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The serum level of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D], the biologically most potent metabolite of vitamin D, is tightly regulated within narrow limits in human healthy adults. 1,25-(OH)2D deficiency is rare and is associated with disturbances in calcium and bone metabolism. We have previously reported a marked decrease in serum levels of 1,25-(OH)2D in human immunodeficiency virus (HIV)-infected patients. The present study was designed to further examine the causes and consequences of severe 1,25-(OH)2D deficiency in these patients. The design was a prospective cohort study. Fifty-four HIV-infected patients clinically classified according to the revised criteria from Centers for Disease Control and Prevention and healthy controls were studied. Parameters related to vitamin D and calcium metabolism as well as immunological and nutritional status were determined. Twenty-nine of the patients (54%) had serum levels of 1,25-(OH)2D below the lower reference limit, and 18 of these had undetectable levels. In contrast, HIV-infected patients had normal serum levels of 25-hydroxyvitamin D and vitamin D-binding protein. HIV-infected patients as a group had modestly depressed serum calcium and PTH levels. There were, however, no correlations between these parameters and serum levels of 1,25-(OH)2D. There were no differences in serum calcium or PTH levels or nutritional status when patients with severe 1,25-(OH)2D deficiency were compared to other patients, but patients with undetectable 1,25-(OH)2D had significantly elevated serum phosphate levels. Furthermore, patients with undetectable 1,25-(OH)2D levels were characterized by advanced clinical HIV infection, low CD4+ lymphocyte counts, and high serum levels of tumor necrosis factor-alpha (TNFalpha). We conclude that inadequate 1alpha-hydroxylation of 25-hydroxyvitamin D seems to be the most likely cause of 1,25-(OH)2D deficiency in HIV-infected patients, possibly induced by an inhibitory effect of TNFalpha. The low 1,25-(OH)2D and high TNFalpha levels observed may impair the immune response in HIV-infected patients both independently and in combination and may represent an important feature of the pathogenesis of HIV-related immunodeficiency. Markedly depressed 1,25-(OH)2D serum levels are also present in certain other disorders characterized by immunological hyperactivity. Thus, the findings in the present study may not only represent a previously unrecognized immune-mediated mechanism for induction of 1,25-(OH)2D deficiency in human disease, but may also reflect the importance of adequate serum levels of 1,25-(OH)2D for satisfactory performance of the immune system in man.

Objective: To assess the influence of malabsorption on nutritional status and energy expenditure in patients at different stages of HIV infection., Design and Methods: Fifty HIV patients were classified into three groups: Group 1, HIV asymptomatic patients (n=17); Group 2, AIDS without opportunistic infection (n=16); Group 3, AIDS patients with active infection (n=17). Clinically-healthy subjects (n=19) were used as controls. Parameters measured were: anthropometry, body composition by tetrapolar bioelectrical impedance; resting energy expenditure (REE) by open-circuit indirect calorimetry; malabsoption by D-xylose absorption and triolein breath tests., Results: Malabsorption (defined as abnormality of xylose and/or fat absorption test) was found in 34 (68%) of patients: 9 (53%) Group 1; 11 (69%) Group 2; 14 (82%) Group 3. Twenty-seven (54%) had sugar malabsorption and 21 (42%) fat malabsorption. A significant relationship was observed between malabsorption and weight loss. REE measured was significantly lower in malabsorptive patients than in non-malabsorptive patients and controls (6006.3+/-846.5 versus 6443.4 + 985.5 versus 6802.1+/-862.7 kJ/day, respectively; P < 0.05). The REE adjusted for fat-free mass was lower in malabsorptive than in non-malabsorptive patients and slightly higher than in controls, although the differences were not statistically significant., Conclusions: The results suggest that malabsorption is a frequent feature in HIV infection and is related to the HIV-related weight loss. Hypermetabolism is not a constant phenomenon in HIV infection since, in the presence of malabsorption, our patients show an appropriate metabolic response with a compensatory decrease in REE.

