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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After a review of causes and symptoms of sugar malabsorption and the usual diagnostic methods, the application is described of a recently developed procedure with high specificity and sensitivity: the hydrogen breath test. Examination of a large number of children shows that its sensitivity is higher than that of the procedures used so far, that lactose malabsorption is present in over 30% of the children with recurrent abdominal pain and/or diarrhoea; that in contrast to the prevailing opinion, malabsorption of sucrose in children is rare.
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PMID:[Diagnosis of carbohydrate malabsorption]. 726 53

To evaluate the role of the lactose breath hydrogen test for the detection of lactose malabsorption in children with chronic nonspecific abdominal complaints, breath hydrogen excretion was measured in 131 children with recurrent abdominal pain (n = 75) or chronic nonspecific diarrhea (n = 56) following a lactose load (2 gm/kg; maximum 50 gm). The data were compared to those obtained from lactose tolerance tests (n = 113) and symptom response following a lactose load (n = 109) performed simultaneously with the lactose breath hydrogen test, and with results from small bowel biopsies obtained in 31 children to determine dissacharidase activity and mucosal histology. The results indicate that an increase in breath hydrogen of greater than 10 ppm above base line values (delta ppm) by 120 minutes ("early increase" response) completely discriminates between biopsy-proven isolated lactase-insufficient and lactase-sufficient children. A similar increase after 120 minutes ("late increase" response) is consistent both with normal mucosal function and partial lactase insufficiency due to mucosal injury. Breath hydrogen responses predicted assayed lactase activity in all patients with isolated lactase insufficiency, but were "falsely negative" in four of ten children whose lactase insufficiency was secondary to mucosal injury. In both clinical groups, lactose malabsorbers report significantly more symptoms than absorbers (P less than .001), but neither symptom reports nor tolerance tests are accurate methods for distinguishing lactose malabsorbers from absorbers. Although the lactose breath hydrogen test provides objective documentation of lactose malabsorption, it is equally predictive of assayed lactase activity in all clinical groups.
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PMID:Mucosal function and breath hydrogen excretion: comparative studies in the clinical evaluation of children with nonspecific abdominal complaints. 732 85

Our objectives were to evaluate children with recurrent abdominal pain for lactose maldigestion and to assess factors which might predict lactose absorption status. One hundred thirty-seven children were referred for specialty evaluation of recurrent abdominal pain of at least three months' duration. Study subjects were evaluated by history and physical examination, dietary interviews, hematologic and biochemical laboratory testing, stool parasite examination, and radiologic or endoscopic structural examinations, as indicated. Lactose hydrogen breath testing was performed after challenge with 1 g/kg lactose 10% aqueous solution). There were 53 males and 84 females, whose ages ranged from 6 to 18 years (9.64 +/- 2.9; mean +/- SD) Lactose maldigestion was detected in 33/137 patients (24%). The prevalence of abdominal pain, bloating, gas, flatulence, diarrhea, and constipation was similar in children with or without lactose maldigestion. The perception of symptoms related to the ingestion of dairy products was similar in both groups. No other clinical parameter predicted lactose maldigestion. However, children with lactose maldigestion had overall clinical improvement with a lactose-restricted diet. Clinical evaluation alone cannot adequately predict the presence of lactose maldigestion in children. Formal evaluation for lactose maldigestion using breath hydrogen testing methods should be considered in children with recurrent abdominal pain.
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PMID:Lactose maldigestion and recurrent abdominal pain in children. 762 74

The effects of octreotide on six normal subjects and five patients with scleroderma were investigated. Changes in intestinal motility and in plasma motilin were examined after a single injection of octreotide. Octreotide stimulated intense intestinal motor activity in normal subjects. Motility patterns in the scleroderma patients were chaotic and non-propagative, but, after octreotide was given, became well coordinated, aborally directed, and nearly as intense as in normal volunteers. Clinical responses and changes in breath hydrogen were also evaluated in the five scleroderma patients who had further treatment with octreotide at a dose of 50 micrograms/day subcutaneously for three weeks. A reduction in symptoms of abdominal pain, nausea, vomiting, and bloating was seen. Additionally, there was an improvement in bacterial overgrowth as objectively measured by breath hydrogen testing. The effects of octreotide (100 micrograms/day subcutaneously) on the perception of rectal distension were investigated in a double blind, placebo controlled study in healthy volunteers. Octreotide was shown to reduce the perception of rectal distension without affecting motor pathways or local rectal reflexes. This enhanced tolerance to volume distension seems to result from inhibition of sensory afferent pathways as shown by electroencephalographic studies showing diminished evoked spinal and cortical potentials after octreotide. In irritable bowel syndrome patients with rectal urgency, octreotide reduces rectal pressures and perception after rectal distension to near normal values.
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PMID:Octreotide in gastrointestinal motility disorders. 820 95

