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)

Ten patients, aged 39-61 years, with hypomagnesaemia due to chronic alcoholism (7 cases) or malabsorption (3 cases), have been investigated by assessing the maximum isometric voluntary contraction force (MVC) of the quadriceps femoris muscle (7 cases), laboratory screening (9 cases) and estimating the electrolyte and metabolite content of biopsy specimens from the quadriceps femoris muscle. The MVC ranged from 0.5 to 34 kp and was significantly lower than in 12 apparently healthy normomagnesaemic controls (p is less than 0.001). The results of the laboratory screening, apart from a significant lowering of the serum magnesium concentration (p is less than 0.01), were mainly within the range of normal values, apart from signs of liver damage, such as an elevated activity of S-OCT (3 cases), alkaline phosphatease(3 cases), S-ALAT (1 case) and an elevation of bilirubin and blood ammonia (2 cases). Low serum iron-binding capacity occurred in 4 cases, a finding reported in protein-calorie malnutrition. Muscle magnesium content was significantly lower than in healthy controls (p is less than 0.001). Muslce sodium and chloride contents were significantly increased (p is less than 0.05). Total H2O content and the extracellular H2O content were both significantly increased (p is less than 0.05). Pyruvate and lactate values were within the normal range. The apparent equilibrium constant for creatine kinase differed significantly ( is less than 0.01). ATP values were within the normal range, but there were slight decreases for ADP (p is less than 0.05) and creatine phosphate ( is less than 0.01), whcih is of interest in view of the lowering of the MVC and the diminished capacity for sustained muscular effort in hypomagnesaemic patients reported earlier.
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PMID:Hypomagnesaemia and muscle electrolytes and metabolites. 85 Oct 37

Chronic consumption of substantial amounts of alcohol is not associated with the expected effect on body weight. Isocaloric substitution of carbohydrates by ethanol results in weight loss, and addition of ethanol to an otherwise normal diet does not produce the expected weight gain. This energy deficit cannot be explained by maldigestion or malabsorption but has been attributed to induction of the microsomal ethanol oxidizing system (a metabolic pathway that oxidizes ethanol without associated chemical energy production), increased sympathetic tone and associated thermogenesis, and/or enhanced ATP breakdown (with increased purine catabolism) secondary to the acetate produced from ethanol. All these hypotheses do not fully explain the lack of weight deficit when alcohol is consumed with a very-low-fat diet, which suggests that an alteration in the energy utilization derived from fat plays a major role, possibly through uncoupling of oxidation with phosphorylation in mitochondria damaged by chronic ethanol consumption.
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PMID:Perspectives: do alcohol calories count? 195 30

Phosphorus is the sixth most abundant element in the body after oxygen, hydrogen, carbon, nitrogen, and calcium. It comprises about 1% of the total body weight of humans. Eighty-five percent of it is stored in the bone in the form of hydroxyapatite crystal; 14% is in the soft tissues in the form of energy-storing bonds with nucleotides (ATP, GTP), nucleic acids in chromosomes and ribosomes, 2,3-DPG in the red blood cells, and phospholipids in the cells' membranes. Less than 1% is in the extracellular fluids. Phosphate balance is maintained by multiple systems. The gut is responsible for the absorption of two thirds of the 4-30 mg/kg/day of phosphate intake. Absorption sites are all along the gut; in humans the most active site is the jejunum. The kidney filters 90% of the plasma phosphate and reabsorbs it in the tubuli. In states of hypophosphatemia the kidney can reabsorb the filtered phosphates very efficiently, reducing the amount excreted in the urine virtually to zero. The healthy kidney can excrete high loads of phosphate and rid the body of phosphate overload. Through the vitamin D-PTH axis the endocrine system regulates the phosphate balance by influencing the kidney, gut, and bone. Other hormones, including thyroid, insulin, glucagon, glucocorticosteroid, and thyrocalcitonin, play a lesser role in regulation of phosphate metabolism. Because of the complex control of phosphate homeostasis, various clinical conditions may lead to hypophosphatemia. These include nutritional repletion, gastrointestinal malabsorption, use of phosphate binders, starvation, diabetes mellitus, and increased urinary losses due to tubular dysfunction. The clinical picture of phosphate depletion is manifested in different organs and is due mainly to the fall in intracellular levels of ATP and decreased availability of oxygen to the tissues, secondary to 2,3-DPG depletion. The various manifestations of phosphate depletion are listed in Table 2. The treatment of hypophosphatemia consists of administering enteral or parenteral phosphate salts. An important aspect of dealing with the potentially serious effects of phosphate depletion is to prevent the depletion from happening in the first place. Hyperphosphatemia can occur in renal failure, hemolysis, tumor lysis syndrome, and rhabdomyolysis. The treatment of hyperphosphatemia usually consists of fluid administration (in the absence of kidney failure). In chronic hyperphosphatemia, phosphate binders such as aluminum and magnesium salts can reduce the phosphate load. The use of these phosphate binders is limited by their potential side effects.
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PMID:Consequences of phosphate imbalance. 306 Jan 61

