Clinically, patients present with nonspecific gastrointestinal symptoms like: abdominal pain, bloating, excessive gas production, diarrhea, weight loss and malabsorption.
The bacterial overgrowth syndrome occurs when there are alterations in intestinal anatomy, gastrointestinal motility, or a lack of gastric acid secretion.. The nutritional consequences of intestinal bacterial overgrowth include vitamin deficiencies, fat malabsorption, and malnutrition.
The goal of treatment is eradication of the bacterial overgrowth (usually with antibiotics) and the correction of nutritional deficiencies.
Saltzman-JR & Russell-RM: Nutritional consequences of intestinal bacterial overgrowth. Compr-Ther. 1994; 20(9): 523-30.
Evaluated whether detailed symptom analysis would help to identify pathophysiologic subgroups in chronic constipation.
In 59 percent of patients, disordered defecation was found, and 27 percent had slow-transit stool. In 6 percent of patients, a combination of both was found; in only 8 percent of patients, there were no pathologic findings. Straining was reported by the vast majority in all groups (82-94 percent).
Infrequent bowel movements and abdominal bloating were more common in slow-transit stool (87 and 82 percent vs. 69 and 55 percent, respectively). Feeling of incomplete evacuation was more common in disordered defecation (84 vs. 46 percent).
However, specificity of these symptoms was discouraging (for slow-transit stool: infrequent bowel movements had a sensitivity of 87 percent and a specificity of 32 percent and abdominal bloating had a sensitivity of 82 percent and specificity of 45 percent; for disordered defecation: feeling of incomplete evacuation had a sensitivity of 84 percent and a specificity of 54 percent).
Definition of chronic constipation by infrequent bowel movements alone is of little value; the symptom "necessity to strain" is much better suited.
Symptoms of chronically constipated patients are not well suited to differentiate between the pathophysiologic subgroups suffering chronic constipation.
Koch A et al., Symptoms in chronic constipation. Dis Colon Rectum, 1997 Aug, 40:8, 902-6.
Investigated the possibility that a variant of the normal colonic flora, a high concentration of methanogens (CH4), influences the host's response to ingestion of nonabsorbable, fermentable materials.
The low CH4 producers had a significantly higher breath H2 concentration than the high producers on the basal diet and after ingestion of sorbitol or oat fiber. Low producers of methane reported significantly increased bloating and cramping after sorbitol ingestion and increased bloating after fiber ingestion, whereas high CH4 producers reported no significant increase in these symptoms.
The presence of a methanogenic flora is associated with a reduced symptomatic response to ingestion of nonabsorbable, fermentable material in healthy subjects. Manipulation of the normal flora could be of therapeutic value in nonmethanogenic patients with irritable bowel syndrome.
Kajs TM et al., Influence of a methanogenic flora on the breath H2 and symptom response to ingestion of sorbitol or oat fiber. Am J Gastroenterol, 1997 Jan, 92:1, 89-94.
Evaluated the gastrointestinal tolerance to an indigestible bulking sweetener containing fructo-oligosaccharides (FOS).
In order to mimic their usual pattern of consumption, FOS were ingested throughout the day either occasionally (once a week, first period) or regularly (every day, second period). In the two patterns of consumption, daily sugar doses were increased until diarrhoea and/or a symptom graded 3 (i.e. severe) occurred, or when subjects did not want to ingest more candies.
In both periods, the first symptom which occurred was excessive flatus (> 30 g FOS/day): borborygmi and bloating appeared at a higher level (> 40 g/day); lastly, abdominal cramps and diarrhoea occurred at a very much higher level (50 g/day).
Chronic consumption of FOS initiated cautiously with subsequent gradual increase did not improve tolerance, nor reduce breath excretion of hydrogen.
Briet-F: Symptomatic response to varying levels of fructo-oligosaccharides consumed occasionally or regularly. Eur-J-Clin-Nutr. 1995 Jul; 49(7): 501-7.
