Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients who present with chronic unexplained upper abdominal pain or discomfort (functional dyspepsia), therapy should ideally be targeted on correcting the individual's disturbed pathophysiology. Here, putative mechanisms implicated in functional dyspepsia and potential approaches to therapy are critically reviewed in order to determine if targeting treatment is of value. Pharmacological therapies reviewed include those that aim to correct disordered gastric emptying (e.g. cisapride, dopaminergic receptor antagonists, macrolides), reduce visceral hypersensitivity (e.g. somatostatin analogues, cholecystokinin antagonists, opioid agonists, serotonin type 3 receptor antagonists), reduce gastric acid secretion (e.g. H2-blockers, acid pump inhibitors), cure Helicobacter pylori infection, enhance muscosal defence (e.g. sucralfate, bismuth) or modify central nervous system processes. It is concluded that the imperfectly understood pathophysiology of functional dyspepsia contributes to the paucity of established efficacious therapies.
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PMID:Review article: functional dyspepsia--should treatment be targeted on disturbed physiology? 760 50

Changes in immunoreactive (ir)-somatostatin, substance P, and calcitonin gene-related peptide concentrations of the human gastric mucosa were examined in subjects with nonulcer dyspepsia (NUD) and peptic ulcer to clarify the relationship between these peptides and dyspeptic symptoms. Fifty-six patients with NUD were divided into two subject subgroups as follows: 22 patients with upper abdominal discomfort, nausea, and/or vomiting (motility disorder group) and 34 patients complaining of upper abdominal pain [ulcer-like disorder (UD) group]. These patients were compared with either an age- and sex-matched group of asymptomatic outpatients without any organic disease (control group: n = 51), or to a group with peptic ulcer (PU group: n = 30). Ir-somatostatin concentrations of the gastric mucosa were significantly higher in UD group than in PU, motility disorder, or control group, and ir-substance P concentrations in the UD group were higher than in the PU group. No difference in ir-calcitonin gene-related peptide concentrations was observed among the four groups. These results indicate that there may be two distinct subgroups in NUD, and that NUD is not just a stage within the spectrum of peptic ulcer disease from the viewpoint of several gastrointestinal-hormone concentrations of the human gastric mucosa.
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PMID:Immunoreactive-somatostatin, substance P, and calcitonin gene-related peptide concentrations of the human gastric mucosa in patients with nonulcer dyspepsia and peptic ulcer disease. 768 83

Chronic pancreatitis should be considered in all patients with unexplained abdominal pain. The importance of small duct disease without obvious radiographic abnormalities is an important new concept. Diagnostic evaluation should begin with simple, non-invasive, inexpensive tests (serum trypsinogen) to be followed by more complicated testing (hormone stimulation test) if needed. Enteric-coated pancreatic enzymes are the drugs of choice for treating steatorrhea, while conventional non-enteric coated enzymes are preferred for managing pain. The somatostatin analogue octreotide may become an important therapy for treating abdominal pain unresponsive to pancreatic enzyme therapy. Endoscopic approaches to the treatment of chronic pancreatitis are experimental and may cause damage to the pancreas. Surgical ductal decompression is appropriate in selected patients.
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PMID:Medical management of chronic pancreatitis. 777 9

The objective of the present study was to measure plasma concentrations of the gastrointestinal hormones gastrin, somatostatin and cholecystokinin in plasma of children with recurrent abdominal pain, since these hormones affect gastrointestinal function. Forty-four children (7-16 years old) with recurrent abdominal pain and 36 control children (matched for age and sex) participated in the study. In a blood sample collected after an overnight fast, gastrin, somatostatin and cholecystokinin concentrations were measured by radioimmunoassay. The children with recurrent abdominal pain had higher plasma cholecystokinin levels (p < 0.001) than the controls. Whether or not this aberration is related to the clinical symptoms of children with recurrent abdominal pain remains to be established.
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PMID:Elevated cholecystokinin concentrations in plasma in children with recurrent abdominal pain. 790 74

