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)

Diarrhea is a common gastrointestinal problem in diabetes, and its prevalence has been underestimated. The cause of diabetic diarrhea is unknown, but it is probably related to gastrointestinal motility disturbances secondary to diabetic autonomic neuropathy. Other causes (especially primary malabsorption syndromes and islet cell tumors) must be excluded. Treatment of diabetic diarrhea is largely symptomatic and only moderately effective. Antidiarrheal agents may ameliorate acute episodes. Broad-spectrum antibiotics and clonidine hydrochloride (Catapres) have had some success in long-term control. Most recently, subcutaneous administration of somatostatin analogues has been shown to be helpful, the main side effects being drowsiness and vomiting.
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PMID:Diabetic diarrhea. An underdiagnosed complication? 160 50

Autonomic nerve function was evaluated in 33 patients with Crohn's disease (age range, 19-66 years; mean, 36 years) by three established non-invasive tests based on the heart reactions to deep breathing (E/I ratio) and to tilt (acceleration and brake indices). Peripheral nerve function was evaluated neurographically and by measuring thresholds to vibration and temperature changes. None of the patients were diabetic, and all had normal thyroid function. In spite of normal peripheral nerve function, almost half of the patients, 48% (16/33), showed signs of autonomic neuropathy (AN). The occurrence of AN was not related to duration or severity of Crohn's disease or to biochemical evidence of inflammation or malabsorption of vitamins and trace elements. We conclude that autonomic nerve dysfunction is a feature of Crohn's disease which may be relevant with regard to the frequent disturbance in bowel function in patients with this disorder.
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PMID:Disturbed autonomic nerve function in patients with Crohn's disease. 203 89

The small intestine is a major target in HIV infection. Chronic diarrhoeal disease associated with malabsorption is the principal clinical manifestation of such infection. Reduced intestinal immunity and opportunistic enteric infections play a major role in clinical disease, but an enteropathy induced by HIV per se has also been implicated. The immunopathology of reduced intestinal immunity and its progression during HIV infection is poorly understood. HIV genome and proteins have been detected reproducibly in cells of the lamina propria resembling macrophages, but direct epithelial infection with HIV is controversial. Another factor which may contribute to diarrhoea is autonomic neuropathy within the jejunum. Small intestinal disease causes malabsorption of fat and disaccharides and may contribute to the weight loss seen in advancing HIV infection. However, malnutrition seen in HIV infection is multifactorial and may occur as a constitutional sign of infection in the absence of overt intestinal disease. Reduced food intake does not appear to be a causative factor in the weight loss in constitutionally well stage IV patients and there is some evidence that release of cytokines (TNF alpha/cachectin) into plasma or locally into tissue may mediate such events. The response of HIV-infected individuals to nutritional support is variable, but it is becoming increasingly apparent that the response is limited by the presence of severe systemic infection. However, aggressive nutrition is an important therapeutic mode which should be offered to all HIV-infected patients.
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PMID:Malabsorption, malnutrition and HIV disease. 228 81

We assessed gastrocolic transit time in 10 diabetic patients with autonomic neuropathy and 10 healthy age-matched controls by measuring breath hydrogen rise and scintigraphic bolus progression after ingestion of an isosmotic lactulose solution containing 99m-Tc-diethylentriamine-pentaacetic acid. Mean transit time in diabetics with autonomic neuropathy was significantly slower with respect to controls, with a good correlation between the two techniques. Moreover, diabetics had a significantly shorter discharge time (defined as the period that elapses between the arrival of the meal into the cecum and the hydrogen increase in the expired air). It is concluded that the selective lipid malabsorption seen in diabetic patients could be the result of cecal-ileal reflux, as a contaminating consequence of the last ileal loop. A possible motor innervation defect of the ileo-cecal valve is postulated in these subjects.
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PMID:Hydrogen breath test and scintigraphic gastrocolic transit time in diabetics with autonomic neuropathy. 843 Feb 46

Chronic intestinal pseudo-obstruction denotes the clinical picture that results due to the failure of intestinal peristalsis to overcome the normal resistance to flow and is characterized by recurrent episodes of signs and symptoms of intestinal obstruction in the absence of any mechanical compromise of the intestinal lumen. The region(s) of the gut affected may be isolated or diffuse. It is not uncommon to find evidence of autonomic neuropathy and smooth muscle dysfunction with extraintestinal manifestations such as urinary symptoms from abnormal ureter or bladder function. Intestinal pseudo-obstruction can be caused by a variety of diseases, and for simplicity, certain authors have divided it into myopathic and neuropathic categories. Intestinal pseudo-obstruction may present at any age with a variable amount of abdominal pain, distension, nausea, diarrhea, or constipation and with laboratory abnormalities usually reflecting the degree of malabsorption and malnutrition present. The radiologic findings are varied but commonly include paralytic ileus or signs of apparent clinical obstruction with dilated loops of bowel. The number of pseudo-obstruction cases is dependent on how one defines the condition. It appears prudent to require radiographic abnormalities consistent with obstruction on a plain film of the abdomen for the diagnosis. More recently, studies have focused on the gastrointestinal manometric abnormalities of the stomach and small intestine in chronic intestinal pseudo-obstruction during fasting and fed states; however, sensitivity and specificity of these abnormalities are not well defined. Treatment is aimed at limiting symptoms and maintaining adequate nutrition. Prokinetic agents should be tried in an attempt to restore normal intestinal propulsion. However, their overall efficacy appears to be variable. It is still too premature to consider intestinal pacing or small bowel transplantation in this condition. Surgical approaches to chronic intestinal pseudo-obstruction should be limited to patients refractory to medical therapy, and even then, an approach focused on the patient's primary presenting symptoms should be considered.
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PMID:Chronic intestinal pseudo-obstruction. 854 80

