOTATOC approximately 6 weeks apart (mean normalized cumulative dose, 165.4 +/- 36.4 mCi/m(2)). Twenty-two of 29 patients were administered a normalized cumulative dose of 200 mCi/m(2) without side effects. Among the 7 patients (6 women, 1 man) administered a normalized cumulative dose greater than 200 mCi/m(2), 5 patients (4 women, 1 man) developed renal failure. Increasing serum creatinine levels were observed within 3 months after the last (90)Y-DOTATOC injection. The evolution was rapidly progressive in 3 patients, resulting in end-stage renal failure within 6 months. The remaining 2 patients developed chronic renal insufficiency (mean serum creatinine level, 300 micromol/L an average 16 months after the end of treatment). Renal biopsies performed in 3 patients showed typical signs of TMA involving glomeruli, arterioles, and small arteries. Patients treated with high-dose (90)Y-DOTATOC internal radiotherapy (cumulative dose > 200 mCi/m(2)) are at high risk to develop severe renal failure caused by TMA lesions. The histopathologic lesions are identical to those found after external radiotherapy, which suggests a causal relationship between (90)Y-DOTATOC and renal TMA.
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PMID:A new cause of renal thrombotic microangiopathy: yttrium 90-DOTATOC internal radiotherapy. 1127 86

We report a case of a female neonate with Beckwith-Wiedemann syndrome who manifested upper airway obstruction soon after birth and suffered from intractable hypoglycemia and abdominal distention caused by nephromegaly. She was delivered at 31 weeks of gestation with 2480 g and was diagnosed as Beckwith-Wiedeman syndrome, manifesting macroglossia, hepatomegaly, nephromegaly and omphalocele. Her trachea was intubated 30 minutes after birth due to upper airway obstruction. At 12 days of life, glossopexy was performed to relieve the airway obstruction. Although tracheal extubation was successfully accomplished 12 days later, 21 days after the glossopexy she manifested apnea and hypoxia and required tracheal intubation and mechanical ventilation again. We suspected hypoglycemia or central apnea to be the cause of apnea and started the administration of somatostatin analog as a treatment for hypoglycemia. In addition to the apnea, abdominal distention caused by nephromegaly exacerbated her respiratory condition. At 69 days of life she died of sepsis complicated with disseminated intravascular coagulation and renal failure. A needle biopsy at autopsy revealed nephroblastomatosis.
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PMID:[A neonate with Beckwith-Wiedemann syndrome who developed upper airway obstruction after glossopexy]. 1184 Jun 63

Hormonal disorders are the permanent symptoms of renal failure. They concern all known hormones and can be due to quantitative changes of the secretory activity and disturbances of endocrine cell functions. The aim of this study was to establish whether experimental thyroparathyroidectomy in uremic animals causes detectable histomorphological changes in endocrine cells of pancreatic islets. Thyroparathyroidectomy was performed in rats 30 days after nephrectomy. Fragments of pancreatic tissue were collected 14 days after the operation. Paraffin sections were stained with H+E and by silver salt impregnation. Immunohistochemical reactions were conducted using antibodies against calcitoningene-related peptide (CGRP), synaptophysin (SPh), somatostatin (ST), neuron-specific enolase (NSE), and chromogranin (CgA). It was shown that endocrine cells of pancreatic islets in thyroparathyroidectomized rats show intensified immunoreactivity to SPh and ST as compared to the control group of animals. Immunocytochemical reactions for NSE, CgA, and CGRP were negative.
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PMID:Preliminary evaluation of pancreatic islets in rats with experimental uremia and after thyroparathyroidectomy. 1205 34

A diabetic patient with chronic renal failure who developed recurrent and prolonged episodes of hypoglycemia associated with use of sulfonylurea agent is presented here. This patient was hospitalized with neuroglycopenic symptoms of hypoglycemia that persisted in spite of large doses of parenteral glucose replacement. On administration of somatostatin analogue octreotide, hypoglycemia resolved and, blood glucose levels were maintained even after cessation of parenteral glucose. The patient received 2 subcutaneous doses of octreotide 12 hours apart, and made a complete recovery. Our experience suggests that use of octerotide to treat refractory or prolonged sulfonylurea-included hypoglycemia in renal failure patients is safe and effective; large prospective studies would be needed to validate these findings.
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PMID:Use of octreotide to treat prolonged sulfonylurea-induced hypoglycemia in a patient with chronic renal failure. 1260 74

