Summary Philadelphia chromosome/BCR‐ABL1 positive chronic myeloid leukaemia (CML) can be successfully treated with Glivec (Imatinib), which is available free of cost through the Glivec International Patient Assistance programme (GIPAP) to patients with proven CML without means to pay for the drug. We review the acquired mutations in the tyrosine kinase encoded by the BCR‐ABL1 gene underlying Glivec failure or resistance in a cohort of 388 imatinib‐treated CML patients (149 Female and 239 male) registered between February 2003 and June 2016 in Nepal. Forty‐five patients (11 female 34 male) were studied; 18 different BCR‐ABL1 mutations were seen in 33 patients. P‐loop mutation, Kinase domain and A‐loop mutations were seen in 9, 16 and 4 patients respectively. Other mutations were seen in five patients. A T315I mutation was the most common mutation, followed by F359V and M244V. Sixteen mutations showed intermediate activity to complete resistance to Glivec. Among the 45 patients evaluated for BCR‐ABL1 mutations, 4 were lost to follow‐up, 14 died and 27 are still alive. Among the surviving patients, 16 are receiving Nilotinib, 5 Dasatinib and 3 Ponatinib, while 3 patients were referred to India, one of who received allogenic bone marrow transplantation. Understanding the spectrum of further acquired mutations in BCR‐ABL1 may help to choose more specific targeted tyrosine kinase inhibitors that can be provided by GIPAP.
Introductions: Kidney biopsy is the standard tool to diagnose glomerular disease (GD). There is lack of national registry of kidney biopsy for the type, incidence and prevalence of GD. We aim to review kidney biopsy at Patan Hospital for profile of GD in local scenario. Methods: This was a chart review of patients who underwent kidney biopsy at Patan Hospital, Nepal, from October 2013 to September 2015. We analyzed the data for indication of kidney biopsy, types of GD and complication of biopsy. Results: There were 117 patients who had kidney biopsies. Immunoglobulin A Nephropathy was seen in 42 (35.8%) and Lupus Nephritis in 38 (32.5%). Sub nephrotic range proteinuria with or without active urinary sediments was found in 75 (64%). Blood transfusion was required in 3 (2.5%) patients after biopsy. There was no surgical intervention or mortality related to biopsy. Conclusions: IgA Nephropathy was the commonest glomerular disease. Kidney biopsy was a safe and effective procedure.
Wegener’s granulomatosis is a form of systemic vasculitis of small to medium sized vessels and affects upper respiratory tract, lungs and kidneys along with various organs. It causes necrotizing granulomatous inflammation of the affected parts and presents with positive antineutrophil cytoplasmic antibodies in more severe forms. Being a systemic disease with the potential to affect any organ-systems with a wide range of clinical presentations, it is associated with a risk of delay in diagnosis with resultant setback in institution of appropriate treatment. Confusion may arise due to an extent of histological similarity between Wegener’s granulomatosis and the more prevalent tuberculosis, both causing granulomatous inflammation of the affected parts. Here, we present two cases of this rare disorder where the diagnosis was missed for several years in the beginning causing a delay in institution of specific therapy which led to the development of complications.DOI: http://dx.doi.org/10.3126/kumj.v9i3.6309 Kathmandu Univ Med J 2011;9(3):218-21
Summary The Glivec International Patient Assistance Programme makes Glivec (Imatinib mesylate) available to Philadelphia chromosome/BCR‐ABL1 positive patients with chronic myeloid leukaemia (CML) in Lower and Middle Income Countries (LMIC). We have established a large cohort of 211 CML patients who are eligible for Imatinib, in Kathmandu, Nepal. Thirty‐one patients were lost to follow‐up. We report on 180 CML patients with a median age of 38 years (range 9–81). Of these 180 patients, 162 underwent cytogenetic testing and 110 were investigated by reverse transcription polymerase chain reaction. One hundred and thirty‐nine of the 180 patients (77·2%) had at least one optimal response. Taken together, our cohort has a 95% overall survival rate and 78% of the patients were still taking Glivec at a median time of 48·8 months (range 3–140 months). The number of patients who actually failed therapy, as defined by the LeukaemiaNet 2013 criteria, was 39 (21·7%). While our cohort has some differences with those in North America or Europe, we have shown Glivec is effective in inducing an optimal response in our patients in Nepal and that it is possible to deliver a clinical service for CML patients using tyrosine kinase inhibitors in resource‐poor settings.
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