The result of a deficiency in intestinal lactase, lactose intolerance affects 50 million Americans, most of whom are African-American, Asian, Hispanic, Native American, or of southern European descent. Undigested lactose can lead to abdominal cramps, bloating, borborygmi, increased flatulence, and other symptoms. Eliminating lactose-containing foods or supplementing the diet with lactose-digestive aids can help this condition. Milk substitutes can be used along with lactase supplements. Calcium and vitamin D may also be important for the lactase-deficient individual. Diagnosis of lactose intolerance includes a diet/symptom diary, hydrogen breath test, intestinal brush border biopsy, stool test for pH and sugars, and a lactose tolerance test.
Griffith, Ceabert J., PA-C: Lactose Intolerance, Physician Assistant, November 1997;56-62.
A standard for the assessment of lactose malabsorption does not exist. As measured by lactose tolerance tests, insufficient increase in blood glucose or increased breath hydrogen (H2) excretion after lactose ingestion is regarded as pathological.
After consumption of 50 g of lactose, blood glucose and breath H2 concentrations were measured. During the test (240 min), the severity of bloating, flatulence, abdominal distention, and diarrhea were semiquantitatively scored as 0, 1, or 2. The individual sum of these four scores was calculated and denoted as the total symptom score (TSS). All subjects were classified according to their TSS to compare symptoms with peak breath-H2 concentration and change in blood glucose concentration, respectively.
The glucose and breath H2 response were pathological in 51 and 40% of cases, respectively.
GI symptoms after a lactose challenge are strongly associated with the amount of H2 excretion. The relationship between the increase in glucose concentration and symptoms after a lactose load is less evident. Thus, the H2 breath test seems to be superior to the measurement of blood glucose increment as a diagnostic tool in lactose malabsorption, although the true predictive value of this test only can be determined after a period of dietary treatment.
Hermans MM et al., The relationship between lactose tolerance test results and symptoms of lactose intolerance. Am J Gastroenterol, 1997 Jun, 92:6, 981-4.
Some people insist that small quantities of milk, such as the amount used with cereal or coffee, cause severe gastrointestinal distress such as abdominal pain, diarrhea, bloating, and flatulence.
A large dose of the milk sugar lactose--for example, the 50-g load in 1 liter of milk--causes symptoms in the majority of people with lactose malabsorption. It is uncertain whether the ingestion of more common doses of lactose, such as the amount in 240 ml (8 oz) of milk, causes symptoms..
The ability to digest lactose was assessed by measuring the subjects' end-alveolar hydrogen concentration after 15 g of lactose in 250 ml of water. Subjects then received either 240 ml of lactose-hydrolyzed milk containing 2 percent fat or 240 ml of milk containing 2 percent fat and sweetened with aspartame to approximate the taste of lactose-hydrolyzed milk; each type of milk was administered daily with breakfast for a one-week period.
Twenty-one participants were classified as having lactose malabsorption and nine as being able to absorb lactose. During the study periods, gastrointestinal symptoms were minimal (mean symptom-severity scores for bloating, abdominal pain, diarrhea, and flatus between 0.1 and 1.2 [1 indicated trivial symptoms; and 2, mild symptoms]).
People who identify themselves as severely lactose-intolerant may mistakenly attribute a variety of abdominal symptoms to lactose intolerance. When lactose intake is limited to the equivalent of 240 ml of milk or less a day, symptoms are likely to be negligible and the use of lactose-digestive aids unnecessary.
Suarez-FL: A comparison of symptoms after the consumption of milk or lactose-hydrolyzed milk by people with self-reported severe lactose intolerance [see comments]. N-Engl-J-Med. 1995 Jul 6; 333(1): 1-4.
This study examined whether small doses of lactose induced symptoms in 39 lactose maldigesters and 15 lactose digesters in a randomized, crossover, double-blind design. The test doses were 200 mL fat-free, lactose-free milk to which 0, 0.5, 1.5, and 7 g lactose was added.
During the study, the maldigesters reported significantly more abdominal bloating (P = 0.0003) and abdominal pain (P = 0.006) than the digesters. There was no difference in the mean severity of the reported symptoms between the test milks and the lactose-free milk in the group of lactose maldigesters, of whom one-third did not experience any symptoms from any of the test doses. The same proportion (64%) of the maldigesters experienced symptoms after both the lactose-free milk and the milk with 7 g lactose. However, the symptoms occurred inconsistently with the different test doses in 59% of the maldigesters.
