Hemorrhagic complications from glaucoma surgery in patients on anticoagulation therapy or antiplatelet therapy.

PURPOSE: To determine the incidence of and risk factors for hemorrhagic complications in patients on anticoagulation (ACT) or antiplatelet therapy (APT) having glaucoma surgery. DESIGN: Retrospective case-control study. METHODS: Medical records of patients who had glaucoma surgery between July 1, 1998 and March 31, 2005 were reviewed. Patients who either used ACT/APT continuously throughout the perioperative period or discontinued its use prior to surgery were compared to case-matched control patients who were not on such therapies. Patients on ACT/APT who experienced postoperative hemorrhagic complications were compared to those who did not. Outcome measures included hemorrhagic complications and thromboembolic events. RESULTS: Three hundred and forty-seven patients (eyes) who were on ACT or APT prior to glaucoma surgery had a higher rate of hemorrhagic complications than 347 control patients (10.1% vs 3.7%, respectively, P = .002). Patients on ACT had a higher rate of hemorrhagic complications than patients on APT (22.9% vs 8.0%, respectively, P = .003). Patients who continued ACT during glaucoma surgery had the highest rate of hemorrhagic complications (31.8%) when compared to patients who discontinued ACT prior to surgery or patients who used APT alone (P = .001). Hemorrhagic complications following glaucoma surgery were more frequently associated with preoperative ACT, arrhythmia, and higher preoperative and postoperative intraocular pressures (IOP). CONCLUSION: Chronic ACT/APT was associated with a statistically significant increase in the rate of hemorrhagic complications, and perioperative ACT and a high preoperative IOP are potential risk factors for hemorrhagic complications in patients undergoing glaucoma surgery.

Effects of metallothionein on isolated rat heart.

To investigate the effects of metallothionein (MT) on isolated rat heart, 16 Wistar rats were randomly divided into 2 groups. In control group (group C), distilled water was injected intraperitoneally and 24 h later isolated hearts were perfused with Langendorff and stored at 4 degrees C for 3 h with histidine-tryptophan-ketoglutarate (HTK) solutions, and then isolated hearts were perfused for 2 h by Langendorff. In experimental group (group E), 3.6% ZnSO(4) was injected intraperitoneally, 24 h later isolated hearts were perfused by Langendorff and stored at 4 degrees C for 3 h with HTK solutions, and then the isolated hearts were perfused for 2 h with Langendorff. MT content, the recovery of hemodynamics, myocardial water content (MWC), lactate dehydrogenase (LDH) and creatine kinase (CK) leakage, adenosine triphosphate (ATP) and malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, myocardial cell Ca(2+) content, Ca(2+)-ATPase activity of mitochondria ([Ca(2+)-ATPase](m)) and its Ca(2+) content ([Ca(2+)](m)), synthesizing ATP activity of mitochondria ([ATP](m)), and the ultrastructure of cells were examined. There were a significant increase in group E in hemodynamic recovery, ATP content, SOD activity, [Ca(2+)-ATPase](m) activity, [ATP](m) activity, and substantial reduction in MWC, LDH and CK leakage, MDA content, myocardial cell Ca(2+) content, [Ca(2+)](m) content, and the ultrastructural injury were obviously milder than that of group C. This study demonstrated that MT has protective effects on isolated rat heart.

Decreased glibenclamide uptake in hepatocytes of hepatocyte nuclear factor-1alpha-deficient mice: a mechanism for hypersensitivity to sulfonylurea therapy in patients with maturity-onset diabetes of the young, type 3 (MODY3).

Diabetes in subjects with hepatocyte nuclear factor (HNF)-1alpha gene mutations (maturity-onset diabetes of the young [MODY]-3) is characterized by impaired insulin secretion. Surprisingly, MODY3 patients exhibit hypersensitivity to the hypoglycemic actions of sulfonylurea therapy. To study the pharmacogenetic mechanism(s), we have investigated glibenclamide-induced insulin secretion, glibenclamide clearance from the blood, and glibenclamide metabolism in wild-type and Hnf-1alpha-deficient mice. We show that despite a profound defect in glucose-stimulated insulin secretion, diabetic Hnf-1alpha(-/-) mice have a robust glibenclamide-induced insulin secretory response. We demonstrate that the half-life (t(1/2)) of glibenclamide in the blood is increased in Hnf-1alpha(-/-) mice compared with wild-type littermates (3.9 +/- 1.3 vs. 1.5 +/- 1.8 min, P