Even excellent clinical function after ileo-anal pouch construction is associated with a variety of physiological abnormalities. Small bowel intestinal motility is essentially normal but the ileal reservoir serves to markedly suppress the ileal motor response both to progressive distension by intestinal contents and to transmitted myoelectrical complexes. As a result, the healthy pouch can accommodate a large volume of intestinal content before the rising baseline pressure and the appearance of large isolated contraction waves produce an urge to defecate. Evacuation in the normal pouch patient is rapid and highly efficient and is achieved by means of the Valsalva maneuver without any evidence of significant intestinal propulsion. External anal sphincter function is fully preserved but internal anal sphincter function is significantly impaired in the immediate postoperative period. Recovery occurs over the next 6 to 12 months but is often incomplete. Bacterial overgrowth in the pouch and prepouch ileum is almost universal and results in the premature deconjugation of primary bile salts and accumulation of secondary bile salts within the pouch. These produce morphologic changes in the ileal mucosa, and their excretion in pouch effluent gradually depletes the bile salt pool. Anerobic organisms also bind with vitamin B12 and the vitamin B12-intrinsic factor complex, resulting in subtle but measurable reductions in vitamin B12 levels in pouch patients. Finally, anerobic fermentation of mucus and undigested carbohydrate results in excessive quantities of short chain fatty acids within the pouch lumen. The clinical significance of these substances is unclear, but they may have an adverse action on both ileal mucosal and smooth muscle function. In essence, however, the pouch surgeon can maximize the likelihood of good clinical function by constructing a large capacity pouch, by avoiding surgery in patients with clearly deficient anal sphincter mechanisms, and by careful attention to pouch-anal anastomotic technique.

Background & Aims: Oral administration of ursodeoxycholic acid (UDCA) and cholesterol causes bile salt malabsorption; the former by competition for and the latter by down-regulation of ileal bile acid transporters. Because ileectomy in rats induces enterohepatic cycling of bilirubin, the hypothesis that dietary steroids might have the same effect was tested., Methods: Male inbred C57L/J mice and Sprague-Dawley rats were fed low doses of UDCA, chenodeoxycholic acid (CDCA), or cholesterol added to laboratory chow with simultaneous chow-fed controls. After 1 week (mice) or 2 weeks (rats), indices of bile salt malabsorption and enterohepatic cycling of bilirubin were measured, including bilirubin secretion rates into bile, serum and intestinal bilirubin and bile salt levels, and urobilinogen levels in cecum, large intestine, and feces., Results: Dietary UDCA and cholesterol, but not CDCA, significantly increased bilirubin secretion rates into bile. In UDCA-fed mice, gallbladder biles contained increased levels of bilirubin conjugates and unconjugated bilirubin, and in 60%, granules of amorphous calcium bilirubinate precipitated. Dietary cholesterol and bile acids, particularly UDCA, increased cecal bile salt levels, unconjugated bilirubin and urobilinogen concentrations, and decreased fecal bilirubin outputs, consistent with colonic absorption., Conclusions: By causing bile salt malabsorption, dietary UDCA and cholesterol induce enterohepatic cycling of bilirubin.

Diarrhea and malabsorption are common findings in patients with the acquired immunodeficiency syndrome (AIDS). The pathogenesis and consequences of malabsorption in human immunodeficiency virus (HIV) infection are similar to those found in non-HIV-related conditions, and are related to both direct intestinal damage and alterations in the coordination of the body's response to feeding. The pathogenesis of malabsorption is multifactorial and includes primary enterocyte injury with partial villus atrophy and crypt hyperplasia, ileal dysfunction with bile salt wasting and fat malabsorption, and exudative enteropathy. Clinical studies show that intestinal cryptosporidiosis leads to excess fecal losses of about 20% for protein and fat. The consequences of malabsorption include decreased appetite; "enterogastrone" effects including dry mouth, decreased gastric acid secretion, decreased rate of gastric emptying, and slowed intestinal transit; anemia resulting from iron, folate, or vitamin B12 malabsorption; and metabolic effects including osteomalacia, gallstones, renal stones, and hypocholesterolemia. Few studies of nutritional therapy have been applied specifically to AIDS patients with malabsorption. Total parenteral nutrition promotes weight gain, although the response to this therapy depends on the underlying clinical problem, with body cell mass repletion noted in patients with malabsorption but predominantly fat gain in patients with systemic infections. Nutritional stabilization also was noted in response to oral administration of a semielemental diet.

Concentrative and facilitative glucose transporters are responsible for the movement of glucose across the plasma membrane of human cells. Defects in concentrative glucose transporters cause renal glycosuria and glucose-galactose malabsorption. Alterations in facilitative glucose transporters explain the newly discovered syndrome of low CNS glucose in the presence of normal blood sugar, causing seizures and developmental delay. Defects in other facilitate glucose transporters also help explain Fanconi-Bickel syndrome, glycogen storage disease type, Id, and non-insulin-dependent diabetes mellitus.

