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Currently employed markers for the detection of acute coronary syndrome are Troponin T, CK (Creatine Kinase) and CKMB activity. CKMB activity measured by immunoinhibition method can give falsely elevated results due to the presence of atypical CK and CKBB and at times lead to the mis-diagnosis of acute coronary syndrome. Hence, CKMB mass (CKMB) measured by electrochemiluminence sandwich principle was employed. In this cross-sectional study 183 samples of 61 patients were analyzed within 6 h of diagnosis of acute coronary syndrome and followed up to 72 h. The correlation coefficient between CKMB activity and CKMBM at 4–6 h was 0.744, while at 12–24 h it was 0.909 and at 48–72 h it was 0.337. Thus there was good association between the two methods at 12–24 h but, statistically for method comparison studies and for replacing one method by another, the two methods need to be in agreement with one another. In this study the two methods are not in agreement with one another and thus analytically not replaceable. Another finding was obtained that CKMBM reached cut off levels prior to CKMB enzyme activity and hence, CKMBM is clinically better than CKMB activity to detect reinfarction.

Aim of this study was to evaluate the role of Myeloperoxidase (MPO) and high sensitive Troponin T in the early diagnosis of acute coronary syndrome (ACS). This was a cross sectional study that comprised of 120 individuals of which 75 were cases and 45 healthy controls. On the basis of clinical history and 12 lead electrocardiogram initial diagnosis of ACS was made in the cases. MPO and high sensitive Troponin T (hs-cTnT) was measured in all the individuals. Levels of MPO were significantly higher in patients of ACS as compared to those in control group [medians: 15.40 (95 % CI 11.06–20.84) vs 5.84 (95 % CI 5.50–6.44)]. By taking the cut off as >11.87 U/mL for MPO, its sensitivity was 87 % (95 % CI 73.7–95.1), specificity was 97.3 % (95 % CI 90.6–99.7), positive predictive value was 94.6 % and negative predictive value was 92.6 %. Positive likelihood ratio was 33.0 while negative likelihood ratio was 0.13, whereas the corresponding values in case of hs-cTnT were 95.6 % (95 % CI 85.2–99.5), 61.3 % (95 % CI 49.5–72.6), 59.7 %, 95.8 %, 2.47 and 0.07 by taking cut off as >14 pg/ml. The area under the ROC curves (AUC) of MPO and hscTnT at 0–6 h were 0.971 (95 % CI 0.92–0.99, P < 0.001) and 0.797 (95 % CI 0.71–0.86, P < 0.001) respectively. The logistic model combining the two markers yielded sensitivity, specificity, positive predictive value and negative predictive value of 95.7, 97.3, 98.2 and 93.7 % respectively. It was concluded that MPO and hs-cTnT may be useful tools for risk stratification of ACS and can be used together with better accuracy in the early diagnosis of ACS.

Background: Hypothyroidism is a progressive disorder that presents with diverse degrees of thyroid failure and metabolic consequences. Purine metabolism can be affected by disturbance in thyroid hormones, which leads to alteration in the uric acid levels, leading to hyperuricemia and subsequently causing gout. Also, hemodynamic changes occur in hypothyroidism that leads to reduction in renal plasma flow and glomerular filtration rate, which also causes increase in the levels of serum uric acid and serum creatinine. Aims and Objective: To determine whether thyroid dysfunction, subclinical and overt, has deleterious effects on renal function. Materials and Methods: This was a cross-sectional study that comprised 108 individuals (56 cases and 52 controls; 52 men and 56 women) aged between 20 and 60 years. Case group comprised suspected cases of hypothyroidism. Serum TSH, T4, T3, uric acid, and creatinine were estimated after applying inclusion and exclusion criteria. Result: Uric acid and creatinine levels were significantly elevated in case group as compared to control group (7.09 ± 0.45 and 1.52± 0.16 mg/dL versus 4.08 ± 0.25 and 0.62 ± 0.05 mg/dL, respectively; p < 0.001). There was insignificant correlation between serum uric acid and creatinine levels with hypothyroidism (r = 0.185, p = 0.172 and r = 0.082, p = 0.550). Also, there was no significant correlation between serum uric acid and creatinine levels with the age in hypothyroidism (r = 0.143; p = 0.292 and r = -20.154; p = 0.257, respectively). Conclusion: Hypothyroidism causes significant increase in serum uric acid and creatinine levels. Therefore, we would emphasize the importance of the routine evaluation of serum uric acid and creatinine levels in patients with hypothyroidism. [Natl J Physiol Pharm Pharmacol 2015; 5(3.000): 232-235]

Background: It is very crucial to recognize infection in immunocompromised patients. The purpose of this study was to explore the diagnostic accuracy of C-reactive protein (CRP) in critically ill immunocompromised patients with sepsis. Aims and Objective: To find out the diagnostic utility of CRP in immunocompromised patients with sepsis. Materials and Methods: This was a cross-sectional study, which included immunocompromised patients with suspected sepsis. Patients were classified into two diagnostic groups: those with nonbacterial sepsis and those with bacterial sepsis, and the values of CRP were estimated. Results: Of 94 patients (63 men and 31 women) with a median age of 56 years (95% CI 53.959.3), 74 (78.5%) had immunosuppression with nonbacterial sepsis and 20 (21.4%) had immunosuppression with bacterial sepsis. CRP concentrations were higher in the group with bacterial sepsis [30.94 ng/ml (95% CI 25.1336.74)] than those with nonbacterial sepsis [7.46 ng/ml (95% CI 7.057.87), P < 0.0001]. CRP concentrations that were >6 mg/L had 93.33% sensitivity but only 63.20% specificity for diagnosing sepsis. The accuracy of diagnosis was 87.23%. The area under the receiver-operating characteristic curve was 0.82 (0.720.92). Conclusion: Despite limited specificity in critically ill immunocompromised patients, CRP concentrations may help to rule out bacterial infection. [Natl J Physiol Pharm Pharmacol 2015; 5(3.000): 166-169]

Leber's Hereditary Optic Neuropathy (LHON) is a maternally transmitted disease of the optic nerve that primarily affects males in their second or third decade. Clinical features include painless acute or subacute loss of vision, deep central scotomas, disc edema, hyperemia and peri-papillary telangiectasia. Patients are otherwise healthy. Mitochondria is a generator of ATP, required for the all the functions of the body. The major types of mutations in this disease are:(1)m.3460G>A (guanine to adenosine); (2)m. 11778G>A (guanine to adenosine); (3)m. 14484T>C (thymidine to cytosine) disrupt key polypeptide subunits of complex I respiratory chain. The final pathological outcome in LHON is apoptotic retinal ganglion cells loss. Objective was to find out the gene mutations in a young male patient with clinical and neurophysiological condition suggestive of LHON, confirmed by genetic testing. A case study was done on 20 year old male patient in neuromedicine OPD in Sri Krishna Hospital, Karamsad after the consent of the patient. Molecular genetic testing for the three common LHON mitochondrial DNA point mutations (targeted mutation analysis) in the patient and his three unaffected sibling sisters were done for confirmation of LHON. Affected male patient on molecular genetic testing revealed mutation on 11778G>A and his three sibling sisters revealed same type of mutation but phenotypically were normal. LHON is a mitochondrial genetic disease characterised by bilateral subacute loss of central vision owing to focal degeneration of the optic nerve. The vast majority of cases are result of one of three mtDNA point mutations. To confirm these mutations molecular genetic testing is now available.