Impact of ocular hypotensive lipids on clinically significant diabetic macular edema

Purpose. To study the impact of ocular hypotensive lipids (OHL) on the incidence, progression, and response to treatment of clinically significant diabetic macular edema (CSDME). Methods. A total of 379 patients (232 female, 147 male) with a history of diabetes mellitus (DM) and primary open-angle glaucoma (POAG) were identified and included in the study. Patients were stratified into groups based on CSDME development and OHL exposure. Main outcome measures included time to development of CSDME, total duration of OHL exposure, and duration of DM and POAG. Results. Seven patients (1.8%) developed CSDME after OHL exposure (group 1A), 15 (4.0%) developed CSDME prior to OHL exposure (group 1B), and 197 (52.0%) were treated with OHL but never developed CSDME (group 2). Of patients not exposed to OHL, 22 (5.8%) developed CSDME (group 3) and 138 (36.4%) did not (group 4). Mean duration of DM was longer (p<0.0001) in patients who developed CSDME (20.2 years) compared to patients who did not (12.4 years). There was no difference (p=0.67) in the amount of OHL exposure between patients who developed CSDME (4.1 years) and patients who did not (4.6 years). Once developed, there was no difference in the interval until CSDME resolution between OHL treated (17.8 mo) and untreated (12.7 mo) patients (p=0.36). Conclusions. The CSDME development correlated most strongly with the duration of diabetes, irrespective of OHL use. Ocular hypotensive lipids treatment of POAG seems not to affect the incidence, progression, or response to treatment of CSDME in diabetes.     

Effect of Grade I and II intraventricular hemorrhage on visuocortical function in very low birth weight infants

The neurological outcome for infants with Grade I/II intraventricular hemorrhage (IVH) is debated. The aim of this study was to determine whether very low birth weight infants (VLBW, <1500 g) with Grade I/II (IVH) have altered visuocortical activity compared with infants with no IVH. We assessed the quantitative swept parameter visual evoked potential (sVEP) responses evoked by three different visual stimuli. Data from 52 VLBW infants were compared with data from 13 infants with Grade I or II IVH, enrolled at 5-7 months corrected age. Acuity thresholds and suprathreshold response amplitudes were compared. Grating acuity (GA), contrast sensitivity (CS) and vernier acuity (VA) were each worse in the Grade I/II IVH compared with the no IVH groups (8.24 cpd in IVH group vs. 13.07 cpd in no IVH group for GA; 1.44% vs. 1.18% for CS and 1.55 arcmin vs. 0.58 arcmin for VA). The slopes of the response amplitude for CS and VA were significantly lower in IVH infants. The spatial frequency tuning function was shifted downward on the spatial frequency axis, without a change in slope. These results indicate that Grade I/II IVH are associated with deleterious effects on cortical vision development and function.     

Relook at lipoprotein (A): Independent risk factor of coronary artery disease in North Indian population

Aims

Lipoprotein (a) [Lp(a)] levels have shown wide ethnic variations. Sparse data on mean Lp(a) levels, its link with clinical variables and severity of coronary artery disease (CAD) in North Indian population needed further studies.

Methods

150 patients, each of single vessel disease (SVD), double vessel disease (DVD) and triple vessel disease (TVD) with 150 healthy controls were drawn for the study. Serum Lp(a) estimation was performed by immunoturbidimetric method.

Results

Lp(a) had a skewed distribution. Median Lp(a) level was significantly raised in cases as compared to controls (median 30.30 vs. 20 mg/dl, p < 0.001). Cases with acute coronary syndrome (ACS, 55.8%) had significantly higher median Lp(a) levels as compared to those with chronic stable angina (35.4 mg/dl vs. 23 mg/dl, p < 0.001). Significant difference in median Lp(a) levels were observed in patients with DVD or TVD versus control (30, 39.05 vs 20 mg/dl, p < 0.008). Lp(a) level was found to be an independent risk factor for CAD (AOR{adjusted odds ratio} 1.018, 95% CI 1.010–1.027; p < 0.001). Analysis using Lp(a) as categorical variable showed that progressive increase in Lp(a) concentration was associated with increased risk of CAD [AOR from lowest to highest quartile (1, 1.04, 1.43 and 2.65, p value for trend = 0.00026)]. Multivariably AOR of CAD for subjects with Lp(a) in the highest quartile (above 40 mg/dl) compared to those with Lp(a) ≤40 mg/dl was 2.308 (95% CI 1.465–3.636, p < 0.001).

Conclusion

Lp(a) above 40 mg/dl (corresponding to 75th percentile)assessed by an isoform insensitive assay is an independent risk factor for CAD. Raised Lp(a) level is also associated with increased risk of ACS and multivessel CAD.     

A critical analysis of the purported role of hypoxaemia in the comorbidity of obstructive sleep apnoea and epilepsy

Obstructive sleep apnoea (OSA) is a globally prevalent sleep disorder of significant health concern and confounded with several comorbidities resulting in adverse effect(s) on quality of life in patients afflicted with it. Of particular interest is the enigmatic high comorbidity of OSA with epilepsy, the exact underlying pathophysiology of which remains elusive despite a multitude of research performed in the last four decades. Hypoxaemia, which is an important characteristic feature found in OSA during apnoeic spells, has been implicated in the high comorbidity of OSA with epilepsy, the basis of which rests upon hypoxaemia‐mediated brain damage, subcortical release phenomenon, oxidative stress and neuroinflammatory reactions. However, several studies present contradictory evidences that potentially refute the hypoxaemia‐based mechanism. Additionally, the role of hypercapnia thatgenerally accompanies hypoxaemia during apnoeic spells, cannot be overlooked and is known to be potentially protective against neuronal hyperexcitability. Thus, hypoxaemia theory implicated in the high comorbidity of OSA and epilepsy appears weak and refutable. This brief paper studies and critically analyses the role of hypoxaemia in conjunction with hypercapnia in the underlying pathophysiology of the comorbidity.