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)

The authors report a case of glucagonoma in a 52 years old man presenting a migratory necrolytic erythema. By conjugated means of arteriography and splenoportography with plasma glucagon assays the tumour was localized in the tail of the pancreas. Surgical excision was easy but hepatic metastases revealed the malignant nature of the tumor. This glucagonoma has been investigated by several approaches including electron microscopy, immunocytochemistry and radioimmunological techniques. The tumor contained scattered glucagon and pancreatic polypeptide immunoreactive cells; insuline, glucagon, somatostatin, pancreatic polypeptide, gastrin and VIP antisera gave negative results. Ultrastructurally, these cells showed atypical secretory granules different from A granules of the normal glucagon cell. Radio immunological determinations carried out after gel permeation chromatography of plasma revealed high molecular weight (4 000, 9 000, 14 000) immunoreactive glucagon peptides. They have been thought to be proglucagon forms which did not react with specific antiglucagon sera used in cytological studies. Reported data are consistent with the classification of this tumor in the category of glucagonoma with the "glucagonoma syndrome".
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PMID:[A human pancreatic glucagonoma, ultrastructural, immunocytochemical and radioimmunological investigations (author's transl)]. 627 65

An open-field provocation, in front of an ordinary TV set, of 2 patients regarding themselves as suffering from skin problems due to work at video display terminals (VDTs) is presented. Using immunohistochemistry, in combination with a wide range of antisera directed towards cellular and neurochemical markers, we were able to show a high-to-very high number of somatostatin-immunoreactive dendritic cells as well as histamine-positive mast cells in skin biopsies from the anterior neck taken before the start of the provocation. At the end of the provocation the number of mast cells was unchanged; however, the somatostatin-positive cells had seemingly disappeared. The reason for this latter findings is discussed in terms of loss of immunoreactivity, increase of breakdown, etc. The high number of mast cells present may explain the clinical symptoms of itch, pain, edema and erythema. Naturally, in view of the present public debate, the observed results are highly provocative and, we believe, have to be taken seriously.
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PMID:Skin changes in patients claiming to suffer from "screen dermatitis": a two-case open-field provocation study. 788 69

A 52-year-old female with metastatic glucagonoma secreting glucagon and chromogranin A was treated with the somatostatin analogue octreotide for 2 years without any additional tumor-reducing interventions. Before therapy plasma glucagon was above 8 micrograms/l (normal < 0.2) and within 2 days 3 x 200 micrograms octreotide daily suppressed plasma glucagon to 2.2-2.5 micrograms/l. Concomitantly, chromogranin A dropped from 0.85 mg/l (normal < 0.1) to 0.2. After 3 weeks the preexisting disabling necrolytic migratory erythema had vanished completely, and weight loss was temporarily stopped. During therapy chromogranin A and plasma glucagon rose, exceeding pretreatment levels after 3 and 14 months, respectively. After 1 year the erythema recurred, responding only transiently to increasing doses of octreotide. The patient died after 2 years of therapy of tumor cachexy despite very high doses of octreotide (4 x 600 micrograms/day). Throughout treatment octreotide did not prevent tumor growth, as demonstrated by computed tomography and sonography. Determination of immunoreactive glucagon before and during octreotide therapy in fractions of plasma samples subjected to gel chromatography revealed a reduction in the ratio of glucagon to preproglucagon from 1.83 (before) to 0.56 (during therapy), indicating inhibition of posttranslational processing of preoproglucagon by octreotide, thereby reducing circulating bioactive glucagon. In summary, octreotide induced a remission of clinical symptoms by inhibiting posttranslational conversion of preproglucagon to glucagon but did not prevent tumor growth. Therefore, octreotide is a valuable therapy for rapid relief of clinical symptoms, thereby improving the possibilities for other tumor-reducing therapies.
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PMID:The long-acting somatostatin analogue octreotide alleviates symptoms by reducing posttranslational conversion of prepro-glucagon to glucagon in a patient with malignant glucagonoma, but does not prevent tumor growth. 818 58

