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Biomedical subjects

J S Fordtran

Publications and source records attributed to J S Fordtran.

At least 19 recordsLinked to original sources
PubMed1992

The self-limited nature of chronic idiopathic diarrhea.

BACKGROUND: Little is known about the clinical presentation and natural history of previously healthy patients in whom chronic idiopathic diarrhea develops. METHODS: We reviewed the case records of 152 patients with chronic diarrhea who had no history of gastrointestinal surgery and who were evaluated in detail as part of a chronic-diarrhea protocol from 1985 to 1990. Patients were considered to have chronic idiopathic diarrhea if they had persistently loose stools for more than four weeks, no systemic illness, and no identifiable cause of diarrhea. RESULTS: Seventeen patients (10 men and 7 women) ranging in age from 33 to 72 years met the criteria for chronic idiopathic diarrhea. Each patient had a history of a relatively abrupt onset of symptoms, often soon after returning home from a trip, starting two to seven months before evaluation. Their diarrhea did not occur during a local outbreak of diarrhea, and other family members did not become ill. Stool frequency ranged from 5 to 25 movements per day, stool weights ranged from 417 to 1480 g per day, and fecal electrolyte and osmolality values were consistent with a diagnosis of secretory diarrhea. The results of biopsies of the small intestine and colon were normal, as were small-bowel roentgenograms. Extensive studies for infectious causes of diarrhea were negative, and no patient responded to antibiotic therapy. In every patient the diarrhea stopped without specific therapy after 7 to 31 months (mean, 15) and did not recur during a follow-up period averaging 38 months. CONCLUSIONS: Sporadic idiopathic chronic diarrhea is a recognizable syndrome that can last many months, but is self-limited.

Adult↗
PubMed1992

Treatment of severe steatorrhea with ox bile in an ileectomy patient with residual colon.

Patients with ileectomy can present with severe steatorrhea due to bile acid depletion. While exogenous bile acid would seem to be ideal therapy for this condition, it is not often used because it is thought that the bile acid would be malabsorbed and would enter the colon, producing a secretory diarrhea. This report describes a patient who had an ileectomy and partial right colon resection for Crohn's disease and then developed severe steatorrhea due to bile acid malabsorption. Although steatorrhea was reduced from 134 to 9 g/24 hr with chronic ingestion of ox bile extract, stool weight did not increase with ox bile (stool weight 669 g/24 hr before therapy and 507 g/24 hr after therapy). In this patient, oral bile acid supplementation reduced fat excretion markedly, but did not aggravate diarrhea, even though the colon was still present. This result may have been due to impaired solubility of bile acid in fecal fluid due to an acid pH or to binding of bile acid with particles of solid stool. Ingestion of ox bile extract does not necessarily increase stool weight in patients with defective fat absorption due to bile acid malabsorption and can be tried with caution in an effort to diminish steatorrhea.

Aged↗
PubMed1992

The effect of diarrhea on fecal fat excretion.

To determine whether diarrhea increases fecal fat excretion, fecal fat output was measured during three consecutive days in normal subjects and in normal subjects in whom diarrhea was purposefully induced. Mean fecal fat output in normal subjects was 3.4 g/day; the upper limit of normal was 6.4 g/day. Twenty-one percent of subjects with mild to moderate diarrhea (fecal weight 200-800 g/day) and 58% of subjects with severe diarrhea (fecal weight greater than 800 g/day) had fecal fat excretion above the upper limit of normal, with values as high as 13.6 g/day. It is concluded that (a) diarrhea itself can induce mild secondary steatorrhea, and (b) when the quantitative fecal fat test is used in patients with diarrhea, mild abnormalities (up to 14 g/day) are not specific for a primary defect in fat digestion or absorption, i.e., they may represent false-positive results.

Adult↗
PubMed1992

Fecal osmotic gap and pH in experimental diarrhea of various causes.

