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 total membrane-bound ATP hydrolytic activity in human epidermis is due to the activities of at least three differently located enzymes, namely Mg++-activated ATPase, phosphomonoesterase and adenyl cyclase. Cytochemical studies on psoriatic epidermis with various inhibitory and stimulatory substances showed reduced activities of ATPase and phosphomonoesterase, and a lack of sensitivity of adenyl cyclase to specific stimulators such as isoproterenol and glucagon. Since no differences of basal adenyl cyclase activity were observed between normal and psoriatic human skin without stimulation, it seems likely that in psoriasis a latent defect of adenyl cyclase may exist, resulting in a deficient response of this enzyme to regulatory agents. In conclusion, the present study reveals that not a single enzyme but the entire membrane-bound nucleotide metabolism is altered in psoriatic keratinocytes, causing a disturbance of the membrane-bound energy utilization, similar to findings in proliferating tumour cells.
Br J Dermatol 1975 Nov
PMID:Ultrastructural localization and differentiation of membrane-bound ATP utilizing enzymes including adenyl cyclase in normal and psoriatic epidermis. 17 85

The glucagonoma syndrome is characterized by dermatitis, stomatitis, elevated serum glucagon levels, abnormal glucose tolerance, weight loss, and anemia--all in association with a glucagon-secreting alpha-cell tumor of the pancreas. A review of 21 cases showed strikingly similar features. A generalized, symmetrical dermatitis initially appeared to be asteatotic or eczematous over the perineum, buttocks, and lower extremities. Gradually, a more characteristic migratory necrolytic erythema with transient bulla formation and erosions developed in intertriginous and dependent areas. Histologically, the most specific features included necrolysis of the upper epidermis, with liquefaction necrosis of the granular cell layer and subcorneal clefting or blister formation. The dermatologist is often first to examine such patients; early recognition of this syndrome with prompt surgical removal of the primary pancreatic lesion may afford cure of the neoplasm.
Arch Dermatol 1977 Jun
PMID:Glucagonoma syndrome. Report of two cases and literature review. 19 36

Glucagon-secreting tumors of the pancreatic islets (glucagonomas) produce a distinctive syndrome in which weight loss, diabetes mellitus, anemia,and prominent mucocutaneous findings occur. The cutaneous component-necrolytic migratory erythema--may be polymorphous, but most commonly manifests as erosions and crusts of the groin, perineum, buttocks, distal part of the extremities, and central area of the face. Alternatively, scaly papules and plaques may predominate in these areas. The eruption may resemble such dermatoses as pemphigus foliaceus, acrodermatitis enteropathica, chronic mucocutaneous candidiasis, psoriasis, and severe seborrheic dermatitis. Two patients with chronic, previously undiagnosed dermatoses had necrolytic migratory erythemia, which led to the discovery of glucagonomas present in each. In one patient surgical resection of the tumor resulted in total clearing of the rash within 48 hours. Awareness of this distinctive entity may lead to early diagnosis and, possibly, cure.
Arch Dermatol 1977 Jun
PMID:Necrolytic migratory erythema. Distinctive dermatosis of the glucagonoma syndrome. 19 37

The glucagonoma syndrome is a rare clinical condition characterized by a distinctive cutaneous eruption associated with a glucagon-secreting islet cell neoplasm of the pancreas. A 19-year-old woman manifested typical features of this condition: a polymorphous skin eruption with characteristic distribution of lesions in perioral and paragenital regions; lesions in sites of cutaneous trauma; a skin biopsy that showed epidermal cleavage; glossitis; weight loss; mild anemia; abnormal glucose tolerance test results. Plasma glucagon levels, determined by radioimmunoassay, were approximately five times normal. Angiography indicated a pancreatic tumor with liver metastases. Islet cell origin was confirmed histologically. It is hoped that wider recognition of the distinctive clinical features of this syndrome will result in earlier detection and possible surgical cure of the underlying malignancy.
Arch Dermatol 1978 Feb
PMID:The glucagonoma syndrome. A distinctive cutaneous marker of systemic disease. 20 56