The gastrointestinal symptoms in most lactose maldigesters are not induced by lactose when small amounts (0.5-7.0 g) of lactose are included in the diet.
Vesa-TH: Tolerance to small amounts of lactose in lactose maldigesters. American-Journal-of-Clinical-Nutrition (AM-J-CLIN-NUTR) 1996 Aug; 64(2): 197-201 (14 ref).
Lactose maldigestion in children
Lactose hydrogen breath testing was performed after challenge with 1 g/kg lactose 10% aqueous solution).
Lactose maldigestion was detected in 33/137 patients (24%). The perception and prevalence of abdominal pain, bloating, gas, flatulence, diarrhea, and constipation was similar in children with or without lactose maldigestion.
No other clinical parameter predicted lactose maldigestion. However, children with lactose maldigestion improved clinically with a lactose-restricted diet. Clinical evaluation alone cannot identify lactose maldigestion in children.
Consider formal evaluation for lactose maldigestion (using breath hydrogen testing) in children with recurrent abdominal pain.
Webster-RB et al: Lactose maldigestion and recurrent abdominal pain in children. Dig-Dis-Sci. 1995 Jul; 40(7): 1506-10.
Small bowel motility disorders
Small bowel motility disorders may result in prolonged or accelerated transit and present clinically with such symptoms as nausea, vomiting, bloating, pain or altered bowel movements.
These disorders result from derangements of neuromuscular control affecting extrinsic nerves, enteric plexuses or smooth muscle, or from structural disorders that may be congenital or acquired.
Management of stasis syndromes is based on restoration of good nutrition, treatment of bacterial overgrowth, prokinetic agents, antiemetics and surgery for localized disease. Patients with fast transit disorders require opioid agonists and, rarely, second-line treatments such as verapamil, clonidine or octreotide.
Camilleri-M: Small bowel motility disorders. Rev-Gastroenterol-Mex. 1994 Apr-Jun; 59(2): 120-6.
To determine whether sodium balance affects expression of menstrual symptoms.
During the luteal phase of the sodium restriction cycle, significant decreases in plasma sodium levels of 1.23 +/- 0.5 mmol/L (from values of 138.8 mmol/L during the follicular phase) and increases in urinary sodium excretion of 27.2 +/- 10 mmol/d (from values of 65.5 mmol/d during the follicular phase) preceded periods when menstrual symptoms were most severe.
Ratings of breast tenderness increased sixfold to eightfold in the late luteal phase and those of swelling or bloating increased twofold to threefold during early menses compared with nadir symptom ratings during each cycle. Sodium cravings increased in the luteal phase of all cycles but were not accompanied by increased sodium intake when access to added salt was allowed.
Breast tenderness and bloating did not result from sodium retention in the luteal phase of the menstrual cycle. During normal and sodium-restricted diet cycles, women actually had urinary sodium loss, not retention , during the luteal phase; severity of menstrual symptoms was unchanged.
Olson, BR et al: Relation between sodium balance and menstrual cycle symptoms in normal women. Ann Intern Med 1996 Oct 1;125(7):564-7.
Normal, healthy, free-living adults ingested either 18 g/d olestra, with or without 1.1 mg tocopheryl acetate/g olestra, or 18 g/d triglyceride placebo, for 16 wk in a double-blind, placebo-controlled study.
Addition of tocopheryl acetate to olestra partially offset the effect of olestra. For the group given 18 g/d olestra plus 1.1 mg tocopheryl acetate/g olestra, serum alpha-tocopherol concentration was 4% less than the placebo value. Olestra reduced serum concentration of beta-carotene by 27%; the other carotenoids were similarly affected.
Clinical observations and laboratory measures indicated no health-related effects of olestra; mild-to-moderate transient gastrointestinal symptoms such as bloating, cramping, loose stools and diarrhea were reported by all groups.
Koonsvitsky BP et al., Olestra affects serum concentrations of alpha-tocopherol and carotenoids but not vitamin D or vitamin K status in free-living subjects. J Nutr, 1997 Aug, 127:8 Suppl, 1636S-1645S.
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