Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The sulphonylureas and the biguanides are widely used as adjuncts to dietary measures in the treatment of non-insulin-dependent (type 2) diabetes mellitus (NIDDM). Adverse effect profiles differ markedly between the sulphonylureas and biguanides, reflecting differences in chemical structure and mode of action. Sulphonylureas are generally well tolerated, although pharmacokinetic differences between these agents have important clinical implications. The main adverse effect associated with sulphonylureas is hypoglycaemia. This effect is a predictable consequence of the principal pharmacological effect of these drugs, i.e. sensitisation of the islet beta-cell to glucose, resulting in enhanced endogenous insulin secretion. Sulphonylurea-induced suppression of hepatic glucose production may cause profound and protracted hypoglycaemia, especially in elderly patients, in individuals with intercurrent illnesses and reduced caloric intake, or when taken in combination with other compounds with hypoglycaemic potential, e.g. alcohol (ethanol). Sulphonylureas with a longer duration of action, notably chlorpropamide and glibenclamide (glyburide), are more liable to induce serious hypoglycaemia, particularly when drug elimination is reduced by renal impairment. Other drugs such as salicylates may potentiate the actions of sulphonylureas, thereby increasing the risk of hypoglycaemia. Biguanide therapy is associated with alterations in lactate homeostasis which under certain clinical circumstances may result in fatal lactic acidosis. Phenformin is associated with a markedly greater risk of lactic acidosis than metformin. Phenformin has been withdrawn in many countries for this reason. All biguanides must be avoided in patients with renal impairment, hepatic dysfunction and cardiac failure--conditions where drug accumulation or disordered lactate metabolism may predispose to lactic acidosis. Phenformin should not be given to individuals who exhibit a severe, genetically conferred hepatic defect of hydroxylation which impedes metabolism of this drug. Less seriously, the biguanides are associated with a relatively high incidence of gastrointestinal adverse effects which limit compliance. Acarbose, a competitive inhibitor of intestinal alpha-glucosidases, has recently been introduced. In contrast to the sulphonylureas and biguanides, acarbose has not been associated with life-threatening adverse effects. This reflects the low systemic absorption of the drug and, predictably, its principal unwanted effects are gastrointestinal disturbances resulting from iatrogenic carbohydrate malabsorption.
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PMID:Comparative tolerability profiles of oral antidiabetic agents. 784 43

Octreotide, a long-acting analog of somatostatin that inhibits insulin release, has the potential to control hypoglycemia in infants with congenital hyperinsulinism. To examine the efficacy and side effects of octreotide, we evaluated therapy between 1988 and 1993 in 16 infants who did not respond to diazoxide. In nine patients with onset of severe hypoglycemia in the first days of life, octreotide was helpful in stabilizing plasma glucose levels and allowed reductions in the rates of glucose infusion; however, glucose control was inadequate to avoid subtotal pancreatectomy. In two of these nine patients postoperatively and in seven other infants, a trial of long-term treatment with octreotide was undertaken. Four were treated successfully for up to 4.3 years. Octreotide therapy was not associated with thyroid deficiency and caused only transient malabsorption. All patients receiving long-term therapy had some decrease in linear growth and two had subnormal plasma concentrations of insulin-like growth factor I and insulin-like growth factor binding protein 3 compatible with suppression of growth hormone by octreotide. Resistance to octreotide therapy, even with increasing doses, occurred in all patients. These results suggest that octreotide may aid in the acute or long-term treatment of congenital hyperinsulinism in a limited number of selected cases.
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PMID:Short- and long-term use of octreotide in the treatment of congenital hyperinsulinism. 841 May 9

Metformin is an oral antihyperglycemic agent that is approved by the Food and Drug Administration for the treatment of noninsulin-dependent diabetes mellitus. It differs from the sulfonylureas in that it is does not enhance insulin secretion and normally does not produce hypoglycemia. Metformin acts to decrease preprandial and postprandial blood glucose concentrations by increasing skeletal muscle uptake of glucose, decreasing gluconeogenesis, and decreasing absorption of glucose. The addition of metformin to maximum dosages of a sulfonylurea may synergistically improve glucose control. The drug may offer other potential benefits, such as weight loss or minimal weight gain, improved blood flow in patients with peripheral vascular disease, reduction of tissue plasminogen activator inhibitor, and improved lipid profiles. It is relatively safe if taken appropriately. Its most common side effects are gastrointestinal (nausea, diarrhea, anorexia), metallic taste, and vitamin B12 malabsorption. Lactic acidosis may also occur, but it is rare if metformin is avoided in patients with contraindications to its use. With careful monitoring, the agent may be considered for the initial treatment of obese patients who fail dietary measures, and those whose disease is refractory to maximum dosages of sulfonylureas or who do not tolerate them.
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PMID:Metformin in noninsulin-dependent diabetes mellitus. 872 92