Splanchnic arterial relaxation is the most important pathology in systemic circulation of portal hypertensive patients. Progressive decline of splanchnic vascular resistance is responsible for development of circulatory dysfunction syndrome (CDS), associated with reduction of effective blood volume within central vascular compartment and compensatory stimulation of vasopressor and natrium retaining hormonal mechanisms. Advanced CDS is characterized by increased cardiac output, tachycardia and low arterial pressure. Complications of CDS have functional nature and comprise: renal failure (hepatorenal syndrome), respiratory failure in context of hepatopulmonary syndrome, cardiac insufficiency produced by portopulmonary hypertension or portal cardiomyopathy, hemorrhages from digestive tract caused by hypertensive portal gastropathy or derangements of brain perfusion. The management of CDS relies on adequate filling of vascular system (albumin), constriction of arterial splanchnic vessels (beta-blocker, analogs of vasopressin and somatostatin), reduction of cardiac output (beta-blocker) and giving support to local vasoprotective mechanisms (prostaglandins, nitric oxide, blockade of ET-A receptors).
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PMID:[Circulatory dysfunction syndrome associated with liver cirrhosis]. 1619 May 66

Gastrointestinal bleeding is a frequent and severe complication of portal hypertension. The most frequent cause of the bleeding is variceal rupture. Despite improvements in prognosis after variceal bleeding over the past two decades, the 6-week mortality rate remains high, ranging from 15 to 30%. Patients die from uncontrolled bleeding, early rebleeding, infection, or renal failure within the first weeks of a bleeding episode. Poor hepatic function, severe portal hypertension with a hepatic venous pressure gradient (HVPG) >20 mmHg, and active bleeding at endoscopy are independently associated with poor prognosis. First-line treatment includes resuscitation, prophylactic antibiotic therapy, the combined use of vasoactive drugs (started as soon as possible), and an endoscopic procedure. Reconstitution of blood volume should be done cautiously to maintain the haematocrit between 25 and 30%. Terlipressin, somatostatin, or octreotide can be used, and drug therapy is maintained from 48 h to 5 days. Ligation is the endoscopic treatment of choice in bleeding oesophageal varices; in gastric varices, obturation with cyanoacrylate is preferable. Uncontrolled bleeding should be an indication for a salvage transjugular portosystemic shunt (TIPS). In patients with Child-Pugh score A, shunt surgery might be an alternative to TIPS. Trials are currently ongoing into the precise indications of early TIPS in selected patients with an HVPG >20 mmHg, and into the usefulness of administration of recombinant activated factor VII when there is an active bleeding at endoscopy.
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PMID:Management of acute bleeding from portal hypertension. 1722 94

