Background:Papillary thyroid microcarcinoma (PTMC) describes a focus of papillary thyroid cancer that is less than 1 cm in size. These tumors are frequently found on histopathological examination of thyroid specimens, operated upon for an indication other than suspected malignancy.Materials and Methods:From 2005 to 2012, 94 of 1300 thyroidectomy specimens in our institution were found to have PTMC. Of these, 77 were isolated PTMC while the others were associated with other differentiated cancers. We studied their clinicopathologic features, treatment and long-term outcome.Results:There were 18 men and 59 women (the male: female ratio was 1:3), their mean age was 44 ± 10.5 years (range: 18-72 years). Multinodular goiter was the most common indication for surgery. Malignancy was suspected in only 31.4% cases. The mean tumor size was 4.1 ± 2.3 mm. Nearly 17% cases had slightly larger tumors measuring >6 but <10 mm. Multifocal tumor was found in 44.1% of cases and among these, multifocal disease restricted to a single lobe was found in 19.5%. Eleven patients (14.2%) had cervical lymph node metastasis, 3 (3.9%) had extra thyroid tumor extension and 2 (2.6%) had evidence of vascular invasion. One patient (1.3%) presented with bone metastasis. Majority of the patients (79.2%) underwent total thyroidectomy with or without lymph node dissection. Sixteen patients (20.7%) who had initially undergone hemithyroidectomy went on to have completion thyroidectomy. Twenty nine patients (36.8%) also received radioactive iodine. The mean duration of follow-up was 20.2 ± 13.5 months. On follow-up one patient developed cervical lymph node recurrence and one died due to a second malignancy.Conclusions:PTMC is often found as an incidental finding on the thyroidectomy specimen. Sometimes they present with regional lymph node metastasis and very rarely with distant metastasis. They have a good prognosis similar to papillary thyroid carcinoma.

IntroductionType 2 Diabetes Mellitus is a modern-day epidemic and dementia has been declared as a global challenge. It is, therefore, worthwhile to investigate the effect that Diabetes has on cognition. Although effective screening is routinely carried out for various complications of Diabetes, its effect on Higher Mental Functions is often overlooked.MethodologyA cross-sectional analytical study to assess Cognitive Impairment was carried out on 800 participants, 400 diabetics and 400 non-diabetics attending a tertiary care center. The Addenbrooke's Cognitive Examination- III was used, which is a validated, highly sensitive tool having a maximum score of 100. Patients with a score &lt; /= 82 were considered to have impaired Cognition. Statistical analysis was done using SPSSv.21. Suitable statistical tests like Mann–Whitney U, t-test, ROC curve and Logistic regression analysis were done.ResultsCognitive Impairment was present in 63.8% of the diabetics when compared to only 10.8% in the non-diabetics, with an Odds Ratio-8.78 (CI-4.47–17.22). The total ACE score in diabetics [median-82 (IQR-4), mean rank-270.06] was less compared to the non-diabetic patients [median- 85 (IQR-3), mean rank-530.94] (U = 27822, p-0.001). Attention, Memory, Language, and Visuospatial domains were significantly lower in the diabetics compared to the non-diabetics. However, the fluency domain was not affected. Hypertension and the presence of macrovascular diseases were significantly associated with Cognitive Impairment (p &lt; 0.005). Those with Cognitive dysfunction also had higher mean RBS values and longer duration of Diabetes (p-0.001). The cut-off value for RBS (to distinguish people with and without Cognitive Impairment) from ROC curve was 142.5 (AUC = 0.834, Youden's Index-0.586, p-0.001) and for duration of Diabetes was 7.5 years (AUC = 0.847, Youden's Index-0.529, p-0.001).ConclusionThis paper highlights that Cognitive Impairment exists in a very high proportion of diabetic patients in Kerala. So, it is important that we do an early assessment of cognitive function in diabetes patients and manage them prudently. Early interventions may prove to be beneficial in the long run, considering the burden of diabetes and cognitive dysfunction associated with the disease.

Catecholamine induced cardiomyopathy in the setting of pheochromocytoma is an unusual clinical entity. Earlier studies have reported left ventricular dysfunction in around 10% of subjects with pheochromocytoma.[1] Catecholamine induced vasoconstriction, direct toxic effect of byproducts of catecholamine degradation and direct receptor-mediated mechanisms are thought to contribute to cardiomyopathy in subjects with pheochromocytoma. The presentation remains a diagnostic challenge as patients may already have hypertensive heart disease and acute coronary syndrome on account of uncontrolled secondary hypertension. We report a case of a 42-year-old male, who presented with features of pheochromocytoma induced cardiomyopathy.

Edwardsiella tarda is very seldom a cause for gastroenteritis in humans. This organism can also cause extraintestinal infections, such as soft tissue infections, meningitis, peritonitis, osteomyelitis, endocarditis and hepatobiliary tract disease, particularly in the setting of compromised immunity. We describe, for the first time a case of E. tarda sepsis with multiple liver abscesses associated with Cushing's syndrome as a result of recreational aquatic exposure.

Various missense mutations in the VHL gene have been reported among patients with familial bilateral pheochromocytoma. However, the p.Arg82Leu mutation in the VHL gene described here among patients with familial bilateral pheochromocytoma, has never been reported previously in a germline configuration. Interestingly, long-term follow-up of these patients indicated that the mutation might have had little impact on the normal function of the VHL gene, since all of them have remained asymptomatic. We further attempted to correlate this information with the results obtained by in silico analysis of this mutation using SIFT, PhD-SNP SVM profile, MutPred, PolyPhen2, and SNPs&GO prediction tools. To gain, new mechanistic insight into the structural effect, we mapped the mutation on to 3D structure (PDB ID 1LM8). Further, we analyzed the structural level changes in time scale level with respect to native and mutant protein complexes by using 12 ns molecular dynamics simulation method. Though these methods predict the mutation to have a pathogenic potential, it remains to be seen if these patients will eventually develop symptomatic disease.