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)

In this age of modern technology and aggressive but noninvasive therapies, the idea of treating an identifiable but discrete bleeding lesion with systemic medical therapy seems an anachronism. But medical therapy can be the treatment of choice for some bleeding vascular lesions of the gut. Though most vascular lesions appear similar endoscopically and are a cause of gastrointestinal bleeding, they consist of various pathologic identities. These different lesions have not only different pathologic appearances, but also different prognoses. The natural history of many of these lesions remains largely unknown. Long-term success in controlling bleeding must be measured in the context of the responsible lesion's frequency of occurrence and recurrence. Medical therapy can include hopeful watchful waiting, routine blood transfusions, or specific medications. Medical therapy has been pursued along two lines. The most common form of medical therapy has been simple supportive care. This may include iron therapy and avoidance of aspirin and other anticoagulants. Transfusions may be necessary, occasionally or on a regular basis. The second form of medical therapy has been the use of estrogens. There have been other medical attempts to control bleeding from intestinal vascular lesions. Somatostatin has been used in an uncontrolled fashion, as has aminocaproic acid. Vascular lesions of the bowel are not all the same. Medical therapy of vascular lesions is contrary to general present practice. Endoscopic or surgical therapy is presently considered best because of its ease, relatively good long-term results, and the lack of a clearly effective, well-tolerated medical therapy. Medical therapy is usually reserved for diffuse vascular diseases of the bowel, for vascular lesions located in relatively inaccessible locations, for patients with continued bleeding despite endoscopic or surgical management, and for patients who are not candidates for either endoscopic or surgical therapy.
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PMID:Medical and hormonal therapy in occult gastrointestinal bleeding. 1036 98

The ciliated hepatic foregut cyst is an unusual solitary cystic lesion of the liver. In a series of 7 cases of hepatic ciliated cysts, we performed a histological, histochemical, and immunohistochemical study to better define the histogenesis of this rare entity. The patients were 4 women and 3 men, aged 39 to 75 years. Four patients presented with abdominal pain. In 3 cases the cyst was discovered incidentally on ultrasonography. The cysts measured from 1 to 4 cm in diameter. Microscopically, the lining of the columnar epithelium was composed of ciliated cells and mucin secreting goblet cells. The wall was composed of bands of smooth-muscle fibers surrounded by an outer fibrous capsule. The goblet cells stained with PAS, alcian blue, and high-iron diamine. The immunohistochemical study showed that endocrine cells were present within the cyst epithelium, positive for chromogranin, synaptophysin, bombesin, and calcitonin, and negative for serotonin, somatostatin, glucagon, insulin, gastrin, and pancreatic polypeptide. In all the cases, immunoreactivity of some cells for CC10 strongly suggested the presence of Clara cells. Our study shows that the epithelium lining ciliated hepatic foregut cysts has histological, histochemical, and immunohistochemical features similar to those observed in the bronchiolar epithelium. This lesion is a developmental ventral foregut abnormality that could arise from a bronchiolar bud of the tracheobronchial diverticulum.
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PMID:The ciliated hepatic foregut cyst, an unusual bronchiolar foregut malformation: a histological, histochemical, and immunohistochemical study of 7 cases. 1068 41

Of the three major functional categories of cardiomyopathies (dilated, hypertrophic, and restrictive), the restrictive cardiomyopathies (RCMs) are the least common in the Western world, but unfortunately often are associated with the greatest morbidity and mortality. Infiltrative disease of the myocardium (often caused by amyloidosis) is a common cause of RCMs and has a significantly lower long-term survival rate when compared to cardiomyopathies of various other causes. Treatment of the RCM is, in general, difficult and often ineffective. Because of the abnormalities of diastolic filling that are characteristic of this condition, general measures to reduce venous and systemic congestion such as with the use of diuretics, are desirable but often result in an attendant reduction in stroke volume and cardiac output. Digoxin, calcium channel blocking drugs, and beta-adrenergic blocking agents are of limited value, although they may be used with benefit to control the heart rate response in the subgroup of patients with atrial fibrillation. Angiotensin-converting enzyme inhibitors are generally ineffective in RCM. Targeted therapy directed against specific causal entities (such as the use of somatostatin analogues in carcinoid syndrome or iron chelation with desferrioxamine in hemochromatosis) may be more effective than simple symptomatic therapy. Differentiation of RCM from constrictive pericarditis is crucial, since constriction may be treated effectively by surgical removal of the thickened pericardium. A limited number of patients appear to have benefited from novel treatment strategies, such as autologous stem cell transplant in amyloidosis, balloon valvuloplasty of stenotic tricuspid or pulmonary valves in cardiac carcinoid syndrome, and cardiac transplantation. Truly effective therapy for RCM is generally lacking, and the best chance for optimizing the clinical outcome is early detection and aggressive medical treatment in an attempt to maintain the highest possible level of patient function for as long as possible.
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PMID:Restrictive Cardiomyopathy. 1109 47

