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PubMedDate not supplied

Malabsorption syndromes.

Malabsorption syndromes are divided according to the underlying cause: maldigestion; bacterial contamination; mucosal abnormalities. One of the main causes of maldigestion are surgical resections. Malabsorption from bacterial contamination is due to a lower effectiveness of one or more of the factors that normally inhibit the growth of pathogens. The most common malabsorption syndrome from mucosal abnormalities is celiac disease for which, with small bowel enteroclysis a specific radiographic pattern has been identified. The gold standard in the diagnosis of diseases associated to malabsorption is represented by mucosal biopsy and histology though some patterns are similar and create difficulties in the differential diagnosis. Among radiologic examinations, small bowel enteroclysis is highly predictive; hopefully, novel diagnostic methods will support radiology.

Bacterial Infections↗
PubMed2002

Overview and diagnosis of malabsorption syndrome.

"Malabsorption" syndrome is the term widely used to describe the end result of either impaired breakdown of nutrients (maldigestion) or defective mucosal uptake and transport of adequately digested nutrients (true malabsorption). The latter may affect a broad range of nutrients (ie, panmalabsorption) or individual nutrients or groups of nutrients (ie, specific malabsorption). This review discusses the etiology and pathophysiology of malabsorption. A diagnostic approach to malabsorption is proposed. Other articles review specific disorders such as celiac disease, bacterial overgrowth, and chronic pancreatitis.

Diagnosis, Differential↗
PubMed1985

Factors related to the incidence of the malabsorption syndrome.

Malabsorption syndrome has been produced in the laboratory with chicks and feed supplied by poultry integrators who had experienced the problem. Feed supplied by one company produced chicks that developed pale shanks and had apparent malabsorption of certain nutrients. One chick source also had a statistically lower pigmentation score than the other.

Animal Feed↗
PubMedDate not supplied

[Usefulness and limitations of edema of the small intestine in malabsorption syndromes].

Malabsorption syndrome is a clinical condition that can be determined by several situations which can ensue by many etiopathogenetic mechanisms. While the diagnostic approach is, for this reason, complex and uses a lot of clinical, laboratory and instrumental techniques, the therapeutic approach could be surgical or medical. The aim of our research is to establish the diagnostic utility of the radiologic examination of the small intestine by enteroclysis, on the basis of our personal experience and the data referred in literature. We took particular care of the radiological study of primitive malabsorption.

Barium Sulfate↗
PubMedDate not supplied

Poult malabsorption syndrome. I. Malabsorption in poult enteritis.

One-day-old poults were placed on littler on which poults had previously developed diarrhea, increased mortality, and stunting. Small intestines, pancreas, and liver were evaluated histologically. Morphometric evaluations were conducted to determine villous length and crypt depth. Poults were evaluated for malabsorption utilizing D-xylose and lipid absorption tests. Compared with controls, the gastrointestinal tract of affected birds was grossly distended, was fluid-filled, and had thin, flaccid walls on days 5 and 8. Ceca were distended with brown watery fluid and gas on days 5, 8, and 12. No histologic lesions were present in the liver, pancreas, or pancreatic ducts, and only mild inflammatory changes were present in the small intestine. Villous atrophy and crypt hypertrophy were present in the small intestine on days 5, 8, 12, 16, and 21. Morphometry revealed significant decreases in villous lengths and increases in crypt depth throughout the trial. D-Xylose and lipid absorption were significantly decreased on days 8 and 11. Intestinal epithelial damage by infectious agents with subsequent villous atrophy is postulated to have produced malabsorptive diarrhea.

Animals↗
PubMed1998

Malabsorption syndromes.

