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)

Relationships between nutrition and infection are generally complex, bidirectional, and not perfectly worked out. Healthy people can adapt to simple decreases in intake or increases in expenditure. However, the imposition of infection with associated cytokines may impair such adaptations, resulting in wasting of lean tissue. In human immunodeficiency virus (HIV) infection, nutritional abnormalities are common. Lean body mass depletion is associated temporally with death in a subset of acquired immune deficiency syndrome (AIDS) patients. Weakness, fatigue, and anorexia are important symptomatic complaints affecting quality of life. Pathophysiologic mechanisms remain speculative, although there is reason to suspect four theoretic factors: decreased intake, malabsorption, hypermetabolism, and altered metabolism. More than one disturbance may be necessary for clinical wasting to develop; ie, a primary abnormality plus a failure of homeostatic adaptation. Excess cytokine production also may be involved, but this is uncertain. Therapeutics remain empiric in the absence of known mechanisms. Current options are restricted to diet adjustments or supplements, treatment of underlying diseases (where possible), and rarely, parenteral alimentation. Promising investigational possibilities include an appetite stimulant (megestrol acetate) and therapies to oppose cytokine production or actions, but definitive beneficial effects on nutritional status, subjective performance, disease activity, or survival have not yet been demonstrated. Advances in clinical therapeutics await an improved understanding of pathophysiologic mechanisms and carefully designed clinical trials testing proposed interventions.
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PMID:Current approach to the treatment of human immunodeficiency virus-associated weight loss: pathophysiologic considerations and emerging management strategies. 225 24

Patients with cystic fibrosis (CF) and pancreatic malabsorption frequently have vitamin E deficiency. Affected patients may develop spinocerebellar degeneration with dysarthria, ataxia, proximal weakness, proprioceptive loss and areflexia. Of a highly selected group of 10 patients with vitamin E levels below 5 micrograms/ml (normal 5-20 micrograms/ml), 7 had abnormal neurological examinations, predominantly affecting vibration and joint position perception with some severely affected patients manifesting diminished visual acuity, tremor, ataxia and diffuse weakness. Evoked potential studies showed marked abnormalities in 3 patients, demonstrating deficits in the optic pathways and in the cervical cord dorsal column pathways. Evoked potential studies may supplement careful neurological examination in patients with CF before and after supplementation with vitamin E to evaluate their progression and response to treatment.
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PMID:Visual and somatosensory evoked potentials in vitamin E deficiency with cystic fibrosis. 245 91

Nontuberculous mycobacteria (NTM) have been frequently identified as opportunistic pathogens in individuals with advanced human immunodeficiency virus (HIV) infection. The majority of these infections have been caused by members of the Mycobacterium avium-intracellulare complex (MAC). Disseminated MAC infection has generally been diagnosed late in the course of HIV infection, and it is often associated with persistent nonspecific symptoms of fever, generalized weakness, and weight loss. Abdominal pain and/or diarrhea with malabsorption may also occur in some patients. Despite frequent isolation of MAC organisms from respiratory secretions in these patients, significant pulmonary involvement has not been seen commonly with disseminated MAC infection. While MAC can be isolated from a variety of clinical specimens in infected individuals, culturing of blood is the single most useful diagnostic procedure to evaluate for MAC infection. The prognosis for disseminated MAC infection in HIV-infected patients has been poor, with a reported median survival of 7.4 months after diagnosis. The overall contribution of MAC infection to mortality in these patients has not been clearly delineated. Treatment of MAC infection in HIV-infected individuals using a variety of drug regimens has not been effective in clearing mycobacteremia or improving overall survival in the majority of patients. However, initiation of drug therapy for MAC may decrease the severity of disease symptoms in some patients. Several NTM other than MAC have also been reported as causing infection in HIV-infected patients. Many of these organisms are ubiquitous in the environment and are frequent colonizers of biologic specimens. Although many NTM are regarded as relatively avirulent, these organisms need to be recognized as potentially important pathogens in HIV-infected patients with significant immunosuppression.
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PMID:Mycobacterium avium complex and other nontuberculous mycobacteria in patients with HIV infection. 266 36

Infection with Capillaria philippinensis has not been reported in Taiwan before. It is characterized by chronic diarrhea, abdominal pain and muscle wasting. Because the infection results in a severe disease with a high mortality, early diagnosis is very important. A 58-year-old housewife from Ar-Lien village, Kao-Hsiung County, was admitted to the National Taiwan University Hospital in July 1988, after suffering from diarrhea, lower leg edema and weight loss for one year. The initial symptom was epigastric pain followed by watery diarrhea. Thereafter borborygmus, frequent loose stool passage and weakness persisted. The cause of her malabsorption syndrome went undetected until the ova, larvae and adult worms of C. philippinensis were detected in the direct smear of the patient's stool in August 1988. She received mebendazole 200mg b.i.d. for 20 days. Capillaria ova were no longer detected following the third day of medication. At the second month follow-up, her body weight returned to her pre-morbid state and all laboratory findings returned to normal with the exception of mild anemia. The infection source was not clear.
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PMID:Intestinal capillariasis: report of a case. 279 62

A 41-yr-old woman with primary biliary cirrhosis developed weakness and wasting in proximal muscles, areflexia, and decreased proprioceptive and vibratory sensation. Investigations revealed law serum levels of vitamin E and electromyographic and muscle biopsy changes consistent with a neuropathy. Sural nerve histology demonstrated axonal dystrophy with patchy demyelination. These features closely resemble a neurologic syndrome associated with chronic cholestatic liver disease and vitamin E deficiency in children. Adults with chronic cholestasis may also be susceptible to neurologic damage from prolonged malabsorption of vitamin E.
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PMID:Neurologic syndrome associated with low levels of vitamin E in primary biliary cirrhosis. 301 81

