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Spindle epithelial tumor with thymus-like differentiation (SETTLE), a rare tumor of the thyroid gland, is difficult to diagnose irrespective of its unique morphology. It is usually misdiagnosed as synovial sarcoma, thymoma, teratoma, or other thyroid carcinomas. In the current case report, we detail a case of a 36-yearold male patient who presented with thyroid swelling that was initially misdiagnosed as papillary thyroid carcinoma instead of SETTLE. Based on fine needle aspiration, the tumor showed a variable pattern with features suggestive of follicular neoplasm in the right lobe and atypia of undetermined significance in the left lobe. Pathological examination showed multiple nodules on both the right and left lobes, with the largest nodule measuring 4.8 x 4.5 x 3 cm. On microscopic examination, a predominant papillary pattern was observed along with spindle cell areas. Immunohistochemistry revealed positive staining for thyroglobulin, CK, HMWCK, CD99, and BCL-2, which led to the diagnosis of SETTLE. The rare nature of the condition and the reduced awareness about it make this tumor a diagnostic challenge. This case report concludes that in case of any biphasic tumor with epithelial and spindle cells in the thyroid gland, it is important to consider the differential diagnosis of SETTLE. Immunohistochemistry is more useful for diagnosing SETTLE, and thus pathologists are encouraged to judiciously advise the patients for immunohistochemistry to establish accurate and efficient diagnosis.

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Risk management constitutes an essential component of the Quality Management System (QMS) of medical laboratories. The international medical laboratory standard for quality and competence, International Standards Organization (ISO) 15189, in its 2012 version, specified risk management for the first time. Since then, there has been much focus on this subject. We authors aimed to develop a practical tool for risk management in a clinical laboratory that contains five major cyclical steps: risk identification, quantification, prioritization, mitigation, and surveillance. The method for risk identification was based on a questionnaire that was formulated by evaluating five major components of laboratory processes, namely i) Specimen, ii) Test system, iii) Reagent, iv) Environment, and v) Testing. All risks that would be identified using the questionnaire can be quantified by calculating the risk priority number (RPN) using the tool, failure modes, and effects analysis (FMEA). Based on the calculated RPN, identified risks then shall be prioritized and mitigated. Based on our collective laboratory management experience, we authors also enlisted and scheduled a few process-specific quality assurances (QA) activities. The listed QA activities intend to monitor new risk emergence and re-emergence of those previously mitigated ones. We authors believe that templates of risk identification, risk quantification, and risk surveillance presented in this article will serve as ready references for supervisors of clinical laboratories.

A 37-year-old North-Indian woman with type-2-diabetes mellitus was enrolled in a clinical study to establish association of promoter mutation ˗132G>A of IAPP (Amylin) gene and hypertension associated with type-2-diabetes mellitus. Patient was diagnosed having type2 diabetes mellitus at the age of 29 years and was diagnosed having hypertension 3 weeks prior to the study enrolment. Her family history was limited to her mother having diabetes. Patient had a BMI of 26.4 kg/m² at enrolment and being treated with insulin, statins and ACEinhibitor.The baseline investigations including blood glucose, blood urea, serum creatinine, fasting lipid profile of patient were done. Results of metabolic chemistry were within reference intervals except for increased levels of postprandial glucose (Postprandial 218 mg/dL; reference interval, <180 mg/dL), total cholesterol (218 mg/dL; reference interval, 150-200 mg/dL), triglycerides (445.75 mg/dL; reference interval, 50-200 mg/dL). The HBA1C value was 12.2% (reference interval, <6.0%). Patient had no micro and macro-vascular complications. All other laboratory results including serum electrolytes, serum lipoproteins, total protein, albumin, are shown in Table 1. Genomic investigation of patient was done and strikingly we identified a novel mutation −99A>T in IAPP (Amylin) proximal promoter region. The mutated sequence had been submitted and published in Genbank (Genbank accession #: KC432757). DiscussionIslet amyloid polypeptide (IAPP) also called as Amylin is a 37 amino acid peptide is a major subunit of amyloid found in insulinomas and pancreatic islet amyloid of patients with type 2 diabetes mellitus [1]. The structural and functional feature of amylin suggests that it has a hormonal control over carbohydrate metabolism in partnership with insulin and other glucoregulatory factors. Immunolocalisation studies of its secretory granules confirmed that amylin is synthesised in, and probably co-secreted from the ß-cells of the Islets of Langerhans [2]. Apart from its pathological role in type-2-diabetes [3,4], amylin also plays a vital role in glycemic regulation by various mechanisms like delaying gastric emptying, stimulating satiety centre in hypothalamus, thereby delaying the rate of appearance of glucose in blood and preventing post-prandial spikes in blood glucose levels [5]. The human amylin gene IAPP which encodes the complete polypeptide is located in short arm of chromosome12; (12p12.1). IAPP has a proximal promoter region, exon1, intron1, exon2, intron2, exon3 (coding regionapproximately 187 bp) and 130 nucleotides following the stop codon [6]. Amylin is probably generated by proteolytic processing similar to that of pro-insulin and other islet pro-hormones. DNA cloning studies in humans and rats had proved that amylin is generated from a precursor called preproamylin with a signal peptide within itself which undergoes proteolytic cleavage to form a small pro-hormone-like sequence called proamylin which is further cleaved proteolytically to form mature amylin [2]. Like ins...