A novel fat absorption test to clarify the malabsorption syndrome was developed using a micronephelometric technique and compared with the classic conventional technique using 131I-triolein. An integrity of time-sequential light scattered from chylomicron-related turbidity in serum was determined between 0 and 300 min after butter fat load, being expressed in terms of the light scattering intensity (LSI). A good correlation was obtained between LSI and the serum level of chylomicron-triglyceride determined by an ultracentrifugation technique (r = 0.819, P < 0.001). The maximal LSI was consistently observed at 180 min after administration of a test meal in the normal group (n = 39), whereas the malabsorption syndrome group (n = 35) was distinctly different and could be further classified according to four patterns of LSI changes. In addition, an inverse correlation was found between this fat absorption test and the 131I-triolein absorption test. It was concluded that the micronephelometric technique which does not use a radionuclide is advantageous in its simple and safe evaluation of fat malabsorption syndrome.

The incidence of intestinal nutrient malabsorption increases with age. Therefore, an important question is whether there are age-related changes in intestinal nutrient absorption which may contribute to a decline in absorptive capacity. Sugar and amino acid transport per mg intestine generally decreases with age. The proximate mechanism underlying this age-related decrease in transport activity is a decrease in number of transporters per mg. This reduction in transporter number can be caused by age-related changes in cell proliferation rates which, in turn, can alter the ratio of absorptive to nonabsorptive cells. The age-related change in proliferation rates typically increases intestinal mass. There seems to be no age-related changes in the steady state levels of transporter mRNA. Aging also modestly impairs the ability of intestinal nutrient transport systems to adapt to changes in dietary conditions. Caloric restriction is the only procedure known to consistently increase the lifespan of mammals. Chronic caloric restriction markedly enhances intestinal nutrient transport per mg without affecting intestinal mass. Since body weight decreases with caloric restriction, there is a dramatic increase in intestinal absorptive capacity normalized to body weight. This suggests that an increase in intestinal nutrient absorption may be a critical adaptation to caloric restriction. There is a need to perform in vivo transport studies during senescence, to distinguish between acute and chronic effects of caloric restriction, and to identify hormones that may mediate aging and caloric restriction effects on intestinal nutrient transport.

The adequate supply of essential fatty acids (EFA) to the body depends upon sufficient dietary intake and subsequent efficient intestinal absorption. Lipid malabsorption is not only a leading cause of EFA deficiency (EFAD), but also occurs secondarily to EFAD. Understanding the relationship between EFAD and lipid malabsorption may be helpful in the development and optimization of oral treatment strategies. Sequential steps involved in EFA absorption, including lipolysis, solubilization by bile, uptake into the enterocyte, and chylomicron secretion into lymph are reviewed, both under physiological and EFAD conditions. EFAD in itself affects the deficiency state by impairment of EFA absorption due to its effects on bile formation and on chylomicron secretion. These processes may be interrelated as decreased phosphatidylcholine secretion into the bile (a consequence of EFAD) is known to result in decreased chylomicron assembly and secretion. Possible treatments of EFAD include increasing dietary amounts of triacylglycerols and/or specifically tailoring lipids (structured triacylglycerols, EFA-rich phosphatidylcholines, EFA-ethyl esters). It is forseen that insights into the relationship between lipid malabsorption and EFAD will refine rational approaches to prevent and treat EFAD in specific patient groups.

Chronic cholestasis is associated with a variety of symptoms and dysfunction of most organs. Among them, jaundice and pruritus are the first to be recognized, usually prompting the patients to see a physician. Besides the skin, however, cholestasis also affects, inter alia, the metabolism of plasma lipids and fat-soluble vitamins, as well as bone and liver. In the following article the pathogenesis and therapy of metabolic disturbances and organ dysfunctions occurring frequently in patients with chronic cholestasis are discussed.

