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)

BAYo1248 and BAYm1099 are two new alpha-glucosidase inhibitors. Postprandial glucose tolerance was significantly improved and postprandial insulin requirements were significantly reduced as compared to placebo after breakfast and lunch when 20 mg BAYo1248 were administered prior to breakfast and after breakfast, lunch and dinner when 50 mg BAYm1099 were given prior to all three main meals. Postprandial breath H2 concentrations were mildly increased when these alpha-glucosidase inhibitors were given and no patient complained of any adverse effects (such as flatulence, abdominal pain or diarrhea). BAYo1248 and BAYm1099 might be useful adjuncts to insulin in the treatment of patients with insulin-dependent diabetes mellitus.
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PMID:Effects of two new alpha-glucosidase inhibitors on glycemic control in patients with insulin-dependent diabetes mellitus. 352 Jan 33

The currently recognized toxic effects of quinine in humans are identified and the problems of management of overdosage of quinine are discussed. Quinine, available therapeutically as sulphate or hydrochloride salts, also is widely used in tonic water, and there are several case reports of allergic reactions to the drug when a patient has consumed the drug in this way. Another unintentional source of poisoning is its use as an adulterant in heroin for "street" use. This appears to be a problem in the US. Quinine, termed a "general protoplasmic poison" is toxic to many bacteria, yeasts, and trypanosomes, as well as to malarial plasmodia. Quinine has local anesthetic action but also is an irritant. The irritant effects may be responsible in part for the nausea associated with its clinical use. In addition it has a mild antipyretic effect. Several features are common to both an acute single overdose in self-poisoning and accumulation of quinine during therapy for malaria: together they are termed cinchonism. Auditory symptoms, gastrointestinal disturbances, vasodilatation, sweating, and headache occur with moderately elevated plasma quinine concentration. As these rise, increasingly severe visual disturbances and then cardiac and neurologic features occur. Mild nausea may be the only symptom, but with large overdoses profuse vomiting, abdominal pain, and diarrhea may occur. These result from a combination of the local irritant effect of quinine on the gut and the central effects of quinine on the chemoreceptor trigger zone. Vasodilatation and sweating are well recognized, and tinnitus is common. Visual symptoms usually are delayed, and blindness may not be discovered for a day or more. Aspirin-sensitive patients, and others, may develop angioedema by nonimmunological mechanisms in response to drugs, and quinine has been reported to produce pseudo-allergic reactions in aspirin-sensitive patients. Quinine also can cause drug-induced thrombocytopenia and purpura. In patients suffering with malaria due to "Plasmodium falciparum," anemia and acute intravascular hemolysis with renal failure are recognized complications. There appears to be little evidence in the literature in support of the folk tradition of quinine as an inducer of abortion. Quinine is known to cause deterioration in patients with myasthenia gravis and erythema multiforme, to stimulate insulin release in patients receiving treatment for falicparum malaria, and to be responsible at times for ataxia following moderate overdosage. Clinically, quinine poisoning is observed in 3 situations: self-poisoning; accidentally; and following use of quinine in excessive doses in the hope of achieving abortion. Treatment courses are reviewed.
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PMID:Quinine toxicity. 354 70

A woman had episodic attacks of flushing associated with severe skin, bone, and abdominal pain, accompanied by mood alterations and anxiety, and followed by an organic psychosis. These symptoms and signs could be induced by small doses of clonidine, L-5-hydroxytryptophan, pentagastrin, insulin, epinephrine, compound 48/80, methacholine, morphine, histamine, or d-tubocurarine. Skin testing showed abnormally sensitive mast cells and an exaggerated axon flare. Cimetidine initially prevented the attacks but became less effective after 18 months. Thyrotropin-releasing hormone stopped the skin pain whereas neurotensin reproduced the burning sensation in the skin without inducing the attack. Both the flush and the organic psychosis were reversed entirely by naloxone or naltrexone, and the hallucinosis could be reversed by vasodilators.
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PMID:A case of episodic flushing and organic psychosis: reversal by opiate antagonists. 618 3

Alcoholic ketoacidosis is a common condition which occurs predominantly in chronic alcoholics. The usual picture is an interval of increased ethanol intake followed by one or more days of abdominal pain, vomiting, dehydration and a marked decrease in caloric intake. Acidosis is frequently as severe as in diabetic ketoacidosis, but the serum Acetest measurement of ketones may be negative or only slightly positive because of the predominance of beta-hydroxybutyrate compared with acetoacetate. Treatment with intravenous glucose and saline are the essentials of management. Insulin, bicarbonate and phosphate are usually not needed. The major cause of morbidity and mortality is not the acidosis but rather failure to adequately treat concurrent medical or surgical conditions.
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PMID:Alcoholic ketoacidosis: clinical and laboratory presentation, pathophysiology and treatment. 634 51

