Endosc Clin N Am 2000 Oct;10(4):739-53, vii
Small intestinal mucosal biopsy for investigation of diarrhea and
malabsorption in adults.
Department of Medicine, University of British Columbia, Vancouver, Canada.
The use of small intestinal biopsy for diagnosis in diarrhea and suspected
malabsorption depends on an optimal interaction between the clinician-endoscopist
and the pathologist. This necessitates open and interactive communication
between involved physicians and an appreciation for correct tissue
handling and biopsy orientation in the endoscopy unit and the pathology
laboratory. Classification of biopsy changes on the basis of architectural
abnormalities in the small intestinal biopsy may be helpful in defining
the diagnosis and include severe (flat) or variably severe (mild or
moderate) abnormalities. For some small intestinal disorders that are
characterized by diarrhea or malabsorption, the biopsy findings may be
distinctive and lead to a specific diagnosis. For others, like celiac
disease, the changes are less specific, and it has become better
recognized that an increasing number of conditions can produce similar
histopathologic changes. Definition of typical gluten-sensitive biopsy
changes in this disorder is critical.
Curr Gastroenterol Rep 2000;2(5):370-7
Malabsorption testing: a review.
Ginsburg PM, Janefalkar P, Rubin DT, Ehrenpreis ED
Department of Gastroenterology, University of Chicago Hospitals, 5841
South Maryland Avenue, MC 4076, Chicago, IL 60637, USA. firstname.lastname@example.org
Malabsorption syndromes often present diagnostic dilemmas to even the most
experienced clinicians. Several malabsorption screening tests are
available, but d-xylose testing is our initial screening method of choice.
Recent innovations such as serum assays for antibodies associated with
celiac sprue are improving the work-up of patients with suspected
malabsorption. In addition, physicians are applying technological advances
in imaging to determine the underlying pathologies responsible for the
occurrence of malabsorption and maldigestion. Breath testing remains a
controversial modality in the work-up of patients with
malabsorption. Tubeless tests of pancreatic function are also the subject
of debate due to a lack of sensitivity for diagnosing mild to moderate
chronic pancreatic insufficiency. This review identifies and provides
critical analysis of new developments in the field of malabsorption
testing. The authors also provide a clinical algorithm for diagnosisng
Paediatr Drugs 2000 May-Jun;2(3):205-22
Control of malabsorption in cystic fibrosis.
Littlewood JM, Wolfe SP
Regional Paediatric Cystic Fibrosis Unit, St James Hospital, Leeds,
Intestinal malabsorption is severe and of early onset in virtually all
people who have cystic fibrosis. The main cause is deficiency of
pancreatic enzymes, but bicarbonate deficiency, abnormalities of bile
salts, mucosal transport and motility, and anatomical structural changes
are other contributory factors. Appropriate pancreatic replacement therapy
will achieve normal or near normal absorption in many patients. It is
important to identify both malabsorption and evidence of a pancreatic
lesion in all patients who are to receive pancreatic enzymes. All who have
evidence of fat malabsorption are deemed pancreatic insufficient and
candidates for enzyme replacement therapy. Effective treatment should
allow a normal diet to be taken, control symptoms, correct malabsorption
and achieve a normal nutritional state and growth. The occurrence of
fibrosing colonopathy in some patients receiving very high doses of those
enzymes that have the copolymer Eudragit L30 D55 in their covering has
resulted in guidelines in the UK to avoid dosages greater than the
equivalent of 10,000 IU lipase/kg/day for all patients and also to avoid
preparations containing this copolymer in children and adolescents. For
patients not responding to 10,000 IU lipase/kg/day, review of adherence to
treatment, change of enzyme preparation, variation of the time of
administration and reduction in gastric acid may improve absorption. The
importance of excluding other gastrointestinal disorders as a cause of the
patient's symptoms and the need for early investigations, rather than
merely increasing the dosage of enzymes, is stressed. With modern enzymes,
adequate control of gastrointestinal symptoms and absorption can be
achieved at dosages of 10,000 IU lipase/kg/day or only slightly more, and
a normal nutritional state and growth rate maintained in most patients
with cystic fibrosis.
J Pediatr Gastroenterol Nutr 2000;30 Suppl:S61-6
Food-induced malabsorption syndromes.
Hospital for Children and Adolescents, University of Helsinki, Finland.