Although the osmotic gap of fecal fluid is often used to distinguish osmotic diarrhea from secretory diarrhea, there has never been a scientific evaluation of the validity of this concept. Similarly, although a low fecal fluid pH value is used to indicate that diarrhea is mediated by carbohydrate malabsorption, the validity of this method is unproven. Therefore, in the present study, diarrhea was induced in normal subjects by different mechanisms and fecal fluid osmotic gap (using an assumed fecal fluid osmolality of 290 mOsm/kg) and pH were measured. In secretory diarrhea caused by phenolphthalein, the osmotic gap was always less than 50 mOsm/kg, whereas in osmotic diarrhea caused by polyethylene glycol, magnesium hydroxide, lactulose, and sorbitol, the osmotic gap always exceeded 50 mOsm/kg. In osmotic diarrhea caused by sodium sulfate, the fecal fluid osmotic gap was less than 50 mOsm/kg, but phenolphthalein-induced secretory diarrhea could be distinguished from sodium sulfate-induced osmotic diarrhea by the fecal chloride concentration. When diarrhea was caused by carbohydrate malabsorption (lactulose or sorbitol), the fecal fluid pH was always less than 5.6 and usually less than 5.3; by contrast, other causes of diarrhea rarely caused a fecal pH as low as 5.6 and never caused a pH less than 5.3. It is concluded that measurement of fecal fluid osmotic gap and pH can distinguish various mechanisms of experimental diarrhea in normal subjects. The concepts on which these tests are based are therefore verified experimentally.

Adult↗
PubMed1992

Subepithelial collagen table thickness in colon specimens from patients with microscopic colitis and collagenous colitis.

Microscopic colitis and collagenous colitis are similar conditions that are differentiated by the presence or absence of subepithelial collagen table thickening. To better understand the relationship between these two disorders and the role of collagen table thickening in the pathogenesis of diarrhea, colonic mucosal biopsy specimens from 24 patients with microscopic or collagenous colitis and 9 control subjects were analyzed using a computer-assisted morphometric method to evaluate the average thickness of the subepithelial collagen table. The collagen table thickness in colitis patients taken together formed a multimodal rather than a unimodal distribution. There was no tendency for collagen table thickening to increase with age or with duration of symptoms. In general, the types and distribution of inflammatory cells were similar in patients with normal and thickened collagen tables. Stool weight correlated with lamina propria cellularity but not with collagen table thickening. The multimodal distribution of collagen table thickening and the lack of correlation with age, duration of symptoms, or inflammation suggest that microscopic colitis and collagenous colitis are discrete conditions, although the inflammatory changes in the two conditions are similar. Moreover, because stool weight correlates with lamina propria cellularity but not with collagen table thickening, diarrhea probably is caused by the inflammatory changes and not by collagen table thickening per se.

Adult↗
PubMed1991

Diagnosis of magnesium-induced diarrhea.

BACKGROUND: There is no specific method of diagnosing magnesium-induced diarrhea. Therefore, the frequency and clinical importance of diarrhea caused by magnesium are unknown. The purposes of this study were to establish a method for diagnosing magnesium-induced diarrhea and to apply it to patients with chronic diarrhea. METHODS: We measured fecal output of soluble magnesium and fecal magnesium concentration in 19 normal subjects with formed stools (15 collection periods), with non-magnesium-induced diarrhea (36 collection periods), and with diarrhea induced by magnesium hydroxide alone (11 collection periods) or in combination with phenolphthalein (3 collection periods), and in 359 patients with chronic diarrhea. RESULTS: The upper limits of fecal output of soluble magnesium and fecal magnesium concentration in normal subjects were 14.6 mmol per day and 45.2 mmol per liter, respectively. When normal subjects had diarrhea due to the ingestion of magnesium hydroxide alone or in combination with phenolphthalein, fecal magnesium output was always abnormally high. For each millimole increase in fecal magnesium output, fecal weight increased by approximately 7.3 g. The fecal magnesium concentration was very high when magnesium was the only cause of diarrhea but only moderately elevated when diarrhea was induced by magnesium hydroxide plus phenolphthalein. Biochemical and clinical evidence indicated that excessive ingestion of magnesium was an important cause of chronic diarrhea in 15 of the 359 patients with chronic diarrhea (4.2 percent), if not the only cause. CONCLUSIONS: Quantitative fecal analysis for soluble magnesium is an accurate method of diagnosing magnesium-induced diarrhea. Some patients with chronic diarrhea ingest excessive amounts of magnesium (in antacids or food supplements), and physicians may fail to discover this before embarking on an expensive and invasive diagnostic evaluation.

Adult↗
PubMed1991

Intestinal absorption of magnesium from food and supplements.

