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Query: UMLS:C0024523 (
malabsorption
)
7,319
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Congenital chloride-losing diarrhea is a recessively inherited disorder due to the absence of chloride-bicarbonate exchange in the small bowel.
Malabsorption
of chloride leads to osmotic diarrhea, electrolyte abnormalities, and dehydration. If left untreated, the infants fail to thrive and have a very high mortality. Clinically, affected patients develop secretory diarrhea in utero resulting in distended bowel loops and polyhydramnios. At birth these infants have profuse watery diarrhea that may be confused with urine. Thus, the correct diagnosis is often missed, and they may be subjected to unnecessary interventions. If diagnosed early, the electrolyte abnormalities are easily corrected and the prognosis is good. We report two patients who were initially evaluated for other conditions but later proved to have congenital chloride-losing diarrhea. The cases emphasize the importance of having a high index of suspicion in patients with a history of polyhydramnios,
prematurity
, and watery stools.
...
PMID:Misdiagnosis of congenital chloride-losing diarrhea. 152 26
The essential effects of Tocopherol are based on its antioxidative capacity. Tocopherol, however, is just one in a group of antioxidants, which are important for the organism. Established indication for therapeutical application of vitamin E in infancy is only vitamin-E-
malabsorption
in connection with chronic cholestasis, pancreatic insufficiency (cystic fibrosis) and short bowel syndrome. In emergency therapy vitamin E is suggested with high dosage in case of shock lung and haemolytic-uraemic syndrome. Positive effects of daily vitamin E application in connection with prophylaxis of retinopathy
prematurity
, bronchopulmonary dysplasia and intraventricular encephalorrhagia of premature infants of severe underweight are not established. Very questionable therapeutic or prophylactic efficiency is opposed to the risk of higher incidence of severe complications in caring for premature infants of severe underweight, such as enterocolitis necroticans and neonatal septicaemia.
...
PMID:[The use of vitamin E in childhood]. 209 6
Copper deficiency developed in a five-month-old prematurely born infant with an abdominal wall closure defect and a small bowel fistula under long-term parenteral nutrition. The first manifestations were typical bone changes including diffuse osteoporosis, delayed bone age, widened cupped metaphyses with beaks and a fracture, subperiosteal hematomas and ossifications in the shafts of long bones, and a diaphyseal fracture. Other findings that confirmed the diagnosis included edema of the limbs with pseudoparalysis, neurologic abnormalities, anemia, leukoneutropenia, and very low serum levels of copper and ceruloplasmin. Following initiation of copper supplementation, clinical, hematological and biological disorders resolved within a few days and roentgenologic bone abnormalities within four months. Copper deficiency develops only in the presence of specific risk factors, that are often combined in a single patient: inadequate stores due to
prematurity
, excessive loss due to chronic diarrhea, exudative enteropathy, a proximal stoma, or a biliodigestive fistula; and inadequate intake due to
malabsorption
or long-term exclusive parenteral nutrition (EPN). Appropriate copper supplementation is needed in all these high risk situations. Early, continuous copper supplementation is required for young children under EPN. Serum copper assays should be included among the periodically monitored biochemical parameters.
...
PMID:[Nutritional copper deficiency. Apropos of a case]. 250 Aug 84
The use of elevated dosages of vitamin E in humans has led to the discovery of vitamin E deficiency syndromes in neurological areas. This evidence comes from careful clinical studies in which elevated vitamin E dosages were applied. In long-term studies it has now been established that retinal and neurological abnormalities are due to vitamin E deficiency and can be ameliorated by therapy with a large amount of the vitamin enterally or parenterally, which can possibly completely prevent the development of clinical manifestations if adequate treatment is given from an early age. It has also become clear that similar neurological and ocular lesions occur in other chronic fat malabsorptive states such as cholestatic liver diseases, cystic fibrosis, and extensive resection of the gut, with respect to an elevated dosage of vitamin E therapy. More recently, several patients with spinocerebellar degeneration from vitamin E deficiency without other evidence of
malabsorption
have been reported on in whom the progression of the diseases is cessated by the vitamin E therapy. Whether or not the use of elevated dosages of vitamin E should be recommended for certain diseases in premature infants is controversial. Previously, it has been thought that newborn infants, especially premature infants, suffer from vitamin E deficiency, because of their low plasma vitamin E concentrations and high susceptibility of erythrocytes to hydrogen peroxide hemolysis test. Furthermore, tocopherol deficiency has been implicated in four neonatal conditions: anemia of
prematurity
, retrolental fibroplasia (RLF), bronchopulmonary dysplasia (BPD), and intraventricular hemorrhage (IVH). A hemolytic anemia, associated with thrombocytosis and edema, which is responsive to vitamin E therapy, is not well recognized and occurs in a minority of preterm infants, who were given high amounts of polyunsaturated fatty acids in their formula. However, prophylactic use of an elevated dosage of vitamin E to prevent anemia in the majority of premature infants is controversial. There is no evidence for beneficial effects in BPD. In addition, the prophylactic use of pharmacological dosages of vitamin E for prevention of RLF and IVH has also had conflicting results. In the course of therapy with elevated dosages of vitamin E, administered either orally, intramuscularly, or intravenously, many problems arose in the infants, such as unexpected death, increased frequency of necrotizing enterocolitis (NEC) and sepsis, and the development of unusual symptoms including hepatic injuries.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Use and safety of elevated dosages of vitamin E in infants and children. 250 8
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.
