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Biomedical subjects

V S Chadda

Publications and source records attributed to V S Chadda.

35 records · Page 2Linked to original sources
PubMed1982

Dermatomyositis.

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Adolescent↗
PubMed1981

A study of estimation of serum alpha-1-antitrypsin in various forms of leprosy.

Study of serum alpha-1 antitrypsin by agar gel electrophoresis was carried out in 25 patients of various forms of leprosy including 9 cases of Erythema nodosum leprosum, and was compared with findings in 25 healthy controls. The level of serum alpha-1 antitrypsin in healthy subjects ranged from 211 mg% to 602 mg% with a mean level of 290.92 mg% +/- 86.82 mg, have p value 0.1, while in leprosy patients of various types ranged from 129 mg% to 702 mg% with mean level of 405.84 mg% +/- 152.70. Nine patients of lepromatous leprosy with ENL had marked elevation of serum alpha-1 antitrypsin and level was 376 to 720 mg% with a mean level of 562.65% +/- 106.62, statistically significant.

Adult↗
PubMedDate not supplied

Bactericidal power of neutrophils in protein calorie malnutrition.

The present study was undertaken to compare the disturbance in bactericidal power of neutrophils in 25 children having protein caloric malnutrition age and sex matched healthy control subjects. There was a highly significant reduction in the percentage of bacteria killed during incubation in children having PCM as compared to healthy control. A direct relationship existed between total serum proteins and bactericidal activity of neutrophils in children having PCM. The impaired bactericidal power of neutrophils can be attributed to impaired synthesis of lysosomal enzymes, glycolytic activity of neutrophils in children having PCM. The exact mechanisms still remain to be elucidated. Decreased bactericidal activity of neutrophils may be one of the mechanisms responsible for infection.

Bacteria↗
PubMedDate not supplied

Cardiac autonomic neuropathy and its correlation with QTc dispersion in type 2 diabetes.

This study was conducted on 50 patients of diabetes mellitus type 2 and 20 healthy controls to correlate severity of diabetic cardiac autonomic neuropathy with QTc interval and QTc dispersion. Five standard cardiovascular response tests were carried out (i.e. Valsalva ratio, expiration-inspiration ratio, immediate heart rate response to standing, fall of systolic blood pressure on standing and sustained hand grip test) to determine the severity of cardiac autonomic neuropathy by scoring system. QTc dispersion was determined by subtracting heart rate-corrected minimum QTc interval (QTc min) from maximum QT interval (QTc max) from standard electrocardiogram. Severity of cardiac autonomic neuropathy strongly correlated with QTc dispersion (r = 0.760; p = 0.0001). Correlation of severity of cardiac autonomic neuropathy with QTc max and QTc mean was also found but weaker than with QTc dispersion (r = 0.663, r = 0.542, p = 0.0001 each) and no correlation was found with QTc min (r = 0.177; p = 0.17). This shows that QTc dispersion is a better predictor of cardiac autonomic neuropathy than any of above three QTc intervals. QTc max, QTc mean and QTc dispersion were significantly higher (p < 0.001) in diabetics with autonomic neuropathy (450 +/- 23, 423 +/- 22 and 57 +/- 12 msec; n = 30) than without neuropathy (407 +/- 14, 397 +/- 15 and 20 +/- 7 msec; n = 20) and control subjects (408 +/- 20, 399 +/- 19 and 19 +/- 7 msec; n = 20) but QTc min remained same in the three groups (393 +/- 21, 387 +/- 12, 388 +/- 19 msec, respectively) (p > 0.05). Correlation of QTc dispersion was stronger with QTc max (r = 0.781; p < 0.001) than QTc mean (r = 0.625; p = 0.001) but not with QTc min (r = 0.097; p = 1.0) which suggests that regional increase in QT interval due to regional autonomic denervation leads to increased QTc dispersion. Thus, QTc dispersion is a sensitive, non-invasive, simple and cost-effective predictor of cardiac dysautonomia.

Adult↗
PubMedDate not supplied

Prognostic implication of hypocalcemia and QTc interval in malaria.

Hundred confirmed cases of malaria were included in the present study to determine the clinical and prognostic implications of hypocalcemia and corrected QT interval (QTc) prolongation in malaria. Peripheral blood smear examination was done to determine the parasite species and the parasite load. Serum calcium level and QTc measurements in electrocardiogram were done for each patient. Fifty patients were of P. falciparum malaria (38 complicated and 12 uncomplicated), 40 of vivax malaria and 10 patients were having mixed (P. falciparum and P. vivax) infection. Hypocalcemia was found in 26 cases in which QTc was prolonged. Ten patients who had convulsions, all of them were having QTc prolongation and eight had hypocalcemia. A total number of eight patients had muscle spasm, of which six had QTc prolongation and four had hypocalcemia. There were 34 cases of cerebral malaria, of which 18 had hypocalcemia as well as QTc prolongation, 12 of them developed renal failure and 14 had high parasitaemia. Four patients died who had hypocalcemia and QTc prolongation due to hepatorenal syndrome. The mean parasite load, QTc interval and serum calcium were 2.69 +/- 1.0, 0.468 +/- 0.055 sec and 8.16 +/- 0.86 mg/dl respectively in complicated falciparum malaria; 1.6 +/- 0.55, 0.442 +/- 0.043 sec and 8.72 +/- 0.97 mg/dl in complicated mixed (Pf + Pv) infection. 1.33 +/- 0.52, 0.435 +/- 0.035 sec and 9.77 +/- 1.34 mg/dl in uncomplicated falciparum malaria and 1.35 +/- 0.58, 0.403 +/- 0.019 sec and 9.68 +/- 0.99 mg/dl in vivax malaria. The difference was significant between complicated falciparum and mixed (Pf + Pv) infection when compared to uncomplicated falciparum and vivax malaria (p < 0.05).

Adolescent↗