Abdominal examination was unremarkable. Rectal exam revealed a small external hemorrhoid and no masses, red blood was found on the exam glove. Stool culture, ova and parasites, and WBCs was negative. The patient discontinued the celecoxib and the bleeding diminished. A flexible sigmoidoscopy demonstrated a few 5 mm ulcers in the descending and transverse colon. Biopsies revealed nonspecific acute and chronic inflammation. No granulomas or crypt abscesses were seen. The bloody diarrhea completely resolved. The patient remains off of the celecoxib. Her back pain remains problematic. IMPLICATIONS/DISCUSSION: Upper GI tract ulceration with hemorrhage is a wellrecognized complication of NSAIDs. This serious side effect prompted the development of the selective COX-2 inhibitors which are touted as being safer in this regard. (However, this claim has recently been questioned.) Less known important GI adverse events attributed to NSAIDs include strictures and ulcerations of the small and large intestine. This case demonstrates symptomatic ulcerations of the colon attributed to celecoxib, a COX-2 specific NSAID. The patient's clinical presentation, and histology are consistent with that described with nonselective NSAIDS. Clinicians must consider NSAIDs in the differential diagnosis of lower GI tract bleeding, ulceration, or strictures. Studies are needed to determine if COX-2 specific inhibitors are safer than non-specific NSAIDs regarding the lower GI tract. This may become especially relevant in assessing the role of COX-2 inhibitors in the prevention of colon cancer. Although she had a family history of diabetes, a previous fasting glucose before beginning olanzapine was 85 mg/dL. Her exam was significant only for a non-obese, dehydrated appearing female who was orthostatic and tachycardic. Total glucose was 1122 mg/dL and measured serum osmolality was 320 mOsm/kg. A venous blood gas showed pH 7.38 and pCO2 41. Other labs included positive serum ACE test, trace urine ketones, and (in mEq/L) serum HCO3 23, sodium 122 and potassium 5.4 (anion gap of 19). IMPLICATIONS/DISCUSSION: As early as 1926, patients with schizophrenia have been known to have an increased risk of developing hyperglycemia, a process which was exacerbated with the introduction of phenothyiazines in 1956 and the atypical anti-psychotics in 1994. Increasingly, non-schizophrenic patients taking atypical anti-psychotics are demonstrating increased episodes of hyperglycemia and the complications thereof. One proposed mechanism for this hyperglycemia is through drug interference with cellular glucose transport proteins leading to increased insulin resistance and impaired glucose utilization in the periphery. This effect is not dose dependent and has its onset from 10 day to 18 months after the initiation of the drug. The literature is replete with examples of DKA in schizophrenic patients taking atypical anti-psychotics but does not specifically report the development of non-ketotic hyperosmolar syndrome. Additionally, patients taking atypical anti-psychotic medicines for diagnoses other than schizophrenia±including bipolar disorder and major depression with psychosis±risk developing hyperglycemia.