The glucagonoma syndrome is a rare disorder characterized by weight loss, necrolytic migratory erythema (NME), diabetes, stomatitis, and diarrhea. We identified 21 patients with the glucagonoma syndrome evaluated at the Mayo Clinic from 1975 to 1991. Although NME and diabetes help identify patients with glucagonomas, other manifestations of malignant disease often lead to the diagnosis. If the diagnosis is made after the tumor is metastatic, the potential for cure is limited. The most common presenting symptoms of the glucagonoma syndrome were weight loss (71%), NME (67%), diabetes mellitus (38%), cheilosis or stomatitis (29%), and diarrhea (29%). Although only 8 of the 21 patients had diabetes at presentation, diabetes eventually developed in 16 patients, 75% of whom required insulin therapy. Symptoms other than NME or diabetes mellitus led to the diagnosis of an islet cell tumor in 7 patients. The combination of NME and diabetes mellitus led to a more rapid diagnosis (7 months) than either symptom alone (4 years). Ten patients had diabetes mellitus before the onset of NME. No patients had NME clearly preceding diabetes mellitus. Increased levels of secondary hormones, such as gastrin (4 patients), vasoactive intestinal peptide (1 patient), serotonin (5 patients), insulin (6 patients, clinically significant in 1 only), human pancreatic polypeptide (2 patients), calcitonin (2 patients) and adrenocorticotropic hormone (2 patients), contributed to clinical symptoms leading to the diagnosis of an islet cell tumor before the onset of the full glucagonoma syndrome in 2 patients. All patients had metastatic disease at presentation. Surgical debulking, chemotherapy, somatostatin, and hepatic artery embolization offered palliation of NME, diabetes, weight loss, and diarrhea. Despite the malignant potential of the glucagonomas, only 9 of 21 patients had tumor-related deaths, occurring an average of 4.91 years after diagnosis. Twelve patients were still alive, with an average age follow-up of 3.67 years.
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PMID:The glucagonoma syndrome. Clinical and pathologic features in 21 patients. 860 27

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.
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PMID:[Glucagonoma: case report and literature review]. 920 30

Neuropeptides (NP) are a heterogeneous group of proteins functioning as neurotransmitters, neuromodulators and neurohormones. More than fifty of these molecules have been described, and some have been detected in human skin through immunochemistry and radioimmunoassay. In this article we attempt to study the role played by some of these substances such as substance P (SP), calcitonin gene related peptide (CGRP), neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), somatostatin (S), and neurotensin (N). Several NP induce inflammatory response with edema and erythema. They can also induce the release of histamine by mastocytes, regulate cutaneous blood flow, and participate in sweat regulation and nociception. They also exert their action over several cells that participate in immunity, acting as mitotic, and chemotactic factors, inhibiting or stimulating inflammatory mechanisms. Specific NP have their receptors on epidermal cells. We will also try to study certain diseases in which NP play an important role in inducing or alleviating lesions, such as psoriasis, atopic eczema, alopecia areata, vitiligo, nodular prurigo, aquagenic pruritus, hypertrophic scars and other entities.
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PMID:[Role of neuropeptides in dermatology]. 927 66

We report three cases of malignant glucagonoma with necrolytic migratory erythema as the first clinical symptom. Long-acting somatostatin analogue was the first step of a multimodal therapeutic strategy which included surgical resection of the primary tumour in every case. Liver metastases which were present in two patients were treated by hepatic arterial chemoembolization and systemic chemotherapy in one case and by liver resection for cytoreduction and hepatic arterial chemoembolization in another case. Skin lesions resolved in all three patients.
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PMID:Necrolytic migratory erythema, first symptom of a malignant glucagonoma: treatment by long-acting somatostatin and surgical resection. Report of three cases. 987 Jul 35

RC-160 (octastatin/vapreotide) is a potent octapeptide analogue of somatostatin with growth inhibitory activity in experimental tumours in vitro and in vivo, including breast cancer. We evaluated the efficacy and tolerability of high-dose RC-160, 3 mg day(-1) on week 1 increased to 4.5 mg day(-1) for weeks 2-4 and subsequently 6 mg day(-1) until the end of treatment, administered by continuous subcutaneous infusion in the management of 14 women with previously treated metastatic breast cancer. The age range was 37-80 years (median 58.5 years) and performance status 0-2. The treatment was well tolerated with no dose reductions being required. No grade 3 or 4 toxicities were seen. Abscess formation developed at the infusion site in eight patients and erythema and discomfort was seen in a further three patients. A significant reduction in IGF-I levels occurred by day 7 and was maintained throughout the treatment. The lowest dose of RC-160 produced the maximal IGF-I response. Although there was no reduction in prolactin levels in patients whose baseline levels were normal, elevated prolactin levels found in three patients fell to within the normal range 7 days after commencing RC-160 treatment. A small but significant rise in fasting blood glucose levels was also recorded, the highest level on treatment being 7.6 mmol l(-1). No objective tumour responses were observed, all patients showing disease progression within 3 months of commencing treatment. These findings demonstrate that high-dose RC-160, administered as a continuous subcutaneous infusion, can reduce serum levels of the breast growth factors IGF-I and prolactin but is ineffective in the management of metastatic breast cancer. Encouraging preclinical anti-tumour activity and the favourable toxicity profile in patients suggest the merit of future studies combining RC-160 with anti-oestrogen, cytotoxic and anti-angiogenic agents.
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PMID:Phase II study of RC-160 (vapreotide), an octapeptide analogue of somatostatin, in the treatment of metastatic breast cancer. 1018 84