The glucagonoma syndrome is characterized by necrolytic migratory erythema, glossitis, ungual dystrophy, diabetes mellitus, anemia, weight loss, elevated plasma glucagon levels and an alpha-cell glucagon-secreting neoplasm of the pancreas. We are reporting a case of this syndrome in a middle-aged woman, in whom the first complaints and signs were cutaneous. The recognition of the distinctive skin manifestations of the syndrome led to early diagnosis and treatment of the underlying malignant pancreatic tumor.
J Dermatol Surg Oncol 1978 Mar
PMID:The glucagonoma syndrome. 20 68

The glucagonoma syndrome is another of those systemic disorders in which skin manifestations provide a clue to the diagnosis. The patient will most often be a middle-aged woman who has the characteristic, indolent skin lesions in the face of diabetes mellitus and additional features to suggest an occult carcinoma. Marked elevation of the levels of plasma glucagon should confirm the suspicion cure of the skin lesions follows cure of the tumor. Two lines of speculation seem promising. Either the initial event is an overproduction of glucagon and all other observations follow. Or the syndrome is another of the polyendocrine disorders. Cases are still too few to resolve either the pathophysiology, prognosis, or even to guess at the true frequency of the syndrome.
Int J Dermatol
PMID:The glucagonoma syndrome. 21 45

Necrolytic migratory erythema is the distinctive cutaneous eruption seen with glucagon-producing tumours of the pancreas. Recognition of this eruption is important because it may lead to the early diagnosis of a glucagonoma. Recently, we saw a patient who had necrolytic migratory erythema, hyperglucagonaemia, and cirrhosis of the liver with no evidence of pancreatic tumour while alive or at autopsy. Serum glucagon levels during the period of observation and during an oral glucose tolerance test suggested that the hyperglucagonaemia was not due to an occult glucagon-producing tumour but may have been the result of advanced hepatic cirrhosis.
Br J Dermatol 1979 Nov
PMID:Hyperglucagonaemia and necrolytic migratory erythema in cirrhosis--possible pseudoglucagonoma syndrome. 51 28

Two patients with clinical and histologic findings consistent with necrolytic migratory erythema are presented. Unlike previously described patients with this disorder, neither patient had substantially elevated glucagon levels nor an associated pancreatic islet cell tumor. The cause of the skin disease in these patients remains unknown but may be related to the underlying small-bowel disorder present in both.
Arch Dermatol 1979 Dec
PMID:Necrolytic migratory erythema without glucagonoma. 53 89

Glucagon and beta-adrenergic compounds such as 1-isoproterenol stimulated the low activity of an ATP-utilizing enzyme located on the cell membranes of normal keratinocytes. Addition of beta-antagonist propranolol to the incubation medium prevented the stimulatory effect of 1-isoproterenol. We considered, therefore, the reaction product being due to epidermal membrane-bound adenyl cyclase activity. In psoriatic epidermis the basal adenyl cyclase activity was low, similar to normal epidermis, however, glucagon and 1-isoproterenol failed to stimulate the enzyme activity in psoriasis under the same conditions. It seems, therefore, that the beta-adrenergic-cAMP cascade as a regulatory epidermal control mechanism of induced proliferation is ineffective in this disease.
Arch Dermatol Res 1975 Sep 12
PMID:[Lack of beta-adrenergic stimulation of membrane bound adenyl cyclase in psoriasis as compared to normal epidermis (author's transl)]. 124 87

The glucagonoma syndrome is characterized by elevated serum glucagon, a pancreatic alpha-cell tumor, anemia, hypoaminoacidemia, and necrolytic migratory erythema. Necrolytic migratory erythema may cause marked morbidity and is frequently misdiagnosed. A 42-year-old white woman with a 1 1/2-year history of refractory dermatitis (most severe on the lower extremities) had the glucagonoma syndrome. Her severe morbidity was markedly relieved with the administration of intravenous amino acids. This therapy was successful in controlling the necrolytic migratory erythema through recurrences after somatostatin (SMS 201-995), surgical debulking, and chemotherapy proved inadequate.
J Am Acad Dermatol 1991 Nov
PMID:Treatment of necrolytic migratory erythema in glucagonoma syndrome. 176 71


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