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)

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

We studied the cellular immune response against malabsorption syndrome (MAS) in two broiler chicken lines, A and B. We determined the number of pan T-lymphocytes (CD3), helper T-lymphocytes (CD4), cytotoxic T-lymphocytes (CD8) and macrophages/monocytes in the small intestine in the first 2 weeks after oral inoculation of two MAS homogenates, MAS80 and MAS97-1. The immune cells were detected on cryostat tissue by immunohistochemistry and counted by villus area. In trial 1, we compared the two broiler lines for weight gain depression, intestinal lesion and number of CD3, CD4, CD8 cells and macrophages/monocytes after MAS80 inoculation. Although there was no significant difference in weight gain depression between the two broiler lines, line B had significantly higher numbers of CD8+ T-cells per villus area than had line A. To confirm part of the results of trial 1, trial 2 was done in which we compared different homogenates in broiler line B. Broiler line B was orally inoculated with either MAS97-1, intestinal homogenate obtained from healthy chickens (healthy homogenate), or phosphate buffered saline (PBS). In this trial, the MAS97-1 homogenate also induced weight gain depression and intestinal lesions, whereas the "healthy homogenate" and PBS did not induce weight gain depression or intestinal lesions. The broilers inoculated with MAS97-1 homogenate had significantly more CD8+ T-cells per villus area than had broilers inoculated with "healthy homogenate" or PBS. Increased CD8+ T-cells per villus area in the affected small intestines of broilers suggests an increase of cytotoxic T-cell activity.
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PMID:Cellular immune response in the small intestine of two broiler chicken lines orally inoculated with malabsorption syndrome homogenates. 1186 67

Attempts to reproduce malabsorption syndrome (MAS) by oral inoculation with several different combinations including intestinal homogenate, reovirus, and hemolytic Escherichia coli obtained from MAS-affected chickens and intestinal homogenate from healthy chickens (healthy homogenate) were performed in 1-day-old specific-pathogen-free (SPF) broilers. The MAS homogenate, serving as a positive control, induced weight gain depression and intestinal lesions such as cystic crypts of Lieberkuhn, villus atrophy, and lymphoid and/or granulocytic infiltration. The healthy homogenate, the formalin-treated MAS homogenate, the formalin-treated healthy homogenate, and phosphate-buffered saline caused neither weight gain depression nor intestinal lesions. We were able to reproduce both weight gain depression and intestinal lesions by inoculation of reovirus either combined with the formalin-treated MAS homogenate or combined with healthy homogenate. Surprisingly, when hemolytic E. coli was added to the combination of reovirus with formalin-treated MAS homogenate, this did not cause weight gain depression although this combination caused the described intestinal lesions. Identical results were obtained with the combination of formalin-treated MAS homogenate with hemolytic E coli or the combination of reovirus with hemolytic E. coli. The intestinal lesions were more severe and developed faster by combinations including reovirus and formalin-treated MAS homogenate. This study indicates that a combination of enteropathogenic reovirus with other agents or substances that are present in an intestinal homogenate from MAS-affected and healthy chickens can induce MAS in SPF broilers. Escherichia coli is not essential for induction of weight gain depression but can play a role in development of intestinal lesions. Furthermore, intestinal lesions alone will not always result in weight gain depression.
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PMID:Experimental reproduction of malabsorption syndrome with different combinations of reovirus, Escherichia coli, and treated homogenates obtained from broilers. 1192 4

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

Inflammatory bowel diseases, most frequently Crohn's disease, are frequently accompanied by decreased bone mineral content (30-70%). The osteopenia is not explained by the side effects of treatment or the secondary malabsorption. There must be a common pathological pathway in the background. The mineral content of bones is most easily measured by dual-ray absorptiometry. The measurement should be performed at the time of the diagnosis of bowel disease. It is useful to perform some routine laboratory examinations (serum calcium and phosphate, urinary calcium excretion level, etc.) and some special tests (serum osteocalcin and crosslaps) to exclude some other pathological pathways as well as to plan the anti-osteoporotic therapy. Appropriate calcium and vitamin-D supplementation is essential in prevention and therapy as well. Several drug-classes have proven useful in the therapy of severe osteoporosis associated with inflammatory bowel diseases such as bisphosphonates, hormone replacement therapy, selective estrogen receptor modulators and calcitonin. The authors provide an algorithm for the therapy of metabolic bone disease in inflammatory bowel disease.
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PMID:[Osteoporosis associated with inflammatory bowel diseases]. 1520 26

Impaired bone metabolism following urinary diversion through intestinal segments has always been a controversial subject of unclear clinical relevance. Whereas the perpetuated pathophysiological considerations seem conclusive in theory, the role of acidosis and malabsorption is less clear in animal experimentation and, even more so, in the clinical reality of modern continent diversion. In hardly any of the available contemporary case series was overt derangement of the acid-base balance, rickets or osteomalacia encountered. No consistent changes in osteotropic serum parameters could be found with normal calcium and phosphate in all patients. The assumption that colonic reservoirs have a higher risk of developing metabolic bone disease could not be confirmed by clinical data. As early correction of base excess is easy and probably a common policy in patients with intestinal urinary reservoirs, it will be virtually impossible to further study the natural history of bone metabolism after urinary diversion. While there is no need for a bone specific follow-up in asymptomatic adults with a normal acid-base balance, particular attention should be paid to children and to all patients with impaired renal function.
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PMID:Bladder, bowel and bones--skeletal changes after intestinal urinary diversion. 1531 38