The purpose of this study was to measure magnesium absorption over the wide range of intakes to which the intestine may be exposed from food and/or magnesium-containing medications. Net magnesium absorption was measured in normal subjects after they ingested a standard meal supplemented with 0, 10, 20, 40, and 80 mEq of magnesium acetate. Although absorption increased with each increment in intake, fractional magnesium absorption fell progressively (from 65% at the lowest to 11% at the highest intake) so that absorption as a function of intake was curvilinear. This absorption-intake relationship was almost perfectly represented by an equation containing a hyperbolic function plus a linear function. Our results are statistically compatible with a magnesium absorption process that simultaneously uses a mechanism that reaches an absorptive maximum, plus a mechanism that endlessly absorbs a defined fraction (7%) of ingested magnesium. Compared to previous studies of calcium absorption, much less magnesium that calcium was absorbed at intakes above 8 mEq/meal, apparently due to greater restriction of intestinal permeability to magnesium. We also found that magnesium from a high magnesium-containing food source, almonds, was just as bioavailable as from soluble magnesium acetate. In contrast, magnesium absorption from commercially available enteric-coated magnesium chloride was much less than from magnesium acetate, suggesting that enteric coating can impair magnesium bioavailability.

Adult↗
PubMed1990

Comparison of endogenous and radiolabeled bile acid excretion in patients with idiopathic chronic diarrhea.

Fecal recovery of radioactivity after ingestion of a bolus of radiolabeled bile acid is abnormally high in most patients with idiopathic chronic diarrhea. To evaluate the significance of this malabsorption, concurrent fecal excretion of both exogenous radiolabeled bile acid and endogenous (unlabeled) bile acid were measured in patients with idiopathic chronic diarrhea. Subjects received a 2.5-microCi oral dose of taurocholic acid labeled with 14C in the 24th position of the steroid moiety. Endogenous bile acid excretion was measured by a hydroxysteroid dehydrogenase assay on a concurrent 72-h stool collection. Both radiolabeled and endogenous bile acid excretion were abnormally high in most patients with chronic diarrhea compared with normal subjects, even when equivoluminous diarrhea was induced in normal subjects by ingestion of osmotically active solutions. The correlation between radiolabeled and endogenous bile acid excretion was good. However, neither radiolabeled nor endogenous bile acid excretion was as abnormal as is typically seen in patients with ileal resection, and none of these diarrhea patients responded to treatment with cholestyramine with stool weights less than 200 g. These results suggest (a) that this radiolabeled bile acid excretion test accurately reflects excess endogenous bile acid excretion; (b) that excess endogenous bile acid excretion is not caused by diarrhea per se; (c) that spontaneously occurring idiopathic chronic diarrhea is often associated with increased endogenous bile acid excretion; and (d) that bile acid malabsorption is not likely to be the primary cause of diarrhea in most of these patients.

Adult↗
PubMed1990

Alpha 1-antitrypsin excretion in stool in normal subjects and in patients with gastrointestinal disorders.

Fecal clearance of plasma alpha 1-antitrypsin is used as a measure of protein leakage into the intestinal tract. In this study, the alpha 1-antitrypsin concentration in stool and the plasma clearance of alpha 1-antitrypsin in normal subjects and in a consecutive series of patients with chronic diarrhea, malabsorption, or unexplained hypoalbuminemia was determined. The normal subjects were studied in their usual state and also when they had diarrhea secondary to ingestion of lactulose, sorbitol, sodium sulfate, or phenolphthalein. The study first concluded that induced diarrhea can cause an increase in alpha 1-antitrypsin clearance; if this is not considered in establishing normal values, there may be an overdiagnosis of excess protein leakage in patients with diarrhea. Second, there is a highly significant statistical correlation (P less than 0.001) between alpha 1-antitrypsin clearance and serum albumin concentration. On average, the serum albumin falls below 3.0 g/dL (30 g/L) when the alpha 1-antitrypsin clearance exceeds 180 mL/day, a value that is about threefold higher than the upper limit of normal. Third, three of nine patients with microscopic/collagenous colitis had elevated clearance of alpha 1-antitrypsin; by contrast, abnormal alpha 1-antitrypsin clearance was not found in 23 patients with idiopathic secretory diarrhea. Fourth, fecal alpha 1-antitrypsin concentration is not a reliable index of abnormal alpha 1-antitrypsin clearance.

Adolescent↗
PubMed1990

A low-sodium solution for gastrointestinal lavage.