Immunoreactive-somatostatin (ir-SS) concentrations of the gastric mucosa and mood state in patients with functional dyspepsia were examined. The subjects were 12 patients with upper abdominal discomfort, nausea and/or vomiting (motility disorder group) and 14 patients complaining of upper abdominal pain (ulcer-like disorder group) for more than a month without any organic upper-gastrointestinal tract disease proven by endoscopy. These patients were compared with either an age- and sex-matched group of asymptomatic outpatients without any organic disease (control group: n = 26) or to a group of patients with peptic ulcer (n = 19). Somatostatin concentrations of the stomach were measured by radio-immunoassay, and the mood state of each subject was assessed by Manifest Anxiety Scale (MAS) and Self-rating Depression Scale test. Immunoreactive-somatostatin concentrations of the gastric mucosa were significantly higher in the ulcer-like disorder group than in the peptic ulcer, motility disorder or control group, and gastric juice levels were higher in the ulcer-like disorder group. The psychometric tests showed that the motility disorder group was more depressive than the ulcer-like disorder group, but there were no differences between the motility disorder, ulcer-like disorder and peptic ulcer group in MAS scores or environmental factors. These results indicate that there may be two different subgroups in functional dyspepsia influenced by both ir-SS concentration of the stomach and/or mood state.
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PMID:Immunoreactive-somatostatin concentrations of the human stomach and mood state in patients with functional dyspepsia: a preliminary case-control study. 810 48

It has been recently reported that pyridostigmine (PD), an indirect cholinergic agonist, probably acting via inhibition of hypothalamic somatostatin, potentiates the GH-releasing hormone (GHRH)-induced GH rise in men, but not in women. The aim of this study was to verify the sex-related, if any, GH response to GHRH (1 microgram/kg, i.v., as a bolus) both alone and preceded by two different doses of PD (120 mg, group A, and 60 mg, group B, given orally 60 min before GHRH) in a large group of volunteers (36 women, aged 18-35 yr, and 48 men, aged 18-35 yrs). In group A, 120 mg oral PD potentiated the GH response to GHRH in both men [area under the curve (AUC), 2579.3 +/- 264.5 vs. 806.2 +/- 99.7 micrograms/L.h; P < 0.00001] and women (AUC, 2273.2 +/- 248.7 vs. 792.6 +/- 72.7 micrograms/L.h; P < 0.00001). Similarly, in the group B, 60 mg oral PD potentiated the GH response to GHRH in both men (AUC, 1929.6 +/- 157.2 vs. 568.2 +/- 81.3 micrograms/L.h; P < 0.01) and in women (AUC, 1655.9 +/- 146.9 vs. 738.2 +/- 105.7 micrograms/L.h; P < 0.01). The GH responses to GHRH, both alone and after 120 and 60 mg oral PD, did not significantly differ in men and women. No sex-related difference was observed in the cholinergic side-effects (mild abdominal pain and muscle fasciculations) that occurred in nearly 30% of the subjects. In conclusion, our results clearly show that there is no sex-related difference in the potentiating effect of PD on GHRH-induced GH release, ruling out the suggestion that women have increased cholinergic activity, leading to reduced somatostatinergic tone.
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PMID:Pyridostigmine potentiates growth hormone (GH)-releasing hormone-induced GH release in both men and women. 843 81