The diagnostic merits of CA 50 and of symptoms indicating pancreatic cancer (pain, jaundice, weight loss, malabsorption) were compared prospectively in 512 consecutive patients. Among the final diagnoses were: exocrine pancreatic cancer, 175; periampullary cancer, 44; other gastrointestinal cancer, 45; and chronic pancreatitis, 64 cases. The suspected diagnoses based on symptoms and signs were correct in 80% of the patients with exocrine pancreatic cancer, in 78% with periampullary, in 76% with other gastrointestinal cancer and in 90% with chronic pancreatitis. CA 50 was pathological in 96% of the cases with exocrine pancreatic cancer, in 70% with periampullary, in 78% with other gastrointestinal malignancies and in 36% with chronic pancreatitis. The sensitivity was 96%, specificity 48%, positive prediction 49% and negative prediction 96%, depending on cut-off level. The single CA 50 value was comparable to symptoms and signs regarding sensitivity and negative prediction. In 28 of 42 cases incorrectly clinically classified, CA 50 alone indicated a benign or malignant diagnosis. If both the modalities 'signs and symptoms' and CA 50 were combined, the sensitivity was 91%, the specificity 92%, the positive prediction 86% and the negative prediction 95%. The initial CA 50 value can help to indicate in which patients a pancreatic malignancy should be suspected.

We report on seven patients in two unrelated consanguineous Bedouin families with Grasbeck-Imerslund syndrome. Pedigree analysis in Family 1 was suggestive of an X-linked mode of inheritance. Intra- and inter-familial heterogeneity was elicited among the affected children in both families. Two of the affected sibs in each family had raised Hb A2 (>4%) while a third in Family 1 had a raised level of Hb F before treatment. One of the patients developed subacute combined degeneration of the cord at the age of 17 years before the correct diagnosis was made. All abnormalities were corrected following the institution of parenteral cobalamin therapy.

A 22-year-old Nepali man presented with a 2-month history of fever, ill health, anorexia, loss of weight and diarrhoea. Apart from an ill-defined lower abdominal mass, physical examination was unremarkable. Investigations showed the picture of malabsorption syndrome with no evidence of structural gastro-intestinal tract involvement on barium meal, small bowel and large bowel enema, upper gastro-intestinal endoscopy, colonoscopy and mucous membrane biopsy. Laparoscopy showed typical features of tuberculous peritonitis. Liver biopsy showed tuberculous granulomatous hepatitis, and peritoneal biopsy showed caseating granulomata. The patient responded rapidly to antituberculosis chemotherapy.

Unlabelled: The aim of this prospective study was to examine the relationship between gastrointestinal ethanol production ("Mei-Tei-Sho" syndrome described in Japan) and biological liver dysfunction associated with intestinal malabsorption syndromes., Methods: Sixty-five patients with malabsorption-diarrhea underwent 98 simultaneous measurements of plasma gamma-glutamyl-transpeptidase and of faecal ethanol concentrations; in 5 cases, ethanolemia and faecal ethanol concentrations were measured after a 250 g rice-meal; in 1, ethanol concentration was measured in a sample of caecal liquid in hours following local instillation of fructose (40 g)., Results: Faecal ethanol was detected at least once in 60/65 patients (74/98 measurements, maximum 3.50 g*L-1), more often (98.0%, P < 0.001) in 51 patients with gamma-glutamyl-transpeptidase above 38 IU/L. Eating rice increased the faecal ethanol concentration in 5 patients, 2 of whom had measurable ethanolemia (0.20 and 0.47 g*L-1). Ileo-caecal ethanol concentration following local fructose instillation was 11.8 g*L-1., Conclusion: Endogenous gastrointestinal ethanol production contributes to elevated gamma-glutamyl-transpeptidase activity observed during malabsorption syndromes.

Objective: The prevalence of lactose malabsorption (LM) in the Caucasian population of northern Europe is estimated to be low. Irritable bowel syndrome (IBS) is a very common diagnosis, and its symptoms are nearly identical to those of LM. Therefore we investigated the prevalence of LM among IBS patients in comparison with healthy volunteers., Design: A double-blind clinical trial compared with healthy controls., Setting: One out-patient gastroenterology clinic in the Netherlands., Patients: 70 Caucasian IBS patients and 35 healthy volunteers (staff members)., Methods: All 105 underwent hydrogen (H2) breath and blood glucose tests, after an oral intake of 50 grams of lactose. The IBS patients were treated with a lactose-restricted diet for 6 weeks. They completed a lactose intake score before, and a symptom score scored by six separate criteria, before, during and after treatment., Results: In 17 out of 70 (24.3%) IBS patients LM was detected, in comparison with 2 out of 35 (5.7%) controls (P < 0.009). There was no difference in the pre-entry mean lactose intake and symptom score between the LM positive and negative IBS patients. The mean symptom score of the LM positive group showed a marked decrease after 6 weeks of dietary therapy (P < 0.001)., Conclusion: A substantial number of IBS patients showed a clinically unrecognized lactose malabsorption, which could not be discriminated by symptoms and dietary history, and which can be treated with a lactose-restricted diet. Therefore LM has to be excluded before the diagnosis IBS is made.

