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)

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

Since the turn of the century, recurrent abdominal pain (RAP) has been a diagnostic dilemma. From the fifties, the work of Apley led to a shift in the thinking i.e., away from organic to psychosomatic causes for the pain. During the past decade, however, better gastroenterological studies have led to a return to a search for organic causes. Psychologically, this may prove salutory to the child with RAP. Based on the history, glucose tolerance and histopathological studies reported elsewhere by the authors, it is suggested that the pain in these children is due to intestinal angina. The angina may be consequent to the master switch of life operating as a glucose homeostatic mechanism in mild viral infections. The role of intravenous glucose in such situations is discussed.
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PMID:Pathogenesis and rationale of treatment of recurrent abdominal pain. 734 67

The clinical features of acute intermittent porphyria (AIP) are described in this chapter. AIP is inherited as an autosomal dominant pattern of inheritance. Prevalence in Japan is 1.5 in 100,000. Attacks are more frequent in women of 20s to 40s. The common clinical pattern of symptom involves acute abdominal pain, psychiatric disturbances, and acute neuropathy. The nerve biopsy shows segmental demyelination and axonal degeneration. Many small vacuolations are distinctively seen in all of the cell components of the nerve. Clinical diagnosis is not difficult when doctors keep the possibility of AIP in their minds in cases of abdominal pain, weakness and mental symptoms. The major trust of treatment is avoidance of acute attacks which is almost entirely dependent upon avoidance of porphyrogenic drugs. The intravenous administration of heme and glucose is important and effective therapy for acute attacks of porphyria.
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PMID:[Acute intermittent porphyria]. 761 56

Medical records of horses that underwent surgical treatment for colic between 1990 and 1992 were reviewed. Horses with a pulse rate of > or = 60 beats/min or signs of abdominal pain, which were also accompanied by a volume of > 2 L of material that refluxed from the stomach during the postoperative period (excluding horses with anterior enteritis), comprised the postoperative ileus (POI) group. Horses that had < 2 L of material reflux during the postoperative period and survived > 3 days after surgery comprised the reference population. The association of preoperative and intraoperative clinical variables with development of POI was evaluated by use of logistic regression analysis. Of 148 horses, 117 were assigned to the reference population, and 31 (21%) developed POI. Multiple logistic regression analysis was used to determine that PCV, pulse rate, type and location of lesion detected during surgery, and serum glucose concentration were the most important variables associated with development of POI. Time of recovery from anesthesia to development of POI was 0.5 to 120 hours (median, 13 hours). Duration of POI was 1 to 7 days (median, 1 day). Four of 31 (13%) horses with POI died. Of 148 horses, only 10 (7%) died; however, 4 of the 10 (40%) deaths in the short-term postoperative period were attributable to POI.
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PMID:Evaluation of factors associated with postoperative ileus in horses: 31 cases (1990-1992) 774 49

Over the period 1983-1993 10,344 stool cultures were undertaken in children with gastrointestinal symptoms at the pediatric department of the Landeskrankenhaus Leoben. Campylobacter jejuni was diagnosed as pathogen in 238 cultures taken from 196 patients aged one month to 16 years. Thus, Campylobacter jejuni infections (2.3% of all stool cultures) were second in frequency to various forms of salmonella (6.1% of all stool cultures; 332 patients). Apart from diarrhea (92% of cases), the most frequent clinical features were fever exceeding 38 degrees C (61%), abdominal pain (58%), blood in the stools (48%) and vomiting (34%). Treatment was based on appropriate diet. Fluid replacement with glucose-electrolyte infusions was required in 24% of the patients and erythromycin was administered orally in 30% of cases.
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PMID:[Infections caused by Campylobacter jejuni in the pediatric department of the Leoben district hospital 1983-1993]. 776 43

Using the noninvasive technique of electrical impedance tomography (EIT), gastric emptying was studied in 12 children, aged 9 months to 17 years, who had undergone gastric transposition (six with pyloroplasty) for oesophageal replacement (seven oesophageal atresia, five severe caustic or peptic damage). In two patients, gastric antral electrical control activity was also studied using surface electrogastrography. Nine patients had problems on oral feeds (respiratory symptoms, feeding difficulties, vomiting, abdominal pain, symptoms suggesting dumping), whilst three were asymptomatic. All 12 patients were tested with a milk meal; in addition four (two with and two without dumping symptoms) were tested with a hypertonic glucose drink; gastric emptying of the milk meal was expressed as the percentage of the meal remaining in the stomach at 60 min (R60). Mean (+/- 2 SD) R60 was 54.6% (+/- 17.4%) in 12 healthy controls and 59.8% (+/- 83.2%) in the 12 patients. Gastric emptying was normal in one patient (R60, 42.6%), delayed in seven (mean R60, 91.2%; range, 74.4-100%), and accelerated in four (R60, 0%). The emptying rate was unrelated to the presence or absence of pyloroplasty. Furthermore, the emptying pattern was extremely irregular, suggesting that gastroesophageal as well as duodenogastric reflux episodes occurred in all patients. The hypertonic glucose drink induced dumping (50% of the meal emptied at 1-3 min) in all four patients, two of whom had delayed emptying of the milk meal, but the gastric antral electrical control activity occurred at the normal frequency of 0.05 Hz.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gastric emptying in children with gastric transposition. 787 94

