Materials and Methods: 154 patients with hypothyroidism were included in the study. They were divided into 4 groups. Group 1 included 66 hypothyroid patients without iron deficiency. They were taken as controls. Group 2 included 66 hypothyroid patients with iron deficiency anemia (IDA). Group 3 included 12 hypothyroid patients with iron deficiency but without anemia (ID). Group 4 included 10 hypothyroid patients which had concomitant iron deficiency with anemia of chronic disorder (ACDC). Ret-He was measured by analyzing blood samples on System XN 350. Thyroid profile, serum ferritin, and biochemical data were measured by an automated analyzer. Statistical analysis was performed by using SPSS 23.
Results: Ret-He was significantly lower with (p < 0.001) in group 2 (hypothyroid patients with IDA), group 3 (hypothyroid patients with ID), and in group 4 (hypothyroid patients with ACDC) as compared to controls in group 1 (hypothyroid patients without iron deficiency). After ROC analysis area under the curve (AUC) of Ret-He for hypothyroid patients with IDA was 0.96 at cutoff 28.5 pg with sensitivity of 93% and specificity of 90%. AUC of Ret-He in the hypothyroid group with ACDC was 0.99 at cutoff 30.8 pg with sensitivity of 90% and specificity of 90%. AUC of Ret-He in hypothyroid patients with ID was 0.97 at cutoff 31.7 pg with sensitivity of 91% and specificity of 70%.
Conclusion: Ret-He is a reliable, rapid, and cost-effective tool for diagnosing iron deficiency in hypothyroid patients.
CASE REPORT: Here we report a case of a 39-year-old lady, with an incidental finding of hyperleukocytosis (white blood cells count: 139.2 x 109/L). Her peripheral blood film revealed 36% of blasts and a bone marrow aspiration showed 53% of blasts. Immunophenotyping showed a population of blasts exhibiting positivity of two lineages, myeloid lineage and B-lymphoid lineage with strong positivity of CD34 and terminal deoxynucleotidyl transferase (Tdt). A conventional karyotyping revealed the presence of Philadelphia chromosome. She was diagnosed with MPAL with t(9,22), BCR ABL1, which carried a poor prognosis. She was treated with acute lymphoblastic leukaemia (ALL) chemotherapy protocol coupled with a tyrosine kinase inhibitor and was planned for an allogeneic stem cells transplant.
CONCLUSION: This MPAL case was diagnosed incidentally in an asymptomatic patient during medical check-up. We highlight this rare case report to raise the awareness about this rare disease. Understanding the pathogenesis of the disease with the underlying genes responsible for triggering the disease, uniform protocols for diagnosis and targeted treatment will help for proper management of these patients.