In order to attain a diagnostic procedure able to detect intestinal malabsorption we studied the effect of rice flour ingestion (30 g) on H2 levels in the expired air of asymptomatic volunteers (n = 12) and in pancreas failure patients, either with (n = 15) or without steatorrhea (n = 13). The excretion of H2 in the expired air from pancreatopathic patients with steatorrhea were well above than those obtained from patients without steatorrhea (P < 0.05). Our results suggest that H2 breath test could be utilized to recognize intestinal malabsorption in individuals with exocrine pancreas disease.

Background/aims: Malabsorption is a frequent complication following pancreatico-duodenectomy (PD) for pancreatic carcinoma. Gastrojejunostomy followed by Billroth I type of reconstruction (PD III) has been advanced to prevent this disorder. We compared postoperative digestion and absorption determined by 131I-triolein, D-xylose and pancreatic function diagnostant (PFD) after extensive PD followed by one of two reconstructive procedures., Material and Methods: Postoperative digestive and absorptive functions in patients operated by Child's method (PD II) were compared with patients in whom the stomach emptied proximal to the pancreas and bile duct (PD III)., Results: The absorption of D-xylose was significantly higher (1.24 +/- 0.36 g vs. 0.72 +/- 0.21 g) in the PD III group. No difference was noted in pancreatic endocrine secretion between the two groups. Biliary scintigraphy revealed increased bile secretion in the PD III group., Conclusions: These results suggest that PD III is superior to PD II following extensive PD.

Major intestinal resection may result in diarrhea and malabsorption, a clinical entity known as the short-bowel syndrome. Nutritional prognosis after a wide intestinal resection depends on the extent of resection, the nature of the intestinal segment removed (ileum or jejunum), the function and the adaptative capacity of the remaining intestine, and the preservation of the colon and the ileocecal valve. Adequate management of this dreadful syndrome requires a multidisciplinary effort between various medical specialties: general and pediatric surgery, intensive care unit, nutrition, psychology, pediatric and adult gastroenterology. Intestinal transplantation is the only chance for a real cure in patients who depend on total parenteral nutrition. Although results of small bowel transplantation have dramatically improved over the last few years, it remains a challenging surgical and immunologic enterprise. Severe rejection and infection are the major obstacles.

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 therapy.

Peptide YY (PYY) is a 36 amino acid peptide that is released from the endocrine cells of the distal ileum, colon, and rectum following a meal. PYY is strongly proabsorptive in the small intestine. We studied the effects of intravenous PYY on colonic water and electrolyte transport in awake dogs. Dogs had 20 cm neurovascularly intact colon Thiry-Vella fistulas (TVS) surgically constructed. Colonic transport was studied in three experimental groups. Group 1 animals received a standard mixed meal. Group 2 animals were unfed and received intravenous PYY and 100 pmol/kg/hr for two hours. This dose of PYY has previously been shown to simulate the plasma levels of PYY normally seen after a meal. Group 3 received intravenous PYY at the same dose in addition to a mixed meal. Our study shows an increase in colonic water, Na+, and Cl- absorption after a meal (P < 0.05). Infusion of PYY at a 100 pmol/kg/hr was significantly proabsorptive beginning at 60 minutes (P < 0.01). Infusion of PYY in addition to a meal further increased absorption (P < 0.05). PYY is a potent proabsorptive agent in the colon of the conscious dog. PYY, or its analogs, may be useful clinical agents in intestinal malabsorptive disorders or after bowel resection.