The absence of ketoacidosis is thought to be characteristic of generalized lipoatrophic diabetes. It is widely believed that lipoatrophic diabetic patients are able to tolerate starvation and therapeutic insulin withdrawal, due to absence of subcutaneous body fat, the substrate essential for ketogenesis. In this article, we document nine episodes of acidosis and accelerated ketone body formation in a 24-yr-old woman whose deterioration followed episodes of dietary excesses without evidence of intercurrent infection or other identifiable forms of metabolic stress. Serum C-peptide measurements demonstrated that an absolute insulin deficiency did not exist. During short-term, experimental, dietary manipulations, excess dietary calories worsened the hyperglycemia and hyperlipidemia but did not reproduce the ketoacidotic state. Excess fat added to the diet was the most poorly tolerated of the food groups, causing ketonuria, hypertriglyceridemia, and abdominal pain. Our experience with this patient suggests that increased food consumption, insufficient insulin relative to an insulin-resistant state, and increased amounts of insulin counterregulatory hormones (stress), acted in concert to cause acidosis and increased ketone body formation.
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PMID:Recurrent ketoacidosis in acquired, total lipodystrophy (lipoatrophic diabetes). 643 2

Severe abdominal pain was the major indication for operation in 85 patients with chronic pancreatitis. Preoperative endoscopic retrograde cholangiopancreatography (50 patients) or intraoperative pancreatic ductograms (44 patients) demonstrated dilated or obstructed major pancreatic ducts in 50 patients (59%), nonvisualization of the distal duct in 10 patients (12%), and normal or small sized ducts in 34 patients (40%). Operative procedures, tailored according to duct morphology, included pancreatic duct drainage (46 patients), subtotal (40% to 80%) pancreatectomy (21 patients), near-total (85% to 95%) pancreatectomy alone (eight patients), and near-total or total pancreatectomy and intrahepatic islet autotransplantation (10 patients). Pancreatic duct drainage resulted in pain relief in 37/46 patients (80%) followed for 6 years. However, 20/46 patients (43%) had continued loss of pancreatic function after duct drainage as measured by the development of insulin-dependent diabetes (16 patients) or steatorrhea (seven patients). Seven years after subtotal pancreatectomy, pain relief was partial in 9/21 patients (43%) and complete in five patients (24%). A higher incidence of hypoglycemic or ketoacidotic complications was noted in patients treated by subtotal pancreatectomy (three patients, 14%) than by duct drainage (one patient, 2%). Near-total pancreatectomy was the most effective surgical procedure in relieving pain, but late sequelae in three patients (38%) included one hypoglycemic death and two ketoacidotic episodes. Five years after near-total pancreatectomy and islet autotransplantation, one patient remained permanently insulin independent; three patients were insulin independent for 4, 5, and 15 months, respectively, but subsequently developed nonketosis-prone diabetes (tested by insulin withdrawal) and require 15 to 30 U of insulin daily; three patients had immediate insulin requirements and currently need 20 to 30 U of insulin per day but are nonketosis prone; and two patients are ketosis prone and require 30 to 60 U of insulin daily. Our analysis suggests that 5-year survival of patients undergoing operation for chronic pancreatitis is similar after treatment by duct drainage, subtotal pancreatectomy, or near-total pancreatectomy, regardless of duct morphology. Five years after duct drainage or subtotal pancreatic resection, a high incidence of diabetes (59% and 48%) and/or continued pain (20%) and (35%) can be expected.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Chronic pancreatitis: long-term surgical results of pancreatic duct drainage, pancreatic resection, and near-total pancreatectomy and islet autotransplantation. 643 70

Endoscopic retrograde cholangiopancreatography (ERCP) is generally regarded as a safe and useful investigation in the diagnosis and management of diseases of the pancreas and biliary tree. Asymptomatic hyperamylasemia is not uncommon following this procedure, but clinical pancreatitis is rare. The authors report on a 56-year-old man who suffered life-threatening acute hemorrhagic pancreatitis 2 weeks after ERCP was performed for the investigation of abdominal pain. He subsequently had insulin-dependent diabetes mellitus, which was not present at the time of ERCP.
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PMID:Acute hemorrhagic pancreatitis and diabetes mellitus following endoscopic retrograde cholangiopancreatography. 674 53