Type 1 diabetes is an intrinsically unstable condition. However, the term "brittle diabetes" is reserved for those cases in which the instability, whatever its cause, results in disruption of life and often recurrent and/or prolonged hospitalization. It affects 3/1000 insulin-dependent diabetic patients, mainly young women. Its prognosis is poor with lower quality of life scores, more microvascular and pregnancy complications and shortened life expectancy. Three forms have been described: recurrent diabetic ketoacidosis, predominant hypoglycemic forms and mixed instability. Main causes of brittleness include malabsorption, certain drugs (alcohol, antipsychotics), defective insulin absorption or degradation, defect of hyperglycemic hormones especially glucocorticoid and glucagon, and above all delayed gastric emptying as a result of autonomic neuropathy. Psychosocial factors are very important and factitious brittleness may lead to a self-perpetuating condition. The assessment of brittle diabetes requires quantification of the variability of blood glucose levels. To quantify instability, measures which have been developed, include Mean Amplitude of the largest Glycemic Excursions (MAGE), Mean Of Daily Differences (MODD), Lability Index (LI), Low Blood Glucose Index (LBGI), Clarke's score, Hyposcore, and continuous blood glucose monitoring. Once psychogenic problems have been excluded, therapeutic strategies require firstly, the treatment of underlying organic causes of the brittleness whenever possible and secondly optimising standard insulin therapy using analogues, multiple injections and consideration of Continuous Subcutaneous Insulin Infusion. Alternative approaches may still be needed for the most severely affected patients. Isolated islet transplantation (IIT), which restores glucose sensing, should be considered in cases of hypoglycaemic unawareness and/or lability especially if the body mass index is < 25, but with current immunosuppressive protocols patients must have normal renal function and preferably no plans for pregnancy. Implantable pumps have advantages for patients who either weigh more than 80 kgs or have abnormalities of kidney or liver function or are highly sensitised.
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PMID:Management strategies for brittle diabetes. 1707 32

Patients with chronic pancreatitis may have abnormal gastrointestinal transit, but the factors underlying these abnormalities are poorly understood. Gastrointestinal transit was assessed, in 40 male outpatients with alcohol-related chronic pancreatitis and 18 controls, by scintigraphy after a liquid meal labeled with (99m)technetium-phytate. Blood and urinary glucose, fecal fat excretion, nutritional status, and cardiovascular autonomic function were determined in all patients. The influence of diabetes mellitus, malabsorption, malnutrition, and autonomic neuropathy on abnormal gastrointestinal transit was assessed by univariate analysis and Bayesian multiple regression analysis. Accelerated gastrointestinal transit was found in 11 patients who showed abnormally rapid arrival of the meal marker to the cecum. Univariate and Bayesian analysis showed that diabetes mellitus and autonomic neuropathy had significant influences on rapid transit, which was not associated with either malabsorption or malnutrition. In conclusion, rapid gastrointestinal transit in patients with alcohol-related chronic pancreatitis is related to diabetes mellitus and autonomic neuropathy.
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PMID:Determinants of accelerated small intestinal transit in alcohol-related chronic pancreatitis. 1939 Sep 66

Along with myasthenia, other paraneoplastic neurological syndromes (PNS) may occur in thymoma. Anti-Hu antibodies and a clinical "anti-Hu syndrome" characterized by encephalitis and/or painful neuropathies have been reported in only three patients at the time of the diagnosis of thymoma. We describe a severe anti-Hu-related autonomic neuropathy with gastrointestinal paresis and intestinal pseudo-obstruction with malabsorption that occurred concomitantly with the worsening of myasthenic symptoms long after the initial diagnosis of thymoma in a young patient. The clinical anti-Hu syndrome preceded the radiological diagnosis of thymoma recurrence. Treatment with plasma exchange led to a transient improvement of neurological symptoms.
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PMID:Thymoma associated with myasthenia and autonomic anti-Hu paraneoplastic neuropathy. 1957 74

Human intestinal microbiota create a complex polymicrobial ecology. This is characterised by its high population density, wide diversity and complexity of interaction. Any dysbalance of this complex intestinal microbiome, both qualitative and quantitative, might have serious health consequence for a macro-organism, including small intestinal bacterial overgrowth syndrome (SIBO). SIBO is defined as an increase in the number and/or alteration in the type of bacteria in the upper gastrointestinal tract. There are several endogenous defence mechanisms for preventing bacterial overgrowth: gastric acid secretion, intestinal motility, intact ileo-caecal valve, immunoglobulins within intestinal secretion and bacteriostatic properties of pancreatic and biliary secretion. Aetiology of SIBO is usually complex, associated with disorders of protective antibacterial mechanisms (e.g. achlorhydria, pancreatic exocrine insufficiency, immunodeficiency syndromes), anatomical abnormalities (e.g. small intestinal obstruction, diverticula, fistulae, surgical blind loop, previous ileo-caecal resections) and/or motility disorders (e.g. scleroderma, autonomic neuropathy in diabetes mellitus, post-radiation enteropathy, small intestinal pseudo-obstruction). In some patients more than one factor may be involved. Symptoms related to SIBO are bloating, diarrhoea, malabsorption, weight loss and malnutrition. The gold standard for diagnosing SIBO is still microbial investigation of jejunal aspirates. Non-invasive hydrogen and methane breath tests are most commonly used for the diagnosis of SIBO using glucose or lactulose. Therapy for SIBO must be complex, addressing all causes, symptoms and complications, and fully individualised. It should include treatment of the underlying disease, nutritional support and cyclical gastro-intestinal selective antibiotics. Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.
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PMID:Small intestinal bacterial overgrowth syndrome. 2057