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Medical therapy for anal fissure is designed to relax the internal anal sphincter, much as is done by sphincterotomy, but reversibly, and thus avoiding long standing minor incontinence. The effectiveness and future of this approach is assessed. Publications were sought in Medline using the search terms: anal fissure randomized, and all articles screened for inclusion. Randomized controlled trials that had at least one arm involving medical therapy for anal fissure were chosen, as were systematic Cochrane reviews of these articles and the quantitative assessment of therapeutic effectiveness reported. In addition, the newer therapies being developed are listed, most of which have not yet been subjected to randomized trials, so their effectiveness is unknown. Lastly, the major problems still facing medical therapy for anal fissure are listed in hope that trials will be conducted that will specifically address these questions. Currently medical therapy for anal fissure is effective in achieving long term cure, whether glyceryl trinitrate ointment, botulinum toxin injection, or calcium channel blockers given orally or topically, but only marginally so. They are far less effective than surgery.

Purpose: To determine factors associated with the development of urinary and fecal incontinence in nursing homes. Design and methods: Residents of Wisconsin skilled nursing facilities reported in the Wisconsin annual nursing home survey continent to both urine and stool in 1992 were re-assessed 1 year later for the development of urinary and/or fecal incontinence. Independent variables were elements of the HCFA minimum data set found to be significantly associated with incontinence in cross-sectional surveys of Wisconsin nursing home residents. Results: Dementia and advancing age were consistently associated with the development of incontinence, but the strongest associations were impairment of activities of daily living and the use of patient restraints. Implication: Adjusting for the major reasons to apply patient restraint: dementia, blindness, arthritis and stroke, along with other risk factors for incontinence, the use of patient restraints is the most significant cause for the development of incontinence in nursing homes.

Nursing home residence is by far the most prominent association with fecal incontinence, with a prevalence approaching 50%. In one major survey, urinary incontinence was the greatest risk factor for developing fecal incontinence, and fecal incontinence was the greatest risk factor for developing urinary incontinence. Immobility, dementia, and the use of physical restraints were also important risk factors. Specific diseases associated with fecal incontinence include diabetes, multiple sclerosis, Parkinson's disease, stroke, and spinal cord injury. The surgical procedures lateral internal sphincterotomy for anal fissure, fistulotomy, and ileal pouch reconstruction can result in fecal incontinence. Children who are born with congenital abnormalities, such as imperforate anus, often experience soiling for many years. Future studies to determine the prevalence and etiology of fecal and urinary incontinence will need to first define these conditions and eliminate referral bias. Epidemiologic investigations of both disorders should be performed jointly because the conditions are so often comorbid.

PURPOSE: Primary repair of penetrating colon injuries is an appealing management option; however, uncertainty about its safety persists. This study was conducted to compare the morbidity and mortality of primary repair with fecal diversion in the management of penetrating colon injuries by use of a meta-analysis of randomized, prospective trials. METHODS: We searched for prospective, randomized trials in MEDLINE (1966 to November 2001), the Cochrane Library, and EMBase using the terms colon, penetrating, injury, colostomy, prospective, and randomized. Studies were included if they were randomized, controlled trials that compared the outcomes of primary repair with fecal diversion in the management of penetrating colon injuries. Five studies were included. Reviewers performed data extraction independently. Outcomes evaluated from each trial included mortality, total complications, infectious complications, intra-abdominal infections, wound complications, penetrating abdominal trauma index, and length of stay. Peto odds ratios for combined effect were calculated with a 95 percent confidence interval for each outcome. Heterogeneity was also assessed for each outcome. RESULTS: The penetrating abdominal trauma index of included subjects did not differ significantly between studies. Mortality was not significantly different between groups (odds ratio, 1.70; 95 percent confidence interval, 0.51–5.66). However, total complications (odds ratio, 0.28; 95 percent confidence interval, 0.18–0.42), total infectious complications (odds ratio, 0.41; 95 percent confidence interval, 0.27–0.63), abdominal infections including dehiscence (odds ratio, 0.59; 95 percent confidence interval, 0.38–0.94), abdominal infections excluding dehiscence (odds ratio, 0.52; 95 percent confidence interval, 0.31–0.86), wound complications including dehiscence (odds ratio, 0.55; 95 percent confidence interval, 0.34–0.89), and wound complications excluding dehiscence (odds ratio, 0.43; 95 percent confidence interval, 0.25–0.76) all significantly favored primary repair. CONCLUSION: Meta-analysis of currently published randomized, controlled trials favors primary repair over fecal diversion for penetrating colon injuries.