A 59-year-old man presented with painful subcutaneous nodules on the anterior surfaces of the legs. He had received oral antibiotics and supportive care for presumed cellulitis and thrombophlebitis, but had minimal improvement. Five months earlier, he had undergone pancreaticoduodenectomy for acinar pancreatic carcinoma; at that time, the serum level of amylase had been normal, but the level of lipase was elevated. The patient denied fever, rigors, arthritis/arthralgia, or pleuritic pain. His medications included aspirin, furosemide, ranitidine, and nortriptyline. He denied any allergies. Physical examination revealed numerous firm, tender, erythematous and violaceous, subcutaneous nodules on the lower extremities, with marked bilateral pitting edema (Fig. 1). Skin biopsy of a representative lesion revealed septal panniculitis, consistent with erythema nodosum (Fig. 2). None of the characteristic changes of pancreatic fat necrosis was present. The patient was treated with aspirin, 650 mg orally, q 6 h, and indomethacin, 50 mg orally, q 12 h, but he continued to develop new nodules; prednisone, 60 mg orally was begun. Although he reported improvement in symptoms, the nodules failed to respond clinically and older nodules ulcerated along the medical aspect of the right leg (Fig. 3). The complete blood count was normal, except for hemoglobin, 10.9 mg per dL. Routine serum biochemical studies were also normal, except for albumin, 3.1 mg per dL, LDH, 312 U per L, and SGOT, 51 U per L. Serum amylase was 14 U per L (normal per 30 to 115 U per L) and serum lipase was 54,160 U per L (normal 0 to 200 U per L). Chest roentgenogram and tuberculin skin test were negative. A CT scan of the abdomen revealed extensive liver metastases. A second biopsy of the skin and subcutis of a necrotic nodule revealed lobular panniculitis with the characteristic picture seen in pancreatic fat necrosis (Fig. 4). The patient was presumed to have metastatic pancreatic carcinoma and pancreatic fat necrosis. Nodules subsequently developed on the thighs, arms, hands, wrists, and fingers. He developed arthritis and arthralgias of the ankles, wrists, and hands, bilaterally, and the right knee. Aspiration of a right knee effusion revealed numerous neutrophils, but no evidence of infection. Treatment was begun with the somatostatin analog, octreotide, in increasing doses. During this therapy, the lesions did not progress and new lesions did not appear. There was no change in the lipase level. Inadvertently, octreotide was omitted at discharge, but reintroduction of octreotide was associated with lack of further progression of the nodules, according to the patient's spouse; however the patient became progressively debilitated and his abdominal pain worsened, requiring continuous sedation. His condition deteriorated and he died several weeks after hospital discharge.
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PMID:Fat necrosis with features of erythema nodosum in a patient with metastatic pancreatic carcinoma. 883 28

We report two patients who had non-surgical management of Pancreatic Pseudocyst. The first patient presented with acute pancreatitis and intestinal obstruction, had laparatomy and found to have hemorrhagic pancreatitis and impacted gallstone in terminal item which was removed. Two weeks after laparatomy U/S and CT showed a dilated CBD and two Pancreatic Pseudocysts. ERCP showed dilated CBD. Endoscopic sphincterotomy and stent insertion in CBD and Cystoduodenostomy was done. A percutaneous drainage was done for the pseudocyst involving the body of the pancreas. The second patient presented abdominal pain and clinically had an abdominal mass which was shown by CT as Pseudopancreatic cyst. This was drained percutaneously and given treatment with somatostatin with good outcome.
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PMID:Non surgical management of pancreatic pseudocyst: two case reports and review of the literature. 890 70

