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Y C Govil

Publications and source records attributed to Y C Govil.

13 recordsLinked to original sources
PubMed2003

Varying role of vitamin D deficiency in the etiology of rickets in young children vs. adolescents in northern India.

The relative importance of calcium vs. vitamin D deficiency in the etiology of nutritional rickets in the tropics may be different in children compared with adolescents. We studied calcium intake, sun exposure, serum alkaline phosphatase, and 25 hydroxyvitamin D in 24 children and 16 adolescents with rickets/osteomalacia. The values were compared with those obtained in control subjects (34 children and 19 adolescents). We found that young children with rickets had lower calcium intake compared with controls (285 +/- 113 vs. 404 +/- 149 mg/day, p < 0.01), but similar sun exposure (55 +/- 28 vs. 56 +/- 23 min x m2/day) and 25 hydroxyvitamin D (49 +/- 38 vs. 61 +/- 36 nmol/l). Sixteen of 24 children with rickets had 25 hydroxyvitamin D above the rachitic range (> 25 nmol/l), in contrast to one of 16 adolescents. Adolescent patients had low calcium intake vs. controls (305 +/- 196 vs. 762 +/- 183 mg, p < 0.001), and lower sunshine exposure (16 +/- 15 vs. 27 +/- 17 min x m2/day, p < 0.01) and serum 25 hydroxyvitamin D (12.6 +/- 7.1 vs. 46 +/- 45.4 nmol/l, p < 0.001). The odds ratio for developing rickets with a daily calcium intake below 300 mg was 4.8 (95 per cent CI, 1.9 - 12.4, p = 0.001). Subjects with rickets were randomized to receive 1 g calcium daily, with or without vitamin D. Children showed complete healing in 3 months, whether they received calcium alone or with vitamin D. Adolescents showed no response to calcium alone, but had complete healing with calcium and vitamin D in 3-9 months (mean 5.3 months). Thus deficient calcium intake is universal among children and adolescents with rickets/osteomalacia. Inadequate sun exposure and vitamin D deficiency are important in the etiology of adolescent osteomalacia.

Adolescent↗
PubMed1998

Predictors of outcome in fulminant hepatic failure in children.

OBJECTIVE: To identify the predictors of outcome in fulminant hepatic failure (FHF) in children. STUDY DESIGN: Prospective cohort study. METHODS: 41 children with FHF were studied. Patient characteristics and findings on examination at the time of hospitalization were noted. Serum biochemistry and screening for hepatotropic viruses (A, B and C) were done in each patient. Patients were treated using a predefined protocol and followed up till death or discharge. Univariate and multivariate analysis was done to find the predictors of outcome. RESULTS: Hepatitis B was the commonest cause of FHF (11 children; 26.9%). Markers for hepatitis A and C viruses were present in one and two patients, respectively. Serology was negative in 27 children (65.9%), of whom two had history of ingestion of hepatotoxins (antitubercular drugs). The overall mortality was 61%. Irrespective of etiology, the following factors were associated with poor outcome on univariate analysis: presence of gastrointestinal (GI) hemorrhage, serum bilirubin more than 10 mg/dL, age 6 years or less, coma of grade 3 or more, presence of infection, prolongation of prothrombin time > 8 s over control, prothrombin concentration < 50%, hypoglycemia (blood glucose < 45 mg/dL), hyponatremia (serum sodium < 125 mEq/L) and hyperkalemia (serum potassium > 5.5 mEq/L). On multiple logistic regression analysis, presence of GI hemorrhage (p = 0.005), degree of coma (p = 0.02) and serum bilirubin level (p = 0.025) were identified as independent predictors of mortality.

Child↗
PubMed1992

Ketotifen.

Explore the source record for details and available documents.

Airway Resistance↗
PubMed1991

Hepatotoxicity of rifampin and isoniazid. Is it all drug-induced hepatitis?

Serologic markers for hepatitis viruses were studied in 40 children who developed acute hepatitis during antituberculosis therapy with rifampin and isoniazid, with the aim of assessing the contributory role of these viruses toward producing hepatic injury. Hepatitis A and B were confirmed in 7.5 and 35% patients, respectively, by IgM antibodies. Epidemiologic evidence suggested the possibility of non-A, non-B hepatitis in at least a few of the remaining 23 children. Hepatitis B was seen more often in children with severe tubercular disease (72%) and was largely (92.8%) parenterally transmitted. The study highlights that the endemicity of viral hepatitis in developing countries, among other factors, could also be responsible for the reported higher incidence of hepatotoxicity from developing countries and also for the increased risk of hepatotoxicity seen in severe tubercular disease.

Chemical and Drug Induced Liver Injury↗
PubMed1990

Ring or disc-like enhancing lesions in partial epilepsy in India.

One-hundred unselected children presenting with partial motor seizures were subjected to clinical work-up and cranial computed tomography (CT scan). Seventy-three children had an abnormal scan. On these, 56 patients had either a ring (35 patients) or a disc-like (21 patients) enhancing lesion which coincided with the probable site of origin of the seizures in all cases. The lesions were surrounded by perifocal oedema which was occasionally severe enough to produce a mass effect. The significance of these disc or ring lesions is discussed in the light of recent literature. All patients with such lesions were put on three-drug anti-tubercular therapy along with anticonvulsants. A repeat scan could be obtained in 20 patients, 10 weeks to 11/2 years after the initial scan. This showed a decrease in size or disappearance of the lesion in the majority (13 patients). Four patients showed a spot of calcification in the area of the original lesion and another two showed a typical 'target sign', i.e. calcification within a ring. It is concluded that these ring or disc lesions represent tuberculomas which are, thus, the commonest cause of partial motor seizures in children in this area.

Brain↗
PubMedDate not supplied

Trends in poisoning in children: experience at a large referral teaching hospital.

BACKGROUND: Poisoning is a major problem in the paediatric population. The offending substances used vary from place to place. Information on poisoning trends in India is meagre and there is an impression among clinicians that there has been a change in the commonly used poisons over the years. This retrospective study aimed to determine the pattern of poisoning in children and to study the nationwide trend over the past five decades. METHODS: Case records of children (age group: 1 month and above) admitted to the Department of Paediatrics, King George's Medical College, Lucknow, Uttar Pradesh in three alternate calendar years, i.e. 1989, 1991 and 1993 were screened. All children were grouped into three categories based on the poison: (i) bites and stings, (ii) medicinal compounds, and (iii) non-medicinal compounds. The Indian literature on poisoning in children was reviewed and decade-wise data from a total of 22 studies (including the present study) were used to determine the changing trend. RESULTS: Childhood poisoning constituted 2.1% of the total paediatric admissions and 1.2% of total deaths. Non-medicinal compounds were the largest contributors (69.2%), of which kerosene alone was responsible for 47% of cases. Medicinal compounds, and bites and stings accounted for 21.6% and 9.2% of these cases, respectively. The case-fatality rate was 9.2%. Comparison of our data, after excluding bites and stings, with a previous study (1977-79) from our institution showed that kerosene poisoning continues to be responsible for a substantial part of the morbidity (51.8% v. 31.5%). Also, poisoning due to insecticides and pesticides has increased (13.7% v. 2.1%) while that due to plant poisons (primarily dhatura) has reduced markedly (4.8% v. 19.2%). CONCLUSION: Mortality due to poisoning in children has remained high over the last five decades (2.9%-4.7%). Kerosene has remained the single largest contributor to childhood poisoning (51.5% in the 1960s v. 52.8% in the 1990s).

Child, Preschool↗