Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The endocrine function and histology of segmental pancreatic autografts with pancreatic exocrine diversion to the esophagus were assessed in nine dogs which survived longer than three years. An original twelve dogs underwent total pancreatectomy followed by a segmental pancreatic graft autotransplanted with pancreatic duct to esophagus anastomosis in the neck. All twelve dogs immediately had normal fasting glucose, nine of which sustained it for more than three years. One of the twelve dogs died on the tenth day from a thrombosis and two others died of causes unrelated to the graft; one of pneumonia and the other of an unknown cause, within the first year of transplantation. An intravenous glucose tolerance test performed three years after the transplantation revealed K values (1.90 +/- 0.37) which were not significantly different from those tested before the transplantation (1.92 +/- 0.42). The patency of the anastomosis between the pancreatic duct and the esophagus was clearly identified in the specimen of a dog sacrificed three years after the transplantation. The mucosa of the esophagus was macroscopically and microscopically almost normal. Histological studies of the autografts done three years after the transplantation showed almost normal pancreatic architecture in the islets and exocrine tissues, while histochemical analysis with immunoperoxidase stains confirmed the presence of insulin, glucagon and somatostatin. It is therefore possible that this new technique could be used for clinical segmental pancreatic transplantation.
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PMID:The long-term function and histology of segmental pancreatic autografts with pancreatic exocrine diversion to the esophagus in dogs. 208 92

Of 18 AIDS patients with Pneumocystis carinii pneumonia treated with pentamidine mesylate parenterally, four developed serious to severe hypoglycaemia, three hypoglycaemia followed by insulin-requiring diabetes, and two others diabetes alone. Hypoglycaemia (blood glucose 2.1 +/- 0.2 (+/- SE) mmol l-1) occurred 9 (2-22) days after starting treatment, and diabetes (initial blood glucose 30 +/- 6 mmol l-1) after 60 (20-90) days. The other patients remained euglycaemic. The dysglycaemic patients (hypo- and hyper-glycaemic) had a higher pentamidine dosage (p less than 0.01), and higher serum creatinine levels at end of treatment (p less than 0.001), consistent with drug accumulation and dose-dependent toxicity. Plasma C-peptide levels were low in the diabetic patients, in the basal state (0.25-0.28 nmol l-1) and following stimulation by IV glucagon (0.35-0.40 nmol l-1), vs 0.80 +/- 0.06 nmol l-1 (basal) and 1.83 +/- 0.16 nmol l-1 (stimulated) in 23 healthy control subjects (mean +/- SE). Islet cell or insulin antibodies were not detected. Serum amylase levels rose abnormally in the dysglycaemic group, and pancreatitis was proved in one, and suspected in another patient. None of 28 similar AIDS patients whose P. carinii pneumonia was treated with cotrimoxazole showed blood glucose disturbance.
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PMID:Hypoglycaemia and diabetes mellitus following parenteral pentamidine mesylate treatment in AIDS patients. 214 64

A prospective study of 18 critically ill patients with community-acquired lobar pneumonia was undertaken at Hillbrow Hospital, Johannesburg, in order to document the initial plasma hormonal and substrate profile as part of the stress response to the infection. The results of these studies, carried out before therapy, were compared with the results in a group of healthy fasting adults. Highly significant (P less than or equal to 0.005) increases in the mean plasma levels of adrenaline, noradrenaline, human growth hormone, cortisol, glucose and free fatty acids were noted in the study group, with a lesser increase in the prolactin concentration (P less than or equal to 0.01). The levels of dopamine, glucagon, insulin and adrenocorticotrophin did not show any significant change. No significant differences were found in the hormonal profile when comparing survivors with non-survivors. The neuro-endocrine hormonal and metabolic responses in pneumonia appear to be similar to those seen in other stress situations and failure of the initial stress response does not appear to contribute to the mortality of critically ill patients with community-acquired lobar pneumonia.
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PMID:Initial hormonal and metabolic profile in critically ill patients with community-acquired lobar pneumonia. 259 84

We have reviewed ten children who underwent surgical therapy for persistent neonatal hypoglycemia over a 5-year period. All had inappropriately high insulin levels in the face of hypoglycemia, and all failed medical management with intravenous glucose, frequent feeds, diazoxide and glucagon. Two groups of five patients each were analysed retrospectively. Group 1 underwent 95% pancreatectomy, leaving a small amount of pancreatic tissue on the duodenum and common bile duct. The only major complication in this group was in one patient with common duct obstruction requiring choledochoduodenostomy. All these children are developing normally, without diabetes, steatorrhea, or recurrent hypoglycemia. Group 2 underwent 85% pancreatectomy, leaving the uncinate process in situ. Two of these children are well. Two required conversion to 95% resection because of recurrent hypoglycemia; one of these required a subsequent total pancreatectomy, at which time the pancreatic remnant had significantly regenerated. The other Group II patient was normoglycemic but died at age 3 from pneumonia. Pathology in nine cases showed islet cell dysplasia; 5 of these also had microadenomatosis. One case had a histologically normal pancreas. We conclude that 95% pancreatectomy is a safe operation with a lower failure rate than less radical resections, and should be used early in the management of this condition.
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PMID:Surgical management of persistent neonatal hypoglycemia due to islet cell dysplasia. 639 33

