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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The development of herbal medicine has follow in line with increased popular interest in ecology. Emphasis has been placed on the safety of natural herbs in contrast with the risks involved with "classical" medicines. But recent publications have revealed that several herbal medicines are toxic for the liver. For example, in France we have observed cases of hepatitis after ingestion of germander (Teucrium chamaedrys). Clinicians should also be aware of other well documented toxic effects of herbs used in popular medicines in Africa, Asia or Central America. The toxicity of pyrrolizidine alkaloids was recognized over 40 years ago. More than 300 plant species, including Heliotropium, Crotalaria, Senecio and Symphytum, are implicated. In Africa or Central America, intoxication is sometimes endemic since these plants are often used for making tea. In Western countries, cases of herb-induced hepatitis have been observed after use of preparations containing Symphytum or Chinese herbs. Pyrrolizidine alkaloids cause obstruction of the hepatic venous system and can lead to hepatonecrosis. Clinical manifestations include abdominal pain, ascitis, hepatomegaly and raised serum transaminase levels. Prognosis is often poor with death rates of 20 to 30% being reported. Atractylis gummifera is another example of herbal toxicity. Twenty-six species of this plant are used for medicinal purposes or for chewing gum. Intoxication usually occurs in the spring and is related to chewing the roots of these plants. Severe hepatocellular lysis may occur less than 24 hours after ingestion. Clinical manifestations are related to the induced hypoglycemia and neurovegetative disorders or subsequent renal failure. These compounds have an inhibitor effect on the Krebs cycle and can lead to severe or fatal liver failure. Other similar cases of fatal liver accidents have been reported after ingesting Callilepis laureola, a herb used by the Zoulous in Natal for medicinal purposes or after use of products containing extracts of Teucrium chamaedrys, which was nevertheless authorized in France in 1986 for use in preparations for weight loss. These examples emphasize the importance of remembering that herbal medicine is not harmless. Faced with the extensive distribution of many herbal preparations and the risk of self-medication, consumers and clinicians alike should be increasingly vigilant with these potentially hepatotoxic products.
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PMID:[Liver involvement in the course of phytotherapy]. 807 73

After a Roux-en-Y gastrojejunostomy patients frequently complain about abdominal pain, fullness, nausea and vomiting, ie, the Roux-en-Y syndrome. Stasis in the Roux limb due to disordered motility is known to be a cause of these complaints. The aim of the present study was to determine whether vagal denervation contributes to the development of motility disturbances and stasis in the Roux limb. Forty-seven patients with a Roux-en-Y gastrojejunostomy after partial gastrectomy were studied. A truncal vagotomy had been performed in 26 of these 47 patients. Transit through the Roux limb was evaluated by radionuclide studies, motility in the Roux limb was studied by manometry, and vagal function was tested by measuring the pancreatic polypeptide response to an insulin-induced hypoglycemia (PP test). On the basis of the PP test patients were classified as having (1) normal, (2) moderately impaired, and (3) severely impaired vagal function. The PP test showed that two of the 26 patients subjected to vagotomy had a moderately impaired vagal function, the other 24 all had a severely impaired vagal function. In the patients not subjected to a vagotomy, vagal function was disturbed in 11 of the 21 patients. Motility disturbances were not observed more frequently in patients with either moderately or severely impaired vagal function than in patients with normal vagal function. Stasis in the Roux limb was seen even more frequently in patients with a normal vagal function than in patients with a severely impaired vagal function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of vagal dysfunction in motility and transit disorders of jejunal Roux limb after Roux-en-Y gastrojejunostomy. 814 49