The objective of the study was to determine the tolerability and effectiveness of the slow release (SR) somatostatin analog lanreotide in active acromegaly. Fifty-seven patients, unselected in terms of their previous responsiveness to octreotide therapy, were included in a prospective, open label study carried out at 6 Italian endocrinological centers. The effects of 6 months of SR lanreotide, given at first every 14 days at a dosage of 30 mg, im, were recorded. In some patients (33%), drug dosage was adjusted by increasing the dose (to 60 mg, im) and/or shortening the time interval (every 10 days) of SR lanreotide administration. Fifty patients completed the 6-month period of therapy; 2 subjects dropped out because of adverse events, and 5 dropped out because of ineffectiveness after changes in drug administration. The first SR lanreotide injection produced more than 50% suppression of GH levels from the basal value in 93% of patients. Thirteen days later, baseline GH levels were reduced by over 50% in 25% of patients. Mean GH values were normalized in 85% of patients after 6 months, whereas insulin-like growth factor I (IGF-I) levels were normalized in 38% of patients. No correlation was found between pretreatment GH levels and GH response to SR lanreotide or between changes in GH and IGF-I during therapy. During treatment, there was a significant reduction in the percentage of patients complaining of joint pain, hyperhydrosis, and paresthesias. Changes in soft tissue swelling were documented by significant decreases in finger measurements. Diarrhea and abdominal pain were the most frequent side-effects when therapy was started; these progressively decreased. After the first month of therapy, moderate, mild, and no side-effects were reported by 3%, 40%, and 53% of patients. A nonsignificant increase occurred in asymptomatic gallstones and amylase levels. Minimal changes were noted in carbohydrate tolerance, consisting of a slight increase in glycosylated hemoglobin, a rise in glucose and a decrease in pre- and postprandial insulin levels. No effects on PRL, free cortisol, TSH, or free thyroid hormone levels were noted. No significant change in the percentage of visual field abnormalities was noted. Decreases in pituitary tumor size occurred in 3 of 17 patients reevaluated after 6 months of therapy. The 6-month period of SR lanreotide therapy was compared, on an anamnestic basis, with a 6-month or longer period of sc octreotide therapy (median, 300 micrograms/day) in 34 patients. There were no differences in effectiveness or tolerability between the 2 somatostatin analogs. These data indicate that SR lanreotide at a dose of 30 mg, im, every 14 days is an effective treatment in most unselected acromegalic patients. When administered to a group of poorly responsive patients, an increase in drug dose (60 mg im) and/or a shortening of the drug interval (10 days) seem to improve the GH/IGF-I response. Tolerability to SR lanreotide therapy is high. The use of a new sustained release formulation of somatostatin analog is clearly advantageous in improving patient compliance with medical treatment for acromegaly.
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PMID:Effectiveness and tolerability of slow release lanreotide treatment in active acromegaly: six-month report on an Italian multicenter study. Italian Multicenter Slow Release Lanreotide Study Group. 895 72

Sphincter of Oddi dysfunction has been reported as a cause of acute idiopathic recurrent pancreatitis (IRP). Octreotide, a long-acting somatostatin analogue, is an antisecretory drug used in the treatment and prevention of acute pancreatitis. Its action on sphincter of Oddi motility is controversial and no data are available for IRP patients. The aim of this study was to assess sphincter of Oddi motor response to acute administration of octreotide in patients with past attacks of acute pancreatitis without identification of any evident aetiological factor. Six patients (four male, two female; mean age +/-SD, 38.8+/-9 years) suffering from acute pancreatitis for at least 3 months before the examination were submitted to sphincter of Oddi manometry. After a basal recording lasting at least 2 min, octreotide, 0.05 mg i.v., was administered and the recording repeated. Intraduodenal pressure was taken as the zero reference and the basal sphincter of Oddi pressure and amplitude and frequency of phasic contractions were calculated before and after octreotide administration. No significant pre- vs post-octreotide differences were observed in basal pressure (41.9+/-24 vs 47.5+/-33 mm Hg, respectively) or in amplitude of phasic contractions (164.6+/-33 vs 170.8+/-18 mm Hg). With a latency of about 1 min, octreotide administration caused a high-frequency phasic activity in all cases (mean frequency, 5.5+/-2.2 contractions/min before and 9.8+/-2 after octreotide; P < 0.04). After the procedure acute pancreatitis (prolonged abdominal pain and serum amylase levels more than three-fold the normal values) developed in five patients. In conclusion, our data suggest that acute administration of octreotide may induce tachyoddia and thus a rise in sphincter of Oddi pressure, with possible impairment of biliary-pancreatic outflow.
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PMID:Effect of octreotide on sphincter of Oddi motility in patients with acute recurrent pancreatitis: a manometric study. 901 48


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