Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endocrine pancreatic tumours (EPTs) are uncommon tumours occurring in approximately 1 in 100,000 of the population, representing 1-2% of all pancreatic neoplasms. Some of the tumours may be part of multiple endocrine neoplasia type one (MEN-1) syndrome or von Hippel-Lindau (vHL) disease. EPTs are classified as functioning or non-functioning tumours on the basis of their clinical manifestation. The biochemical diagnosis of EPT is based on hormones and amines released. Besides specific markers such as insulin, there are also general tumour markers such as chromogranin A, which is the most valuable marker and has been reported to be increased in plasma in 50-80% of patients with EPTs and correlates with tumour burden. The location of endocrine tumours of the pancreas includes different techniques, from endoscopic investigations to scintigraphy (e.g. somatostatin receptor scintigraphy) and positron emission tomography. The medical treatment of endocrine pancreatic tumours consists of chemotherapy, somatostatin analogues and alpha-interferon. None of these can cure a patient with malignant disease. In future, therapy will be custom-made and based on current knowledge of tumour biology and molecular genetics.
Best Pract Res Clin Gastroenterol 2005 Oct
PMID:Endocrine tumours of the pancreas. 1625 99

Gallstone disease is common: >700,000 cholecystectomies and costs of approximately 6.5 billion dollars annually in the U.S. The burden of disease is epidemic in American Indians (60-70%); a corresponding decrease occurs in Hispanics of mixed Indian origin. Ten to fifteen per cent of white adults in developed countries harbour gallstones. Frequency is further reduced in Black Americans, East Asia and sub-Saharan Africa. In developed countries, cholesterol gallstones predominate; 15% are black pigment. East Asians develop brown pigment stones in bile ducts, associated with biliary infection or parasites, or in intrahepatic ducts (hepatolithiasis). Certain risk factors for gallstones are immutable: female gender, increasing age and ethnicity/family (genetic traits). Others are modifiable: obesity, the metabolic syndrome, rapid weight loss, certain diseases (cirrhosis, Crohn's disease) and gallbladder stasis (from spinal cord injury or drugs like somatostatin). The only established dietary risk is a high caloric intake. Protective factors include diets containing fibre, vegetable protein, nuts, calcium, vitamin C, coffee and alcohol, plus physical activity.
Best Pract Res Clin Gastroenterol 2006
PMID:Gallstone disease: Epidemiology of gallbladder stone disease. 1712 83

Several risk factors for cholesterol gallstone formation in the general population have been identified. There is a strongly increased risk of gallstone disease during prolonged fasting, rapid weight loss, total parenteral nutrition, and somatostatin(-analogue) treatment. The annual risk of biliary colic and gallstone complications in asymptomatic gallstone carriers has been investigated sparsely. In asymptomatic and symptomatic gallstone carriers, treatment with the hydrophilic bile salt ursodeoxycholic acid (UDCA) has been claimed to reduce the risk of biliary colic and gallstone complications such as acute cholecystitis and acute pancreatitis. Also, prophylactic cholecystectomy could be beneficial in certain subgroups of asymptomatic gallstone carriers. However, randomized, double-blind, placebo-controlled trials are lacking. In this review, strategies for the prevention of gallstone formation in the general population and in high-risk conditions are dealt with. Also, strategies for the prevention of biliary colic and gallstone complications in asymptomatic and symptomatic gallstone carriers are discussed.
Best Pract Res Clin Gastroenterol 2006
PMID:Gallstone disease: Primary and secondary prevention. 1712 88