Four patients, treated with pentamidine because of Pneumocystis carinii pneumonitis, displayed severe fasting hypoglycemia during this treatment. Diabetes mellitus appeared later, requiring insulin therapy in the three of them who survived more than a few weeks. The metabolic study, performed in two cases during the hypoglycemic period, demonstrated inappropriately high insulin levels in the postabsorptive state. 28 +/- 1 microunits/ml (blood glucose 41 +/- 4 mg/dl) and 86 +/- 5 microunits/ml (blood glucose 15 +/- 5 mg/dl) vs. 15 +/- 3 microunits/ml in 10 control subjects and 55 +/- 3 microunits/ml in 6 patients with a verified B-cell tumor, respectively. Poor B-cell secretory responses followed the stimulations by oral glucose (maximal increment over basal: +5 microunits/ml vs. + 40 microunits/ml in control group and +77 microunits/ml in the insulinoma group), by i.v. arginine (maximal increment + 10 and +28 microunits/ml, respectively, vs. +55 in the controls and +90 microunits/ml in the insulinoma group) and by i.v. glucagon (+10 and +23 microunits/ml, respectively) vs. +40 microunits/ml in both the control and the insulinoma groups). Plasma cortisol and glucagon, and the A-cell response to arginine were higher than normal. These high, nonsuppressible, nonstimulable insulin levels and the sequence of hypoglycemia followed by insulin-dependent diabetes mellitus is consistent with the hypothesis of a selective toxicity turned towards the B-cells. In vitro incubation of islets with pentamidine 10(-10) M produced a passive release of insulin, followed by a significant decrease in B-cell response to glucose + theophylline. It is suggested that pentamidine can induce hypoglycemia because of an early cytolytic release of insulin, and then diabetes mellitus because of B-cell destruction and insulin deficiency.
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PMID:Diabetes mellitus following pentamidine-induced hypoglycemia in humans. 675 11

The pancreatic islets from 112 infants (66 males and 46 females) who died of SIDS during the years 1990-1992 have been studied. The control group consisted of endocrine pancreas tissue from 19 infants who died of a clear cause of death (pneumonia, drowning, sepsis, etc.). The mean age of the SIDS group was 5.1 months. We found histologically normally developed organs in all the SIDS cases. By evaluating the relative endocrine cell area of the pancreas by immunohistochemical investigations, A-cells were found to make up 10-30%, B-cells 30-60%, D-cells 10-30% and pancreatic polypeptide cells less than 10% in the SIDS group and in the controls with a small increase in glucagon and insulin cells among SIDS cases. The morphometric evaluation revealed that cell enlargement and cytoplasm shrinking occurred slightly more often in the SIDS group than in the control group. The diameter of the islets was normal and the maximal volume was not enlarged. The results did not show significant differences so that a relationship between alterations of the endocrine pancreas and sudden infant death syndrome could not be demonstrated.
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PMID:Morphology, immunohistochemistry and morphometry of pancreatic islets in cases of sudden infant death syndrome (SIDS). 927 44

The aim of the study was to verify the effects of the administration of an inhibitor of the release of endogenous vasodilators together with a vasoconstrictor agent in patients with hepatorenal syndrome (HRS). This new medical perspective was compared with a traditional medical approach for HRS, such as the infusion of nonpressor doses of dopamine to produce renal vasodilation. Thirteen patients with type 1 HRS were enrolled in the study. Five of them were treated with the oral administration of midodrine and the parenteral administration of octreotide. In addition, the patients received 50 to 100 mL of 20% human albumin solution daily for 20 days. Midodrine and octreotide were dosed to obtain a stable increase of at least 15 mm Hg of mean arterial pressure. Eight patients were treated with the intravenous administration of nonpressor doses of dopamine (2-4 micrograms/kg/min) and the same daily amount of albumin. After 20 days of treatment with midodrine and octreotide, an impressive improvement in renal plasma flow (RPF), glomerular filtration rate, and urinary sodium excretion was observed in patients. This was accompanied by a significant reduction in plasma renin activity, plasma vasopressin, and plasma glucagon. No side effects were observed. Three patients were discharged from the hospital. One of them successfully underwent liver transplantation. One of the two remaining patients is still alive after 472 days with a preserved renal function, and the other died from terminal liver failure after 76 days. One of the two patients who were not discharged from the hospital successfully underwent liver transplantation, and the other died from pneumonia after 29 days. Seven out of eight patients who were treated with dopamine experienced a progressive deterioration in renal function and died during the first 12 days. Only one patient recovered renal function and underwent liver transplantation. In conclusion, the long-term administration of midodrine and octreotide seems to be an effective and safe treatment of type 1 HRS in patients with cirrhosis.
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PMID:Reversal of type 1 hepatorenal syndrome with the administration of midodrine and octreotide. 1034 9