Few gastrointestinal functions decline to an important extent as a result of old age alone and there is little clinical evidence that significant malnutrition occurs in any normal elderly person as a result of the aging process itself. Nevertheless, decreased gastrointestinal reserve makes older people highly sensitive to minor insults and decompensation can rapidly occur. Drugs appreciably affect taste sensation, which is already blunted and psychological as well as physical disability can have a major impact on appetite. Malabsorption can be caused by gastric hypochlorhydria with small bowel bacterial overgrowth and while gastrointestinal dysmotility can be caused by subclinical hypothyroidism, it can improve in response to physical exercise. Evidence is now mounting that thorough investigation of gastrointestinal disturbances in elderly patients coupled with intensive nutritional support can make a very real impact on their outcome. Gastroenterologists should therefore seek out and actively treat gastrointestinal disorders in the elderly and not just ascribe them to old age.

Malnutrition resulting from chronic congestive heart failure (cardiac cachexia, CC) is not uncommon and contributes to mortality and morbidity especially of elderly people. The aetiology of cardiac cachexia is probably multifactorial. We have assessed whether malabsorption of fat is associated with CC and if so whether it is due to small-bowel bacterial overgrowth. Three groups of subjects were studied: 29 (20 women) patients (mean age 76.1 years) with controlled congestive heart failure and weight loss (CC); 14 (seven women) patients (mean age 74.0 years) with controlled congestive heart failure and no weight loss (non-cachexia, NON-CC); and 29 (20 women) healthy controls (mean age 74.9 years). Fast absorption was quantified using the cumulative 6 h 14CO2 exhalation in the 14C-triolein breath test and small-bowel bacterial overgrowth was quantified using the cumulative 8 h 14CO2 exhalation in the 14C-glycocholic acid breath test. The cumulative 6 h 14CO2 exhalation in the triolein breath test was reduced in the CC group (p = 0.001) implying impaired fat absorption. There was no evidence of small-bowel bacterial overgrowth in any group. Impaired absorption of fat was related to the clinical severity of heart failure and its duration. Impaired fat absorption is associated with cardiac cachexia. It is not due to small-bowel bacterial overgrowth. The aetiology of fat malabsorption in heart failure requires further studies.

Massive intestinal resection produces malabsorption which, in the suckling rat, reduces growth. Our aim was to determine whether the proliferative action of neurotensin, can reduce the negative effects on growth induced by bowel resection. Fifteen days old suckling Wistar rats were used. Twenty rats underwent 90% midgut resection and twelve were used as controls. Half the animals were treated with neurotensin (600 micrograms/kg-day) until sacrifice 30 days later. Body and bone weight were measured and mucosal samples obtained. All resected animals lost body weight and bone weight. Neurotensin treatment reduced femur weight loss. After bowel resection, significant trophic effects were observed at mucosal level (crypt and villous size) but only in the jejunum of resected animals neurotensin treatment had a trophic effect. In conclusion, neurotensin favors intestinal adaptation after resection without improving mid-term growth in the suckling rat.

The type, incidence, and severity of malabsorption in patients with pancreatic cancer were investigated. The following absorption tests were performed; pancreatic function diagnostant (PFD) test, measurement of serum carotene levels, and 5 g D-xylose absorption test. Rates of abnormality in the tests were 75.7% of 37, 54.2% of 48, and 54% of 50 patients with pancreatic cancer, respectively. In particular, a marked decrease of values in the xylose absorption test was characteristic and more often recognized in patients with carcinoma of the pancreas with occlusion of the superior mesenteric vein. The presence of malabsorption (disturbed transport through the portal vein), in addition to maldigestion of nutrients, is suggested to induce severe malnutrition in patients with pancreatic cancer.

Background: The aim of the study was to elucidate the degree and the pathophysiology of abdominal symptoms, malnutrition and malassimilation after total gastrectomy., Methods: In 174 consecutive patients, with potentially curative total gastrectomy for gastric malignancy, subjective symptoms and objective parameters of malassimilation were evaluated., Results: Abdominal symptoms were present in 86% of the patients. In spite of a high daily calorie intake (median 37.8 kcal/kg body weight) mean body mass index had been decreasing since good health. Anaemia was found in 46%, sideropenia in 31% and oesophagitis in 26%. Mean faecal fat excretion was 17.4 (1.4) g/day and mean fat malassimilation 14.8% (1.1) of the intake. A shortened small-bowel transit was measured in 21.7% of the patients, and bacterial overgrowth was present in 37.7%., Conclusions: Malassimilation post total gastrectomy seems to be multifactorial. Shortened small-bowel transit and subsequent dyssynchrony of pancreatic enzyme supply seem to be of major importance.

