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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The main purpose of this work was to study changes in the balance of fluids, electrolytes and blood metabolites in neonatal piglets with severe transmissible gastroenteritis. Six two day old conventional piglets were infected with transmissible gastroenteritis virus while six others were used as normal controls. Blood samples were collected in heparin when the infected piglets were moribund. The following variables were measured: packed red cell volume, total plasma protein and bicarbonate, blood pH, blood urea nitrogen and plasma glucose, creatinine, chloride, inorganic phosphorus, sodium, potassium, magnesium and calcium. Vomiting and diarrhea appeared 12 to 24 hours postinoculation in the infected piglets and they were moribund one or two days later. Before becoming moribund, most of the piglets fell rapidly into a lethargic and comatose state. The most evident changes in their blood variables were an increase in packed cell volume, total protein, blood urea nitrogen, phosphorus and magnesium levels and a decrease in pH and bicarbonate concentration as well as a severe hypoglycemia. The results suggest that severe hypoglycemia coupled with metabolic acidosis and dehydration might be an important factor contributing to the high mortality rates caused by transmissible gastroenteritis in neonatal piglets. The hypoglycemia results from a combination of the inadequate glucose metabolism inherent to neonatal piglets and the acute maldigestion and malabsorption resulting from the diffuse and severe villous atrophy induced by the virus.
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PMID:Hypoglycemia: a factor associated with low survival rate of neonatal piglets infected with transmissible gastroenteritis virus. 647 97

Nutritional status indicators were assessed chemically in blood and urine taken from 625 Transkeians drawn from three age-groups in each of two regions: one with a moderate risk for esophageal cancer and one with a very high risk. Aggregate mean values for protein, albumin, vitamin A, and phosphorus were generally acceptable, but many subjects had inadequate (though not necessarily deficient) values for nicotinic acid (74% of subjects), magnesium (60%), vitamin C (55%), carotene (53%), riboflavin (41%), calcium (35%), and zinc (27%). Groups at highest risk for esophageal cancer had markedly lower serum magnesium and carotene concentrations and mildly depressed hemoglobin and hematocrit values, but such findings are not necessarily associated with esophageal cancer etiology. Possible intestinal malabsorption in the populations at highest risk may be associated with the unusually high fiber and phytate intake of the high-risk populations as well as with exposure to necrotizing mycotoxins. Thus, while protein and energy nutriture seem generally adequate, both the high- and moderate-risk populations had high incidences of multiple micronutrient malnutrition.
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PMID:Nutritional status of African populations predisposed to esophageal cancer. 684 45

Rickets, hypocalcemia, hypophosphatemia, and hyperparathyroidism were found in a low-birth-weight premature infant. The concentration of plasma calcitriol (1,25-dihydroxyvitamin D) was 145 pg/mL. With additional exogenous calcitriol (37.5 ng/kg/24 hr) given for eight weeks, the biochemical abnormalities were corrected and healing of rickets was evident. Three months later, while receiving only 400 IU of ergocalciferal daily, the patient had normal levels of serum calcium, phosphate, and alkaline phosphatase with a serum calcitriol concentration of 36 pg/mL. These observations suggest that rickets of prematurity may involve a malabsorption of calcium and phosphorus with an elevated calcitriol level needed to overcome this inadequate absorption. Additional doses of calcitriol may be of benefit in these infants, although it must be given carefully. Furthermore, the role of phosphate supplementation in these infants requires consideration.
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PMID:Rickets of prematurity. Supranormal levels of serum 1,25-dihydroxyvitamin D. 696 86

After successful renal transplantation there is continuing malabsorption of calcium and phosphorus. This is due in part to impaired glomerular filtration rate, and in part to the action of steroid on calcium and phosphorus absorption. The effect of steroids is most marked over the first 18 months after transplantation and causes significant malabsorption of calcium and phosphorus even though good graft function is established. Calcium and phosphorus malabsorption can be improved by exogenous 1,25-dihydroxy vitamin D (oral 1 alpha-OH D3 or 1,25-[OH]2D3).
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PMID:Factors influencing the intestinal absorption of calcium and phosphorus following renal transplantation. 699 70