Golytely is a sodium sulfate-based solution used for lavage cleansing of the colon. Although most patients and physicians prefer Golytely lavage over other methods of bowel cleansing, its highly salty taste is a drawback. This report describes the development of a modified lavage solution that has a barely perceptible salty taste. This solution was developed by removing sodium sulfate, increasing the concentration of polyethylene glycol, and making minor adjustments in the concentration of other salts. Golytely, reduced sodium sulfate Golytely (Golytely-RSS), and a balanced electrolyte solution were infused into the stomachs of normal subjects. After steady-state lavage conditions were established, the rates of fluid and electrolyte absorption were measured. Average fluid absorption rate was 791 ml/h with the balanced electrolyte solution, compared with only 63 and 45 ml/h with Golytely and Golytely-RSS, respectively. Golytely-RSS was studied at 3 infusion rates, from 0.9-1.8 L/h, and the time and volume of solution required for colon cleansing was determined; the lower infusion rate (0.9 L/h) took longer but required less solution to cleanse the colon. In conclusion, Golytely-RSS has the essential feature of Golytely; i.e., lavage is associated with negligible salt and water absorption. The less-salty taste of Golytely-RSS may make it less difficult to drink and thereby enhance patient compliance; the total volume of solution required for cleansing is less when the solution is ingested at 0.9 L/h than when the ingestion rate is 1.8 L/h.

Colon↗
PubMed1990

Carbohydrate malabsorption. Its measurement and its contribution to diarrhea.

The major purpose of this research was to gain insight into the effect of carbohydrate malabsorption on fecal water output. To do this we measured daily fecal output of total carbohydrate, reducing sugars, and organic acids (a product of bacterial fermentation). Normal subjects were studied in their native state and when diarrhea was induced by mechanisms that did and did not involve carbohydrate malabsorption. Patients with malabsorption syndrome were also studied. We concluded that: (a) Excretion of carbohydrate and its breakdown products can be expressed as a single number by converting organic acids to their monosaccharide equivalents. (b) Diarrhea per se causes only a trivial increase in fecal carbohydrate excretion. (c) The molar output of osmotic moieties in feces due to unabsorbed carbohydrate can be determined by adding fecal reducing sugars to organic acids and their obligated cations. This expression parallels almost exactly the effect of increasing doses of lactulose (a nonabsorbable sugar) on fecal water output; one excreted millimole obligates 3.5 g of stool water. This relationship can be used to predict the effect of carbohydrate malabsorption on stool water output in patients with diarrhea. (d) 12 of 19 patients with malabsorption syndrome due to various diseases had excessive fecal excretion of carbohydrate and its breakdown products; of the diseases that cause malabsorption syndrome, combined small and large bowel resection is most likely to result in excessive fecal excretion of carbohydrate and monosaccharide equivalents. In 6 of these 19 patients carbohydrate malabsorption appeared to be the major cause of diarrhea.

Carbohydrate Metabolism↗
PubMed1990

In vivo intestinal absorption of calcium in humans.

We reviewed data on calcium absorption in humans, mainly focusing on concentrations of soluble calcium in the gut, kinetics of absorption, correlation of net absorption with serum 1,25-(OH)2-vitamin D, and adaptation to different intakes. We conclude: (a) most of the unabsorbed food calcium is insoluble when it reaches the terminal ileum; (b) calcium absorption in jejunum is both active and passive with active component being dependent on vitamin D; ileal absorption is also highly dependent on vitamin D, but it is uncertain whether this action is on the active or passive component; (c) the relative role of vitamin D-dependent and vitamin D-independent mechanisms to dietary calcium absorption depends upon serum 1,25-(OH)2-D level and calcium intake; (d) over short periods, the gut reduces calcium absorption much more in response to a high-calcium diet than it increases absorption in response to a low-calcium diet. We also evaluated the measurement of 'true' calcium absorption by isotopic methods. By ignoring isotopic equilibration, these methods overestimate both the amount of calcium secreted into and absorbed from the gut. Since altered gut physiology and pathology can variably affect isotopic equilibration, 'true' absorption may not reflect absorption of dietary calcium in an individual patient. Moreover, only net absorption has metabolic and nutritional significance.

Adaptation, Physiological↗
PubMed1989

Effect of the time of administration of calcium acetate on phosphorus binding.

