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Alcohol-Related Diarrhea
Abstract
Diarrhea related to alcohol abuse may be either acute or chronic. Acute diarrheas are the result of dietary indiscretion,
transient anatomic or motility changes of the stomach or small intestine, impaired nutrient absorption, mucosal barrier function
or pancreatic secretion as well as hormonal/cytokine abnormalities related to alcohol hangover. Chronic diarrheas may result
from alcohol withdrawal, pancreatic or hepatobiliary dysfunction, morphologic or motility changes of the gastrointestinal
tract, or macro- or micronutrient malabsorption with resulting deficiencies. Treatment of acute alcohol-related diarrhea includes
ceasing alcohol ingestion, avoiding milk products, rehydration, and replacement of micronutrients, and use of antidiarrheals
and NSAIDS. In addition to the above, treatment of chronic alcohol-related diarrheas includes assessing and treating for alcohol
withdrawal, nutritional deficiencies, pancreatic or hepatobiliary dysfunction, as well as diagnosing and treating small bowel
bacterial overgrowth.
Key WordsAlcohol-Ethanol-Diarrhea-Intestinal permeability-Endotoxin-Pancreatic insufficiency-Bile salt-Malabsorption-Bacterial overgrowth-Steatorrhea
... It was hypothesized that opioid use might have played a moderating role between alcohol use and compensatory behaviors because of the constipating effect of opioids (Bruera et al., 1994) and the laxative effects of alcohol. Specifically, moderate-to-heavy alcohol use can have a concomitant diuretic and laxative effect (Reddy, Singal, & Powell, 2010) and opioids can conversely have a constipating effect (Camilleri, et al., 2014). Operating under the assumption that individuals would engage in compensatory behaviors including the use of laxatives and diuretics, it was hypothesized that opioid use might have been used to better regulate any exacerbated gastrointestinal effects incurred from simultaneous supplement and alcohol use. ...
Objectives: To estimate the prevalence of compensatory eating behaviors in relation to alcohol consumption in a clinical sample, to assess the moderating capabilities of opioid use in relation to alcohol use and compensatory behaviors, and to examine the predictive capabilities of gender-specific binge drinking in relation to compensatory behaviors.Methods: The Compensatory Eating Behaviors in Relation to Alcohol Consumption Scale (CEBRACS), an opioid use survey, and the Alcohol Use Disorders Identification Test (AUDIT) were administered to residents at an addiction treatment facility (n = 77) over a period of 6 months.Results: Morphine was the only opioid to have significant relationships with the CEBRACS alcohol effects (r = - .33), diet/exercise (r = - .38), and restrictive eating (r = - .31), subscales (all p < .001), but not with the bulimic subscale. Heroin had the strongest correlations with all other opioids. Opioid use did not have a significant moderating effect between alcohol frequency and the CEBRACS in a single moderating regression analysis (b = .84, t(73) = .43, p = .67). Men (Mdn = 27.00) and women (Mdn = 33.00) did not differ on the CEBRACS, although women ranked higher than men (U = 678.00, z = - .68, ns, r = .08). Binge drinking predicted CEBRACS scores in both males (b = .50, t(38) = 3.59, p < .001) and females (b = .60, t(35) = 4.46, p < .001).Conclusions: Individual dietary habits fluctuate throughout alcohol consumption and the goals of the individual are crucial in discerning specific substance use vs disordered eating motivations.
Alcohol has pervasive effects on the gastrointestinal tract and pancreas, ranging from subtle microscopic changes to devastating clinical sequelae. As the portal of entry into the body, the digestive tract is vulnerable to the effects of alcohol. The effect of alcohol on the pancreas is mediated by less direct mechanisms. The association between alcohol and liver disease is discussed in Chapter 14 and that with gastrointestinal cancer is discussed in Chapter 18.
Background
The effectiveness acamprosate (calcium bisacetylhomotaurinate) as a treatment to maintain abstinence in alcohol-dependent patients was assessed for 1 year.Methods:
After short-term detoxification, 272 patients participated in a randomized, double-blind, placebo-controlled study. Patients received routine counseling and either the study medication or placebo for 48 weeks; they were followed up for another 48 weeks without medication. Statistical analysis was performed according to the intention-to-treat principle.Results:
Patients who were receiving acamprosate showed a significantly higher continuous abstinence rate within the first 60 days of treatment compared with patients who were assigned to placebo treatment (67% vs 50%) until completion of the treatment period (43% vs 21%, log rank P=.005), and they had a significantly longer mean abstinence duration of 224 vs 163 days, or 62% vs 45% days abstinent (P<.001); however, there was no difference in psychiatric symptoms. Of the patients who were receiving acamprosate, 41% had dropped out, whereas 60% of the placebo-treated patients dropped out of the study. Few side effects (mainly diarrhea and headache) were recorded. At the end of a further 48 weeks without receiving study medication, 39% and 17% of the acamprosate- and placebo-treated patients, respectively, had remained abstinent (P=.003).Conclusion:
Acamprosate proved to be a safe and effective aid in treating alcohol-dependent patients and in maintaining the abstinence of patients during 2 years.
