A case of childhood hemiplegia due to idiopathic hypereosinophilic syndrome is reported. There was no cardiac lesion. The neurological complications associated with hypereosinophilic syndrome and the pathophysiological mechanism of neurotoxicity of human eosinophils are discussed. It is likely that the neurological deficit was due to eosinophilic neurotoxicity.

Introduction:BCR-ABL1 kinase domain mutations represent the most frequent mechanism of resistance to tyrosine kinase inhibitor (TKI) therapy, being detected in 40%–50% of imatinib-resistant patients with chronic myeloid leukemia in chronic phase (CML-CP). Over 100 BCR-ABL1 single-point mutations have been reported in patients with imatinib-resistant CML. There were few studies reported from India on BCR-ABL kinase mutations in imatinib failure patients. We present our data on imatinib resistance mutation analysis (IRMA) and use of imatinib dose hike and 2nd-generation TKI at our institute.Materials and Methods:All patients with a diagnosis of CML in a university hospital from June 2003 to July 2016 and who were tested for IRMA in view of imatinib failure, those in CP, and age <18 years were included in the study.Results:A total of 2110 cases of CML reviewed and 269 cases of CML with imatinib failure were analyzed. The male to female ratio was 1.7:1. The median age at presentation was 36 years (range: 18–66 years). Among these, 26% were primary failures and 74% were secondary failures. The treatment was modified either as imatinib dose hike or nilotinib/dasatinib. Molecular response at 12 months was achieved in 25.7% in imatinib dose hike, 46.6% in nilotinib, and 53.8% in dasatinib arms. The 4-year overall survival in mutation detected group was 37.5% and in nonmutated group was 87.7%.Conclusion:Imatinib-resistant mutations were more common in the cases with secondary failure though not statistically significant. T315I mutation was the common mutation found in the study. Imatinib dose hike to the failure cases resulted in optimal hematological response rates.

Introduction:Renal cell carcinoma (RCC) is the most common cancer of the kidney accounting for 85% of renal tumors. Metastatic RCC (mRCC) had a poor prognosis and with the introduction of tyrosine-kinase inhibitors, such as sunitinib, pazopanib the outcomes improved. There is only one study reported from India on the use of sunitinib in mRCC. We present our analysis of mRCC and use of sunitinib at our institute over 5 years.Materials and Methods:All patients with mRCC receiving sunitinib were analyzed with respect to patient characteristics, response, toxicity, and outcomes.Results:A total of 108 patients were seen during the study period. The male to female ratio was 9.8:1. The median age of patients at presentation was 58 years (range: 15–80 years). Of the 108 patients, 68.51% had metastatic disease at initial presentation. The most common sites of metastases were lung followed by bone. Of the 97 patients eligible for sunitinib, only 76 received at least one cycle of sunitinib, out of which only 48 received further cycles (range: 2–36). The median progression-free survival (PFS) and overall survival (OS) in our patients were 10.2 and 28.2 months, respectively. The most common adverse effect noticed in our population was mucositis followed by hand-foot syndrome.Conclusion:Sunitinib is an option for the treatment of mRCC and shows a good PFS in Indian patients. Median OS and PFS in this study are similar to other reported studies despite the presence of poor risk factors in the patient population. The pitfall in this study is significant attrition due to poor compliance to treatment and follow-up, which is a major factor in the clinic thereby compromising outcomes.