Medicine

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Idiopathic pancreatitis: is it a consequence of an altering spectrum of bile nucleation time?
(BMJ Publishing, 2009) Abeysuriya, V.; Deen, K.I.; Navarathne, N.M.M; Kumarage, S.K.
INTRODUCTION: The pathogenesis of idiopathic pancreatitis (IP) remains poorly understood. Our hypothesis is that IP is a sequel of the microcrystallisation of hepatic bile. AIMS AND METHODS: A prospective case–control study compared 55 patients (symptomatic cholelithiasis, 30: 14 men, 16 women, median age 36 years, body mass index (BMI) 25.1 ¡ 0.33 kg/m2 ; gallstone pancreatitis, nine: six women, three men, median age 35 years, BMI 24.86 ¡ 0.23 kg/m2 ; and idiopathic pancreatitis, 16: seven women, nine men, median age 34 years, BMI 23.34 ¡ 0.2 kg/m2 ) with 30 controls (15 men, 15 women, median age 38 years, BMI 24.5 ¡ 0.23 kg/m2 , undergoing laparotomy and who had normal gallbladder and no demonstrable stones on ultrasonography). Ultrafiltered bile from the common hepatic duct in patients and controls was anaerobically incubated and examined by polarised light microscopy, for nucleation time (NT). Ethical approval was obtained. RESULTS: Patients were similar to controls. Mean NT in all groups of patients was significantly shorter than controls (established gallstones cumulative mean NT, 1.73 ¡ 0.2 vs controls, 12.74 ¡ 0.4 days vs, p = 0.001, t test and IP patients mean NT, 3.1 ¡ 0.24 days vs controls, 12.74 ¡ 0.4 days, p = 0.001, t test). However, NT in those with IP was significantly longer compared with those with established gallstones (mean NT in IP, 3.1 ¡ 0.24 SEM days, vs cumulative mean in patients with established symptomatic gallstones, 1.73 ¡ 0.2 days, p = 0.002, t test). CONCLUSION: NT in bile in patients with IP is abnormal and is intermediate in NT of lithogenic and non-lithogenic bile.
Anorectal physiology and transit in patients with disorders of thyroid metabolism
(Blackwell Scientific Publications, 1999) Deen, K.I.; Seneviratne, S.L.; de Silva, H.J.
BACKGROUND: Data on anorectal physiology in patients with disordered thyroid metabolism are lacking. This prospective study was performed to evaluate anorectal physiology in patients with either hyperthyroidism and diarrhoea, or hypothyroidism and constipation in order to assess slow transit in hypothyroid patients. METHODS: Thirty patients with hypothyroidism and constipation (24 females, median age 59 years, range 23-80) and 20 patients with hyperthyroidism and diarrhoea (12 females, median age 46 years, range 36-62) were evaluated by anal manometry, rectal balloon sensation and whole-gut transit markers. Data were compared with anorectal physiology and whole-gut transit in 22 healthy controls (13 females, median age 51 years, range 24-65). RESULTS: In the hypothyroid patients, maximum resting pressure (MRP) and maximum squeeze pressure (MSP) were similar to controls (patients, median MRP 55 mmHg (18-98); controls, median MRP 41 mmHg (20-105) and patients, median MSP 83 mmHg (39-400); controls, median MSP 88 mmHg (30-230); P 0.05 for both resting and squeeze pressures). In hyperthyroid patients, median MRP and MSP were significantly lower than controls (patients, MRP 33 mmHg (8-69); controls MRP 41 mmHg (20-105) P = 0.04 and patients, MSP 60 mmHg (26-104); controls, MSP 88 mmHg (30-230); P = 0.03). Threshold sensation for impending evacuation in hypothyroid patients was significantly higher than controls, while in hyperthyroid patients, threshold sensation was significantly lower compared with controls. Maximum tolerable rectal volumes in hypothyroid patients was significantly lower compared with controls, while no significant difference was found between maximum tolerable rectal volumes in hyperthyroid patients and controls. Prevalence of delayed whole-gut transit in both hypothyroid and hyperthyroid patients was similar to controls. Furthermore, 33 percent of hypothyroid patients and 40 percent of hyperthyroid patients experienced symptoms of bowel dysfunction prior to the onset of their thyroid disorder. CONCLUSIONS: Patients with altered thyroid function and bowel dysfunction demonstrated abnormalities of anal manometry and rectal sensation.
The Recto-anal inhibitory reflex: abnormal response in diabetics suggests an intrinsic neuroenteropathy
(Blackwell Scientific Publications, 1998) Deen, K.I.; Premaratna, R.; Fonseka, M.M.D.; de Silva, H.J.
As electrical stimulation of the rectum has been shown to result in reflex internal sphincter inhibition mediated by intrinsic nerves, we aimed to evaluate the integrity of these nerves in the rectum of diabetic patients. Anal canal pressure, recto-anal inhibitory reflex (RAIR) and continence were evaluated in 30 diabetic patients (male:female 13:17, median age 57 years, range 37-70) and these data were compared with similar data obtained from 22 age- and sex-matched healthy controls (male:female 9:13, median age 51 years, range 19-65 years). Median duration of diabetes was 8 years (range 3-30). Twelve (40 percent) of the 30 diabetics had impaired continence for gas (n = 12) and liquid faeces (n = 3). None of the controls had incontinence. Median maximum resting anal canal pressure (MRP) was: patients 30 mmHg (range 20-75 mmHg) versus controls 40 mmHg (range 20-105 mmHg, P = 0.61). Median maximum squeeze pressure (MSP) was 65 mmHg (range 30-150 mmHg) in patients versus 84mmHg (range 35-230 mm Hg) in controls (P = 0.59). Median threshold rectal mucosal electrosensation (RMES-T) was 27mA (5-40 mA) in patients versus 13 mA (5-28 mA) in controls (P = 0.03). Maximum tolerable rectal mucosal electrosensation was 40 mA (20-60) in patients versus 20 mA (10-30), in controls (P = 0.042, all comparisons using the Wilcoxon rank test). Recto-anal inhibitory reflex was present in eight, abnormal in five (one incontinent) and absent in 17 (11 incontinent) diabetics, while it was present in 18 and abnormal in four controls (test of proportion, P = 0.031). Blood glucose in diabetics on the day of the procedure was 98 mg/dL (70-165 mg/dL). Rectal mucosal electrosensitivity and RAIR were impaired in significantly more patients with diabetes than controls, implying impairment of intrinsic neuronal function. The recto-anal inhibitory reflex was either impaired or absent in all diabetic patients with incontinence.

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