Pancreatic steatorrhea and pancreatic diabetes are the dominant symptoms of patients in the decompensated stage of chronic pancreatitis (CP). In this stage, the nutritional state is greatly disturbed and hypoglycemia and labile infection are involved. Pancreatic enzyme replacement therapy is the principal treatment method for pancreatic steatorrhea. Before initiating this therapy, dietary fat intake must be determined and pancreatic lipase and bicarbonate secretion function must be evaluated. Upper small intestinal pH is regulated by gastric acid secretion, and abnormal gastric emptying changes lipolysis. In addition, precipitation of bile acids in the upper small intestine and ileal brakes due to undigested fats and carbohydrates must be considered. Porcine pancreatin, bacterial lipase, and acid-resistant fungal lipase are used as enzymes for replacement therapy. Conventional, entero-coating, and enteric-coated microsphere preparations of porcine pancreatin are available for treatment and are formulated to protect against gastric acids, to dissolve enzymes at optimum pH, and to be emptied simultaneously with food from the stomach. Gastric acid secretion suppressants, such as H2 blockers or a proton pump inhibitor, can also be used concomitantly with pancreatin preparations. In consideration of both strengths and weaknesses of these preparations, types and dosages of enzyme replacement therapy should be carefully prescribed, and fecal fats should be examined repeatedly by a simple and rapid method during treatment. Attention should also be paid to changes in body weight and nutritional indices (e.g., nutritional parameters, fat-soluble vitamins). The relationship between carbohydrate maldigestion/malabsorption in CP patients and treatment of pancreatic diabetes are topics for future research.
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PMID:Pancreatic dysfunction and treatment options. 954 75

Necrolytic migratory erythema is characterized by waves of irregular erythema in which a central bulla develops, and subsequently erodes and becomes crusted. It usually occurs in patients with an alpha-islet cell tumor of the pancreas. However, necrolytic migratory erythema has also been observed in patients without an associated glucagonoma. We describe a woman with iatrogenic necrolytic migratory erythema. She received intravenous glucagon for hypoglycemia associated with an insulin-like growth factor II-secreting hemangiopericytoma. After chemotherapy, she developed necrolytic migratory erythema. The characteristics of the previously reported patients with nonglucagonoma-associated necrolytic migratory erythema are reviewed. In patients with nonglucagonoma-associated necrolytic migratory erythema, the dermatosis-related conditions most commonly observed were celiac disease or malabsorption, cirrhosis, malignancy, and pancreatitis; less common conditions included hepatitis, inflammatory bowel disease, heroin abuse, and odontogenic abscess. Although the pathogenesis of necrolytic migratory erythema remains unknown, hyperglucagonemia appears to have had a causative role in the development of this dermatosis in our patient. Patients who develop necrolytic migratory erythema should be evaluated for the presence of a glucagonoma; if a glucagonoma is ruled out, evaluation for other conditions known to occur with necrolytic migratory erythema, such as liver disease, malabsorptive disorders, and nonislet-cell tumors is warranted.
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PMID:Iatrogenic necrolytic migratory erythema: a case report and review of nonglucagonoma-associated necrolytic migratory erythema. 959 6

In childhood, coeliac disease (gluten enteropathy) tends to show itself with failure to thrive and growth retardation; in adult life with malabsorption syndromes. We report six cases in adults who presented atypically, with features including clotting disorder, hypoglycaemia, weight loss, anaemia and angina pectoris, all of which responded to gluten withdrawal.
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PMID:Coeliac disease in adults: variations on a theme. 1069 14