A 62-yr-old woman with idiopathic hypoparathyroidism was admitted to our hospital for severe anemia (Hb 5.6 gr/dl) and hypoalbuminemia (3.2 gr/dl). Hypoparathyroidism was diagnosed when she was 33 yr old, because of repeated hypocalcemic tetanic crises, low calcium and high phosphate levels. Since then she has been treated with oral calcium gluconate and calcitriol, with satisfactory clinical balance and normalization of calcium serum levels. After menopause, despite this therapy, the patient still had frequent hypocalcemic tetanic crises, resolving with iv administration, in high doses, of calcium gluconate. The anemia, for which the patient came to our attention, was hypochromic microcytic and in the past she had been treated with iron and transfusion therapy. The patient's recent history also revealed recurrent long lasting episodes of diarrhea, hyporexia and weight loss. The clinical presentation seemed related to a malabsorption syndrome: a celiac disease (CD) diagnosis was confirmed, based upon the finding, at duodenal biopsy, of a severe villous atrophy. A bone mineral density (BMD) evaluation showed a limited reduction of femoral values classified as osteopenia according to the World Health Organization (WHO) criteria. Thereafter, the patient was instructed to follow a gluten-free diet which rapidly led to an improvement of the nutritional parameters and to a reduction of calcium and vitamin D requirements. Difficult clinical and metabolic control in hypoparathyroidism patients may suggest the possible co-existence of both endocrine and extra-endocrine autoimmune diseases, such as CD. Moreover, bone density, normally reduced in celiac patients, seems to be preserved (maintained) by the lack of parathyroid secretion.
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PMID:Hypoparathyroidism and co-existing celiac disease. 1563 34

In order to examine the etiology of refractory rickets, we evaluated the case records of patients presenting between 1990 and 2002. Subjects with impaired renal functions were excluded. Of 131 patients, 25.9 % each had hypophosphatemic rickets and distal renal tubular acidosis (RTA), 19.6 %vitamin D dependent rickets (VDDR), 11.3 % proximal RTA, 9.1 % liver disease and 6.1 % malabsorption. A significant proportion of patients with VDDR and proximal RTA showed deformities in the first year of life, whereas those with distal RTA and hypophosphatemic rickets presented later. Patients with hypophosphatemic rickets had predominant involvement of lower limbs; hypercalciuria was found in 4. Distal RTA was associated with marked rickets and normal levels of alkaline phosphatase. Hypophosphatemia and low tubular reabsorption of phosphate, though characteristic of hypophosphatemic rickets, was also seen in patients with VDDR (19.2%) and distal RTA (17.6 %). Our findings suggest that application and interpretation of appropriate investigations are useful in determining the cause of non-azotemic refractory rickets allowing initiation of specific therapy.
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PMID:Non-azotemic refractory rickets in Indian children. 1569 54

Vegetarians may have subtle nutritional deficiencies which have been related to the occurrence of an unrecognized malabsorption syndrome. The excess phytate content in cereals, nuts, legumes and oilseeds which represent the mainstay of their food intake, seems to play a central role in the pathogenesis of this malabsorption syndrome as an inverse relationship has been shown to link the phytate content of the diet with the intestinal absorption of trace minerals and proteins. We postulate that manipulating the endogenous digestive microflora of subjects on a vegetarian diet through administering probiotic lactic bacteria would represent an innovative tool to counteract the occurrence of the malabsorption syndrome dependent on the high phytate content of their diet. Even though there are no data about the composition of endogenous digestive microflora in subjects on a vegetarian diet, we expect that probiotic lactobacilli can interact with or affect distinct yet interrelated components within the intestinal milieu, such as epithelial cells, enteric flora, and/or mucosal immune cells. This would ultimately translate into the correction of the unregulated mechanisms implicated in the altered intestinal absorption of trace metals and proteins commonly seen in vegetarians. Clinical experience with probiotic therapy of patients with inflammatory bowel disease fully agrees with this view. One additional point of interest is that probiotic lactobacilli, and other species of the endogenous digestive microflora as well, are an important source of the enzyme phytase which catalyses the release of phosphate from phytate and hydrolyses the complexes formed by phytate and metal ions or other cations, rendering them more soluble ultimately improving and facilitating their intestinal absorption. The regular intake of probiotic preparation, may represent a cheap and safe tool in order to convert a diet with a low potential for bioavailability of trace minerals and proteins, such as the vegetarian diet, into a diet with a high bioavailability potential. The benefit of such an approach would not be restricted to vegetarians.
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PMID:Probiotic lactobacilli: an innovative tool to correct the malabsorption syndrome of vegetarians? 1609 46

Magnesium deficiency is a common clinical problem. Dietary malabsorption and renal wasting are the commonest causes. Hypomagnesemia induces a state of functional hypoparathyroidism due to decreased secretion of parathormone (PTH) as well as resistance to its action. Contrary to typical autoimmune hypoparathyroidism, it is associated with decreased levels of serum phosphate. We report a patient who presented with hypocalcemic tetany associated with hypomagnesaemia due to renal wasting. Subsequently, he improved with magnesium supplementation of therapy.
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PMID:Hypomagnesaemia masquerading as hypoparathyroidism. 1690 43


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