Although the endocrine pancreas appears to play an important role in the pathophysiology of sickle cell disease, very little is known about the morphologic changes in this tissue. Our study was initiated to delineate the microscopic features of the endocrine pancreas in a large autopsy series of sickle cell hemoglobinopathies. From more than 650 cases archived at the Centralized Pathology Unit for Sickle Cell Disease (Mobile, AL), 224 autopsy cases were identified for review of clinical and gross autopsy findings and/or for microscopic studies, including histochemical stains (trichrome, reticulin, iron), and immunohistochemical stains (insulin, glucagon, somatostatin, and pancreatic polypeptide). The gross examinations were recorded as unremarkable in 65% of the autopsies. In childhood and adolescence (< or = 18 years), pancreas weights (50.76 +/- 5.16SE gm) were significantly greater (p < 0.0001) than age-matched controls (30.42 +/- 3.59SE gm). In adulthood, pancreas weights (108.34 +/- 5.29SE gm) were not significantly different from controls (110 gm). Microscopic findings included vascular congestion (48%), edema (65%), siderosis (31%), and nesidioblastosis (76%), which included islet cell dispersion (53%), hyperplasia (23%), and hypertrophy (25%). Analysis by age groups suggested that islet cell dispersion/hyperplasia persists unchanged, whereas diameters of compact islets tend to increase with age. These findings may be related to local tissue hypoxia and/or increased metabolic energy needs in sickle cell disease.
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PMID:Nesidioblastosis in sickle cell disease. 1267 39

Glucagonoma of the pancreas is a rare tumor with distinct clinical manifestations, such as necrolytic migratory erythema,weight loss, anemia, diabetes mellitus, and hypoamino-acidemia. We report the case of a 68-year-old Japanese man who underwent curative resection for malignant glucagonoma of the pancreas diagnosed through anemia and diabetes mellitus. The patient had had diabetes mellitus for 20 years. Anemia was diagnosed in 1998. On admission, the hemoglobin level was 8.3g/dl, but the levels of serum iron, vitamin B12, and erythropoietin and, the number of reticulocytes were within normal limits. The levels of carcinoembryonic antigen (CEA), carbohydrate antigen (CA)19-9, and DUPAN-2 were also within normal limits, and exocrine function of the pancreas (PFD, 75%) was normal. Ultrasonography (US) revealed a hypoechoic tumor in the distal pancreas. Computed tomography (CT) demonstrated a high-density area 4 cm in diameter with calcification. The serum glucagon level was very high (2360 pg/ml), but the levels of other hormones such as somatostatin or gastrin were within normal limits, while insulin was low. Glucagonoma of the pancreas was diagnosed, and distal pancreatectomy with splenectomy was performed. Histological examination revealed a malignant endocrine tumor,which was immunohistochemically positive for chromogranin A and glucagon. Two months after the operation, the serum glucagon level had decreased to within normal limits and the hemoglobin level had increased to 10.4 g/dl. The case of glucagonoma reported here was found through diagnostic examinations of anemia and treated by surgical resection, by which the patient's anemia was largely alleviated. Therefore, we recommend checking patients who have diabetes mellitus and anemia in order to diagnose and treat glucagonoma in its early stage.
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PMID:Malignant glucagonoma of the pancreas diagnoses through anemia and diabetes mellitus. 1291 65

Portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE) are two distinct gastric mucosal lesions that may cause acute and/or chronic upper gastrointestinal hemorrhage in patients with cirrhosis. Whereas PHG is associated with portal hypertension, GAVE may present in patients without portal hypertension or liver disease. Diagnosis is made upon visualization of the characteristic lesions with upper gastrointestinal endoscopy, although the differential may be difficult at times. PHG is characterized endoscopically by a mosaic pattern with or without red signs and a proximal distribution. PHG mainly causes chronic blood loss and anemia in patients with cirrhosis but also can cause acute hemorrhage. First-line therapy for chronic hemorrhage from PHG is a nonselective beta-blocker (propranolol or nadolol) and iron supplementation. If bleeding/anemia are not controlled with these measures and the patient is transfusion-dependent, shunt therapy (transjugular intrahepatic portosystemic shunt or shunt surgery) should be considered. Management of acute bleeding from PHG, an infrequent event, should be accomplished with a vasoactive drug, somatostatin (or its analogues) or terlipressin. If bleeding responds, the patient must be switched to a nonselective beta-blocker. Shunt therapy should be considered in patients who rebleed or continue to bleed despite adequate beta-blocker therapy. GAVE is less common than PHG. It is characterized by red spots without a background mosaic pattern, typically in the gastric antrum. When lesions have a linear distribution, the lesion is called "watermelon stomach." GAVE is a cause of chronic gastrointestinal bleeding and anemia in patients with cirrhosis. If lesions are localized, first-line therapy is argon plasma coagulation. In more diffuse lesions, therapy with argon plasma coagulation is more complicated. Preliminary data suggest that cryotherapy may be a reasonable option for diffuse GAVE lesions. Neither beta-blockers nor TIPS reduces the bleeding risk in patients with GAVE and thus should not be used in this setting.
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PMID:Treatment of gastropathy and gastric antral vascular ectasia in patients with portal hypertension. 1822 9