In this paper 85 cases of relapsing Parotiditis are presented, with the aim to ascertain the degree of accuracy provided by treatments with vitamin B complex, anti-inflammatory drugs or catchers of free radicals. Perusal of the bibliography and proposal of considering the malady divided in two stages. The first one would be characterized for metabolic alterations of the saccharoid cycle with scarce yielding of energy (ATP). Therefore failure of the Na/L bomb, which phenomenon is linked to an enzymatic protein deficiency and/or coenzyme of the B complex vitamins, being this condition provoked for a dietetic deficiencies, intestinal malabsorption due to alcoholic oedema, excessive expenditure of energy among drug-addicts, anemia, diabetes, etc. From this moment on appears the second stage--the inflammatory--with the whole metabolic and biochemical courtship of structural and functional irreversible damages.
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PMID:[Relapsing parotiditis: its etiopathology and treatment]. 809 46

In the rapidly increasing elderly population, diarrhoea as a result of drug therapy is an important consideration. The elderly consume a disproportionately large number of drugs for multiple acute and chronic diseases. Drugs can compromise both immune and nonimmune responses. Aging decreases the quality and proportion of T cells which in turn reduces the production of secretory IgA, the primary immune response of the gut. Acid production in the stomach decreases with increasing age and this compromise its vital 'self-sterilising' function, thus increasing the risk of diarrhoea due to viral, bacterial and protozoal pathogens. Other nonimmune defence mechanisms include the motility of the small intestine and the host-protective commensal bacteria of the colon. Drug induced hypomotility may result in bacterial overgrowth, deconjugation of bile salts and diarrhoea. Less commonly, diarrhoea may occur due to hypermotility because of a cholinergic-like syndrome. In the colon the host-protective commensal bacteria provide a powerful defence against pathogens. Disruption of this commensal population by antibiotic therapy may result in Clostridium difficile supra-infection which causes diarrhoea through toxin production. This is especially important in the elderly patient on chemotherapy for malignancy and those with multiple diseases. The organism responds to vancomycin, metronidazole and bacitracin. Metronidazole is the suggested drug of choice, with vancomycin reserved for relapses. Drugs also cause diarrhoea by interfering with normal physiological processes. Drugs impair fluid absorption by activating adenylate cyclase within the small intestinal enterocyte which increases the level of cyclic AMP. This causes active secretion of Cl- and HCO3-, passive efflux of Na+, K+ and water and inhibition of Na+ and Cl- into the enterocyte. Examples of these drugs (secretagogues) are bisacodyl, misoprostol and chenodeoxycholic acid (used to dissolve cholesterol gallstones). Drugs may also affect a second mechanism that regulates water and electrolyte transport, the Na+, K+ exchange pump. The energy for this pump is provided by the ATPase mediated breakdown of ATP. ATPase may be inhibited by digoxin, auranofin, colchicine and olsalazine. A number of drugs cause osmotic diarrhoea including antacids containing magnesium trisilicate or hydroxide. Lactulose is being used increasingly in compensated liver disease to increase protein tolerance and prevent hepatic encephalopathy. Sorbitol, an osmotic laxative agent also used in some liquid pharmaceutical preparations, induces diarrhoea by virtue of its osmotic potential. Another mechanism by which drugs cause diarrhoea is by mucosal damage of the small and large bowel. In the small intestine mucosal damage causes diarrhoea and fat malabsorption, as may occur with neomycin and colchicine. In the colon, for example, gold salts and penicillamine cause colitis of varying severity. Though the causes of diarrhoea are diverse, a drug-associated aetiology should always be considered and actively sought and addressed to prevent the complications of dehydration, electrolyte imbalance and undernutrition.
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PMID:Mechanisms of drug-induced diarrhoea in the elderly. 978 28

