Rickets: a cause of delayed walking in toddlers.

OBJECTIVE: Children with complaints of not able to walk were investigated for rickets by appropriate history, clinical examination, serum biochemistry and radiology. METHODS: Children more than 1 yr were included. Each child was evaluated keeping in mind the possible causes of delayed walking. Also each child was thoroughly examined and diagnosed by combination of clinical, radiological, biochemical findings and response to treatment. RESULTS: Out of forty-two non-walkers during the study period, 25 patients turned out to be affected by nutritional rickets (60%). On follow-up at 3 weeks of treatment, all 25 patients (100%) showed radiological and biochemical response. Five patients were lost to follow-up after 3 weeks of treatment. Seventeen patients started walking within 3 months of treatment. Two patients did not start walking even after complete biochemical and radiological resolution. Radiological resolution, with limiting factor being the healing of lower end of ulna, averaged 5 months. CONCLUSION: The study reveals that majority of ricketic non-walkers start walking within 2 to 5 months of appropriate treatment.

Factors associated with treatment failure in childhood tuberculosis.

We retrospectively reviewed records of 541 children (315 boys) suffering from tuberculosis, median age 95 (range 2-180) months, to determine factors associated with treatment failure. 256 (47.3%) children had pulmonary tuberculosis (PTB) while 285 (52.7%) had extrapulmonary tuberculosis (EPTB). 459 (84.8%) children were cured and 82 (15.5%) had treatment failure. On bivariate analysis, AFB positivity [OR= 2.13 (95% CI 1.18- 3.85)], non-receipt of BCG vaccination during infancy [OR=1.73 (1.02- 2.91)] and EPTB [1.9 (1.16- 3.11)] were associated with treatment failure. On multivariate analysis, only extrapulmonary tuberculosis was significantly associated with treatment failure.

Montelukast in pediatric asthma management.

Leukotriene modifiers (receptor antagonist and biosynthesis inhibitor) represent the first mediator specific therapeutic option for asthma. Montelukast, a leukotriene receptor antagonist is the only such agent approved for use in pediatric patients. Montelukast modifies action of leukotrienes, which are the most potent bronchoconstrictors, by blocking Cysteinyl leukotriene receptors. Systemic drug like mountelukast can reach lower airways and improves the peripheral functions which play a crucial role in the evolution of asthma. Review of existing literature showed that montelukast compared to placebo has proven clinical efficacy in better control of day time asthma symptoms, percentage of symptom free days, need for rescue drugs and improvement in FEV 1. Studies also demonstrated improvement in airway inflammation as indicated by reduction in fractional exhaled nitric oxide, a marker of inflammation. Studies comparing low dose inhaled corticosteroids (ICS) with montelukast are limited in children and conclude that it is not superior to ICS. For moderate to severe persistent asthma, montelukast has been compared with long acting beta agonists (LABA) as an add-on therapy to ICS, montelukast was less efficacious and less cost-effective. It has beneficial effects in exercise induced asthma and aspirin-sensitive asthma. Montelukast has onset of action within one hour. Patient satisfaction and compliance was better with montelukast than inhaled anti-inflammatory agents due to oral, once a day administration. The recommended doses of montelukast in asthma are- children 1-5 years: 4 mg chewable tablet, children 6-14 years: 5mg chewable tablet, ADULTS: 10mg tablet; administered once daily. The drug is well tolerated. Based on the presently available data montelukast may be an alternative treatment for mild persistent asthma as monotherapy where ICS cannot be administered. It is also an alternative to LABA as an add-on therapy to ICS for moderate to severe persistent asthma. The other indications for use of montelukast include: allergic rhinitis, exercise induced bronchoconstriction and aspirin-induced asthma.