Day-old male, meat-type chicks raised in brooder batteries were infected by orally administering an inoculum prepared from intestines of broiler chicks infected with stunting syndrome (SS). Naive controls were kept in a parallel room. The chicks were fed a commercial starter diet supplemented with two levels of enzyme preparations to 14 d of age. The experiment was continued to the age of 6 wk in order to estimate compensatory feed intake and growth. In a parallel study, digestibility of the feed was determined from 1 to 3 wk of age with control or inoculated chicks. The enzymes amylase and proteases were produced by Bacillus subtilis and Penicillium emersonii. Enzyme supplementation had no effect on feed intake, growth, or feed utilization, or on digestibility of fat, starch, protein, or energy. Because enzyme supplementation did not consistently affect performance of chicks and no interactions were observed between enzyme supplementation and infection status, data are presented for effects of infection only. Inoculation of SS-infective material reduced performance to 4 wk. Compensatory growth and feed intake were observed from the age of 4 wk onward. At the age of 6 wk the slight retardation of the inoculated chicks was not significant. On Week 1, retention of fat, starch, protein, and energy was significantly depressed in the inoculated chicks. At the age of 2 wk, retention of starch was not depressed, and at the age of 3 wk, the only consistent depression was that observed for fat. The proventriculus weight and content were consistently higher in inoculated chicks, as were the small intestine and intestinal content. The pH of the gizzard content was higher, and that of the small intestine content was lower, in the inoculated birds than in their control counterparts. Stunting syndrome infection was accompanied by a significant depression of trypsin activity in the pancreas at the age of 1 and 2 wk. At these periods, amylase and chymotrypsin were not affected. At 6 wk of age, the activities of amylase, trypsin, and chymotrypsin in the pancreas were higher in the inoculated than in the control birds. In the intestinal chime, amylase, trypsin, and chymotrypsin activities were lower in the inoculated birds on Week 1 and 2 (NS for amylase on Week 1). On Week 6, the activity of all enzymes assayed was higher in the inoculated birds (NS for amylase). It is suggested that the main factors depressing feed intake and growth in SS-infected birds are most probably beyond those of digestion.

Objective: To determine if a single-step noninvasive stable isotope method of assessing digestive function could separate normal subjects from subjects with pancreatic insufficiency (maldigestion) or small bowel dysfunction (malabsorption) and to see if subjects with maldigestion could be simultaneously separated from subjects with malabsorption., Methods: Forty (40) normal volunteers, 18 adults with cystic fibrosis and four adults with celiac sprue, ingested a liquid test meal along with bentiromide, [13C6]PABA, and xylose (PABAX test). Serum was collected at 1 h and analyzed for PABA, [13C6]PABA, and xylose by stable isotope dilution methods using gas chromatography mass spectrometry., Results: All subjects with cystic fibrosis had abnormal pancreatic function test results, whereas three of four adults with sprue had normal values of pancreatic function. All subjects with sprue had abnormal small bowel absorption tests, whereas all adults with cystic fibrosis had apparently normal intestinal function., Conclusion: The one-step, 1-h PABAX test can reliably separate normal subjects from those with either maldigestion or malabsorption and can also separate subjects with maldigestion from those with malabsorption.

The complained gastrointestinal symptoms in PSS are probably caused by several complex disturbances like intestinal transit disturbances (ITD), bacterial overgrowth of the small intestine caused malabsorption of bile acids and altered kinetics of intestinal hormones. 25 patients with PSS and eleven healthy controls were tested for the existence of ITD by use of the metal-detector test (MDT). Twelve patients were also tested for a malabsorption of primary bile acids by radioimmunological measurement of clolylglycine serum levels before and after a meal. In addition serum concentrations of gastrin (nine patients) and plasma concentrations of cholecystokinin (CCK) (eight patients) and motilin (eleven patients) were measured by radioimmunoassay pre- and postprandial. Interdigestive gastric emptying was accelerated in patients with PSS (53 +/- 3 min. vs. 73 +/- 7 min.; p<0.01). Small intestinal transit times were similar in both groups (115 +/- 17 min. vs. 121 +/- 13 min.). Colonic transit in patients with PSS was significant prolonged (63 +/- 6 h vs. 39 +/- 5 h; p<0.05). There were no significant differences between the two groups concerning the pre- and postprandial levels of cholylglycin. Basic and postprandial levels of gastrin, CCK and motilin were higher in the PSS group. In contrast to scintigraphic studies using semisolid meals gastric emptying of the copper pellet in PSS was accelerated. A general malabsorption of primary bile acids was not found. Prolonged colonic transit times correlate well with frequently complained obstipation. Gastric hypacidity could be the reason of elevated gastrin levels. The high motilin-levels in PSS could be due to a lack of the feed-back inhibition as a result of diminished phase-III activity of the interdigestive migrating motor complex. The elevation of CCK-levels could reflect compensation of neurogenic or myogenic disturbances of gallbladder contraction.