Gastrointestinal bleeding is a frequent and severe complication of portal hypertension. The most frequent cause of the bleeding is variceal rupture. Despite improvements in prognosis after variceal bleeding over the past two decades, the 6-week mortality rate remains high, ranging from 15 to 30%. Patients die from uncontrolled bleeding, early rebleeding, infection, or renal failure within the first weeks of a bleeding episode. Poor hepatic function, severe portal hypertension with a hepatic venous pressure gradient (HVPG) >20 mmHg, and active bleeding at endoscopy are independently associated with poor prognosis. First-line treatment includes resuscitation, prophylactic antibiotic therapy, the combined use of vasoactive drugs (started as soon as possible), and an endoscopic procedure. Reconstitution of blood volume should be done cautiously to maintain the haematocrit between 25 and 30%. Terlipressin, somatostatin, or octreotide can be used, and drug therapy is maintained from 48 h to 5 days. Ligation is the endoscopic treatment of choice in bleeding oesophageal varices; in gastric varices, obturation with cyanoacrylate is preferable. Uncontrolled bleeding should be an indication for a salvage transjugular portosystemic shunt (TIPS). In patients with Child-Pugh score A, shunt surgery might be an alternative to TIPS. Trials are currently ongoing into the precise indications of early TIPS in selected patients with an HVPG >20 mmHg, and into the usefulness of administration of recombinant activated factor VII when there is an active bleeding at endoscopy.
Best Pract Res Clin Gastroenterol 2007
PMID:Management of acute bleeding from portal hypertension. 1722 94

Several circulating or urinary tumour markers can be used for the diagnosis and follow-up of functioning and clinically non-functioning neuroendocrine tumours of the pancreatic islet cells and intestinal tract. Among the specific tumour markers are serotonin and its metabolites--e.g. 5-hydroxyindoleacetic acid (5-HIAA)--in carcinoid tumours and the carcinoid syndrome, insulin and its precursors or breakdown products in insulinoma, and gastrin in gastrinoma. Plasma vasointestinal polypeptide (VIP) determinations have been used in the diagnosis of VIPoma, plasma glucagon for glucagonoma, and serum somatostatin for somatostatinoma. Among the tumour-non-specific markers are: chromogranins, neuron-specific enolase (NSE), alpha-subunits of the glycoprotein hormones, catecholamines, pancreatic polypeptide (PP), ghrelin and adrenomedullin.
Best Pract Res Clin Endocrinol Metab 2007 Mar
PMID:Biochemistry of neuroendocrine tumours. 1738 64

The diagnosis of neuroendocrine tumours (NETs) and monitoring of therapy in many patients relies mainly on morphological imaging techniques such as computed tomography (CT), ultrasound (US) and magnetic resonance imaging (MRI). However, functional imaging modalities--such as somatostatin receptor scintigraphy (SRS)--have great impact on patient management by providing tools for better staging of the disease, visualization of occult tumour, and evaluation of eligibility for somatostatin analogue treatment. Positron emission tomography (PET) using (18)F-fluoro-deoxy-glucose (FDG) is a powerful functional modality for oncological imaging. Unfortunately, FDG is not accumulated in NETs except in the case of dedifferentiated tumours and tumours with high proliferative activity. Based on the concept of amine precursor uptake and decarboxylation (APUD), the (18)F- and (11)C-labelled amine precursors L-dihydroxyphenylalanine and 5-hydroxy-L-tryptophan (5-HTP) have been utilized for PET imaging of NETs. In comparative studies of patients with a variety of NETs, (11)C5-HTP-PET proved better than CT and SRS by visualizing additional small lesions. With carbidopa premedication orally before (11)C5-HTP-PET examination the tumour uptake could be increased and the urinary radioactivity concentration considerably reduced. This concept may also be applied to (18)F-L-DOPA-PET, a method which in a limited number of studies has gained additional diagnostic information in NET patients compared to SRS and morphological imaging. (68)Ga is available from an in-house generator and has been utilized for labelling of somatostatin analogues for PET imaging of NETs with promising results in a small number of patients. However, SRS is an established functional imaging method for patients with NETs, whereas the role for PET in the clinical routine needs further evaluation in comparative studies in larger groups of patients.
Best Pract Res Clin Endocrinol Metab 2007 Mar
PMID:Nuclear imaging of neuroendocrine tumours. 1738 66