An 8-yr-old intact male Grant's zebra (Equus burchelli bohmi) was referred to the Veterinary Medical Teaching Hospital of the University of California-Davis after being found in the owner's pasture obtunded and in lateral recumbency. The animal was hypothermic, weak, and unwilling to rise. There was no evidence of trauma, and the zebra had seemed normal the preceding evening. There was no extensor rigidity, and cranial nerve reflexes were normal. Flexor and extensor reflexes were weak upon initial examination. A complete blood count and serum biochemistry analysis revealed a mild leukocytosis, hyperfibrinogenemia, hypoglycemia, hyponatremia, hypochloremia, hypocalcemia, and hypoalbuminemia. Urinalysis was normal, and a urine toxicology screen for alkaloids was negative. No toxic substance was found in the hay or pasture grasses although the owner reported the presence of yellow star thistle and mushrooms in the pasture. The cerebrospinal fluid cytologic and biochemical analyses were normal, but antibodies to Sarcocystis neurona were detected. The zebra died despite aggressive supportive therapy over a 4-day period. The necropsy demonstrated severe gastrointestinal nematodiasis that could account for hypoalbuminemia and electrolyte abnormalities. Histopathologic examination of the nervous system revealed focal areas of perivascular cuffing in the brainstem that were comprised mainly of lymphocytes, monocytes, and plasma cells. Immunohistochemical staining identified the presence of S. neurona merozoites associated with the lesions. This zebra probably died from severe endoparasitism that resulted in malabsorption, weakness, and recumbency rather than from encephalitis associated with S. neurona merozoites. Equine protozoal myeloencephalitis has not been reported previously in nondomestic equids.
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PMID:Detection of Sarcocystis neurona in the brain of a Grant's zebra (Equus burchelli bohmi). 1088 30

Liver chronic pathologies often courses with metabolic abnormalities of macronutrients leading to or aggravating a protein-energy malnutrition status. This review raised the major pathophysiological mechanisms related to the protein-energy malnutrition in chronic liver patients. By large the reduced dietary intake is the most accepted cause particularly among alcoholic patients. Moreover during the treatment prevails the iatrogenic anorexia by unpalatable (restricted) diets interpolated with long-lasting fastings of hospitalized patients. Intestinal fat malabsorption is a common finding whereas hypermetabolism can be found associated with an acute alcoholism. Hypoglycemia or insulin resistance, hypertriglyceridemia and liver steatosis are common findings as well as lower plasma proteins along with higher levels of ammonia, aromatic and sulphur amino acids leading to neurological outcomes. The knowledge of these metabolic changes allow proper dietary interventions toward reduced morbi-mortality of those patients.
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PMID:[Nutritional consequences of metabolic impairment of macronutrients in chronic liver disease]. 1096 19

A six-month-old beagle was presented with a three-month history of failure to gain weight, lethargy, intermittent vomiting and seizures. Hypoglycaemia, portosystemic shunt, lead intoxication, gastrointestinal diseases and hereditary metabolic disorders were considered. Laboratory test results of low serum cobalamin (Cbl) concentrations, anaemia, leucopenia and methylmalonic aciduria while the dog was receiving a balanced commercial canine diet were suggestive of a congenital selective Cbl malabsorption. Treatment with repeated injections of parenteral cyanocobalamin (CN-Cbl) at 50 microg/kg every two weeks corrected the Cbl-deficient state and reversed all the clinical abnormalities. Selective Cbl malabsorption has previously been described in giant schnauzers and border collies and represents a unique readily treatable hereditary metabolic disorder.
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PMID:Persistent cobalamin deficiency causing failure to thrive in a juvenile beagle. 1102 27

We report a total of 23 novel mutations of the SLC2A2 ( GLUT2) gene in 49 patients with a clinical diagnosis of Fanconi-Bickel syndrome (FBS). Molecular genetic analysis has now been performed in more than 50% of the 109 FBS cases from 88 families that we have been able to locate world-wide since the original report in 1949. In these 49 patients, 33 different SLC2A2 mutations (9 missense, 7 nonsense, 10 frameshift, 7 splice-site) have been detected. Thus, our results confirm that mutations of SLC2A2 are the basic defect in patients with FBS. Mutations of SLC2A2 were detected in historical FBS patients in whom some of the characteristic clinical features (hepatorenal glycogen accumulation, glucose and galactose intolerance, fasting hypoglycemia, a characteristic tubular nephropathy) and the effect of therapy were described for the first time. Mutations were also found in patients with atypical clinical signs such as intestinal malabsorption, failure to thrive, the absence of hepatomegaly, or renal hyperfiltration. No single prevalent SLC2A2 mutation was responsible for a significant number of cases. In a high percentage (74%) of FBS patients, the mutation is homozygous, so we conclude that the prevalence of SLC2A2 mutations is relatively low in most populations. No mutational hot spots within SLC2A2 or even within homologous sequences among the genes for facilitative glucose transporters were detected.
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PMID:The mutation spectrum of the facilitative glucose transporter gene SLC2A2 (GLUT2) in patients with Fanconi-Bickel syndrome. 1181 Feb 92


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