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

We report the cases of two adult patients with cystic fibrosis affecting the pancreas and liver, who also had severe vitamin E deficiency and neurologic disease. The most prominent clinical features were abnormal eye movements, diminished reflexes, decreased vibratory and position sense, ataxia, and muscle weakness. Treatment with intramuscular injections of vitamin E partially corrected the neurologic deficits. Vitamin E absorption tests documented severe malabsorption, which was later alleviated by the addition of dessicated ox bile to the regimen of alpha-tocopheryl acetate. These studies suggest that a decreased intraluminal concentration of bile salts is an important factor in the development of severe vitamin E deficiency and in the poor response to oral replacement therapy that is seen in some patients with cystic fibrosis.
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PMID:Vitamin E deficiency and neurologic disease in adults with cystic fibrosis. 359 48

The authors describe their experience with four cases of dural arteriovenous malformation (AVM) which led them to analyze the clinical aspects of these lesions in an attempt to understand their pathophysiology. An additional 191 previously reported cases of dural AVM's were reviewed with special attention to the mechanism of intradural, central, and peripheral nervous system manifestations. Apart from the peripheral cranial nerve symptoms, which are most likely due to arterial steal, the central nervous system (CNS) symptoms appear to be related to passive venous hypertension and/or congestion. Generalized CNS symptoms can be related to cerebrospinal fluid malabsorption due either to increased pressure in the superior sagittal sinus, to venous sinus thrombosis, or to meningeal reaction resulting from minimal subarachnoid hemorrhages. These phenomena are not related to the anatomical type of venous drainage. On the other hand, focal CNS symptoms are specifically indicative of cortical venous drainage. Seizures, transient ischemic attacks, motor weakness, and brain-stem and cerebellar symptoms can be encountered depending on the territory of the draining vein or veins. Therefore, the localizing value of focal CNS symptomatology relates to the venous territory and not to the nidus or to the arterial supply characteristics of dural AVM's. Furthermore, the venous patterns of various dural AVM's at the base of the skull are expressed by differences in their clinical presentation. Dural AVM's of the floor of the anterior cranial fossa and of the tentorium are almost always drained by the cortical veins and, therefore, have a high risk of intradural bleeding. The remarkable similarities in the manifestations of dural and brain AVM's and the differences in the manifestations of dural and spinal dural AMV's are pointed out. High-quality angiograms and a multidisciplinary approach to the study of dural AVM's will provide the best understanding of their symptoms and, therefore, the most appropriate treatment strategy.
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PMID:Neurological manifestations of intracranial dural arteriovenous malformations. 370 21

We describe nine patients with fat malabsorption in whom a spectrum of vitamin E deficiency was present. Early deficiency was generally asymptomatic, and intermediate deficiency produced some impairment. Ataxia, weakness, reflex changes, impaired vision, and pigment retinopathy were associated with chronic, advanced deficiency. In the last group, delayed central somatosensory conduction and amplitude reduction of the electroretinogram were present. In adults, a severe vitamin E deficiency state existed for more than 5 years before producing measurable neurologic damage. The clinical picture is less homogeneous than previously suggested, and electrophysiologic abnormalities need not predate clinical dysfunction.
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PMID:The spectrum of neurologic disorder from vitamin E deficiency. 371 53

The results of clinical, laboratory and therapeutic observations conducted over a seven year period in 40 expatriates from the tropics who presented in New York City with overt tropical sprue have been described. The majority of subjects presented with symptoms referable to the gastrointestinal tract, weight loss and weakness. Only nine were symptomatic at the time of arrival; the remainder developed symptoms within several months to 14 years after arrival. Thirty-five subjects had a megaloblastic anemia; this was a secondary to a combined deficiency of folate and vitamin B12 in 25 and to deficiency of only one of these vitamins in the other ten. Serum concentrations of albumin, calcium, and cholesterol were subnormal in approximately one-half and the serum carotene concentrations were low in all but two subjects. Serum values of one or more immunoglobulin were reduced in 19. All 40 subjects had malabsorption of xylose; 12 of 19 tested had malabsorption of a pharmacologic dose of folic acid; 27 of 28 tested had malabsorption of vitamin B12; and 23 of 27 persons tested had steatorrhea. Jejunal morphology was abnormal in 34 of 35 subjects biopsied prior to treatment; villi were completely absent in four and showed changes of moderate severity in 30. Treatment with pharmacologic doses of folic acid or vitamin B12 produced a clinical remission in 18 of 21 patients. This remission was sustained in all 14 subjects who were followed for periods of from one to four years and reevaluation of intestinal morphology and function in nine showed improvement in all, but return to normal in less than one-half. Treatment with oral tetracycline for three weeks resulted in clinical improvement in 11 of 12 subjects, a hematologic response in nine of the ten cases who had a megaloblastic anemia, increased absorption of xylose and cessation of steatorrhea in all, and improved jejunal morphology in 11. Vitamin B12 absorption remained subnormal in nine. Continued antibiotic therapy for six months in eight patients was associated with additional weight gain, further improvement in jejunal morphology and xylose absorption in all, and return of vitamin B12 absorption to normal in all except one. Fifty asymptomatic expatriates from the West Indies were surveyed for abnormalities of intestinal function. The absorption of xylose was reduced in six (24%) of 25 subjects who had been resident in a temperate climate for less than one year but in only one (4%) of 25 persons who had been away from the tropics for more than a year.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Tropical sprue in expatriates from the tropics living in the continental United States. 495 Dec 35


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