BACKGROUND/AIMS: Malabsorption syndromes commonly result from a pathological interference of the normal digestive process. There have been major advances in the last 4 years. The purpose of this review is to highlight in the form of a brief summary the most outstanding information available. METHODS: The review was performed based on a medical literature search using MEDLINE (1993-1997), bibliographic reviews of book chapters and review articles. As a consequence of the extensive information incorporated in the period and the limited scope of this review, the review will focus in three aspects: (1) an overview on some clinical aspects of malabsorption; (2) diseases in which predominates the disturbed mucosal phase of the digestive process, and (3) providing information on diagnostic testing regarding malabsorption. RESULTS: Major advances on celiac disease, Whipple's disease, giardiasis, tropical sprue, malabsorption of oligo- and disaccharides, vitamin B12 and bile salts are discussed. New aspects on diagnostic procedures for malabsorption are also presented. CONCLUSION: Although major advances have given a great support to the investigation of malabsorption, yet the syndrome remains a major diagnostic dilemma. Based on the limited availability of most diagnostic tests, a simple and practical diagnostic algorithm is presented.

Bile Acids and Salts↗
PubMed2001

Primary systemic amyloidosis: a cause of malabsorption syndrome.

PURPOSE: Although malabsorption syndrome is encountered frequently by general internists and gastroenterologists and is common to various underlying disease processes, primary amyloidosis is often overlooked during medical evaluation. We describe the diagnosis, natural history, and laboratory features of a subgroup of patients with primary amyloidosis who presented predominantly with gastrointestinal symptoms and with evidence of a malabsorption syndrome. SUBJECTS AND METHODS: We reviewed all patients diagnosed with amyloidosis and malabsorption syndrome who had been seen at the Mayo Clinic from 1960 through 1998. Nineteen patients with small bowel biopsy results showing primary amyloid and with laboratory evidence of a malabsorption syndrome were studied. RESULTS: The most common symptoms were diarrhea or steatorrhea in 95% of patients (n = 18), anorexia in 42% (n = 8), and dizziness in 32% (n = 6). The most common signs included weight loss in all 19 patients, with a median weight loss of 30 pounds (range, 2 to 134 pounds) and hypotension or orthostatic changes in 10 patients (53%). The median time from symptom onset to diagnosis was 7 months. Most patients had evidence of amyloid involvement of other organs. Only 3 patients (16%) were diagnosed correctly upon initial presentation. Serum or urine protein electrophoresis results were positive in 95% of patients (n = 18). Median survival was 11 months from histologic diagnosis. CONCLUSIONS: Primary systemic amyloidosis should be considered in the differential diagnosis of malabsorption syndrome. All patients over 30 years of age with a malabsorption syndrome should have screening serum and urine immunofixation before undergoing a small bowel biopsy.

Adult↗
PubMedDate not supplied

[Vitamin D metabolism in children with malabsorption syndrome].

In 16 children with malabsorption syndrome, out of which 5 had impaired lipid absorption or diarrhoea, and in 14 children in the control group the concentrations of vitamin D and 25 OH D3 were determined after oral administration of vitamin D in dose of 1200 U/kg.b.wt. or 12000 U/kg.b.wt. No decrease in initial 25 OH D3 concentrations was noted in children with malabsorption syndrome (40,5 +/- 0,7 ng/ml) in comparison with the control group (40,0 +/- 0,4 ng/ml). In children with impaired lipid absorption and diarrhoea the 25 OH D3 concentration was 33,6 +/- 2,4 ng/ml. After oral administration of vitamin D in small doses no differences were noted in the increase in vitamin D and 25 OH D3 concentrations in children with malabsorption syndrome or the control group. After administration of vitamin D in the dose 10 times higher no difference in the increase in vitamin D concentration was noted in children with malabsorption syndrome and the control group. However the increase in 25 OH D3 concentration in children with malabsorption syndrome was 49,8 +/- 1,2 ng/ml and 145,0 +/- 3,5 ng/ml in the control group. In the children with impaired lipid absorption and diarrhoea decreased vitamin D and 25 OH D3 concentrations were noted. This means that physiological doses of vitamin D in children with malabsorption syndrome are sufficient to supply vitamin D. Diarrhoea and impaired lipid absorption however, are indications for stimulation of skin synthesis of vitamin D.

Atrophy↗
PubMed1992

[Morphologic appearance of intestinal microvilli in children with coeliac disease and secondary malabsorption syndromes after gluten-free diet and gluten challenge].