Lactoferrin is a glycoprotein expressed by activated neutrophils. The aim of this study was to determine the sensitivity and specificity of fecal lactoferrin concentrations for inflammatory bowel disease (IBD) or irritable bowel syndrome (IBS) versus healthy controls.Methods
Fresh stool samples were collected from outpatients with ulcerative colitis (UC), Crohn’s disease (CD), or IBS. Clinical disease activity for IBD was assessed using a modified Harvey–Bradshaw Activity Index. Fecal lactoferrin concentrations were determined using a polyclonal antibody-based enzyme linked immunoassay. Mean fecal lactoferrin concentrations for each group and sensitivity and specificity of the assay were determined.ResultsOne hundred-four CD patients, 80 UC patients, 31 IBS patients, and 56 healthy controls were recruited. The mean ± SE fecal lactoferrin concentration (μg/g fecal weight) was 440 ± 128 for CD patients, 1125 ± 498 for UC patients, 1.27 ± 0.29 for IBS patients, and 1.45 ± 0.4 for healthy controls. Fecal lactoferrin was 90% specific for identifying inflammation in patients with active IBD. Elevated fecal lactoferrin was 100% specific in ruling out IBS.Conclusions
Fecal lactoferrin is sensitive and specific for detecting inflammation in chronic IBD. This noninvasive test may prove useful in screening for inflammation in patients presenting with abdominal pain and diarrhea.
Despite the ease in inducing hangover, only a few trials have studied treatment of hangover symptoms. Bogin and coworkers (10) compared propranolol with placebo but found no effect. In their crossover study, 10 healthy college students drank enough alcohol to reach a blood alcohol level of at least 0.1 g/dL. On the night the alcohol was consumed, 5 of the students received a long-acting oral preparation of 160 mg of propranolol; the remaining students received placebo. The study was repeated on a second occasion with a switch in treatment assignment. The morning after each night of alcohol consumption, researchers assessed the vital signs of each participant and calculated a score on a hangover severity scale. Objective analysis of hand tremor, blood pressure, and cardiac rate and rhythm showed no significant differences. On a scale of 1 to 5, the mean (±SD) severity of hangover was 2.9 ± 1.1 in participants who received propranolol and 2.8 ± 0.9 in those who received placebo (CI for the mean difference, −0.84 to 1.04). The authors concluded that propranolol does not produce a clinically important benefit in the symptoms of hangover. However, the study's power was only 50% for the hypothesized primary finding, at a two-sided α value of 0.05 (10).
Two trials have investigated the effect of simple carbohydrates on hangover severity. Seppala and colleagues (29) assigned 40 healthy men to receive one of six treatments. Participants received 1.75 g/kg of alcohol from 6:00 p.m. to 9:00 p.m. and an oral glucose or fructose solution (0.5 g/kg or 1 g/kg). The participants in the two control groups received alcohol or glucose but not both. All patients subjectively assessed their hangover severity and underwent psychomotor tests that determined reaction time, coordination, and attention span. Administration of glucose at the time of alcohol ingestion reduced mistakes by 50% on the choice reaction test (which was given 15 hours later) but slightly increased mistakes on the coordination test. Hangover severity was not affected. The study was limited by the small number of participants (n = 5) in each treatment group. Moreover, the statistical analysis did not account for multiple comparisons. Ylikahri and coworkers (37) used a similar design to study 109 healthy men (1.75 g/kg of alcohol administered orally over 3 hours, followed by 1 g/kg of oral glucose or fructose). Patients who received glucose or fructose had lower serum levels of free fatty acids and ketones but no change in subjective or objective hangover symptoms.
The effects in vivo of a biguanide (Metformin) on intestinal enzyme activities and vitamin B12 and folic acid absorption can be summarized as follows. 1. The enzyme activities of the brush border of the mucosal cell of the upper intestine were influenced. 2. The disaccharidase activities were reduced, although not to such an extent as to be expected to impair disaccharide absorption. 3. Vitamin B12 absorption was significantly reduced, as measured by Schilling test. 4. Serum folic acid levels were significantly reduced, possibly due to a decreased intestinal absorption of dietary folic acid.
The relationship between celiac disease and many autoimmune disorders has been explained by the sharing of a common genetic factor. In a multicenter national study, we examined the relationship between the prevalence of autoimmune disorders in celiac disease and the duration of exposure to gluten.
Over a 6-month period, 909 patients with celiac disease (group A; mean age, 16.1 +/- 3.8 years; grouped according to age at diagnosis into three subgroups [group A1, <2 years; group A2, 2-10 years; and group A3, >10 years]), 1268 healthy controls (group B; mean age, 20.8 +/- 4.5 years), and 163 patients with Crohn's disease (group C; mean age, 28.8 +/- 10 years) were evaluated for the presence of autoimmune disorders.
Prevalence of autoimmune disorders in group A was significantly higher than in group B (14% vs. 2.8%; P < 0.000001) but not higher than in group C (12.9%). Prevalence of autoimmune disorders in celiac disease increased with increasing age at diagnosis: 5.1% in group A1, 17% in group A2, and 23.6% in group A3 (P = 0.000001). In group A3, the prevalence of autoimmune disorders was significantly higher than in group C. In a logistic regression model, age at diagnosis was the only significant predictor variable of the odds of developing an autoimmune disorder (r = 0.3; P < 0.000001).
Our data show for the first time that the prevalence of autoimmune disorders in celiac disease is related to the duration of exposure to gluten.