Three prospective randomised studies and a clinical experiment were performed to study postoperative weight, body mass index, nutritional and immunological laboratory parameters, gut motility, lipid and carbohydrate absorption, quality of life and gastrointestinal hormone production after total gastrectomy with different reconstructions. The first trial compared Roux-en-Y to a newly introduced aboral pouch construction, while the second study compared these two methods and the aboral pouch reconstruction with a preserved duodenal passage version. Improved lipid absorption and quality of life was detected for the aboral pouch reconstruction. In addition to these, the duodenal passage preserving version resulted in a better iron metabolism, too. The third study compared the aboral pouch to conventional oral pouch, both with duodenal passage preserving versions. No significant difference was detected between these two groups. In the fourth study, a clinical experiment was performed examining pre- and postprandial glucose, insulin, cholecystokinin and somatostatin levels in patients recruited from the first two randomised trials. Significant differences were demonstrated between the various reconstruction types: the duodenal passage preserving reconstruction provided close to physiological cholecystokinin and somatostatin productions, while with duodenal exclusion these levels were abnormally raised.
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PMID:[Searching for the optimal reconstructive methods following total gastrectomy]. 1842 14

This study was undertaken to investigate the in vitro effect of islet labeling with iron oxide nanoparticles for MRI on islet viability, insulin secretion, and gene expression. Isolated rat islets were labeled with Resovist (25-200 microg Fe/mL, a clinically approved MRI contrast agent) in the presence or absence of poly-l-Lysine (PLL, 1.5 microg/mL) for 48 h. The iron content of labeled islets was found to increase in a dose-dependent manner. More than 90% of the islets were labeled with 100 microg Fe/mL. We confirmed the localizations of iron oxide nanoparticles within islet beta-cells by insulin immunostaining. As the concentration of Resovist increased, T(2) values as determined by T(2)-weighted MRI on a 1.5 Tesla MR scanner decreased. Labeling of 100 islets in a medium containing 100 microg Fe/mL of Resovist in the absence of PLL provided sufficient contrast for islet visualization on T(2)-weighted MRI. MTT assays showed that the viability of labeled islets was not different from that of unlabeled islets. No statistical difference was observed between labeled (2.91 +/- 0.36) and unlabeled islets (2.83 +/- 0.61) in terms of the ability to secrete insulin, as determined by the glucose stimulation index. We also evaluated the effect of iron oxide incorporation on the gene expressions in islet cells using RT-PCR (reverse transcriptase PCR). Insulin expression in labeled islets was significantly elevated (1.83 +/- 0.25 fold vs. unlabeled; p = 0.005), but not the expression of somatostatin (1.39 +/- 0.18 fold vs. unlabeled; p = 0.085) or glucagons (1.28 +/- 0.13 fold vs. unlabeled; p = 0.09). Expression of an important transcription factor for insulin gene transcription, BETA2 (beta-cell E-box trans-activator), was increased in labeled islets (1.67 +/- 0.15 fold vs. unlabeled; p = 0.029). The findings of this study indicate that Resovist provides a satisfactory means to image islets and has no deleterious effect on islet function or gene expression.
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PMID:Magnetic resonance imaging and biological properties of pancreatic islets labeled with iron oxide nanoparticles. 1948 18

Anaemia may be multifactorial in origin. We present a woman with autoimmune hepatitis and secondary warm autoimmune haemolytic anaemia and most likely also concomitant anaemia of chronic disease. A relapse of autoimmune haemolysis was successfully treated with steroids and high-dose intravenous immunoglobulin. At the same time, bleeding from angiodysplasia in the coecum was masked by unauthorised perorally administrated iron. No other cause of bleeding was found. During that period, she required extensive blood transfusions, up to several times per month. Surgical or endoscopic treatment of the bleeding angiodysplasia was not possible. Alloimmunisation developed as a complication to the large number of transfusions, despite the use of steroids. Treatment with somatostatin analogue markedly reduced the need of our patient for blood transfusions for a follow-up period of more than one year, and she has not experienced any side effects. We do not know how long the haemostasis achieved will last, however, we believe that this treatment may be an alternative for other patients as bleeding from angiodysplasia is not uncommon and is often difficult to eradicate.
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PMID:[A woman in her 60s with multifactorial anaemia]. 2256 31

The most widely used anticancer drugs are platinum-based. Their efficacy might be improved by carriers which can transport large numbers of Pt centres, shield the drug from premature activation, and/or deliver Pt specifically to cancer cells using vectors which recognise specific targets. We describe recent progress using functionalized carbon nanotubes (CNTs) and nanorods, hollow Prussian blue (HPB), magnetic iron oxide and gold nanoparticles, liposomes, nanogels and polymers, as well as active targeting by conjugation to biodegradable proteins and peptides (e.g. EGF, heparin, herceptin, somatostatin and TAT). Spatially targeted activation of Pt(IV) prodrugs using light is also a promising approach. Interestingly, use of these new delivery and targeting systems for platinum drugs can lead to species with unusual reactivity which can kill cancer cells by new mechanisms.
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PMID:Targeted delivery of platinum-based anticancer complexes. 2339 52


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