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

Nine patients with Type 2 diabetes receiving insulin therapy were treated with acarbose 100 mg thrice daily for 1 week to investigate the effect of acarbose on blood glucose control. Daily blood glucose profiles contained fewer excursions during acarbose administration and low levels were maintained. The M-value, an indicator of blood glucose fluctuation, decreased significantly from a run-in period value of 37.6 +/- 8.7 (SEM) to 16.7 +/- 4.0 during the acarbose period (p < 0.05) and rose again to 28.9 +/- 6.7 (p > or = 0.05) in the follow-up period. The 24-h urinary glucose excretion similarly decreased during acarbose administration. As expected, no decrease in HbA1C was observed due to the short treatment period. The 24-h urinary C-peptide excretions and serum lipids were not influenced by acarbose therapy. Frequent episodes of clinical hypoglycaemia were experienced while on acarbose therapy, indicating a decrease in insulin requirements. Adverse events such as flatulence and abdominal distention were observed in six out of nine cases. Symptoms were generally mild and well tolerated, only one patient dropped out because of diarrhoea and abdominal pain. We conclude that acarbose could usefully be administered to Type 2 diabetic patients treated with insulin to improve blood glucose control and reduce insulin requirement if the appropriate selection criteria were met.
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PMID:The effect of acarbose on blood glucose profiles of type 2 diabetic patients receiving insulin therapy. 850 20

A hemodialysed patient with abdominal pain, severe lactic acidosis and prolonged hypoglycemia is described. The diagnosis of acute necrotizing pancreatitis was delayed and the patient died from both systemic and peripancreatic complications of the acute pancreatitis. The article deals with the problem of diagnosing acute pancreatitis in an end-stage renal failure (ESRF) patient; on the possible surgical options open to the physician in the management of acute pancreatitis and on a pathophysiological explanation behind both the lactic acidosis and hypoglycemia in this patient.
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PMID:Acute necrotizing pancreatitis, lactic acidosis and prolonged hypoglycemia in a hemodialysed patient--a logical but unfortunately fatal combination. 879 36

Autonomic nervous dysfunction has recently been considered to be an etiological factor in syncope and sudden death in cases of hypertrophic cardiomyopathy. However, the precise mechanism is still unknown. A 73-year-old woman with obstructive hypertrophic cardiomyopathy was hospitalized with complaints of impaired consciousness; faintness 3 to 4 h after meals, lightheadedness while walking, and syncope during and after defecation and micturition. Faintness was induced by alimentary hypoglycemia related to gastrectomy performed 5 years previously. Lightheadedness and syncope were accounted for by autonomic nervous failure combined with an impairment of alpha 1-adrenoceptor in vasoconstriction and the carotid sinus hypersensitivity which accompanied preceding events such as abdominal pain, defecation and micturition, which could enhance the vagally-mediated baroreceptor reflex.
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PMID:A case of hypertrophic obstructive cardiomyopathy associated with autonomic nervous dysfunction. 884 4

The chemistry, pharmacology, pharmacokinetics, and clinical efficacy of acarbose, a new antidiabetic agent, are reviewed. Acarbose reversibly inhibits intestinal alpha-glucosidases, enzymes responsible for the metabolism of complex carbohydrates into absorbable monosaccharide units. This action results in a diminished and delayed rise in blood glucose following a meal, resulting in a reduction in post-prandial hyperglycemia, area under the glucose concentration-time curve, and glycosylated hemoglobin. Other effects include a reduction in postprandial insulin and variable changes in plasma lipid concentrations. In placebo-controlled trials, acarbose caused significant improvements in glycemic control indicators, including glycosylated hemoglobin. Acarbose has demonstrated additional glycemic control when added to other antidiabetic therapies, including sulfonylureas and insulin. Efficacy of acarbose appears to be comparable to or slightly less than that of sulfonylureas or metformin, although it has not been compared with maximal dose of these agents. The most commonly reported adverse drug reactions with acarbose are abdominal pain, diarrhea, and flatulence, which tend to lessen with time. Acarbose may affect the bioavailability of metformin and may be less effective when used in conjunction with intestinal adsorbents and digestive enzyme preparations. Concurrent use with hypoglycemic agents (sulfonylureas and insulin) may cause an increased frequency of hypoglycemia. Acarbose should not be used in individuals with certain intestinal disorders, including inflammatory bowel disease. The dosage should start at 25 mg one to three times daily given with the first bite of each main meal and should be adjusted to a maximum of 50 mg three times daily for patients weighing up to 60 kg or 100 mg three times daily for heavier patients. Acarbose may be considered for first-line antidiabetic therapy in certain patients and may be useful as combination therapy in selected instances. Acarbose is efficacious in improving metabolic control in non-insulin-dependent diabetes mellitus. Further evaluation of its effects on the long-term complications of diabetes is needed.
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PMID:Acarbose: an alpha-glucosidase inhibitor. 889 66