A case of acute pancreatitis with hyperlipemia and hyperglycemia induced by alcohol abuse is reported. The case is a 34-year-old man who was admitted to our hospital with a complaint of severe abdominal pain. He had been drinking 700ml approximately 1400ml of whisky daily prior to admission. At the time of admission, his serum amylase was elevated to 1833 U. Abdominal computerized tomography revealed edematous swelling of the pancreas. His serum glucose level was 926 mg/dl, cholesterol 754 mg/dl and triglyceride 3,530 mg/dl. Following successful treatment of acute pancreatitis and hyperglycemia with gabexate mesilate and insulin, his serum glucose, lipid and pancreatic enzyme levels decreased to the normal range. This case is considered to be one of acute pancreatitis with diabetic lipemia induced by alcohol abuse.
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PMID:A case of acute pancreatitis with hyperlipemia and hyperglycemia induced by alcohol abuse. 801 72

Twenty-six patients presenting with 33 episodes of Diabetic Ketoacidosis (DKA) and managed on a protocol oriented system were analysed. Diabetes mellitus was newly diagnosed at presentation in 18% of the 33 episodes. The presenting symptoms were polyuria and polydipsia (58%), nausea and vomiting (52%), change in sensorium (24%), hyperventilation (24%), and abdominal pain (18%). The main clinical findings at admission were dehydration (97%), acidotic respiration (67%), coma and confusion (61%), a clinically detectable source of sepsis (49%), fever (33%) and hypotension (9%). Blood sugar levels at admission ranged between 351 mg/dl and 1200 mg/dl (mean = 633 mg/dl). The mean serum potassium at diagnosis was 5.1 mmol/l and the mean calculated serum osmolality was 320 mOsm/kg. The mean serum osmolality was higher in those with disturbed conscious level. Infections, particularly those of the urogenital tract, were the main precipitating cause for the DKA. Only 12 of the 19 patients with sepsis had fever. Eight of the episodes were attributed to patients' non-compliance with insulin. Four patients died during the 33 hospitalisations, giving a mortality rate of 10%. Death occurred despite glucose control and stabilisation of the ketoacidotic state and was due to uncontrolled septicaemia. The mean duration of hospitalisation was 11 days. The ketoacidosis state was reversed after a mean duration of 9.5 hours, with an average soluble insulin requirement per patient of 52.4 units.
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PMID:Diabetic ketoacidosis--a study of 33 episodes. 815 79

When glucose utilisation is impaired due to decreased insulin effect, ketones are produced by the liver from free fatty acids to supply an alternate source of energy. This adaptation may be associated with severe metabolic acidosis and tends to occur in patients with type I (insulin-dependent) diabetes mellitus. In addition, hypovolemia is an almost invariable finding with marked hypoglycemia and is primarily induced by the associated glucosuria. Ketoacidosis stimulates both the central and peripheral chemoreceptors controlling respiration, resulting in alveolar hyperventilation (Kussmaul's respiration). With the ensuing fall in pCO2 the patient tries to raise the extracellular pH. A fruity odor of acetone on the patient's breath sometimes suggests that ketoacidosis is present. The classical triad of symptoms associated with hyperglycemia are polyuria, polydipsia, and weight loss. Circulatory insufficiency with hypotension is not uncommon due to the marked fluid loss and acidemia. In more severely affected patients, neurologic abnormalities may be seen, including lethargy, seizures or coma. Some patients also have marked vomiting and abdominal pain. The history and physical examination may provide important clues to the presence of uncontrolled diabetes mellitus. Once suspected, the diagnosis can be easily confirmed by measuring the plasma glucose concentration. Glucosuria and ketonuria can be semiquantitatively detected with reagent sticks. Blood gas analysis and anion gap give objective information as to the severity of the metabolic acidosis. Therapy must be directed toward each of the metabolic disturbances: hyperosmolality, ketoacidosis, hypovolemia and potassium, and phosphate depletion. The mainstays of therapy are the administration of low-dose insulin and volume repletion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ketoacidotic diabetic metabolic dysregulation: pathophysiology, clinical aspects, diagnosis and therapy]. 817 67

A case of hereditary coproporphyria was reported, he was a 21-year-old farmer, presenting with abdominal pain and fever. His manifestations were composed of all classical symptoms of acute hepatic porphyrias i.e. convulsions, psychosis, hypertension and respiratory failure as well as dark red urine with positive Watson-Schwartz test. Because of lack of cutaneous photosensitivity and strikingly increased urinary coproporphyrin, diagnosis of hereditary coproporphyria was most likely. Precipitating factor could not be identified. He responded well to glucose and other symptomatic treatment during the first admission but not in the second. He died from respiratory failure.
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PMID:Hereditary coproporphyria: a case report. 822 95


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