A component of ATP, phosphate is at the hub of the energy-related mechanisms operative in muscle cells. Together with calcium, phosphate is involved in bone tissue mineralization: thus, a chronic alteration in the metabolism of phosphate can induce bone and joint disorders. Diagnosis of chronic hypophosphatemia. Serum phosphate, calcium, and creatinine should be assayed simultaneously. Serum calcium is increased in hypophosphatemia caused by hyperparathyroidism and decreased in osteomalacia. Urinary phosphate excretion should be measured in patients with a normal serum calcium level and a serum phosphate level lower than 0.80 mmol/L. A decrease in urinary phosphate excretion to less than 10 mmol/24 h strongly suggests a gastrointestinal disorder, such as malabsorption, antacid use, or chronic alcohol abuse. In patients with a urinary phosphate excretion greater than 20 mmol/24 h, the maximal rate of tubular reabsorption of phosphate (TmPO4) and the ratio of TmPO4 over glomerular filtration rate (GFR) should be determined to look for phosphate diabetes. Manifestations and causes of phosphate diabetes in adults. Moderately severe phosphate diabetes in adults manifests as chronic fatigue, depression, spinal pain, and polyarthralgia, with osteoporosis ascribable to increased bone resorption. Although many cases are idiopathic, investigations should be done to look for X-linked vitamin D-resistant rickets missed during childhood, a mesenchymatous tumor, or Fanconi's syndrome with renal wasting of phosphate, glucose, and amino acids. Management of phosphate diabetes. Phosphate supplementation and, in patients with normal urinary calcium excretion, calcitriol produce some improvement in the symptoms and increase the bone mineral density. Whether dipyramidole is clinically effective remains unclear.
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PMID:Phosphate, the renal tubule, and the musculoskeletal system. 1139 20

In this case report, a 56-year-old woman with a reversible multiple organ disease with septic fever, arthritis, rash, weight loss, thrombocytopenia, severe disturbance of liver function, renal tubular dysfunction, general muscular weakness, pleural and pericardial effusions and elevated CRP, leukocytosis and a striking hyperferritinemia is presented. An autoimmune disease and a septic process were excluded. Because of the significantly decreased plasma phosphorus concentration (0.2 mmol/l), caused by malabsorption after Whipple's operation with lowered vitamin D and secondary hyperparathyroidism and by chronic alcoholism, severe phosphate deficiency was diagnosed. By substitution of phosphorus, all symptoms disappeared and laboratory findings normalized. Except for the patient's age, all criteria for the diagnosis of Still's disease were fulfilled. So we reflected upon Still's disease to be rather a disturbance of energy metabolism with secondary immunologic changes than an inflammatory rheumatic disease. Significant weight loss in Still's disease and osteopenia might be signs of decreased energy supply. Besides hypophosphatemia, deficiency of magnesium, which is involved in all ATP-dependent processes, and mitochondrial diseases cause disturbances of energy metabolism.
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PMID:[Adult Still's disease as a manifestation of severe hypophosphatemia. Still's disease--a disturbance of energy metabolism?]. 1282 5