In the period from 1990 to 1992 542 children aged 0-15 years were examined by the breath hydrogen test for abdominal pain and chronic nutritional disorder. The results of lactose tests were pathological in 107 children with abdominal pain and 95 with chronic nutritional disorder. The authors followed 107 children with abdominal pain and directed their attention to its relationship to lactose intolerance. It was confirmed to be the only cause of abdominal pain in twenty-six children (24.3%). In spite of the well known pathogenetic mechanism of lactose intolerance leading to abdominal pain and metheorism and loose stools, an atypical clinical course was observed in these patients. There were no complaints associated with the intake of milk in history, the abdominal pain being the leading symptom in all patients but four who had loose stools. There was an improvement of clinical symptoms after the low-lactose diet.
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PMID:[Lactose intolerance in the differential diagnosis of abdominal pain in children]. 829 91

We conducted blinded, controlled crossover studies to determine the effect of daily lactose feeding on colonic adaptation and intolerance symptoms. The initial study with nine lactose maldigesters showed a threefold increase in fecal beta-galactosidase activity after 16 d of lactose feeding. To determine the effects of this adaptation on breath hydrogen and intolerance symptoms, 20 lactose-maldigesting adults were randomly assigned to lactose or dextrose supplementation for 10 d (days 1-10), crossing over to the other period for days 12-21. The sugar dosage was increased from 0.6 to 1.0 g.kg-1.d-1, subdivided into three equal doses, by adjusting the dose every other day. Symptoms during lactose supplementation and comparison of symptoms during the lactose and dextrose feeding periods showed no significant differences. On days 11 and 22, challenge doses of lactose (0.35 g/kg) were administered after an overnight fast, and breath hydrogen and intolerance symptoms (abdominal pain, flatulence, and diarrhea) were carefully monitored for 8 h. Frequency of flatus passage and flatus severity ratings after the lactose challenge decreased 50% when studied at the end of the lactose period compared with the dextrose period. The sum of hourly breath-hydrogen concentrations (1-8 h) was significantly reduced after the lactose feeding period (9 +/- 38 ppm.h) compared with after the dextrose period (385 +/- 52 ppm.h, P < 0.001). We conclude that there is colonic adaptation to regular lactose ingestion and this adaptation reduces lactose intolerance symptoms.
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PMID:Colonic adaptation to daily lactose feeding in lactose maldigesters reduces lactose intolerance. 869 25

Patients who met International Congress of Gastroenterology criteria for irritable bowel syndrome (IBS) and had breath hydrogen lactose testing were interviewed to determine whether detection of lactose maldigestion (LM) had an impact on their symptoms. Of 199 patients initially evaluated, 161 (81%) were contacted and asked to rate their symptoms. At baseline, 47 (29%) of the IBS group had LM. Before testing, 23 (49%) were aware that ingestion of lactose-containing food was associated with their gastrointestinal symptoms. Lactose-maldigesting IBS subjects (IBSLM, n = 47) and those who had IBS and no LM (n = 114) were similar in terms of age, sex, and ethnic background. Interviews performed 41 +/- 1.1 (SEM) months after baseline evaluation revealed no significant differences in abdominal pain, altered bowel habits, bloating/distension, mucus, and relief with defecation among those with IBS or LMIBS. Overall symptoms resolved, improved, did not change, or worsened in a manner not statistically different between IBS and IBSLM groups. IBSLM subjects (a) felt that identifying LM helped them gain awareness of food-symptom relationships (78.7%), (b) experienced some improvement in symptoms (83%), (c) were avoiding lactose foods (87.2%), or (d) used lactase enzyme supplements (38.3%). Identifying LM did not significantly affect rated variables.
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PMID:Does lactose maldigestion really play a role in the irritable bowel? 883 92