Several case reports have emphasized that esophageal carcinoid tumors are associated with a poor prognosis. To expand our knowledge about the pathology and biologic behavior of these rare tumors, we reviewed the clinicopathologic and immunohistochemical findings of four cases of primary esophageal carcinoid. The age of the patients ranged from 48 to 82 years (mean 63 years; median 61 years). The lower segment of the esophagus was involved in two cases and the mid segment was involved in one case. The sizes of the tumors ranged from 0.3 cm to 3.5 cm. Two tumors were confined to the lamina propria and two invaded into the muscular wall. Two tumors appeared polypoid, whereas the remaining two were incidental findings and associated with adenocarcinoma arising in a background of Barrett esophagus. The adenocarcinoma was superficially invasive in one case, whereas it penetrated the muscular wall in the other. All four carcinoid tumors were immunoreactive with chromogranin and synaptophysin. There was focal expression of serotonin in two cases, glucagon in one case, and pancreatic polypeptide in one case. Endocrine cell hyperplasia was noted in both the Barrett esophagus and the invasive adenocarcinoma. One patient died secondary to postoperative pneumonia. Three patients are alive and disease free at 1, 6, and 23 years status post therapy. None of the patients had metastatic disease. These findings show that esophageal carcinoids are associated with a favorable prognosis. They arise in two settings: (1) a single large polypoid tumor or (2) an incidental finding and in association with adenocarcinoma arising in the background of Barrett esophagus. The presence of endocrine cell hyperplasia in the Barrett mucosa and the adenocarcinoma supports the hypothesis that these lesions arise from a common stem cell.
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PMID:Carcinoid tumor of the esophagus: a clinicopathologic study of four cases. 1191 32

Diabetic ketoacidosis (DKA) is the most common hyperglycemic emergency in patients with diabetes mellitus. DKA most often occurs in patients with type 1 diabetes, but patients with type 2 diabetes are susceptible to DKA under stressful conditions, such as trauma, surgery, or infections. DKA is reported to be responsible for more than 100 000 hospital admissions per year in the US, and accounts for 4-9% of all hospital discharge summaries among patients with diabetes. Treatment of patients with DKA uses significant healthcare resources and accounts for 1 out of every 4 healthcare dollars spent on direct medical care for adult patients with type 1 diabetes in the US. Recent studies using standardized written guidelines for therapy have demonstrated a mortality rate of less than 5%, with higher mortality rates observed in elderly patients and those with concomitant life-threatening illnesses. Worldwide, infection is the most common precipitating cause for DKA, occurring in 30-50% of cases. Urinary tract infection and pneumonia account for the majority of infections. Other precipitating causes are intercurrent illnesses (i.e., surgery, trauma, myocardial ischemia, pancreatitis), psychological stress, and non-compliance with insulin therapy. The triad of uncontrolled hyperglycemia, metabolic acidosis and increased total body ketone concentration characterizes DKA. These metabolic derangements result from the combination of absolute or relative insulin deficiency and increased levels of counter-regulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). Successful treatment of DKA requires frequent monitoring of patients, correction of hypovolemia and hyperglycemia, replacement of electrolyte losses, and careful search for the precipitating cause. Since the majority of DKA cases occur in patients with a known history of diabetes, this acute metabolic complication should be largely preventable through early detection, and by the education of patients, healthcare professionals, and the general public. The frequency of hospitalizations for DKA has been reduced following diabetes education programs, improved follow-up care, and access to medical advice. Novel approaches to patient education incorporating a variety of healthcare beliefs and socioeconomic issues are critical to an effective prevention program.
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PMID:Diabetic ketoacidosis: risk factors and management strategies. 1587 46

The fluoroquinolones can cause severe hypoglycemia in older individuals with diabetes who are taking oral hypoglycemic agents. We describe a patient without diabetes who had new-onset hypoglycemia when given oral levaquin for pneumonia that developed after cardiac bypass surgery. The condition manifested with profound neurologic disturbances and required intravenous dextrose and parenteral glucagon for treatment. No other cause could be identified, and the problem remitted a few days after administration of the antibiotic was stopped. Laboratory evaluation showed relatively inappropriate insulin elevation at the time of the hypoglycemic episodes, consistent with pancreatic beta-cell stimulation. The report highlights glucose-lowering as an adverse effect of the fluoroquinolone class of antibiotics in persons without diabetes or taking hypoglycemic medication. Although levaquin is useful as broad-spectrum therapy in a variety of situations, clinicians should be cognizant of the occurrence of potentially serious or even fatal hypoglycemia with its use.
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PMID:Levofloxacin-induced hypoglycemia in a nondiabetic patient. 1677 43


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