Risk factors for stricture development after caustic ingestion.

BACKGROUND/AIMS: Stricture of the upper digestive tract is the most feared sequelae of caustic ingestion. Determinant risk factors for its development are not entirely known. The aim of this study was to investigate the risk factors associated with the development of fibrotic strictures induced by caustic ingestion. METHODOLOGY: Clinical, laboratory, radiological and endoscopic data from 48 patients admitted to our department for caustic ingestion were reviewed. All cases were submitted to emergency endoscopy and caustic lesions were graded according to Zargar's classification. Twenty-three patients with severe endoscopic lesions (grade IIb/grade III) and/or acute severe complications (gastrointestinal bleeding, respiratory failure) were admitted to an intensive care unit. After hospital discharge, all patients were followed-up (mean follow-up time: 4.1 +/- 1.8 years). RESULTS: Twelve patients (25%) developed caustic strictures. Four patients (8%) were submitted to surgery for stricture resolution. Factors significantly associated with development of caustic stricture were hematemesis (p = 0.002), serum lactic dehydrogenase > 600 U/L (p = 0.008), grade III lesions (p = 0.0002) and involvement of the entire esophagus (p = 0.0003). CONCLUSIONS: Severe endoscopic lesions, involvement of the entire length of the esophagus, hematemesis and increased serum lactic dehydrogenase represent risk factors for the development of fibrotic strictures induced by caustic ingestion. Assessment of these parameters may contribute to prevent this complication.

Screening for pancreatic exocrine insufficiency in patients with diabetes mellitus.

OBJECTIVES: Fecal elastase 1 (E1) is a relatively sensitive and specific indirect test of pancreatic exocrine function. Despite the high functional reserve of the pancreas, it is recognized that a significant proportion of diabetic patients may also have a deficit of the exocrine function. The aim of this study was to screen patients with diabetes mellitus (DM) for pancreatic exocrine insufficiency. METHODS: A total of 80 patients were enrolled in this prospective study, including 42 patients with DM and 38 nondiabetic controls. Exclusion criteria were as follows: age >75 yr; alcohol intake >40 g/day; intake of orlistat or acarbose; and history of diarrhea, pancreatitis, GI surgery, immunodeficiency, or cancer. All patients underwent the same study protocol, which included clinical evaluation, determination of fecal E1, plain x-rays of the abdomen, and abdominal ultrasound. An immunoenzymatic method (ScheBoTech, Wettenburg, Germany) was used for E1 determination. Diagnosis of pancreatic insufficiency was established for a fecal E1 <200 microg/g. RESULTS: The DM and control groups were comparable regarding age (62 +/- 10 yr vs 56 +/- 10 yr), sex (18 men and 24 women vs 15 men and 23 women), and proportion of patients with excess weight (50% vs 42%). Patients had DM diagnosed for 11.5 +/- 8 yr, with structural changes of the pancreas detected on ultrasound in three cases and calcifications in one case. There was no relationship between E1 determination <200 microg/g and the duration or the type of therapy for DM. Fifteen patients (36%) in the DM group had a fecal E1 <200 microg/g, compared with two patients (5%) in the control group (p < 0.05). In the DM group (n = 42), 11 patients with excess weight presented a fecal E1 <200 microg/g, whereas four patients with a BMI <25 presented this result (p < 0.05). CONCLUSIONS: Pancreatic exocrine insufficiency occurs more frequently in diabetic patients than in controls. Diabetic individuals with excess weight (BMI >25) may be at increased risk for underlying exocrine pancreatic insufficiency.