Search

Autoimmune thyroid dysfunction (AITD) is a significant autoimmune disorder affecting the population across age groups. The clustering of autoimmune diseases tends to occur within the same patients and families. Thus, this study aimed to determine the association of Type 1 diabetes and other autoimmune ailments in patients with autoimmune thyroid disorders.We performed a cross-sectional study, evaluating 500 subjects with a diagnosis of AITD (130 with Graves' disease; 370 with Hashimoto's thyroiditis) on presentation to our tertiary care centre to ascertain the prevalence of associated autoimmune disorders.The frequency of Type 1 diabetes and other autoimmune disorders was 18.5% in Graves' disease and 27.8% in Hashimoto's thyroiditis patients. Coeliac disease (8.8%) (found in 6.9% of Graves' disease and 9.5% of Hashimoto's thyroiditis patients) and type 1 diabetes (7.8%) (found in 3.1% of Graves' disease and 9.5% of Hashimoto's thyroiditis patients) were the most common coexisting autoimmune disorders. Rheumatoid arthritis was the most common non-endocrine autoimmunity (2.8%). Female sex and duration of AITD more than five years were associated with increased odds of associated autoimmune disorders.A high prevalence of associated autoimmune disorders was observed in subjects with autoimmune thyroid dysfunction. We suggest the patients who remain symptomatic and those who develop other symptoms even with appropriate treatment undergo screening for associated autoimmune disorders, thus preventing a delay in diagnosis.

Subclinical hypothyroidism (SCH) is defined as a mildly reduced function of the thyroid gland having elevated serum thyroid-stimulating hormone (TSH) level and normal concentrations of free tri-iodothyronine (FT3), free tetra-iodothyronine (FT4), T3 and T4. It occurs due toThis study was planned to evaluate and compare the efficacy ofPatients having serum TSH levels between 5 and 10 mlU/L and normal T3 and T4 values were diagnosed as SCH. A total of 30 patients were registered and randomly divided into two groups. In group A, patients were treated withTen patients in group A and 11 in group B could complete the course of treatment. The findings revealed that therapy in group A and B showed decrease of 16.61% (

Autonomic activity may be deranged in thyroid dysfunctions and may lead to cardiovascular morbidity and mortality. Myopathy is a common manifestation in thyroid disorders and may be associated with raised serum creatine kinase (CK). We hypothesized that cardiovascular abnormality in thyroid dysfunction may manifest as raised CK-MB. This study was designed to investigate the correlation of CK and its isoform CK-MB with thyroid profile and linear parameters of heart rate variability (HRV). The study was conducted on 35 hypothyroid and hyperthyroid patients each, and 25 age-matched healthy controls. Autonomic activity was assessed by simple short term 5-min HRV. Biochemical evaluation of serum thyroid profile, CK-NAC and CK-MB were estimated in all the subjects. Our results demonstrated low HRV in hypo- as well as hyperthyroid patients. We observed significantly higher serum CK levels in hypothyroid patients when compared to hyperthyroids and controls. However, no significant differences were observed in CK-MB levels in the three groups. Significant positive correlation of CK with TSH and negative correlation with some HRV parameters (LF power, HF power, total power, SDNN, RMSSD) was observed in hypothyroid patients. Whereas correlation of CK-MB with thyroid profile as well as HRV parameters was non-significant in all the groups. Based on the CK and CK-MB findings and their correlation, we conclude that the cardiovascular changes seen in thyroid dysfunctions may primarily be due to autonomic imbalance without apparent cardiac muscle involvement. Whereas, raised CK levels indicate predominantly skeletal muscle involvement in hypothyroid patients.