...
PMID:Rickets of prematurity. Supranormal levels of serum 1,25-dihydroxyvitamin D. 696 86
Disturbances of the excretion and reabsorption of bile acids are discussed. Disturbances in bile acid metabolism can be found after terminal ileum resections, in contaminated small bowel syndrome, Crohn's disease localized in terminal ileum, ileostoma, non-specific diarrhoea of infancy, bulky small bowel contents, coeliac disease, cystic fibrosis,
prematurity
, intra- and extrabiliary obstruction. They can cause or increase
malabsorption
. Total bile acid and cholylglycine in serum and duodenal fluid can be used in diagnosing
malabsorption
. Estimation of serum bile acids and triglycerides after an oral fat loading test may provide information about the localization of small intestinal dysfunction.
...
PMID:[Bile acids and malabsorption; physiology, pathology and diagnosis]. 726 54
In this retrospective study carried out covering the period, 1978-1991, 62 neonates were seen, diagnosed and treated for intestinal atresia which included: duodenal atresia and stenosis, small bowel atresia and atresia of large bowel. Locations of obstruction were duodenal in 17 patients, jejunal in 25 patients, jejuno-ileal in 5 and colon in two. Duodenal atresia was noted in 9 infants and duodenal stenosis due to annular pancreas, Ladd's bands with malrotation of bowel in 8. Associated anomalies which were observed were anorectal malformations in 2 and malrotation in 2 infants. Birth weights ranged from 1450 gm to 3000 gm.
Prematurity
was recorded in 11 infants. Diagnosis of intestinal atresia in our patients was made clinically and radiologically. Intestinal atresia in neonates was differentiated from other causes of obstruction such as Meconium Ileus, Hirschsprung's disease, neonatal volvulus, rectal atresia in anorectal malformations. Treatment of infants with intestinal atresia was surgical. Surgical techniques used depended on pathological findings. In 36 patients, complications such as functional obstructions with vomiting and failure to thrive,
malabsorption
, aspiration, bronchopneumonia, sepsis were observed. Overall mortality rate in our cases was 25 (41.9%) out of 62 patients.
...
PMID:Intestinal atresia and stenosis as seen and treated at Kenyatta National Hospital, Nairobi. 818 36
Cholelithiasis is an extremely unusual finding in infancy. Hemolytic disease, bile duct abnormalities,
intestinal malabsorption
have been implicated. Recently, an association of
prematurity
, bronchopulmonary dysplasia, total parenteral nutrition and furosemide has been reported. Rarely, sonographic discovery of idiopathic gallstones and their subsequent spontaneous disappearance has been reported. We report a case of an 11-week-old infant whose initial sonogram displayed evidence of true gallstone, that later showed resolution on follow-up examinations. In the absence of clinical or imaging evidence of biliary tract disease, we suggest an initial conservative management and follow-up sonograms.
...
PMID:Spontaneous resolution of cholelithiasis in an infant. 924 33
Overt copper deficiency is not believed to be a widespread public health concern for most population groups. However, a variety of case studies suggest that under certain circumstances, clinical conditions may predispose individuals to the risk of copper deficiency or copper excess. Acquired copper deficiency has been documented in conditions predisposing to inadequate copper intakes, in
prematurity
, in
malabsorption
syndromes, and in conditions predisposing to excessive copper losses. In contrast, increases in copper concentrations have been reported in response to stress, inflammation, and infection; in Parkinson disease and diabetes mellitus; and in conditions involving an obstruction to bile flow.
...
PMID:Clinical conditions altering copper metabolism in humans. 958 45
Nenatal necrotizing enterocolitis (NEC) is a disease mainly affects premature infants. It is well known that
prematurity
, enteral formula feeding, and bacterial colonization are three major risk factors for NEC. Acetic acid, propionic acid and butyric acid are short chain fatty acids (SCFAs), which are produced mainly in the colon by bacterial fermentation of undigested carbohydrates. Although luminal production of modest quantities of SCFAs is essential for normal colonic mucosal function, excessive production/accumulation of SCFAs may arise in premature infants due to increased luminal carbohydrates
malabsorption
and poor gastrointestinal motility, and may have deleterious effects on mucosal integrity. Therefore, it is proposed that too much luminal short chain fatty acids cause neonatal NEC.
...
PMID:Too much short chain fatty acids cause neonatal necrotizing enterocolitis. 1496 41
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