Peptide receptor radionuclide therapy with radiolabelled somatostatin analogues is an emerging and convincing treatment modality for patients with unresectable, somatostatin-receptor-positive neuroendocrine tumours. Using radiolabelled somatostatin analogues for imaging became the gold standard for staging of neuroendocrine tumours. The somatostatin receptor is strongly over-expressed in most tumours, resulting in high tumour-to-background ratios. Consequently, the next step was to try to treat these patients by increasing the radioactivity of the administered radiolabelled somatostatin analogue in an attempt to bring about tumour cure. Many patients have been treated successfully with this approach, roughly 25% of them achieving objective tumour shrinkage >50%. Serious side-effects have been rare. This article reviews the effectiveness and safety of the different radiolabelled somatostatin analogues used. Furthermore, clinical issues--including indication and timing of therapy--are discussed. Finally, important directions for future research are mentioned to illustrate new strategies for increasing therapy efficacy.
Best Pract Res Clin Endocrinol Metab 2007 Mar
PMID:Neuroendocrine tumors. Peptide receptor radionuclide therapy. 1738 68

In patients with advanced neuroendocrine tumours, surgery is curative in only a minority of cases, whilst the anti-tumour effect of somatostatin analogues, despite efficient symptom control, is limited. Systemic chemotherapy has been proved to be effective only in certain tumour types. Although metastatic midgut carcinoids and well-differentiated gastrointestinal carcinoids are relatively insensitive to chemotherapy, pancreatic neuroendocrine tumours show a response rate of around 40% to streptozotocin-based combinations, particularly with fluorouracil and doxorubicin. Poorly differentiated tumours respond even better, especially to a combination of cisplatin and etoposide. In patients with predominant liver disease, ischaemia of tumour lesions induced by vascular occlusion by particle embolization or chemoembolization may be considered. This may have clinical and biochemical responses up to 80%, and objective responses up to 60%, in disease which is progressive despite previous treatments. Potential adverse effects and short duration of response should be taken into account.
Best Pract Res Clin Endocrinol Metab 2007 Mar
PMID:Cytotoxic treatment including embolization/chemoembolization for neuroendocrine tumours. 1738 69

This review gives an introduction to the classification and staging of neuroendocrine tumors, as the prognostic implications of these classifications influence therapeutic decisions. The indications for biotherapy are given, together with a short update on the mechanism of somatostatin analogs and interferon-alpha therapy. This is followed by an in-depth description of the use of biotherapy, its results with respect to symptomatic and antiproliferative treatment, as well as its side-effects.
Best Pract Res Clin Endocrinol Metab 2007 Mar
PMID:Neuroendocrine tumors. Biotherapy. 1738 70

Carcinoid and islet-cell carcinoma are often also known as low-grade neuroendocrine carcinomas. They are often slow-growing but can be resistant to standard therapy. While somatostatin analogues are often used to control hormonal syndromes, there is currently no therapy approved in the US for control of carcinoid tumor growth. For islet-cell carcinoma, streptozocin-based chemotherapy may induce tumor shrinkage, but second-line option are limited. This chapter reviews the molecular biology of neuroendocrine tumors, including the roles of MENIN, TSC2, NF-1, vHL, p53, bcl-2, bax, VEGF, IGF, PDGF, EGFR, and mTOR. Recently, there has been interest in developing molecularly targeted therapy for this group of diseases. Phase-II studies with imatinib, bevacizumab, sunitinib, gefitnib, temsirolimus, and everolimus (RAD001) have completed accrual. Encouraging results have been observed in studies with VEGF and mTOR inhibitors. Phase-III study of bevacizumab is planned in the US. Large-scale multinational phase-II and -III studies of everolimus are under way.
Best Pract Res Clin Endocrinol Metab 2007 Mar
PMID:Neuroendocrine tumors. Molecular targeted therapy for carcinoid and islet-cell carcinoma. 1738 71


<< Previous 1 2 3 4 5 Next >>