Phosphorus binders are given to patients with renal failure to increase gastrointestinal excretion of phosphorus. To determine the relative importance of the binding of dietary as compared with endogenous phosphorus and to determine the optimal dose schedule, we gave either 4.4 g of calcium acetate (25 mmol of calcium) or a placebo to six normal subjects on each of seven different schedules in a randomized sequence. The net gastrointestinal balance of phosphorus and calcium was determined by a one-day lavage technique. After a meal containing approximately 12 mmol of phosphorus, the mean phosphorus absorption (+/- SE) measured 9.17 +/- 0.36 mmol (78 percent) with placebo but decreased to 3.81 +/- 0.58 mmol (31 percent) when calcium acetate was given immediately before the meal (representing binding of 5.36 +/- 0.77 mmol of phosphorus). Similar binding was observed when calcium acetate was given immediately after the meal and when half the dose was given before and half after the meal. In contrast, when calcium acetate was given two hours after the meal or while the subject was fasting, phosphorus binding was reduced to 2.00 +/- 0.52 mmol and 1.81 +/- 0.84 mmol, respectively. Calcium absorption from calcium acetate averaged 21 +/- 1 percent when the binder was given with a meal; absorption from calcium acetate averaged 40 +/- 4 percent when the binder was given while the subject was fasting. We conclude that calcium acetate increases fecal excretion of phosphorus by binding both dietary and endogenous phosphorus, but the binding of dietary phosphorus is quantitatively much more important. For the most efficient phosphorus binding, calcium (and presumably other phosphorus-binding cations) should be given with meals.

Acetates↗
PubMed1989

Loss of absorptive capacity for sodium chloride as a cause of diarrhea following partial ileal and right colon resection.

Previous studies have emphasized the role of bile acid and fat malabsorption as the cause of the diarrhea that may follow ileal and right colon resection; unabsorbed bile acids and fat are believed to reduce sodium chloride and water absorption in the remaining colon. In this paper we report studies in eight patients with severe postresection diarrhea, in search of a more basic defect in sodium chloride absorption, ie, a loss of sodium chloride absorptive capacity as a direct consequence of resection of sodium chloride absorption sites. First, we determined whether or not diarrhea persisted during a 48-hr fast; in all patients diarrhea and large fecal electrolyte losses continued during a fast. Second, we measured sodium chloride and water absorption rates during total gut perfusion with a balanced electrolyte solution; compared to normal controls, the patients absorbed 23-31% less water, sodium, and chloride. In three patients who could be studied further, the absorptive defect was markedly accentuated when the perfusing solution was such that sodium chloride absorption had to take place against a concentration gradient. These observations indicate that postresection diarrhea patients have a reduced capacity to absorb sodium chloride, particularly when there is a concentration gradient between lumen and plasma. Although all of these patients had malabsorption of radiolabeled taurocholic acid, there was only a modest and statistically insignificant reduction in daily stool weight during treatment with large doses of cholestyramine, suggesting that bile acid malabsorption was not responsible for a major part of their diarrhea.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Calcium acetate, an effective phosphorus binder in patients with renal failure.

Calcium salts are increasingly used as phosphorus binders in patients with chronic renal failure. Calcium carbonate is the principal salt presently utilized, however, other calcium salts may be more effective and safer phosphorus binders. Theoretical calculations, in vitro experiments, and in vivo studies in normal subjects have shown calcium acetate to be a more effective phosphorus binder than other calcium salts. This salt has not previously been studied in patients with chronic renal failure. We used a one-meal gastrointestinal balance technique to measure phosphorus absorption, calcium absorption and phosphorus binding in six patients with chronic renal failure. Calcium acetate was compared with calcium carbonate and placebo. Equivalent doses (50 mEq Ca++) of calcium acetate bound more than twice as much phosphorus (106 +/- 23 mg) as calcium carbonate (43 +/- 39 mg) P less than 0.05. When phosphorus binding was factored for calcium absorption, calcium acetate bound 0.44 mEq HPO4 =/mEq absorbed Ca++ compared with 0.16 mEq HPO4 = bound/mEq Ca++ absorbed with calcium carbonate. More efficient phosphorus binding permits serum phosphorus concentration to be controlled with lower doses of calcium salts. The higher phosphorus binding/calcium absorption ratio coupled with a lower dose indicates that less calcium will be absorbed when calcium acetate is used for phosphorus control. Markedly positive calcium balance, hypercalcemia and ectopic calcification should be less likely to occur with this drug than other calcium salts.

Acetates↗