Background Selenium (SE) has been inversely associated with colon cancer risk. Two potential mechanisms of this effect were examined in a rodent short-term carcinogenesis assay: whether dietary SE deficiency altered the initiation aspect of carcinogenesis in the colon, and whether SE altered carcinogen metabolism. Setting Animal laboratory. Subjects 52 Sprague-Dawley rats, divided into a SE diet deficient group (0.002 parts per million; ppm) and a SE sufficient (0.2 ppm) group. Endpoints Weight, serum SE concentration, and karryorhectic index (Kl), which is a measure of acute carcinogen induced nuclear toxicity in the colonic mucosa. Methods After three weeks of acclimation to the diets, eight animals from each dietary group were injected with one of the following: dimethylhydrazine (DMH), a colon specific carcinogen, its metabolite, methylazoxymethanol (MAM), or 0.9% sodium chloride. Twenty-four hours after injection the colons were removed, blood drawn, and the stained colons assayed for nuclear aberrations. Results No weight differences were generated by the dietary variations. Low-dietary SE resulted in serum SE declining markedly in the study period to 6 ng/ml versus 33 ng/ml in the SE sufficient group. Diet alone, and variations in weight gain, did not alter the Kl. Both carcinogens greatly increased the Kl in both the left and right colon. A SE-deficient diet was associated with a higher Kl in both carcinogen groups in the right colon, with statistical significance for both the left and right colon in the MAM injection group. Conclusions Dietary SE deficiency is associated with increased Kl of the colon in MAM treated rats. SE, therefore, has a protective effect in the initiation phase of carcinogenesis.

Screening of the average-risk individual for disease creates a different relationship between practitioner and subject than the normal doctor-patient relationship. Screened individuals are asymptomatic, have a whole range of motivations from denial to neurosis, and, for the most part, derive no benefit from the screen, as they are destined never to contract the disease. Rewards to the few must clearly outweigh the risks to the many. The screening strategy must be economical when applied to a large population, safe, and effective in achieving the ultimate goal, which, in the case of colorectal cancer, is reduction in the mortality rate. Prediagnostic screening of asymptomatic adults over the age of 45 years for primary disease has been shown to fulfill all of these criteria. Postoperative screening of asymptomatic individuals after curative resection of colorectal cancer for recurrence has been shown to fulfill none of them.

Intestinal exposure to ingested iron may be a principal determinant of human colorectal cancer risk. Evidence exists associating iron with both the initiating and promoting phases of carcinogenesis as well as somatic defenses against early cancers through hypoferremia (progression or proliferation). Iron intake and the ingestion of associated foods that greatly affect iron bioavailability and absorption (phytate, tannin, ascorbate, and alcohol) vary widely between high-risk and low-risk countries as well as within the United States. These variances in intake may explain not only the gradients in risk between populations, but the crossover in risk between sexes related to age within the United States. Human and rodent studies support the above hypothesis and are reviewed herein, however they are few in number and in many cases lack key data.

PURPOSE: This study investigated the relationship between bone mineral density (BMD) and mortality in men using data from the NHANES I Epidemiologic Follow-up Study, which tracked participants from enrollment in 1971–1974 through 1992. METHODS: This analysis included 1,130 men aged 50–74 when first contacted for NHANES I in 1971–1974 who had baseline BMD measurements as part of their first NHANES visit. Mortality rates were calculated by age-adjusted quartile of BMD. RESULTS: Tests for trend showed that lower baseline BMD was significantly associated with total (p CONCLUSIONS: We conclude that low BMD appears to be a marker for cardiac and cancer mortality; delineation of the causal pathway awaits further studies.

A case of hypoglycemic coma and benign pleural mesothelioma is described. Serum insulin levels, as measured by insulin radioimmunoassay, were appropriately suppressed and consistent with hypoglycemia. Assay of the tumor showed insulin to be undectable. The mechanisms for hypoglycemia probably included increased glucose consumption by the tumor and, more important, the inhibition of lipolysis and hepatic gluconegenesis caused by tumor release of L-tryptophan and its metabolites and/or possibly nonsuppressible insulin-like activity, soluble in acid-ethanol(NSILA-s).

Summary A case of congenital cystic lung disease with the clinical, roentgenologic and pathologic findings of partial bronchial obstruction is reported. A brief description of the findings in the disease is given, and a possible explanation for the symptoms offered.