The relationship between exposure to electromagnetic fields (EMFs) and human health is more and more in focus. This is mainly because of the rapid increasing use of such EMFs within our modern society. Exposure to EMFs has been linked to different cancer forms, e.g. leukemia, brain tumors, neurological diseases, such as Alzheimer's disease, asthma and allergy, and recently to the phenomena of 'electrosupersensitivity' and 'screen dermatitis'. There is an increasing number of reports about cutaneous problems as well as symptoms from internal organs, such as the heart, in people exposed to video display terminals (VDTs). These people suffer from subjective and objective skin and mucosa-related symptoms, such as itch, heat sensation, pain, erythema, papules and pustules. In severe cases, people can not, for instance, use VDTs or artificial light at all, or be close to mobile telephones. Mast cells (MCs), when activated, release a spectrum of mediators, among them histamine, which is involved in a variety of biological effects with clinical relevance, e.g. allergic hypersensitivity, itch, edema, local erythema and many types of dermatoses. From the results of recent studies, it is clear that EMFs affect the MC, and also the dendritic cell, population and may degranulate these cells. The release of inflammatory substances, such as histamine, from MCs in the skin results in a local erythema, edema and sensation of itch and pain, and the release of somatostatin from the dendritic cells may give rise to subjective sensations of on-going inflammation and sensitivity to ordinary light. These are, as mentioned, the common symptoms reported from patients suffering from 'electrosupersensitivity'/'screen dermatitis'. MCs are also present in the heart tissue and their localization is of particular relevance to their function. Data from studies made on interactions of EMFs with the cardiac function have demonstrated that highly interesting changes are present in the heart after exposure to EMFs. One could speculate that the cardiac MCs are responsible for these changes due to degranulation after exposure to EMFs. However, it is still not known how, and through which mechanisms, all these different cells are affected by EMFs. In this article, we present a theoretical model, based upon observations on EMFs and their cellular effects, to explain the proclaimed sensitivity to electric and/or magnetic fields in humans.
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PMID:A theoretical model based upon mast cells and histamine to explain the recently proclaimed sensitivity to electric and/or magnetic fields in humans. 1085 62

Gastroenteropancreatic (GEP) neoplasms originate from any of the various cell types belonging to the neuroendocrine system. A general characteristic of GEP endocrine tumours is that the vast majority produce and secrete a multitude of peptide hormones and amines. Many patients with malignant metastasising tumours present clinical symptoms related to hormone hyperproduction. These include the so-called carcinoid syndrome, characterised by flushing, diarrhoea, wheezing and right heart disease, which is predominantly associated with the serotonin- and tachykinins-producing carcinoids of the midgut. Several types of syndrome associated with GEP endocrine tumors are caused by overproduction of a specific hormone. For instance, the well-known Zollinger-Ellison syndrome is gastrin-mediated. The so-called 'insulinoma syndrome' depends on excessive production of insulin and proinsulin, resulting in hypoglycemia. The 'glucagonoma syndrome' is characterised by necrolytic migratory erythema, diabetes and diarrhoea. The Verner-Morrison syndrome, which is brought about by high circulating levels of vasointestinal peptide (VIP). produces severe secretory diarrhoea. Finally the 'somatostatinoma syndrome' involves gallbladder dysfunction and gallstones, diarrhoea with or without steatorrhea, and impaired glucose tolerance. The biochemical diagnosis of endocrine digestive tumors is based on general and specific markers. The best general markers are chromogranin A (CgA) and pancreatic polypeptide (PP). Specific markers for endocrine tumors include insulin, gastrin, glucagon, vaso intestinal polypeptide (VIP), somatostatin and the primary cathabolic product of serotonin, 5-hydroxyndoleacetic acid (5-HIAA). Localisation procedures commonly applied, in the diagnosis of endocrine tumours include ultrasound (US), computed tomography (CT) and somatostatin receptor scintigraphy (SRS).
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PMID:Epidemiology, clinical features and diagnosis of gastroenteropancreatic endocrine tumours. 1176 60


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