A syndrome of chronic diarrhea, vomiting, and failure to thrive was
described 35 years ago. The syndrome was caused by damage in the jejunum
after ingestion of cow's milk. Symptoms appeared in young infants shortly
after introduction of cow's milk formula. Patients had moderate
steatorrhea, decreased absorption of D-xylose, and, often, iron-deficiency
anemia and hypoproteinemia. They had strong IgA and IgG antibodies to
cow's milk. IgE antibodies to cow's milk were negative, as a rule.
Indicators of cell-mediated immune reaction to cow's milk proteins were
often positive. Patients were tolerant to cow's milk by the age of 3 years.
Malabsorption was due to damage to the jejunal mucosa: Varying villus
atrophy was associated with inflammation in surface epithelium and lamina
propria. The epithelial cell renewal rate increased. Surface epithelial
cells decreased in height, with short, furry microvilli and large
aggregates of lysozymes. The number of intraepithelial lymphocytes was
markedly increased, but normalized during cow's milk elimination. Most of
these lymphocytes had alpha/beta T-cell receptors, and many were cytotoxic.
Some specimens had an increase in gamma/delta T-cell receptor-bearing
cells. In the lamina propria, CD4+ cells predominated, and some of them
were activated. IgA- and IgM-containing cells were markedly increased
during cow's milk exposure, but IgE cells were not abnormal. The density
of eosinophils was moderately increased. Secretion of interferon-gamma by
cells isolated from patients' intestines was markedly increased.
Morphologic and immunologic findings suggest that T-cell-mediated reaction
to proteins in cow's milk is present in the small intestines of patients
with this syndrome and causes this enteropathy.
Nutrition 1999 Feb;15(2):167-9
The mechanisms of fat malabsorption in cystic fibrosis patients.
Kalivianakis M, Verkade HJ
Am J Physiol 1998 Nov;275(5 Pt 1):G879-82 [Texto
I. Glucose galactose malabsorption.
Physiology Department, University of California School of Medicine, Los
Angeles, California 90095-1751, USA.
Glucose Galactose Malabsorption is a genetic disorder caused by a defect
in glucose and galactose transport across the intestinal brush border.
Normally, lactose in milk is broken down into glucose and galactose by
lactase, an ectoenzyme on the brush border, and the hexoses are
transported into the cell by the Na+-glucose cotransporter SGLT1. The
mutations causing the defect in sugar transport have been identified in
patients from 33 kindreds, and functional studies have established how
these mutations cause the disease.
Hosp Med 1998 May;59(5):404-7
Malabsorption in the elderly. II: Treatment and further investigations.
Hossain J, Lewis RR
William Harvey Hospital, Ashford, Kent.
After the initial assessment of elderly patients suspected of having
malabsorption, as discussed in the first of this pair of articles, more
specific investigations may be necessary. These are described in this
article, together with the main treatment options that are available.
Hosp Med 1998 Apr;59(4):277-80
Malabsorption in the elderly. 1: Examination, history and investigation.
Hossain J, Lewis RR
William Harvey Hospital, Ashford, Kent.
Malabsorption in elderly patients has varied presentations, and can be
overlooked. A high index of clinical suspicion is required. This, the
first of two articles, discusses the principal causes, clinical features
and initial investigations of malabsorption in the elderly.
Digestion 1998 Aug;59(5):530-46
Universidad del Salvador, and Hospital de Gastroenterologia 'Dr. Carlos
Bonorino Udaondo', Buenos Aires, Argentina.
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.
Gastroenterol Hepatol 1997 Aug-Sep;20(7):386
[A malabsorption syndrome, gastrointestinal leishmaniasis and HIV
[Article in Spanish]
Alguacil GF, Moreno J, Ortolano A, Hallal H
Review of reported cases
Pancreas 1997 May;14(4):323-33
Pancreatic steatorrhea, malabsorption, and nutrition biochemistry: a
comparison of Japanese, European, and American patients with chronic
Nakamura T, Takeuchi T
Third Department of Internal Medicine, Hirosaki University School of
Medicine, Aomori, Japan.
