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J Med Genet. 1994 Aug;31(8):602-6. ["OMIM","window.top.location='Laxative online source: www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=pubmed_omim&from_uid=7815416'","",""],
Long segment and short segment familial Hirschsprung's disease: variable clinical expression at the RET locus.

Edery P, Pelet A, Mulligan LM, Abel L, Attie T, Dow E, Bonneau D, David A, Flintoff W, Jan D, et al.

Service de Genetique Medicale, Enfant INSERM U-393, Paris, France.

Hirschsprung's disease (aganglionic megacolon, HSCR) is a frequent condition of unknown origin (1/5000 live births) resulting in intestinal obstruction in neonates and severe constipation in infants and adults. In the majority of cases (80%), the aganglionic tract involves the rectum and the sigmoid colon only (short segment HSCR), while in 20% of cases it extends toward the proximal end of the colon (long segment HSCR). In a previous study, we mapped a gene for long segment familial HSCR to the proximal long arm of chromosome 10 (10q11.2). Further linkage analyses in familial HSCR have suggested tight linkage of the disease gene to the RET protoncogene mapped to chromosome 10q11.2. Recently, nonsense and missense mutations of RET have been identified in HSCR patients. However, the question of whether mutations of the RET gene account for both long segment and short segment familial HSCR remained unanswered. We have performed genetic linkage analyses in 11 long segment HSCR families and eight short segment HSCR families using microsatellite DNA markers of chromosome 10q. In both anatomical forms, tight pairwise linkage with no recombinant events was observed between the RET proto-oncogene locus and the disease locus (Zmax = 2.16 and Zmax = 5.38 for short segment and long segment HSCR respectively at 0 = 0%) Multipoint linkage analyses performed in the two groups showed that the maximum likelihood estimate was at the RET locus. Moreover, we show that point mutations of the RET proto-oncogene occur either in long segment or in short segment HSCR families and we provide evidence for incomplete penetrance of the disease causing mutation. These data suggest that the two anatomical f

Gastroenterology. 1995 Feb;108(2):350-9.
Hyperglycemia inhibits mechanoreceptor-mediated gastrocolonic responses and colonic peristaltic reflexes in healthy humans.

Sims MA, Hasler WL, Chey WD, Kim MS, Owyang C.

Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor.

BACKGROUND/AIMS: The effects of hyperglycemia on colonic motor function are unknown. Therefore, colonic neuromuscular function was tested in normal volunteers as a model for constipation in diabetes. METHODS: Extended (gastrocolonic response) and local (peristaltic reflex) neural responses and colonic muscle contractility were tested under control, hyperglycemic clamp, and euglycemic, hyperinsulinemic clamp conditions with placement of barostat-regulated balloons in the descending colon to measure changes in tone as differences in balloon volume. RESULTS: Hyperglycemic clamping to 274 +/- 3 mg/dL blunted increases in colon tone evoked by gastric distention (gastrocolonic response) (100-300 mL) but did not affect gastric tone. Three descending colonic balloons in series assessed the peristaltic reflex. Inflation of the middle stimulus balloon increased proximal tone, an increase that was blunted by hyperglycemia, but produced distal relaxation followed by increases in tone that were unaffected by hyperglycemia. Euglycemic, hyperinsulinemic clamping had no effect on the gastrocolonic response or peristaltic reflex. Tonic increases evoked by bethanechol (5 mg administered subcutaneously) were unaffected by hyperglycemic clamping. CONCLUSIONS: Hyperglycemia blunts mechanoreceptor-mediated gastrocolonic responses and ascending contractions but not descending components of the peristaltic reflex in humans, effects not caused by hyperinsulinemia or direct muscle actions. These inhibitory effects on long and short neural reflexes that modulate colonic motility may contribute to constipation in diabetes.

Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7835576&dopt=Abstract constipation laxative colon cleansing

Dis Colon Rectum. 1995 Feb;38(2):166-71.
Pudendal neuropathy in evacuatory disorders.

Vaccaro CA, Cheong DM, Wexner SD, Nogueras JJ, Salanga VD, Hanson MR, Phillips RC.

Department of Colorectal Surgery, Cleveland Clinic Florida, Fort Lauderdale.

PURPOSE: Aims of the present study were to assess frequency of pudendal neuropathy in patients with constipation and fecal incontinence, to determine its correlation with clinical variables, anal electromyographic assessment, and anal manometric pressures, and to determine usefulness of the pudendal nerve terminal motor latency assessment in evaluation of these evacuatory disorders. METHODS: From 1988 to 1993, 395 patients (constipated, 172; incontinent, 223) underwent pudendal nerve terminal motor latency, electromyography, and anal manometry. Pudendal neuropathy was defined as a pudendal nerve terminal motor latency greater than 2.2 ms. RESULTS: Patients were a mean age of 60.7 (range, 17-88) years. Overall incidence of pudendal neuropathy was 31.4 percent (constipated, 23.8 percent; incontinent, 37.2 percent; P < 0.05). Incidence of pudendal neuropathy dramatically increased after 70 years of age in both groups (22 percent vs. 44 percent; P < 0.05). Moreover, subjects with pudendal neuropathy were older than those without pudendal neuropathy (mean age, 67 vs. 57 years; P < 0.05). The presence of pudendal neuropathy was associated with decreased motor unit potentials recruitment in patients with incontinence (P < 0.01). Patients with and without pudendal neuropathy had a similar mean squeezing pressure in both groups. CONCLUSION: Pudendal neuropathy is an age-related phenomenon. Although pudendal neuropathy is associated with abnormal anal electromyographic findings in patients with incontinence, no association with anal manometric pressures was found. Pudendal nerve terminal motor latency assessment is a useful tool in the evaluation of patients with fecal incontinence, but its role in the assessment of constipated patients remains unk

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