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We conducted this study to determine the role of iron deficiency as a risk factor for first febrile seizure in children. Fifty children between 6 months to 6 years with first febrile seizure (Cases) and 50 children with febrile illness but without convulsions (Controls) were enrolled from the pediatric ward of a tertiary care hospital. Iron deficiency was determined by estimation of hemoglobin, red blood cell indices and serum ferritin. The mean serum ferritin level (microg/L) was significantly low in Cases (31.9 +/- 31.0) as compared to Controls (53.9 +/- 56.5) with P = 0.003. Iron deficiency could be a potential risk factor for febrile seizure in children.

Neurotoxoplasmosis is a major cause of morbidity and mortality, especially in immunocompromised patients. Definitive diagnosis is invasive and difficult thereby requiring a therapeutic trial. We herein report a case of an 11-year-old boy who presented with a tuberculoma on computerized tomography (CT) brain and did not show any clinical improvement on anti-tuberculous drugs. Subsequently, reviewing the CT scans and with supportive serology, a diagnosis of neurotoxoplasmosis was considered. A trial of antitoxoplasmosis therapy was given to which the child fully responded in two weeks. Three weeks later, his magnetic resonance imaging showed complete resolution of the lesion. This report provides an insight into the significance of therapeutic trial in neurotoxoplasmosis.

We report a 10-year-old female child with hypothyroidism and limb muscle pseudohypertrophy (i.e. Kocher-Debre-Semelaigne syndrome) with pericardial effusion. The child presented with generalized swelling, breathlessness and difficulty in walking and in getting up from sitting position (of chronic duration). She had bradycardia, dull facies, marked hypertrophy of both calf muscles and nonpitting edema of legs. Pericardial effusion was detected clinically and confirmed on investigations. Muscle pseudohypertrophy was a striking feature and hypothyroidism was confirmed on thyroid studies. The response to thyroxine replacement was excellent, with resolution of the pericardial effusion and clinical improvement. The unusual presence of pericardial effusion in Kocher-Debre-Semelaigne syndrome is discussed in the report.

Moyamoya syndrome has rarely been reported in association with Down syndrome. We report a case of an 11-year-old female child with Down syndrome who presented with hemiparesis and facial palsy. Imaging investigations (magnetic resonance angiography and digital subtraction angiography) revealed the classical Moyamoya pattern. Work-up for prothrombotic and autoimmune disorders was negative. The neurological deficits recovered well. The association of Moyamoya syndrome in patients with Down syndrome has been highlighted. The possible causes for the association and management have been reviewed briefly.

Pulmonary arteriovenous malformations rarely present in childhood. Two cases are presented in this report. Both the cases presented clinically with cyanosis and clubbing without a cardiac murmur. The second case had cerebral abscess in addition. Both the cases underwent a contrast-enhanced echocardiography which suggested the presence of pulmonary arteriovenous malformations. The first case also underwent 99mTc radionuclide scan and pulmonary angiography. The cases are being reported for their characteristic clinical features and for emphasizing the role of non-invasive modalities like contrast-enhanced echocardiography and radionuclide scan in reaching the diagnosis.

Glanzmann's thrombasthenia (GT) is an uncommon cause of bleeding in children. We diagnosed two siblings as having GT on the basis of flow cytometric studies. Both had cutaneous bleedings and epistaxis since early childhood. Hematological investigations revealed prolonged bleeding time and a normal platelet count. Both the patients had absence of aggregation of platelets with the agonist adenosine diphosphate. Absence of the GPIIb/IIIa receptor was confirmed by flow cytometry. A short review of the disorder is presented.

A case of parkinsonism is reported in a 5-years-old male child following prolonged use of chloroquine. The patient presented with reduced spontaneous movements and speech with an expressionless face and a parkinsonian gait but no tremors. His investigations including CT scan brain, CSF study and serum ceruloplasmin were normal. Chloroquine was discontinued and the patient was started on oral trihexyphenidyl. The patient showed gradual recovery and the drug was successfully withdrawn. The toxic manifestations were only transient and reversible.