In adults, slow-transit constipation is a well-established form of constipation with abdominal pain and an empty rectum on examination. Marker studies in these patients, mainly women, show a markedly slowed transit time in all colonic segments. No studies in constipated children are available that assess the existence of slow-transit constipation. In a prospective study, a total of 94 referred constipated pediatric patients, 63 boys and 31 girls (median age, 8.0 years), underwent colonic-transit-time measurements using radioopaque markers to evaluate the pattern of transit. In addition, orocecal-transit-time measurements using the hydrogen breath (lactulose) test, anorectal manometry, and behavior studies using the Child Behavior Checklist were performed in all children. Based on the upper limit (mean + 2 SD) of total colonic transit time (CTT) in constipated children, we arbitrarily separated patients into two groups. Children with CTTs > 100 h were said to have pediatric slow-transit constipation (PSTC), while patients with CTTs < 100 h were said to have normal- or delayed-transit constipation (NDTC). In 94 constipated children, PSTC was found in 24 children; in 70 children, total CTT was < 100 h (NDTC). Total and segmental CTTs were significantly prolonged in PSTC (median, 189 h; range, 104.4-384) versus NDTC (median, 46.8 h; range, 3.6-99.4) hours. No significant differences were found in orocecal transit time. Significant clinical differences in children with PSTC versus those with NDTC existed regarding nighttime soiling (71 vs. 11%); daytime soiling episodes (14 vs. 7 each week, median), and nighttime soiling episodes (5 vs. 0 each week, median); absent urge to defecate (33 vs. 14%); and palpable abdominal (71 vs. 39%) and/or rectal (71 vs. 13%) masses. All manometric parameters were comparable in the two groups, except for a significantly lower maximal squeeze pressure with PSTC. Using the Child Behavior Checklist, both groups differed significantly from controls (26 and 43%, respectively), with no significant differences in behavior problems found between the NDTC and the PSTC groups. In conclusion, based on objective marker studies, our findings suggest the existence of pediatric slow-transit constipation. This entity can be recognized by clinical features, most importantly nighttime soiling and a palpable rectal mass. The probability of PSTC with both of these symptoms was 0.82; in the absence of these two symptoms, it was 0.07. It is of interest that CTTs in PSTC are comparable with CTTs in adults with slow-transit constipation, although the clinical presentation is clearly different. Further studies are needed to investigate whether the prolonged CTT characterizes a distinct form of constipation in children or is an epiphenomenon of the underlying constipation itself. The mechanisms responsible for the slow transit in these children and the appropriate therapeutic approach need to be studied.
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PMID:Colonic transit time in constipated children: does pediatric slow-transit constipation exist? 889 73

Breath hydrogen (H2) studies have made clear that small intestinal absorption of fructose is limited, especially in toddlers. Malabsorption of fructose may be a cause of recurrent abdominal pain and chronic nonspecific diarrhea (toddler's diarrhea). Fructose absorption is facilitated by equimolar doses of glucose and, as we have found, amino acids (especially L-alanine); the mechanism underlying this effect remains unclear. To study fructose absorption in a more direct way, we combined breath H2 studies with breath 13CO2 studies. Gastric emptying was studied by using L-glycine-1-13C in 4 children from 12.1 to 16.0 years of age. After 25 gm of fructose and 27.5 gm of glucose, when given together, gastric emptying was significantly (p<0.05) slower than with either sugar alone. In a second series of experiments, 5 children from 12.0 to 15.9 years of age were tested with 25 gm of fructose, alone and with equimolar doses of glucose and L-alanine, and 4 younger children from 3.1 to 6.1 years of age were tested with 2 gm/kg (max 37.5 gm) fructose, alone or with an equimolar dose of L-alanine. All fructose solutions were enriched with 15 mg of D-fructose-13C-6. In all 9 children, fructose was malabsorbed as judged by breath H2 increases > or = 20 ppm, and the addition of glucose or L-alanine resulted in significantly lower breath H2 increases (p < or = 0.005 for glucose, p < or = 0.001 for alanine). In contrast, the addition of alanine or glucose did not change the pattern of breath 13CO2 excretion in the 5 older children, whereas in the 4 younger children (with relatively higher doses), L-alanine addition resulted in significantly lower increases in breath 13CO2. In the latter group, for each time point, breath H2 and 13CO2 concentrations after fructose were compared with those after fructose plus L-alanine; in 20 out of 24 points, both H2 and 13CO2 were higher after fructose. These results suggest that 13CO2 not only originated from the oxidation of absorbed substrate but also, at least in part, from colonic bacterial metabolism. For the detection of [correction of or] fructose malabsorption--as opposed to, for instance, lactose--the 13CO2 breath test seems to be of limited value.
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PMID:Evaluation of 13CO2 breath tests for the detection of fructose malabsorption. 927 64

Recurrent abdominal pain of childhood affects 10 to 15% of school-aged children and leads to disability and learning difficulties. Lactose maldigestion may be a causative or contributory factor that when identified may lead to improvement. Thus, formal diagnostic testing using breath hydrogen lactose challenge methods is encouraged. This review focuses on this important condition and management options.
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PMID:Recurrent abdominal pain and lactose maldigestion in school-aged children. 938 61


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