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

The features of 41 proven or suspected cases of pancreatic glucagonoma and one possible case of renal glucagonoma have been reviewed. Glucagonoma is one form of islet cell neoplasm and involves pancreatic alpha cells. It may occur more frequently in women and is more likely to be malignant than insulinoma. Patients may present with glucose intolerance, an erythematous, eczematous dermatitis, glossitis, stomatitis, vaginitis and unexplained weight loss. Anemia, hypoproteinemia, hypoaminoacidemia and hypolipidemia may also be present. Malignant glucagonoma metastasizes frequently to liver. An evaluation for possible glucagonoma may be considered in a patient with the characteristic eczematous dermatitis, glossitis or stomatitis and glucose intolerance, an unusual or atypical history of diabetes mellitus, or hepatomegaly with other characteristics of glucagonoma. Initial evaluation may include measurement of fasting plasma glucagon concentration, and an oral glucose tolerance test with measurements of plasma glucose and glucagon levels. Extreme fasting hyperglucagonemia, and a paradoxical rise in plasma glucagon concentrations after glucose ingestion should strongly suggest the presence of glucagonoma. Radiographic demonstration of pancreatic glucagonoma is best carried out by celiac arteriography. Surgical excision of the tumor is the treatment of choice. Nonresectable lesions may respond to chemotherapy with streptozotocin. Treatment for the various dermatologic or metabolic complications of glucagonoma which include glucose intolerance, hypoproteinemia, hypocholesterolemia and anemia may not be satisfactory. Glucose intolerance is usually mild and may be adequately treated with dietary or insulin therapy. Rarely, glucagonoma with massive destruction of the pancreas or other factors may induce severe glucose intolerance. In contrast, the anemia, skin rash, and hypoproteinemia do not respond to conservative therapies tested thus far. Glucagonoma is a model for studying the importance of glucagon in causing the hyperglycemia of diabetes mellitus. Study of patients with glucagonoma does suggest that glucagon has some role in the etiology of hyperglycemia in diabetic states; however, as in studies on diabetes, investigations on glucagonoma do not demonstrate that glucagon has a primary role in producing severe glucose intolerance.
 ...
PMID:Clinical and metabolic aspects of glucagonoma. 698 81

Glucagonoma is a rare pancreatic tumor, necrolytic migratory erythema is its distinctive feature and it is often associated with diabetes mellitus, weight loss, anemia, hypoaminoacidemia, glossitis and stomatitis. We reported a case of glucagonoma misdiagnosed as "eczema" and "benign hepatic anginoma" for 3 years. His blood glucagon level was 1,758 ng/L. The results of abdominal B-mode ultrasonography and CT scan were negative, but selected arteriogram showed a tumor mass between the pancreatic body and tail. Before operation, treatment with octreotide and supply of amino acids were given with improvement of the skin lesion. After resection of the tumor from pancreas, necrolytic migratory erythema disapeared, but his blood level of glucagon and amino acids did not improve. It is suggested that any diabetic patient with chronic skin damage should be checked for blood glucagon level. In suspected cases, selected arteriogram will be helpful for location of the tumor. Vigorous resection of the pancreatic tumor should be done as soon as possible, even though there is already metastases.
 ...
PMID:[Report of a case of glucagonoma misdiagnosed as "eczema" and "hepatic angioma" for three years and review of literature]. 764 42

Erythropoietin (EPO) therapy is widely used to correct the anemia of end-stage renal disease. It has been reported that this treatment affects various hormonal systems. The aim of the present study was to evaluate the effects of EPO therapy on glucose tolerance. Anemia was corrected with EPO in 10 patients on chronic hemodialysis therapy. Oral glucose tolerance tests (OGTT) were performed before and after correction of anemia. The following measurements were made: the areas under the glucose curves (AUCglue), the areas over basal glucose values (OABVglue), the areas under the insulin curves (AUCins) and the areas over basal insulin values (AOBVins). Hemoglobin concentration increased from 70 +/- 1.4 milligrams to 111 +/- 1 milligram. Fasting plasma glucose, insulin and glucagon levels were were not affected by correction of the anemia. Following administration of EPO, AOBVglue increased by 19%, from 2101 +/- 243 to 2508 +/- 230 mmol.min/l (p < 0.02), while AOBVins remained unchanged. AUCins and AUCglue remained unchanged. These data show that correction of anemia with EPO in hemodialyzed patients causes an increase in the glycemic response to an oral glucose load while not affecting the insulin response.
 ...
PMID:Effects of erythropoietin on glucose tolerance in hemodialysis patients. 788 4

