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)

A 15 year old girl with a family history of type 1 multiple endocrine adenomatosis presented with reversible neurological disturbances, hypoglycaemia and hyperinsulinaemia. Initial radiology was normal, but portal venous sampling suggested an insulinoma in the tail of the pancreas which was removed with conservation of the spleen. Hypoglycaemia persisted despite high doses of diazoxide and intravenous dextrose. A second laparotomy revealed a pancreatic endocrine tumour and sub-total pancreatectomy was performed. Histology revealed islet cell microadenomatosis. Hypoglycaemia persisted despite treatment with somatostatin analogues and 40% intravenous dextrose was required to maintain normoglycaemia. A possible lesion near the splenic hilum on computed tomographic scan was reported as a splenunculus although further peripheral, hepatic and portal venous sampling suggested hepatic or systemic lesions. A positron emission scan and selective visceral angiography suggested a lesion in the left upper quadrant. Acute lactic acidosis, rhabdomyolysis and renal failure supervened. Post mortem revealed the putative 'splenunculus' to be a residual insulinoma, whilst the splenic vein was thrombosed, accounting in part for discrepant venous sampling data. Hyperinsulinaemia in type 1 multiple endocrine adenomatosis may require more aggressive surgical and hormonal intervention than when dealing with solitary insulinomas. Insulinomas may mimic developmental abnormalities on computed tomographic scanning.
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PMID:Difficulties in localization and treatment of insulinomas in type 1 multiple endocrine adenomatosis (MEA). 135 Mar 44

Dichloroacetate (DCA) is gaining use as an alternative to bicarbonate therapy in the treatment of lactic acidosis. To determine the mechanism(s) by which DCA lowers blood lactate levels, we studied its effect on the kinetic interrelationships between pyruvate, lactate, alanine, and glucose in the hindlimb of dogs during hormonal stimulation of pyruvate production (Ra) and its conversion to lactate. Three groups of dogs (n = 6) were infused with 1-13C-pyruvate to measure whole body pyruvate Ra, and pyruvate Ra and utilization (Rd) across the hindlimb during either a 4-hr infusion of saline (controls), or somatostatin, glucagon, and epinephrine (SGE), or SGE plus dichloroacetate (SGE + DCA). Pyruvate Ra was used as an index of rate of glycolysis and Rd as an index of pyruvate oxidation. In the controls, all kinetic parameters were constant during the saline infusion. Hindlimb pyruvate Ra and Rd were almost equal, and lactate release negligible. Compared to controls, SGE administration significantly increased (P < 0.05) wholebody pyruvate Ra (48.5 +/- 6.2 vs 33.6 +/- 2.4 mumol/kg/min) and blood lactate levels (P < 0.05). Hindlimb pyruvate Ra increased by approximately 150%, but Rd remained unchanged resulting in marked increases in lactate and alanine effluxes. Adding DCA to the SGE infusion significantly reduced wholebody pyruvate Ra (P < 0.05) and blood lactate levels (P < 0.01). In the hindlimb, however, there was no decrease in lactate output, despite a 91% increase in pyruvate utilization because pyruvate Ra also increased. These results suggest that during stimulation of rate of glycolysis, DCA lowers lactate levels by reducing the overall availability of pyruvate for lactate synthesis. This is accomplished by suppressing the rate of glycolysis in tissues other than skeletal muscle and stimulating pyruvate oxidation.
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PMID:Mechanisms by which dichloroacetate lowers lactic acid levels: the kinetic interrelationships between lactate, pyruvate, alanine, and glucose. 790 82

The mechanism and response to treatment of severe life-threatening hypoglycaemia (plasma glucose 1.15 +/- 0.73 mM/l [+/- SD]) was studied in eight Thai patients with falciparum malaria. Plasma insulin concentrations were inappropriately high (range 1.0-21.8 mU/l), lactic acidosis was common (arterial blood lactic acid concentration 1.44-17.8 mM/l), but the glucose counterregulatory response, indicated by plasma cortisol, growth hormone, catecholamines and glucagon concentrations, was intact. Hyperinsulinaemia was successfully treated in five patients by a continuous intravenous infusion of the long-acting somatostatin analogue Sandostatin (SMS 201-995), 50 micrograms/h. In volunteer studies a single intramuscular injection of Sandostatin (100 micrograms) suppressed quinine-induced hyperinsulinaemia within 15 min; this effect was maintained for 6 h. These results suggest that Sandostatin may be a safe and effective way of correcting the hyperinsulinaemic hypoglycaemia complicating quinine treatment of falciparum malaria. This treatment could be particularly useful in fluid-overloaded patients with recurrent hypoglycaemia despite dextrose infusions.
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PMID:Hypoglycaemia and counterregulatory hormone responses in severe falciparum malaria: treatment with Sandostatin. 832 38

A case is reported of a chronic intestinal pseudoobstruction with lethal outcome in a 6-year-old boy. The clinical symptoms and radiology examination showed ileus without mechanical obstruction. During the observation the patient developed left sided mydriasis and grand mal seizures with lactacidosis. He was treated conservatively which included total parenteral nutrition, fluid-sodium supplements, intravenous erythromycin and somatostatin, correction of acidosis. On the 48th day he died suddenly of cardiac failure at the intensive care unit. The gastrointestinal and neurologic symptoms with lactacidosis suggested the possibility of mitochondrial myopathy. Postmortem histopathology showed visceral myopathy. Molecular genetic analysis could not confirm the presence of the mDNA mutation.
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PMID:[Chronic intestinal pseudoobstruction due to visceral myopathy]. 1761 Nov 83