A metabolic and physiological assessment was carried out in 14 patients who had undergone restorative proctocolectomy with ileal reservoir more than six months previously. The haemoglobin was normal in all but one and plasma electrolytes and serum albumin, calcium, phosphorus, and red cell folate estimations were normal in all. Five patients had low serum iron levels of whom one had an iron deficiency anaemia. The 24 hour faecal fat output was normal in all patients and there was no case of vitamin B12 malabsorption as judged by the Schilling test, although four patients had marginally low values. These were not associated with increased bacterial counts in the faeces within the reservoir and there was no evidence to support a diagnosis of stagnant loop syndrome. Inflammation of the reservoir mucosa was, however, associated with higher counts of aerobic bacteria than in cases where inflammation was absent. Subtotal villous atrophy or inflammation was seen in biopsies of the reservoir in six patients. The mean faecal output per 24 hours was 659 +/- 259 g and the mean reservoir volume was 330 +/- 78 ml. Mean resting anal canal pressure was significantly lower in patients with a mucous leakage per anum than in those without, while manometry of the reservoir showed no alteration of pressure over a period of one hour before and after a meal. A positive rectosphincteric reflex was observed in nine patients.
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PMID:Restorative proctocolectomy with ileal reservoir: a pathophysiological assessment. 726 23

A 60-year-old woman was evaluated for bone pain and incapacitating weakness. Initial laboratory studies showed a serum calcium level of 10.1 mg/dL, severe hypophosphatemia (1.1 mg/dL), and an elevated alkaline phosphatase level. X-ray films showed changes consistent with osteomalacia. Further studies revealed hypercalciuria (448 mg/24 hr) but absent urinary phosphorus. These data indicated phosphate malabsorption. Excessive use of an aluminum hydroxide-containing antacid was the cause of this patient's failure to absorb dietary phosphate. The features of this syndrome are reviewed to increase physicians' awareness of this illness, which occurs particularly in the elderly and is easily treated.
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PMID:Osteomalacia and weakness from excessive antacid ingestion. 743 92

One hundred and four children aged 0-15 years, with suspicion of malabsorption were studied. They had a proximal jejunal biopsy and, at the same time, the following measurements: 25-hydroxycholecalciferol (25-OH-CC), calcium, phosphorus and serum alkaline phosphatase, bone age on X-ray of the left hand and wrist, cortical thickness of the 2nd, 3rd, 4th metacarpal bones. For the analysis of the results, the patients were divided into two groups according to the season (winter vs. summer). None of the patients in either group had clinical or radiological signs of rickets. The following results were obtained: 1. The 25-OH-CC serum levels were significantly lower during the winter than during the summer months. This was observed more frequently in the cases with atrophy of the jejunal mucosa. 2. During the summer, the 25-OH-CC serum levels were not different in the cases with normal or pathological mucosa. This demonstrates the importance of the skin synthesis of vitamin D during the summer months. 3. The mean of the serum calcium levels was significantly lower in the group of children with atrophy of the jejunal mucosa than in children with normal intestinal biopsy. The serum calcium levels were not correlated with the serum 25-OH-CC levels. 4. The serum phosphorus levels were significantly lowered during the winter months in the children aged 0-3 years with pathological jejunal biopsy. 5. The serum alkaline phosphatase levels were lowered in cases of total atrophy of the jejunal epithelium cells. 6. Cortical thickness of the metacarpal bones becomes thinner with the progression of the alteration of the jejunal epithelium cells, independently of season or age. However, only the group of children aged 0-3 years studied during the winter months and with total atrophy of the jejunal mucosa have a significantly diminished cortical thickness of the metacarpal bones. The lowering of the calcium levels and the decrease of the cortical thickness are probably secondary to an impaired intestinal absorption of calcium. In the syndrome of malabsorption, the integrity of the jejunal epithelial cells seems to play a more important role than a vitamin D deficiency in the genesis of this calcium malabsorption.
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PMID:[Phosphorus-calcium metabolism and plasma 25-hydroxycholecalciferol in intestinal malabsorption]. 745 Dec 35