As already reported short-term rHuEpo treatment influences plasma insulin, glucagon, pancreatic polypeptide (PP), and gastrin secretion in haemodialysed patients. The present study aimed to assess the influence of long-term rHuEpo treatment on secretion of above mentioned hormones. A total of 27 haemodialysed patients and nine healthy subjects were examined. Nine patients with uraemic anaemia were treated with rHuEpo for 12 months (Epo group) while another nine patients did not receive rHuEpo (non-Epo group), but were monitored biochemically and clinically as patients of the Epo group. The third group (HD) comprised nine haemodialysed patients with a haematocrit value of > or = 30% without rHuEpo therapy. In all subjects plasma levels of insulin, glucagon, gastrin, and PP were estimated before and after administration of a test meal. Patients of the Epo group were examined before and after 6 and 12 months of rHuEpo treatment (patients of the Epo group) or clinical monitoring (patients of the non-Epo group) respectively, while only one test was performed in patients of the HD group and healthy subjects. Six months of rHuEpo treatment was followed by an increase of fasting insulinaemia and a decrease of basal plasma level of glucagon and PP. At that time point rHuEpo therapy also increased the response of insulin, glucagon, and gastrin to the test meal.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Influence of long-term erythropoietin treatment on insulin, glucagon, pancreatic polypeptide, and gastrin secretion in haemodialysed patients. 807 22

Glucose, insulin, glucagon and fructosamine were measured in the plasma of control (n = 34) and of Rh fetuses (n = 22) before the first and subsequent transfusion. Prior to treatment, Rh fetuses, compared to controls, had raised concentrations of glucose (p = 0.01), glucagon (p = 0.04) and fructosamine (p = 0.004). Fetal insulin levels were not significantly different. Before subsequent transfusion, despite correction of anemia, Rh fetuses were clearly hyperinsulinemic even after correction for gestation (p = 0.002) and had low glucagon concentrations (p = 0.01) when compared with values at the first transfusion. This metabolic milieu appears similar to that of fetuses of diabetic mothers which have increased plasma glucose and insulin during most of the last third of gestation.
 ...
PMID:Carbohydrate metabolism in fetuses with Rh alloimmunization. 826 74

The study aimed to assess the influence of long-term rhuEPO treatment on secretion of pancreatic hormones (insulin, glucagon). A total of 27 haemodialyzed and 9 healthy subjects were examined. Nine patients with uraemic anaemia were treated with rhuEPO for 12 months (EPO group) while another nine patients did not receive rhu-EPO (non-EPO group), but were monitored biochemically and clinically as patients of the EPO group. The third group (HD) comprised nine haemodialyzed patients with a haematocrit value of > 30%, without rhu-EPO therapy. In all subjects plasma levels of glucose, insulin (IRI) and glucagon (Glu) were estimated before and after administration of the test meal. Patients of the EPO and non-EPO group were examined before and after 6 and 12 months of rhu-EPO treatment (EPO group) or clinical monitoring (non-EPO group) respectively, while only one test was performed in patients of the HD group and healthy subjects. During the observation period fasting glicaemia did not change. Six months of rhu-EPO therapy was followed by an increase of fasting insulinaemia and decrease of basal plasma level of glucagon. At that time point rhu-EPO therapy also increased the response of IRI and Glu to the test meal and the insulin/glucose index. After 12 months of rhu-EPO therapy basal insulinaemia and insulin/glucose index returned to the pretreatment value while plasma level of glucagon and the response to the test meal were lower than pretreatment one. Our results suggest that rhu-EPO treatment exerts a profound effect on carbohydrate metabolism and secretion of IRI. Glu, which seems to be dependent upon duration of rhu-EPO therapy and not only, or exclusively to improvement of the haematological status.
 ...
PMID:[Influence of long-term treatment with human recombinant erythropoietin on secretion of hormones regulating carbohydrate metabolism in hemodialyzed patients with chronic uremia]. 861 11

