Arterial switch operation without coronary translocation: mid-term results

We innovated a technique of arterial switch operation without coronary translocation in 1995, which avoids problems related to coronary artery translocation with good mid-term results. It is a better alternative for surgeons who are not well versed with coronary translocation of conventional arterial switch operation and with difficult coronary anatomy. This report deals with the mid-term results of our new technique.     

An association study of thrombospondin 1 and 2 SNPs with coronary artery disease and myocardial infarction among South Indians

Introduction

Thrombospondin 1 and 2 are multidomain calcium-binding extracellular glycoproteins and they play a role in platelet aggregation, inflammatory response and assembly of connective tissue extracellular matrix. The association of thrombospondins (TSP) in the pathogenesis of coronary artery disease (CAD) and myocardial infarction (MI) is well established. The association of the TSP-1 (Asn700Ser, 2210A → G, rs2228262) and TSP-2 un-translated region (UTR) (3949 T → G, rs8089) gene variations among South Indian CAD and MI patients has been examined in the present study.

Materials and Methods

We analyzed the thrombospondin polymorphisms in unrelated CAD patients (n = 511) and a subgroup with an event of MI (n = 173) compared with controls (n = 522). The polymorphisms were assessed using polymerase chain reaction, restriction fragment length analysis and the circulating TSP concentration were measured using enzyme linked immune-sorbent assay.

Results

The prevalence of TSP-1 and TSP-2 alleles did not show any significant difference statistically, when compared controls against CAD/MI patients. The rare GG genotype of the N700S polymorphism was not observed among the studied population. Further, multiple regression analysis revealed that there was no significant risk for CAD (OR = 1.68; 95% CI 0.927 - 3.055; p = 0.087) or MI (OR = 1.84; 95% CI 0.846 - 4.007; p = 0.124) for the GA genotype. The GA genotype showed no impact on clinical characteristics of the CAD patients and their circulating TSP-1 levels. A similar non-association was observed for the TSP-2 in 3949 T → G polymorphism (GG genotype) for CAD (OR = 0.64; 95% CI 0.278 - 1.455; p = 0.636) and MI (OR = 0.53; 95% CI 0.166 - 1.675; p = 0.278).

Conclusions

Our data suggests that the presence of thrombospondin-1 (rs2228262) and thrombospondin-2 (rs8089) variants need not be considered a risk for coronary artery disease or myocardial infarction among South Indians.     

Molecular diversity of Glanzmann thrombasthenia in southern India: new insights into mRNA splicing and structure-function correlations of alphaIIbbeta3 integrin (ITGA2B, ITGB3)

The molecular basis of Glanzmann thrombasthenia (GT) was studied in 40 families from southern India. Of 23 identified mutations (13 in the alphaIIb (ITGA2B) gene and 10 in the beta3 (ITGB3) gene), 20 were novel and three were described previously. Three mutations in the beta3 gene-p.Leu143Trp (Leu117Trp), p.Tyr307Stop (Tyr281Stop), and p.Arg119Gln (Arg93Gln)-were detected in 12, three, and two families, respectively, with definite founder effects observed for the first two mutations. Alternative splicing was predicted in silico for the normal variant and a missense variant of the beta3 gene, and for 10/11 frameshift or nonsense mutations in alphaIIb or beta3. The prediction was confirmed experimentally for a c.2898_2902dupCCCCT mutation in exon 28 of the alphaIIb gene that induced exon skipping. Seven out of nine missense mutations substituted highly conserved amino acids buried in the proteins' cores, predicting structural abnormalities. Among these, a beta3 substitution, p.Cys39Gly (Cys13Gly) was found to cause intracellular degradation of the beta3 subunit, in contrast to previous findings that mutations at Cys435, the partner of Cys13 in a disulfide bond, cause constitutive activation of alphaIIbbeta3. The two patients with a beta3 Arg93Gln mutation had normal clot retraction, consistent with a recent finding that this substitution is associated with normal surface expression of alphaIIbbeta3. In conclusion, this study demonstrates that a variety of mutations account for GT in southern Indian patients, provides new insights into mRNA splicing, and highlights the role of specific amino acids in structure-function correlations of alphaIIbbeta3.     

Delayed Macular Hole Closure

Purpose

The presented case raises questions regarding the favorable scheduling of planned postoperative care and the ideal observation interval to decide for reoperations in macular hole surgery. Furthermore a discussion about the use of short- and long-acting gas tamponades in macular hole surgery is encouraged.

Methods

We present an interventional case report and a short review of the pertinent literature.

Results

We report a case of spontaneous delayed macular hole closure after vitreoretinal surgery had been performed initially without the expected success. A 73-year-old male Caucasian patient presented at our clinic with a stage 2 macular hole in his left eye. He underwent 23-gauge pars plana vitrectomy and internal limiting membrane peeling with a 20% C₂F₆-gas tamponade. Sixteen days after the procedure, an OCT scan revealed a persistent stage 2 macular hole, and the patient was scheduled for reoperation. Surprisingly, at the date of planned surgery, which was another 11 days later, the macular hole had resolved spontaneously without any further intervention.

Conclusions

So far no common opinion exists regarding the use of short- or long-acting gas in macular hole surgery. Our case of delayed macular hole closure after complete resorption of the gas tamponade raises questions about the need and duration of strict prone positioning after surgery. Furthermore short-acting gas might be as efficient as long-acting gas. We suggest to wait with a second intervention at least 4 weeks after the initial surgery, since a delayed macular hole closure is possible.Key words: Macular hole, Vitrectomy, Gas tamponade     

Prevalence of early stages of chronic kidney disease in healthy army personnel

Introduction: Chronic kidney disease (CKD) is associated with significant morbidity and mortality. Screening and detection of early stages of CKD can help institute interventions that may delay the progression of the disease. One aim was to study the prevalence of early stages of CKD in the Army.Methods: A cross-sectional study ofArmy Personnel in an Army cantt in Central India was carried out. All participants filled a structured questionnaire and anthropometric data was collected. Investigative profile included routine urine exam, semi-quantitative microalbuminuria (MAU), serum creatinine, lipid profile and fasting blood glucose. Glomerular Filteration rate (eGFR) was calculated using the Modification of Diet in Renal Diseases (MDRD) study equation.Result: A total of 1920 subjects were examined with 731 (38.07%) from Arms and 1189 (6I.93%) from Services. 348 were excluded and of the remaining 1572 subjects, 141 (8.97%) had MAU and 157 (9.99%) had deranged Albumin Creatinine Ratio (ACR). Mean eGFR by MDRD equation was 102 ± 25.84 ml/min/1.73m². Early CKD was seen in 150 (9.54%) with 84 (5.34%) in stage I CKD, 55 (3.5%) in stage II and 11 (0.7%) in stage III. Multiple logistic regression showed BMI > 23, the presence of DM and HTN were independent risk factors for CKD.Conclusion: 9.54 % of healthy army personnel were found to have early stages of CKD. Institution of screening programs can result in early detection of CKD.