Hypocalcaemia mimicking long QT syndrome: case report

We describe a teenage girl who presented with syncope on exertion and prolonged QT on electrocardiogram (ECG). She was found to be hypocalcaemic due to hypoparathyroidism. Following oral calcium and vitamin D supplementation, there were no further episodes of syncope with normalization of the QT segment. This case highlights the need to consider all causes of a long QT segment.     

Effect of sustained-release long-acting intravitreal dexamethasone implant in patients of non-proliferative diabetic retinopathy undergoing phacoemulsification: A randomized controlled trial

Purpose:Cataract and diabetes, both being a major health care problem, an intervention evaluated for the combination of the two attains paramount importance. The purpose of the study was to determine the role of intraoperative intravitreal dexamethasone implant in patients with diabetic retinopathy with/without macula edema undergoing phacoemulsification.Methods:The study was a two-arm, single-center, randomized, assessor-blinded trial of 151 patients with type-2 diabetes mellitus and cataract. It had two groups: dexamethasone group (DEX) versus standard of care (SOC) group, i.e. phacoemulsification and intraocular lens (IOL) implantation without injection of dexamethasone drug delivery system (DDS). The number of rescue interventions required, central macular thickness by optical coherence tomography (OCT), Early Treatment Diabetic Retinopathy Study (ETDRS) score, laser flare meter (LFM) values, intraocular pressure (IOP), and grade of diabetic retinopathy (DR) were recorded until three months follow up. Macular thickness and number of rescue medications between the treatment groups were the co-primary outcomes.Results:A statistically significant interaction was present between treatment and time on OCT score (P < 0.001). The requirement of rescue interventions in the dexamethasone DDS group [40.2% (33/82)] was lesser as compared to the SOC group [49.3% (34/69)] at the end of 12 weeks [odds ratio (OR), 0.70 (0.36–1.33)] follow up although not statistically significant (P = 0.343). A statistically significant interaction was present between treatment and time on LFM score (P = 0.003). No statistically significant interaction was present between the treatment and time on visual acuity score (P = 0.08) and IOP score (P = 0.375).Conclusion:Dexamethasone implant may have potential as a valuable therapy for patients undergoing cataract surgery with DR with/without macular edema with effects lasting for at least three months.     

Hypercalcemia stimulates expression of intrarenal phospholipase A2 and prostaglandin H synthase-2 in rats. Role of angiotensin II AT1 receptors.

In chronic hypercalcemia, inhibition of thick ascending limb sodium chloride reabsorption is mediated by elevated intrarenal PGE2. The mechanisms and source of elevated PGE2 in hypercalcemia are not known. We determined the effect of hypercalcemia on intrarenal expression of cytosolic phospholipase A2 (cPLA2), prostaglandin H synthase-1 (PGHS-1), and prostaglandin H synthase-2 (PGHS-2), enzymes important in prostaglandin production. In rats fed dihydrotachysterol to induce hypercalcemia, Western blot analysis revealed significant upregulation of both cPLA2 and PGHS-2 in the kidney cortex and the inner and outer medulla. Immunofluorescence localized intrarenal cPLA2 and PGHS-2 to interstitial cells of the inner and outer medulla, and to macula densa and cortical thick ascending limbs in both control and hypercalcemic rats. Hypercalcemia had no effect on intrarenal expression of PGHS-1. To determine if AT1 angiotensin II receptor activation was involved in the stimulation of cPLA2 and PGHS-2 in hypercalcemia, we treated rats with the AT1 receptor antagonist, losartan. Losartan abolished the polydipsia associated with hypercalcemia, prevented the increase in cPLA2 protein in all regions of the kidney, and diminished PGHS-2 expression in the inner medulla. In addition, losartan completely prevented the increase in urinary PGE2 excretion in hypercalcemic rats. Intrarenal levels of angiotensin II were unchanged in hypercalcemia. These data indicate that hypercalcemia stimulates intrarenal cPLA2 and PGHS-2 protein expression. Our results further support a role for angiotensin II, acting on AT1 receptors, in mediating this stimulation.     

Efficacy of Ozurdex implant in recalcitrant diabetic macular edema—a single-center experience

The purpose of this study is to report the efficacy of intravitreal Ozurdex implant in managing recalcitrant diabetic macular edema. Retrospective interventional non-randomized study of patients with recalcitrant diabetic macular edema who received intravitreal Ozurdex implant. Main outcome measures were change in the central macular thickness, visual acuity, and intraocular pressure. Sixty-seven eyes of 52 patients with recalcitrant diabetic macular edema with a mean duration of 45.4 ± 22.5 months (range 6–96 months) were studied. Mean central macular thickness decreased from 514.2 ± 177.8 µm at baseline to 394.3 ± 152.2 µm (p = 0.007), 301.8 ± 93.0 µm (p < 0.000), 316.4 ± 115.6 µm (p < 0.000), and 419.9 ± 186.3 µ (p = 0.03) at 1, 6, 12, and 24 weeks, respectively. Mean best corrected visual acuity changed from 0.82 ± 0.46 log MAR to 0. 69 ± 0.44 log MAR (p = 0.122), 0.61 ± 0.40 log MAR (p = 0.007), 0.65 ± 0.37 log MAR (p = 0.024), and 0.68 ± 0.49 log MAR (p = 0.091) at 1, 6, 12, and 24 weeks, respectively. Single injection of intravitreal Ozurdex implant led to progressive decrease in central macular thickness with maximum percentage decrease at 6 weeks (41.2 %) from the baseline which was maintained up to 12 weeks. Eight eyes showed transient rise in intraocular pressure at 2 months which was controlled by antiglaucoma medications.