This article reports on steatorrhea, daily food intake, and fecal
substances other than fecal fat (e.g., neutral sterols, bile acids, short-chain
fatty acids) in pancreatic exocrine dysfunction arising from chronic
pancreatitis (CP) in Japanese. European, and American patients. Changes in
upper small intestinal pH and lipase secretion, plasma fatty acid profiles,
serum fat-soluble vitamin levels and symptoms of their deficiency, and
nutritional status are discussed in detail. Treatment of pancreatic
steatorrhea is described. Throughout this study, we compared
characteristics of maldigestion and malabsorption in these patient
populations and our study revealed that fecal fat excretion reflected
quantitative differences in fat consumption, plasma fatty acid profiles
reflected quantitative and qualitative differences in fish oil consumption,
and there were no differences in pancreatic exocrine dysfunction among
these three groups. Since differences in fecal fat excretion and plasma
fatty acid profiles appear to depend on dietary fats, the pathology and
treatment of CP patients should be evaluated and the findings used to
J Clin Invest 1997 Apr 15;99(8):1807-8 [Texto
Point mutations in the ileal bile salt transporter cause leaks in the
enterohepatic circulation leading to severe chronic diarrhea and
Am J Clin Nutr 1997 Feb;65(2):564-7
Dairy sensitivity, lactose malabsorption, and elimination diets in
inflammatory bowel disease.
Department of Medicine, McGill University, Montreal, Quebec, Canada.
The ability of inflammatory bowel disease (IBD) patients to tolerate dairy
products and the guidance they receive from physicians and nutritionists
on this subject are important considerations in the management of their
IBD. Although most affected persons are able to consume a glass of milk
daily without discomfort, additional consideration must be given to
specific factors that can be relevant to certain individuals. The
declaration by patients that they are "dairy sensitive" may be
related to lactose intolerance or malabsorption, the long-chain
triacylglycerol content of milk, allergy to milk proteins, as well as
psychologic factors and the misconception that dairy products can be
detrimental to their health. The prevalence of lactose malabsorption is
significantly greater in patients with Crohn disease involving the small
bowel than it is in patients with Crohn disease involving the colon or
ulcerative colitis. In the latter colonic conditions the prevalence of
lactose malabsorption is mainly determined by ethnic risk, which is based
on genetic factors. In addition, lactose malabsorption in Crohn disease of
the small bowel may be determined by factors other than lactase enzyme
activity, such as bacterial overgrowth and/or small bowel transit time.
Physicians differ widely in the advice they give their patients: some
dogmatically advise avoidance of dairy products when the diagnosis is made
whereas others discount the possible role of dairy in the management of
IBD. IBD patients avoid dairy products more than they would need to based
on the prevalence of lactose malabsorption and/or milk intolerance,
probably partly because of incorrect patient perceptions and arbitrary
advice from physicians and authors of popular diet books. Adequate
scientific and clinical information is now available to permit
recommendations about the intake of dairy products for each IBD patient.
Pediatr Clin North Am 1996 Apr;43(2):307-31
Chronic diarrhea and malabsorption.
Branski D, Lerner A, Lebenthal E
Department of Pediatrics, Shaare Zedek Medical Center, Hebrew University,
Diarrhea is one of the major causes of infant morbidity and mortality
worldwide. Major advances in understanding the pathophysiology of chronic
diarrhea and malabsorption have taken place during the past three decades.
Analysis of absorptive and secretory functions of the intestine has
provided some insight into the possible causes of diarrhea. This article
summarizes some of the specific causes of malabsorptive diarrhea in
infancy and childhood, with emphasis on pathophysiology and approaches to
Pediatr Clin North Am 1995 Aug;42(4):899-915
Ushijima K, Riby JE, Kretchmer N
Department of Pediatrics and Child Health, Kurume University Medical
Center, Fukuoka, Japan.
Carbohydrate malabsorption is a very important clinical entity,
particularly in pediatrics, where, if untreated, it can lead to
malnutrition and failure to thrive. Malabsorption that can be treated
readily with elimination of the offending carbohydrate. Knowledge by the
physician of the specific mechanisms involved in the physiology of
carbohydrate absorption and digestion will help in the handling of the
clinical situation of malabsorption.
Gut 1994 May;35(5):582-6
Persisting diarrhoea and malabsorption.
Hospital for Tropical Diseases, London.
Semin Gastrointest Dis 1994 Apr;5(2):78-87
Malabsorption syndromes and celiac disease.
Rosensweig JN, Perman JA
Department of Pediatrics, Johns Hopkins University, School of Medicine,