The gross and metabolizable energy values of artificial enteral and parenteral feeds have been calculated from detailed composition data for amino acid, fatty acid, saccharide and other oxidizable substrates and compared with similar values calculated for conventional foods. The background to the derivation and application of calorie conversion factors is briefly reviewed. There is evidence of widespread inappropriate application of calorie conversion factors for carbohydrates and amino acid mixtures. Appropriate digestibility or availability factors for the oxidizable fractions of artificial feeds is discussed for normal adult man and the intrinsic difficulty of obtaining availability values for subjects with varying types of malabsorption or urinary and tissue losses is emphasized. The nitrogen:protein conversion ratio and the availability of energy at a biochemical level (i.e. net ATP yield per calorie) is also considered. Finally, a more uniform and appropriate approach to calculating energy values for artificial feeds for the purposes of labelling, product description and estimating energy intake of patients is called for.
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PMID:Food energy values of artificial feeds for man. 1683 15

Cobalamin (Cbl, vitamin B(12)) deficiency in humans is a cause of hematologic and neurologic disorders. We show here that the cellular export of Cbl, in contrast to the carrier- and receptor-dependent cellular import of Cbl, occurs by transmembrane transport of "free" Cbl. Screening of candidate transporters by cellular gene silencing showed a role in cellular Cbl efflux of the ATP-binding cassette (ABC)-drug transporter, ABCC1, alias multidrug resistance protein 1 (MRP1), which is present in the basolateral membrane of intestinal epithelium and in other cells. The ability of MRP1 to mediate ATP-dependent Cbl transport was confirmed by vesicular transport experiments, and a physiologic role of MRP1 in mammalian Cbl homeostasis is indicated by the phenotype of knockout mice with targeted disruption of MRP1. These animals have a reduced concentration of Cbl in plasma and in the storage organs liver and kidney. In contrast, Cbl accumulates in the terminal part of the intestine of these mice, suggesting a functional malabsorption because of a lower epithelial basolateral Cbl efflux. The identification of this Cbl export mechanism now allows the delineation of a coherent pathway for Cbl trafficking from food to the body cells.
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PMID:Identification of multidrug resistance protein 1 (MRP1/ABCC1) as a molecular gate for cellular export of cobalamin. 2151 66

The use of proton pump inhibitors (PPIs) in the treatment of gastrointestinal diseases has evolved over recent years. Initially intended for short-term use, PPIs are increasingly being used, often inappropriately, as long-term maintenance medications. The mechanism of action of PPIs is suppression of gastric basal and stimulated acid secretion by inhibiting the parietal cell H+/K+ ATP pump with a resultant increase in gastric pH and hypo- or achlorhydria. Although short-term use is related to few adverse effects, long-term use is associated with numerous complications. We present the case of a 58-year-old man with severe iron deficiency anemia due to malabsorption suspected to be caused by long-term PPI use. An extensive medical work up failed to reveal any definitive source of bleeding. An iron malabsorption test confirmed that iron was not being absorbed from the gastrointestinal tract. The Naranjo Adverse Drug Reaction Probability Scale and the Horn and Hansten Drug Interaction Probability Scale are suggestive of an association between long-term PPI use and the observed iron deficiency anemia. However, the patient's death and lack of an autopsy prevented confirmatory follow-up data from being obtained to connect long-term PPI use as the culprit. Although there are currently no recommendations regarding screening for iron deficiency and/or anemia in patients on long-term PPI therapy, physicians should be aware of this potential side effect and consider monitoring in high-risk patients.
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PMID:A Case of Severe Iron Deficiency Anemia Associated with Long-Term Proton Pump Inhibitor Use. 2876 72


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