Sucrose (100 g) loading tests were performed in 10 healthy volunteers before and during the intake of an alpha-glucosidehydrolase inhibitor (acarbose) for 8 weeks (3 X 200 mg daily) and serum levels of glucose, immunoreactive insulin (IRI), and immunoreactive gastric inhibitory polypeptide (IR-GIP) were measured. The addition of 200 mg of acarbose to the sucrose load attenuated the sucrose-induced glycaemia and IRI response and completely abolished the IR-GIP release. The volunteers complained about meteorism and abdominal pain during the intake of the inhibitor. These side effects became less marked at the end of the study. The attenuation of complaints cannot be explained by a decreasing sucrase inhibition, since the increase of glucose, IRI, and IR-GIP after sucrose loading at the beginning and after 4 and 8 weeks was equally impaired by acarbose.
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PMID:Response of serum levels of gastric inhibitory polypeptide and insulin to sucrose ingestion during long-term application of acarbose. 703 56

DT, a 63-year-old white male with insulin-dependent diabetes mellitus and severe peripheral vascular disease, was admitted with a five-day history of vague abdominal pain and diarrhea. On the day of admission he vomited three times, was noted to have a bloody stool, and came to the emergency room. DT denied hematemesis, fever, or chills. He had bilateral leg amputations and had sustained three myocardial infarctions, the last one 15 months before this admission. He had never experienced symptoms of abdominal angina. Of significance was his history of congestive heart failure, mitral regurgitation, and atrial fibrillation. His medications on admission included digoxin 0.25mg per day, furosemide 40mg per day, and NPH insulin 15 units per day. On admission to the hospital his oral temperature was 38 degrees C, pulse was 90/min, respiratory rate was 24/min, and blood pressure was 134/80mmHg. Abdominal examination revealed a distended abdomen with hypoactive bowel sounds and mild tenderness. Chest x ray revealed cardiomegaly. The electrocardiogram demonstrated atrial fibrillation. A plain film of the abdomen was positive for gallstones and edema of the bowel wall (thumb-printing). Laboratory results included blood urea nitrogen 48mg%, creatinine 1.2mg%, hemoglobin 18g/dl, and hematocrit 52.9%. White blood cell count was 11,900 cells/cc with 33% polymorphonuclear leukocytes, 47% bands, 8% lymphocytes, 11% monocytes, and 1% atypical lymphocytes. The prime considerations for differential diagnosis were mesenteric ischemia and infectious gastroenteritis. While it was appreciated that mesenteric ischemia, if present, might warrant surgical intervention, the risk of anesthesia itself in this patient was felt by his attending physicians to exceed 30%. Furthermore, the clinical findings were only "suggestive" of mesenteric eschemia. They were certainly not "diagnostic." In view of this dilemma, a consultation with the Division of Clinical Decision Making was requested.
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PMID:Abdominal pain, atherosclerosis, and atrial fibrillation. The case for mesenteric ischemia. 716 38

Unless renal function is impaired or rhabdomyolysis is severe, hyperkalemia is a relatively uncommon metabolic complication of poisoning. In contrast, marked hypokalemia is a more common problem and may have serious sequelae. Most potassium disturbances in acute poisoning are due to disruption of extra-renal control mechanisms, notably the activity of Na+/K+ ATPase and K+ channels. Hypokalemia occurs because of increased Na+/K+ ATPase activity (e.g. beta 2 agonist, theophylline or insulin poisoning), competitive blockade of K+ channels (e.g. barium or chloroquine poisoning), gastrointestinal losses and/or alkalosis. Hyperkalemia follows inhibition of Na+/K+ ATPase activity (e.g. by digoxin), increased uptake of potassium salts, disruption of intermediary metabolism (e.g. cyanide poisoning), activation of K+ channels (e.g. fluoride poisoning), and the presence of acidosis and rhabdomyolysis, particularly if the latter is complicated by renal failure. Hypokalemia results in generalized muscle weakness, paralytic ileus, ECG changes (flat or inverted T waves, prominent U waves, ST segment depression) and cardiac arrhythmias (atrial tachycardia +/- block, AV dissociation, VT, VF). Hyperkalemia is associated with abdominal pain, diarrhea, muscle pain and weakness, ECG changes (tall peaked T waves, ST segment depression, prolonged PR interval, QRS prolongation) and cardiac arrhythmias (VT, VF). Significant disturbances of potassium homeostasis are often unrecognized and may cause considerable morbidity and mortality. Prompt recognition and appropriate treatment of these disturbances could be life-saving.
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PMID:Disturbances of potassium homeostasis in poisoning. 762 96


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