OBJECTIVE -We sought to study the optimal management of hyperglycemia in nonintensive care unit patients with type 2 diabetes, as few studies thus far have focused on the subject.RESEARCH DESIGN AND METHODS -We conducted a prospective, multicenter, randomized trial to compare the efficacy and safety of a basal-bolus insulin regimen with that of sliding-scale regular insulin (SSI) in patients with type 2 diabetes. A total of 130 insulin-naive patients were randomized to receive glargine and glulisine (n ϭ 65) or a standard SSI protocol (n ϭ 65). Glargine was given once daily and glulisine before meals at a starting dose of 0.4 units ⅐ kg Ϫ1 ⅐ day Ϫ1 for blood glucose 140 -200 mg/dl or 0.5 units ⅐ kg Ϫ1 ⅐ day Ϫ1 for blood glucose 201-400 mg/dl. SSI was given four times per day for blood glucose Ͼ140 mg/dl. RESULTS -The mean admission blood glucose was 229 Ϯ 6 mg/dl and A1C 8.8 Ϯ 2%. A blood glucose target of Ͻ140 mg/dl was achieved in 66% of patients in the glargine and glulisine group and in 38% of those in the SSI group. The mean daily blood glucose between groups ranged from 23 to 58 mg/dl, with an overall blood glucose difference of 27 mg/dl (P Ͻ 0.01). Despite increasing insulin doses, 14% of patients treated with SSI remained with blood glucose Ͼ240 mg/dl. There were no differences in the rate of hypoglycemia or length of hospital stay.CONCLUSIONS -Treatment with insulin glargine and glulisine resulted in significant improvement in glycemic control compared with that achieved with the use of SSI alone. Our study indicates that a basal-bolus insulin regimen is preferred over SSI in the management of non-critically ill, hospitalized patients with type 2 diabetes. Diabetes Care 30:2181-2186, 2007H yperglycemia in hospitalized patients is a common, serious, and costly health care problem with profound medical consequences. Increasing evidence indicates that the development of hyperglycemia during acute medical or surgical illness is not a physiologic or benign condition but is a marker of poor clinical outcome and mortality (1-3). Extensive evidence from observational studies, including our own, indicates that in hospitalized patients with critical illness, hyperglycemia is associated with an increased risk of complications and mortality (3-9). Prospective randomized trials in critically ill patients have shown that intensive glucose control reduces the risk of multiorgan failure, systemic infections, and short-and longterm mortality. Effective management of hyperglycemia is also associated with a decreased length of intensive care unit and hospital stay (4,6,8 -10) and decreased total hospitalization cost (11). The importance of glycemic control on outcome is not limited to patients in critical care areas but also applies to patients admitted to general surgical and medical wards. In such patients, the presence of hyperglycemia has been associated with prolonged hospital stay, infection, disability after hospital discharge, and death (1,5,12). In general surgery patients, the relative risk for serious postopera...

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W e studied less well-investigated components of the calf muscle pump failure associated with venous disease, including muscle, nerve, movement, and gait abnormalities. 1 We investigated sensory neuropathy and ambulatory foot pressures in patients with chronic venous insufficiency (CVI) to further elucidate the pathogenesis and mechanisms of venous ulceration. Methods. After institutional review board approval and informed consent, 10 patients with active noninfected venous ulcers or a history of such ulcers (CEAP [Clinical-Etiologic-Anatomic-Pathophysiologic] 1 clinical classification 5 or 6) were recruited. No recruited patient had a history of neuropathy or predisposing conditions for neuropathy. Ten age-, sex-, and weight-matched control patients without diabetes or venous disease were also recruited from the same population. All patients had good arterial circulation and walked without assistance. A medical history was obtained and foot, leg, and ulcer examinations were performed on all patients. To evaluate symptoms of peripheral sensory neuropathy, the validated neuropathy symptom score (NSS) 2 was determined. To measure quantitative objective neuropathic changes, we performed quantitative sensory testing of the feet using the validated neuropathy disability score (NDS). 2 As part of the NDS, we used a 10-g monofilament to perform sensory testing of the feet at 6 sites.

The effects of 17 beta-estradiol and progesterone were evaluated separately and in combination, on the growth, survival, and cell cycle dynamics of SW-13 human adrenal carcinoma cells in culture. Both hormones significantly decreased cell survival, with dose response curves at four days demonstrating EC (50)s estimated at 1.2 x 10 (-5) M for 17 beta-estradiol and 4.8 x 10 (-6) M for progesterone. Flow cytometry studies of these cultures indicated a strong G2/M blocking effect of both steroids, either individually or in combination; the effects of progesterone and of both agents together were substantially greater than the effect with 17 beta-estradiol alone. The sub-G1 region of the flow cytometry profile was significantly enhanced by exposure to 17 beta-estradiol and even more by progesterone. Sub-G1 "apoptosis" was confirmed by fragmented and condensed nuclear chromatin staining using a standard DAPI fluorescence assay. The expression of the critical cell cycle regulatory proteins cyclin B1 and D1 were significantly decreased by each hormone, with the influence of progesterone again predominating. These data demonstrate that high doses of 17 beta-estradiol and progesterone have inhibitory and apoptotic effects on SW-13 human adrenal carcinoma cells IN VITRO. The observed effects are associated with declines in cyclin B1 and D1 expression as well as a block in G2/M.