Peptide Receptor Radionuclide Therapy (PRRT) with radiolabelled somatostatin analogues is a promising treatment option for patients with inoperable or metastasised neuroendocrine tumours. Symptomatic improvement may occur with all of the various (111)In, (90)Y, or (177)Lu-labelled somatostatin analogues that have been used. Since tumour size reduction was seldom achieved with (111)Indium labelled somatostatin analogues, radiolabelled somatostatin analogues with beta-emitting isotopes like (90)Y and (177)Lu were developed. Reported anti-tumour effects of [(90)Y-DOTA(0),Tyr(3)]octreotide vary considerably between various studies: Tumour regression of 50% or more was achieved in 9 to 33% (mean 22%). With [(177)Lu-DOTA(0),Tyr(3)]octreotate treatments, tumour regression of 50% or more was achieved in 28% of patients and tumour regression of 25 to 50% in 19% of patients, stable disease was demonstrated in 35% and progressive disease in 18%. Predictive factors for tumour remission were high tumour uptake on somatostatin receptor scintigraphy and limited amount of liver metastases. The side-effects of PRRT are few and mostly mild, certainly when using renal protective agents: Serious side-effects like myelodysplastic syndrome or renal failure are rare. The median duration of the therapy response for [(90)Y-DOTA(0),Tyr(3)]octreotide and [(177)Lu-DOTA(0),Tyr(3)]octreotate is 30 months and more than 36 months respectively. Lastly, quality of life improves significantly after treatment with [(177)Lu-DOTA(0),Tyr(3)]octreotate. These data compare favourably with the limited number of alternative treatment approaches, like chemotherapy. If more widespread use of PRRT is possible, such therapy might become the therapy of first choice in patients with metastasised or inoperable gastroenteropancreatic neuroendocrine tumours. Also the role in somatostatin receptor expressing non-GEP tumours, like metastasised paraganglioma/pheochromocytoma and non-radioiodine-avid differentiated thyroid carcinoma might become more important.
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PMID:Peptide Receptor Radionuclide Therapy with radiolabelled somatostatin analogues in patients with somatostatin receptor positive tumours. 1765 93

Polycystic kidney diseases (autosomal dominant and autosomal recessive) are progressive renal tubular cystic diseases, which are characterised by cyst expansion and loss of normal kidney structure and function. Autosomal dominant polycystic kidney disease (ADPKD) is the most common life- threatening, hereditary disease. ADPKD is more prevalent than Huntington's disease, haemophilia, sickle cell disease, cystic fibrosis, myotonic dystrophy and Down's syndrome combined. Early diagnosis and treatment of hypertension with inhibitors of the renin-angiotensin-aldosterone system (RAAS) and its potential protective effect on left ventricular hypertrophy has been one of the major therapeutic goals to decrease cardiac complications and contribute to improved prognosis of the disease. Advances in the understanding of the genetics, molecular biology and pathophysiology of the disease are likely to facilitate the improvement of treatments for these diseases. Developments in describing the role of intracellular calcium ([Ca(2+)](i)) and its correlation with cellular signalling systems, Ras/Raf/mitogen extracellular kinase (MEK)/extracellular signal-regulated protein kinase (ERK), and interaction of these pathways with cyclic adenosine monophosphate (cAMP) levels, provide new insights on treatment strategies. Blocking the vasopressin V(2) receptor, a major adenylyl cyclase agonist, demonstrated significant improvements in inhibiting cytogenesis in animal models. Because of activation of the mammalian target of rapamycin (mTOR) pathway, the use of sirolimus (rapamycin) an mTOR inhibitor, markedly reduced cyst formation and decreased polycystic kidney size in several animal models. Caspase inhibitors have been shown to decrease cytogenesis and renal failure in rats with cystic disease. Cystic fluid secretion results in cyst enlargement and somatostatin analogues have been shown to decrease renal cyst progression in patients with ADPKD. The safety and efficacy of these classes of drugs provide potential interventions for experimental and clinical trials.
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PMID:Potential pharmacological interventions in polycystic kidney disease. 1803 88

Hepatorenal syndrome is a form of acute or sub-acute renal failure which develops in patients with chronic liver disease. In contrast to other forms of acute renal failure it may be reversible using pharmacological agents. The pathogenesis involves splanchnic vasodilatation and intense renal vasoconstriction. Increasing intravascular volume and prolonged treatment with vasoconstrictor drugs reverses renal failure in a significant proportion of patients. Agents currently used include the vasopressin analogues terlipressin and the alpha1-adrenoceptor agonist midodrine. The somatostatin analogue octreotide has been used in combination therapy but is ineffective as monotherapy. Intravenous albumin is an important adjunctive treatment both in the prevention and treatment of hepatorenal syndrome. Increasing intravascular volume using TIPS (transjugular intrahepatic stent shunt) is effective in some patients and may be useful in maintaining patients who have initially responded to pharmacological therapy. Despite improvements in survival, long term prognosis is still poor and generally depends on the degree of reversibility of the underlying liver disease or access to liver transplantation.
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PMID:Management of hepatorenal syndrome. 1853 34


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