Health effects of methyl isocyanate (MIC) exposure were mostly reported on the one-time acute exposure in Bhopal population. Epidemiological survey conducted by the Indian apex body of health research has been reported as Technical Reports, which were lacking in peer review by the expert epidemiologic scientists. The present pilot survey was aimed to measure the health effects 30 years post disaster in MIC-exposed survivors. Questionnaire-based survey has captured every health complaint in 168 individuals and grouped as systemic functions for interpreting the long-term effects of MIC. Key health parameters, including reproductive outcome and respiratory/orthopedic/general morbidity, were prevalent among the severely exposed population compared to control and moderately exposed groups. The collective incidence of diabetes, hypertension, and cancer also was prevalent in the severely exposed group. Ophthalmic morbidity was almost similar in the three groups, rather with higher incidence in the control group, though not statistically significant. Among all health parameters, reproductive, ophthalmic, and respiratory effects were prevalent over others. Although the incidence of health problems has been declined among the survivors, long-term effect is apparent as scars of one-time acute exposure might trigger sequel of long-term effects. Additionally, acquisition of genetic rearrangements, survival of T cell sub-populations, variable latency of chemical effect on DNA nucleosides, nutritional status, occupational exposure, living environment, lifestyle, and overall gene-environment interaction might perturb individual immunity and favor onset of long-term illness in a scenario of background exposure to MIC. However, the exercise should be continued on a larger sample size for drawing a conclusive result on long-term MIC effect on survivors' health.
Purpose:
The chronic myeloid leukemia (CML) is characterized by the presence of t(9;22)(q34;q11) that results in chimerization of BCR and ABL genes on the rearranged chromosome 22 or Philadelphia chromosome (Ph). Imatinib has been established as the first line of therapy for CML; in case of Imatinib failure or resistance, other second or third generation tyrosine kinase inhibitors (TKIs) are considered. However, acquisition of additional clonal abnormalities (ACAs) interferes in management of CML. We described a complex scenario of cytogenetic remission, relapse, response to TKIs and behavior of ACAs in a case of CML.
Materials and Methods:
Conventional G-banding and FISH cytogenetics, and quantitative PCR studies were conducted in the bone marrow for diagnosis and follow up (FU) of the changes of BCR-ABL gene and ACAs at different time intervals.
Results:
Ph− chromosome disappeared within 6 months of Imatinib therapy, and re-appeared within a year. Subsequent change of TKI to dasatinib eliminated the Ph+ clone, but established an ACA with trisomy 8 (+8). Further change to Nilotinib, eliminated +8 clone, but re-emergence of Ph+ clone occurred with an ACA with monosomy 7 (−7). Reinstate of Dasatinib eliminated Ph+ and −7 clones, but with gradual reappearance of Ph+ and +8 clones. The patient discontinued FU, though participated in a long term examination.
Conclusion:
The complexity of ACAs and Ph+ clones needs frequent monitoring with changes of TKI and technologies.
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