The glycocalyx and the structure of the microvilli were analysed in electron microscopy in 122 children with coeliac disease and secondary syndromes of malabsorption. Slight differences were noted in glycolayx structure between both groups of children. In children with coeliac disease its reduction was noted (after gluten challenge). Changes were observed also in the structure of the microvilli. They were lower and often with abnormal shape in coeliac disease, while they were high and of normal structure in secondary malabsorption syndromes.

Celiac Disease↗
PubMed1983

Nutritional aspects of malabsorption syndromes.

Therapy of the malabsorption syndrome centers on adequate diagnosis of the underlying pathology, with vigorous therapeutic efforts directed at correcting this and thereby preventing ongoing losses of nutrients. Dietary therapy includes a high-protein, high-calorie, low-fat diet often supplemented with MCTs in an effort to minimize steatorrhea. Water-soluble vitamin deficiency is rare, but supplementation with small daily doses is innocuous and probably should be prescribed. Significant fat-soluble vitamin deficiencies are seen more commonly and can be monitored by physical examination and the prothrombin time. Calcium, magnesium, and vitamin D deficiencies are more common than originally suspected. Adequate therapy requires monitoring of the serum calcium, magnesium, parathyroid hormone levels, and, optimally, 24-hour urinary collections for calcium. Supplementation of these mineral deficiencies requires ongoing close observation to prevent hypercalcemia. Iron deficiency can be easily diagnosed by available serum iron determination, and replacement with oral supplements is curative. Trace metal deficiencies occur, but our capabilities of detecting and treating them is still in its infancy. Figure 3 outlines our approach to the evaluation and treatment of the patients suspected of having the malabsorption syndrome.

Dietary Carbohydrates↗
PubMedDate not supplied

A comparative study of the pathogenesis of malabsorption syndrome in broilers.

Five malabsorption syndrome (MAS) homogenates from The Netherlands and Germany were used to reproduce MAS in broilers. We studied the histopathology after inoculation of 1-day-old broiler chicks and the agents that might be involved. Generally, the MAS homogenates induced signs that differed in severity and pathobiology. We could distinguish and classify the inoculated groups best by histopathology: proventriculitis, lesions in the small intestines in combination with proventriculitis, or lesions of the small intestines only. Lesions in the small intestine had more impact on weight gain depression than lesions in the proventriculus. In three out of five inoculated groups, microscopic lesions of the pancreas were found. Reovirus was detected in the inoculated groups by virus isolation and seroconversion, and reoviral antigen was detected by immunohistochemistry of the small intestine. Also, enteroviruslike particles were detected in three of the five inoculated groups, although not in the most affected group. Additionally, bacteriophages and bacteria (hemolytic Escherichia coli, Pasteurella hemolytica, and Enterococcus durans) were isolated from inoculated chicks. The role these agents play in pathogenesis of MAS is still unsolved.

Animals↗
PubMed1989

Effect of malabsorption syndrome on pancreatic function in broilers.

The effect of "malabsorption syndrome" on pancreatic function was studied in newly hatched broiler chicks orally inoculated during the first few hours of life with intestinal homogenates from birds with naturally occurring malabsorption syndrome. The control groups were treated with saline. Tissue samples were collected at 0, 2, 4, 6, 9, 13, 17, and 29 days of age from both groups. The BW of inoculated birds decreased significantly relative to that of controls as early as 9 days of age. Pancreatic amylase activity was significantly greater than that in controls by 2 days. Protease activity of inoculated birds increased significantly over that in controls on the 2nd day and decreased significantly on the 6th and 9th days. Reoviruses were detected in the fecal samples of inoculated birds on the 2nd and 3rd days and did not appear in control samples. Reoviruses were also isolated from the pancreatic tissue of two inoculated birds on the 3rd day. Symptoms characteristic of malabsorption syndrome may be elicited by maldigestion; in the present study, this probably resulted from reduced digestive enzyme production of the pancreas. Similarities of changes in plasma triiodothyronine and pancreatic protease levels suggested a possible relationship between thyroid and pancreatic dysfunction in the condition of the malabsorption syndrome.

Amylases↗