Inflammatory bowel disease (Crohn's disease and ulcerative colitis) is associated with decreased bone mineral density and increased risk of osteoporosis. However, the pathogenesis of this bone loss is not yet fully understood. In the present study we measured lumbar bone mineral density (by dual photon absorptiometry), serum levels of parathyroid hormone (PTH) and vitamin D metabolites, and serum markers of bone turnover (alkaline phosphatase and osteocalcin) in 15 patients with Crohn's disease and in 4 patients with ulcerative colitis. The median duration of the disease was 4 years and the median lifetime steroid dose was 10g of prednisone. We compared our results to a control group of 19 normal persons, who were matched for age and sex to the patients. We found that lumbar bone density was reduced by 11% in patients compared with control persons (Z-score -0.6 +/- 0.6 versus -0.1 +/- 0.8; p < 0.05). In patients, the serum levels of PTH, 25-hydroxyvitamin D3, and calcitriol (1,25(OH)2D3) were significantly reduced compared with control persons. Serum alkaline phosphatase activity (AP) was significantly higher in the patients and was inversely related to lumbar bone density. Osteocalcin values were not different between patients and control persons. There was also no difference in serum levels of calcium between the two groups, whereas phosphorus levels were higher in patients. We conclude that malabsorption of calcium was not a primary cause of bone loss in our patients, because we did not find secondary hyperparathyroidism. Accordingly, we did not find a severe vitamin D deficiency, since 25-hydroxyvitamin D3 levels were within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bone mineral density and calcium regulating hormones in patients with inflammatory bowel disease (Crohn's disease and ulcerative colitis). 800 8

Hypophosphatemia due to parenteral nutrition has been described frequently. It was attributed to the lack of phosphorus content in parenteral nutrition solutions. With modern parenteral nutrition regimens containing phosphorus, this problem has been virtually eliminated. Enteral nutrition solutions contain adequate phosphate for patients with normal phosphate stores. Hypophosphatemia has therefore rarely been reported in enteral nutrition. We describe two patients with protein-energy malnutrition who developed severe hypophosphatemia during tube feeding with phosphorus-containing formula diets. Chronic alcoholism and vitamin D deficiency due to malabsorption because of Crohn's disease were additional risk factors in these two patients. Patients with depleted phosphate stores and high metabolic demand have a higher daily requirement for phosphorus than is available in routine isotonic enteral formulas. This case report emphasizes the importance of monitoring serum phosphate concentration daily during the first week of refeeding.
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PMID:Enteral supplementation of phosphate does not prevent hypophosphatemia during refeeding of cachectic patients. 820 56

1. The best way to prevent early growth failure in children with renal disease is by the use of specified nutrition and appropriate buffer, activated vitamin D, and calcium-containing phosphate binders as needed. With prenatal diagnosis of anatomically abnormal kidneys available, this type of early intervention may be much more feasible in the 1990s. 2. Supplemental sodium and water in children with polyuria and intravascular volume depletion may prevent growth failure. Cow milk is detrimental in this group of individuals because of high solute and protein load, often causing intravascular volume depletion, hyperphosphatemia, and acidosis. 3. Children with acquired glomerular disease may need sodium restriction and, if treated with steroids, a diet low in saturated fat. 4. Children with nephrotic syndrome and severe edema should be evaluated for malabsorption and subsequent malnutrition. Protein intake should be supplemented only at the RDA and to replace ongoing losses. Long-term sodium restriction is appropriate. Hyperlipidemia should be monitored: if nephrosis is chronic, a low saturated fat diet should be instituted. Angiotensin-converting enzyme inhibitors can decrease urinary protein loss and may ameliorate hyperlipidemia. Children resistant to therapy can have very high morbidity. 5. Children with <50 % of normal creatinine clearance should have PTH measured and activated vitamin D therapy should be started if PTH is elevated more than two to three times normal. Thereafter careful monitoring of calcium, phosphorus, and PTH is crucial to prevent renal osteodystrophy, low turnover bone disease, and hypercalcemia with hypercalciuria and nephrocalcinosis. 6. Children with tubular defects with severe polyuria also may benefit from low-solute, high-volume feedings. 7. All physicians caring for children with renal disease should have pediatric nephrology consultation available. Prevention of growth failure is much more cost effective than pharmacologic therapy. Before initiating growth hormone treatment for growth retardation, assiduous treatment of co-existing renal osteodystrophy and provision of optimal nutritional intake should be accomplished.
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PMID:Nutritional management of the child with mild to moderate chronic renal failure. 876 44


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