A rare case of severe acute hepatitis A complicated by pure red cell aplasia (PRCA) is reported. A 60-year-old man with jaundice and hepatomegaly was diagnosed as having acute hepatitis A by positive IgM anti-hepatitis A antibody (anti-HAV). Severe anemia rapidly developed 3 weeks after admission, and the patient was diagnosed with PRCA by both bone marrow smears and erythrocyte survival study. The anemia was transient and bone marrow recovered within 1 week. However, concomitant with bone marrow recovery, the hepatitis worsened. He became drowsy and disoriented and severe jaundice, ascites, prolonged prothrombin time, increased transaminase levels, and abnormal electroencephalogram (EEG) were exhibited. Plasma exchange transfusion and glucagon-insulin (GI) therapy improved the consciousness level, but bilirubin, transaminase levels, and IgM anti-HAV titer remained high. Intravenous administration of lipophilized prostaglandin E1 (lipo-PGE1) was added to the GI therapy. Bilirubin and transaminase levels were normalized in the 8th week after the initiation of this combination therapy (17 weeks after admission). The combined use of lipo-PGE1 with plasma exchange and GI therapy appeared to be useful for the prolonged severe hepatitis in this patient.
 ...
PMID:Severe acute hepatitis A associated with acute pure red cell aplasia. 884 89

Within four years a 44-year-old man developed a glucagonorma syndrome with insulin dependent diabetes mellitus, weight loss, diarrhea, anemia and a marked superinfected eczema. He developed an organo-cerebral psychosyndrome with cognitive retardation and syncoptic disturbance of consciousness, followed by a tetraspasticity with tetraparesis, micturition difficulties and fecal incontinence. There were a general cerebral atrophy as verified by means of MRT and signs of a demyelinating cerebral disease. The plasma concentration of glucagon was 48 fold elevated to 8,536 ng/l. By means of ultrasonography, CT, ERCP, and angiography a tumorous mass of the corpus and tail of the pancreas, 61 x 32 mm in size, was found with signs of infiltration into the region of the aorta and the splenic vein. Furthermore the liver showed diffuse partially cystic metastases. The diagnosis was certified by fine needle biopsy and histologic examination with Grimelius straining. A thrombosis of the femoral vein was detected by CT. The patient was treated by a debulking resection of the corpus and cauda of the pancreas combined with splenectomy and a drug therapy using octreotide. All paraneoplastic symptoms could be widely reduced. Plasma glucagon concentration decreased from 2,200 ng/l to 600 ng/l. Because of a liver enlargement due to the growth of metastases he was successfully treated with dacarbazine 250 mg/m2 per day during six monthly cycles for five days and interferon-alpha 3 x 3 millions units per week for six months followed by a normalization of the liver volumen.
 ...
PMID:[Paraneoplastic spastic tetraparesis in glucagonoma syndrome. Successful therapy with octreotide, dacarbazine and interferon-alpha]. 892 39

Glucagonoma is a neuroendocrine tumor of pancreatic alpha cells manifested by necrolytic migratory erythema, hyperglucagonemia, glucose intolerance, weight loss, anemia and hypopaminoacidemia. We report a case of glucagonoma in a 38 years-old patient diagnosed by the presence of a pancreatic tumor, liver metastasis, weight loss, glucose intolerance, necrolytic migratory erythema, hyperglucagonemia (1400 pg/ml; normal < 200 pg/ml) and histologic demonstration of glucagon and neurospecific enolase by immunocytochemical reaction. Actual therapeutic of glucagonoma includes surgery, chemotherapy, somatostatin or octreotide for control of the symptoms, and more recently alpha-interferon was suggested.
 ...
PMID:[Glucagonoma: case report and literature review]. 920 30

Glucagonoma is a relatively rare pancreatic islet cell tumor. Historically, these tumors present a typical constellation of symptoms including diabetes, weight loss, anemia, necrolytic migratory erythematous rash, and propensity for thrombosis. This clinical presentation is described as the glucagonoma syndrome. The syndrome can be confirmed with the use of serum measurements of glucagon levels and immunohistochemical assay of the tumor. Variations from the classic syndrome have been described, and serum measurements of glucagon in patients with suspected islet cell tumors can identify subsets of patients with glucagonoma who do not exhibit the classic syndrome. In our case, the unusual presentation of glucagonoma included the previously unreported component of an intravascular venous extension of tumor.
 ...
PMID:Intravascular tumor: a previously unreported finding of glucagonoma. 922 1


<< Previous 1 2 3 4 5 6 7 Next >>