Clinical conditions in which secondary maldigestion associated with exocrine pancreatic insufficiency occur include chronic pancreatitis, cystic fibrosis, pancreatic cancer, partial or total gastrectomy, and pancreatic resection. Maldigestion can cause serious weight loss, nutritional deficiencies, and subjective complaints associated with steatorrhea. The various causes of exocrine pancreatic insufficiency may be associated with cause-related changes in gastrointestinal physiology, such as changes in gastrointestinal intraluminal pH, bile acid metabolism, gastric emptying, and intestinal motility. Therefore, to optimize the efficacy of treatment, the management of exocrine pancreatic insufficiency must be individually tailored to account for both the underlying cause and any associated disturbance in gastrointestinal physiology. In addition, the properties of the pancreatic enzyme preparations and adjuvant drugs need to be taken into consideration. This paper reviews the pathophysiological mechanisms of maldigestion in exocrine pancreatic insufficiency, discusses the efficacy of different therapy regimens, and gives guidelines for a cause-related and patient-tailored treatment with respect to both drug therapy and dietary counselling.

Cystic fibrosis often combines an infectious pathology with a syndrome of malabsorption, both potentially capable of favoring the deleterious effects of reactive oxygen species. This study was a simultaneous evaluation of the main antioxidant systems dependent on micronutrients and of lipid peroxidation products in 27 children with cystic fibrosis and 17 healthy children. Plasma of cystic fibrosis patients showed very low concentrations of beta-carotene (0.30 +/- 0.2 vs 1.63 +/- 0.5 mumol/g cholesterol, P < 0.0001) and a lower activity of selenium-dependent glutathione peroxidase (263.6 +/- 42 vs 296.9 +/- 57 U/L, P = 0.028). In parallel, the higher plasma concentrations of organic hydroperoxides (171.5 +/- 54.4 vs 122.6 +/- 23.3 mumol/L, P = 0.001) and of thiobarbituric acid reactants (2.9 +/- 0.6 vs 2.4 +/- 0.3 mumol/L, P = 0.004) reflected oxidative stress in this pathology. In addition, in these patients the major substrates of lipoperoxidation were significantly lower, whether they be linoleic acid (2.26 +/- 0.8 vs 3.60 +/- 0.9 mmol/L, P < 0.0001) or arachidonic acid (0.55 +/- 0.2 vs 0.74 +/- 0.2 mmol/L, P = 0.006). These results suggested that nutritional deficiencies resulting from malabsorption could considerably amplify disorders related to toxicity of reactive oxygen species. These nutritional deficits could also be aggravated by the destruction of antioxidant compounds by the inflammatory process.

Whipple's disease is a chronic systemic infectious disease caused by Tropheryma whippelii that typically involves the small intestine and causes malabsorption. Extraintestinal manifestations such as arthritis and fever are common and often exist prior to the onset of gastrointestinal symptoms. Involvement of the central nervous system can occur and lead to permanent sequelae. Weight loss, hyperpigmentation, and lymphadenopathy are frequent findings. The definitive diagnosis is made by biopsy of the small intestine mucosa which reveals infiltration of the lamina propria of the small intestine with periodic acid-Schiff positive macrophages. Treatment with trimethoprim combined with sulfamethoxazole for 1 year usually results in clinical remission and an excellent prognosis. Recent advances using molecular techniques to identify the uncultured bacillus of Whipple's disease should lead to a better understanding of the pathophysiology and allow for the development of a sensitive noninvasive diagnostic test.

The differential diagnosis for a 57-year-old man with joint pain, bruising, and diarrhea is discussed in the setting of a Clinical Pathological Conference at Louisiana State University Medical Center in Shreveport, La. The pathophysiology and etiology of malabsorptive states are presented.