In adults with diabetes mellitus, hepatomegaly and abnormalities of liver enzymes occur as a consequence of hepatocellular glycogen accumulation, as has been well described in children. During periods of hyperglycemia glucose freely enters the hepatocytes driving glycogen synthesis, which is augmented further by administration of insulin to supraphysiologic levels. The accumulation of excessive amounts of glycogen in the hepatocytes is a function of intermittent episodes of hyperglycemia and hypoglycemia and the use of excessive insulin. Hepatic glycogenosis occurs in patients with poorly controlled insulin-dependent type I or type II diabetes. The clinical manifestations of this phenomenon may include abdominal pain and obstructive symptoms such as early satiety, nausea, and vomiting. Ascites has rarely been reported. The typical biochemical findings are mildly to moderately elevated aminotransferases, with or without mild elevations of alkaline phosphatase. Liver synthetic function is usually normal. All these abnormalities, including the hepatomegaly, are readily reversible with sustained euglycemic control. The other major cause of hepatomegaly in patients with diabetes is steatosis. This is a function of the body habitus and state of insulin resistance rather than glycemic control. However, the distinction between steatosis and glycogenosis is important: whereas steatosis may progress to fibrosis and cirrhosis, glycogenosis does not, but reflects the need for better diabetic control. Glycogenosis and steatosis cannot be distinguished reliably on ultrasound examination. The histology, however, is definitive. In glycogenosis, as in primary glycogen storage diseases, there is excess glycogen in the cytoplasm, and often also in the nucleus, of hepatocytes. The hepatocytes throughout the lobule appear pale and swollen with clearly defined cell boundaries. Ultrastructural examination reveals cytoplasmic glycogen in clumps displacing organelles to the periphery of the cell, and there is little if any steatosis. We have shown that hepatomegaly due to glycogenosis in adults with diabetes is similar in all respects to the condition seen in children. As in children, liver enzyme abnormalities are unreliable in predicting the presence or the extent of glycogenosis. Hepatic glycogenosis can occur at any age, and therefore should be included in the differential diagnosis of hepatomegaly in all insulin-requiring diabetics.
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PMID:Hepatomegaly and abnormal liver tests due to glycogenosis in adults with diabetes. 898 49

An 18-year-old white woman had nausea, vomiting, weight loss, and a diagnosis of anorexia nervosa. Copper-colored skin was noted on physical examination, and serum chemistry values were normal. Subsequent fever, disorientation, and confusion led to the discovery of Addison's disease, which responded well to corticosteroid replacement therapy. Addisonian and anorexic patients exhibit clinical similarities, including nausea, vomiting, weight loss, abdominal pain, cold intolerance, hypothermia, and orthostasis. Other commonalities include prolongation of electrocardiographic PR and QT intervals and generalized slowing on electroencephalogram. Important differences include a brown color to the skin in Addison's disease instead of a yellowish color in anorexia. Addisonian patients also display hypocortisolism, hypoglycemia, and hyperkalemia, in contrast to the hypercortisolism, hyperglycemia, and hypokalemia seen in anorexia.
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PMID:Prompt differentiation of Addison's disease from anorexia nervosa during weight loss and vomiting. 949 78

Although the basic pathophysiology of insulin-dependent diabetes remains unchanged, regardless of age, diabetes among adolescents is affected by certain biologic and psychosocial developments, such as reduced insulin sensitivity and compliance with treatment regimens. Emergent and urgent conditions associated with adolescent diabetes include hypoglycemia, ketoacidosis, abdominal pain, painful foot syndrome, eating disorders, and ophthalmologic problems. Diagnosis, etiology, and treatment of each are discussed in detail.
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PMID:Adolescents with Insulin-Dependent Diabetes. 1035 6


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