Re:Fructose Intolerance (malabsorption)

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Jan A pubmed search from 06-07 revealed some of the following that may interest

you:

Dig Dis Sci. 2007 Nov;52(11):2999-3004. Epub 2007 Mar 15.

Division of Gastroenterology, Department of Medicine, Sir Mortimer B.

Jewish General Hospital, McGill University, Montreal, Quebec, Canada.

aszilagy@...

Fructose malabsorption is linked to gastrointestinal and other unusual symptoms.

Polymers of fructose are also recognized prebiotics. While some prebiotics can

self-adapt when consumed regularly (resulting in decreased breath hydrogen and

symptoms), we wondered whether self-adaptation occurs with basic fructose. We

evaluated 90 subjects (61 females). Each completed a diet questionnaire and

underwent a fructose challenge. Breath hydrogen and quantified symptom scores

were recorded. Group comparisons for sum of breath hydrogen and total symptom

scores were evaluated with the Mann-Whitney U test. Spearman's correlation

coefficient and chi(2) or Fisher's exact test were used as appropriate.

Malabsorption occurred in 29 patients (32.2%) and low-grade symptoms without

malabsorption in 30 (33%). Women complained of symptoms more frequently (p =

0.04) and exhibited more fructose malabsorption (p = 0.0527). Breath hydrogen

correlated with symptoms (r = 0.516, p = 0.0037). Adaptation with increasing

pretest fructose intake was absent. We conclude that gender may influence

fructose malabsorption and there is no adaptation to regular consumption.

Aliment Pharmacol Ther. 2007 Feb 15;25(4):349-63. Epub 2007 Jan 8.

Department of Gastroenterology and Monash University Department of Medicine, Box

Hill Hospital, , Australia. peter.gibson@...

Fructose is found widely in the diet as a free hexose, as the disaccharide,

sucrose and in a polymerized form (fructans). Free fructose has limited

absorption in the small intestine, with up to one half of the population unable

to completely absorb a load of 25 g. Average daily intake of fructose varies

from 11 to 54 g around the world. Fructans are not hydrolysed or absorbed in the

small intestine. The physiological consequences of their malabsorption include

increasing osmotic load, providing substrate for rapid bacterial fermentation,

changing gastrointestinal motility, promoting mucosal biofilm and altering the

profile of bacteria. These effects are additive with other short-chain poorly

absorbed carbohydrates such as sorbitol. The clinical significance of these

events depends upon the response of the bowel to such changes; they have a

higher chance of inducing symptoms in patients with functional gut disorders

than asymptomatic subjects. Restricting dietary intake of free fructose and/or

fructans may have durable symptomatic benefits in a high proportion of patients

with functional gut disorders, but high quality evidence is lacking. It is

proposed that confusion over the clinical relevance of fructose malabsorption

may be reduced by regarding it not as an abnormality but as a physiological

process offering an opportunity to improve functional gastrointestinal symptoms

by dietary change.

Gastrointest Endosc Clin N Am. 2006 Apr;16(2):317-27.

Department of Medicine I (Gastroenterology, Hepatology, Pneumonology and

Endocrinology), University Hospital, Ulmenweg 18, Erlangen 91054, Germany.

Norbert.Krauss@...