To determine the various factors influencing glycemic response to pioglitazone monotherapy in newly diagnosed Asian Indian T2DM patients. Thirty T2DM patients (age 53.23 +/- 8.067 yrs, M: F ratio 14:16) were treated with pioglitazone for at least 14 weeks. Relationship between its glucose lowering effect and following patient parameters was studied: BMI, W:H ratio, HOMA-R, HOMA-beta and Pro12Ala polymorph of PPAR-gamma gene. Glycemic targets could be achieved in 20 (66.67%) subjects. All the parameters were comparable among responders and non-responders at the start of therapy. All the participants were homozygous for Pro allele of Pro12Ala polymorph of PPAR-gamma gene. There was a significant positive association between glycemic response to pioglitazone and W: H ratio (beta = 0.426, P = 0.034) and HOMA-R (beta = 0.563, P = 0.008). Primary pioglitazone failure cannot be explained on the basis of body fat and its distribution, insulin resistance and secretory function and Pro12Ala polymorph of PPAR-gamma gene. Among responders central obesity and high insulin resistance were associated with better glycemic response.

This book is the 24th volume of the ongoing series ‘Endocrine Development’, edited by P. -E. Mullis. This book comprises 14 articles contributed by different authors and is a compilation of presentations during the workshop on ‘Hormone Resistance and Hypersensitivity: From Genetics to Clinical Management’ held in Genoa, Italy, in May 2012. In the preface, the editors have rightly emphasized that the meeting provided a unique opportunity for an updated and perspective view of this exciting topic. Though disorders of end organ resistance and hypersensitivity to hormones are rare, but availability of powerful genetic/epigenetic technologies has catalysed translational research in the field of pathogenesis of these disorders. The clinical application of their findings is the development of highly sensitive and specific molecular diagnostic tests for these disorders. This book is an excellent compilation of genotype-phenotype correlations of these paediatric endocrinology disorders. Each of the articles in this book is on a specific hormone disorder. Each article describes the pathophysiology and clinical phenotype first, followed by compilation of available evidences of molecular genetic defects underlying the hormone resistance syndrome and lastly genotype-phenotype correlations and their therapeutic implications are discussed. The first article is on thyroid hormone transporters and resistance. Physiology of thyroid hormone action, transportation specifically by MCT8 and MCT10 and their mutations are discussed. A brief overview of the thyroid hormone receptor is also given in this article. The second article is about the pseudohypoparathyroidism types-I and II and genetics and epigenetics of GNAS complex and PRKAR locus. The pathophysiologic role of their mutations and altered expression due to epigenetic changes is described. The third and fourth chapters are respectively on gonadotropin and androgen insensitivity and outline the clinical and genetic correlations between their receptor mutations and various reproductive hormonal disorders. The next three chapters are respectively on the molecular mechanism of glucocorticoid receptor action from sensitivity to resistance, ACTH resistance and its defects and generalized glucocorticoid resistance (Chrousos syndrome) and sensitivity. The eighth chapter is on pseudohypoaldosteronism (PHA) and describes its three types and renal sodium channel, and NR3C2 mutations underlying PHA1 and PHA2, respectively. The subsequent five chapters are on growth hormone releasing hormone (GHRH), growth hormone (GH) and growth hormone–insulin like growth factor (IGF-I) axis resistance disorders. Mutations in genes coding GHRH, growth hormone receptor, GH signal transduction pathway like STAT5b pathway, IGF-1 and its receptor are described. The associated clinical phenotype and therapeutic implications with human growth hormone and IGF are discussed. A limitation of this book is that there is only one article on insulin resistance and that is on loss of function mutation PLIN1 gene and its association with severe partial lipodystrophy. Though this book contains an overview of specific hormone resistance syndrome genetics and phenotype, it does not include any article on the general aspects of the molecular basis of hormonal action and genetic/genomic techniques used. Despite the shortcomings, the book is a good attempt to present information on clinical genetics of hormone resistance and sensitivity disorders. This information is usually not available in most of the clinical endocrinology books. This book is primarily recommended for clinical endocrinologists and postgraduates in this superspeciality, however, it is also recommended for experts interested in planning research in this area.