Because of the wide variations in the clinical presentation of celiac disease

and because treatment exists that is effective in most cases, screening of the

general population for celiac disease has been considered. There is still no

evidence that patients who have symptom-free celiac disease are at increased

risk of small intestinal lymphoma or other complications. Prevention of

osteoporosis seems to be the strongest indicator for widespread screening today

[22].The major cause of failure to respond to a gluten-free diet is continuing

ingestion of gluten, but other underlying diseases must be considered.Many

different drugs (eg, anti-tumor necrosis factor [TNF]-alpha) have been used in

patients who have RCD [23]. Steroid treatment has been reported to be effective

even in patients who have underlying early EATL.Histologic recovery in patients

who have celiac disease usually takes several months but can take up to 1 year,

even if the patient remains on a strict gluten-free diet. Some patients report

celiac-related symptoms for months after a single gluten intake.The definitions

for RCD in literature vary. The authors consider the definition give by Daum and

colleagues [24] suitable. They defined true RCD as villous atrophy with crypt

hyperplasia and increased IELs persisting for more than 12 months in spite of a

strict gluten-free diet.If a patient is not responding well to a gluten-free

diet, three considerations are necessary: (1) the initial diagnosis of celiac

disease must be reassessed;(2) the patient should be sent to a dietician to

check for errors in diet or compliance problems, because problems with the

gluten-free diet are the most important cause for persisting symptoms; (3) other

reasons for persisting symptoms (eg, pancreatic insufficiency, irritable bowel

syndrome, bacterial overgrowth, lymphocytic colitis, collagenous colitis,

ulcerative jejunitis, protein-losing enteropathy,T-cell lymphoma, fructose

intolerance, cavitating lymphadenopathy, and tropical sprue) should be

considered.Other causes for villous atrophy are Crohn's disease, collagenous

sprue, and autoimmune enteropathy.Abdulkarim and colleagues [25] examined 55

patients who had a diagnosis of nonresponsive celiac disease. He found that 6

did not have celiac disease, and25 still had some gluten ingestion.Tursi and

colleagues [26] reported 15 patients who had celiac disease with persisting

symptoms. Because histology improved in all patients after several months, RCD

was excluded. Of the 15 patients, 10 had small intestinal bacterial overgrowth,

2 showed lactose malabsorption causing the described symptoms, 1 had mistakenly

taken an antibiotic containing gluten, and 1 patient each had Giardia lamblia

and Ascaris lumbricoides. Thus, other entities must be considered in patients

who have celiac disease and ongoing symptoms.In a follow-up clinical trial, 158

patients who had celiac disease underwent follow-up small intestine biopsies

within 2 years after starting a gluten-free diet.Eleven patients (7.0%) with

persisting (partial) villous atrophy were considered to have RCD; 5 of them

developed EATL [27].RCD type I is characterized by normal expression of T-cell

antigens and polyclonal TCR gene rearrangement.RCD type II is characterized by

an abnormal IEL phenotype with the expression of intracytoplasmic CD3e, surface

CD103, and the lack of classic surface T-cell markers such as CD8, CD4, and

TCR-alpha/beta. This clonal IEL population can be considered crypt IEL [24]. RCD

II has a poor prognosis, which is a problem for therapy.Clonal TCR gene

rearrangements and loss of T-cell antigens such as CD8 and TCR-beta in IELs may

indicate the development of an EATL in patients who have RCD.The markers for an

overt EATL are a positive stool blood test, increased lactate dehydrogenase, or

beta2-microglobulin [24]. If an overt lymphoma is suspected, upper and lower

endoscopy, an ear, nose, and throat work-up, CT scan, capsule endoscopy, and

possibly double-balloon enteroscopy should be performed.Most reports of the

difficulties in treating patients who have true RCE are casereports. and

colleagues [28] reported on an induction of remission by useof the

anti-TNF-alpha antibody infliximab and maintenance with prednisoloneand

azathioprine. Olaussen and colleagues [29] and Mandal and colleagues [30]tried a

nonimmunogenic elemental diet.Gillet and colleagues [31] reported successful

treatment of a patient who hadRCD using anti-TNF-alpha antibodies (infliximab)

for induction and azathioprinefor maintenance.Maurino and colleagues [32]

studied seven consecutive patients diagnosed ashaving refractory sprue and no

response to oral or parenteral steroids. Aftertreatment with azathioprine (2

mg/kg/d) and oral prednisone (1 mg/kg/d), fivepatients had a complete clinical

remission. Two patients who did not respond totreatment at any time died.Goerres

and colleagues [33] described 18 patients who had RCD, 10 of whomhad type I RCD,

and 8 of whom had type II RCD. Treatment consisted ofazathioprine combined with

prednisone for 1 year. Consistent with reports byother investigators, the

response rates in the two groups differed. Eight of the10 patients who had type

I RCD had a histologic response. Seven of the eightpatients who had type II RCD

died, and six of the eight developed a lymphoma.At present there is no effective

treatment for type II RCD.Fig. 3 presents a proposed algorithm for monitoring

patients who have ce-liac disease.

Clin Nutr. 2006 Oct;25(5):824-31. Epub 2006 Jan 10.

CONCLUSIONS: Sugar malabsorption and intolerance seem to be frequent in patients

with functional abdominal bloating and gas-related complaints. A malabsorbed

sugar-free diet might be a long-term effective therapy in a high percentage of

patients. Further controlled clinical trials are warranted

K.athy J. Shattler, M.S.,RD

Director of Nutrition Services, CEU4U.COM

Http://www.ceu4u.com

kshattler@...

Virtual Continuing Education University