{"title":"Correlation of Altered Lipid Profile, Uric Acid and Fasting Plasma Glucose Levels in Females with Hypothyroidism","authors":"Koley Satyajit, Sur Arindam","doi":"10.4172/2161-1017.1000275","DOIUrl":"https://doi.org/10.4172/2161-1017.1000275","url":null,"abstract":"Introduction: Hypothyroidism is a common endocrinal disorder in which thyroid gland does not produce enough thyroid hormones. The disease mainly occurs in female and its prevalence rises with age. Hypothyroidism may be the underlying cause of dyslipidemia and alteration of plasma glucose levels as thyroid hormones plays a key role in lipid and carbohydrate metabolism. It also helps in the growth and development of kidney; hence hypothyroidism may alter the uric acid level in serum due to altered secretion of uric acid at renal tubules. Aims and Objectives: To evaluate if there is any significant correlation between lipid parameters, uric acid, fasting plasma glucose with thyroid parameters in female. Methodology: We included 35 cases and 35 controls (Aged between 20-45 years) and estimated their serum TSH, FT4 by ELISA method and total cholesterol, triglycerides, LDL-c, HDL-c, VLDL-c, uric acid and fasting plasma glucose levels by chemical methods using random access auto-analyzer. Results: Results showing positive and negative correlation of TSH and FT4 with TC, TG, LDL-C and VLDL-C in cases compared to controls, whereas, HDL-C, UA and FPG didn’t show any positive/negative correlation with hypothyroid parameters in either cases or controls. Conclusion: Hypothyroid status is associated with dyslipidemia. So, earlier biological screening for lipid profile can be done in those patients.","PeriodicalId":11670,"journal":{"name":"Endocrinology and Metabolic Syndrome","volume":"15 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80120573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Gestational Prooxidant-Antioxidant Imbalance may be at Higher Risk for Postpartum Thyroid Disease","authors":"Ahmed Rg","doi":"10.4172/2161-1017.1000279","DOIUrl":"https://doi.org/10.4172/2161-1017.1000279","url":null,"abstract":"Thyroid hormones (THs) regulate many features of fetal development [1-29]. Also, the balance between antioxidants/ prooxidants is critical for the cellular homeostasis and for the development [30,5-10]. This protection might be facilitated by the maternofetal thyroid states [2,5,6,31,32]. Additionally, the defense mechanisms against free radical-induced oxidative stress involve [2,33] (1) preventative mechanisms; (2) repair mechanisms; (3) physical defences; and (4) antioxidant defenses. Alternatively, it was also stated that reactive oxygen species (ROS) may play critical roles in several developmental and physiological processes, however when being in excess ROS can cause oxidative damage [2,5,6].","PeriodicalId":11670,"journal":{"name":"Endocrinology and Metabolic Syndrome","volume":"6 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84833353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Age of Menarche and Related Factors","authors":"A. Arzumanyan, R. Markosyan","doi":"10.4172/2161-1017.1000278","DOIUrl":"https://doi.org/10.4172/2161-1017.1000278","url":null,"abstract":"The time of first menarche is an important milestone in female sexual maturation. Some studies have shown that menarche is occurring earlier in previous decades. The onset of menarche depends on many factors including genetic, social, and environmental and ethnicity. In recent years, obesity defined the factor in menarche age. The possible contribution of prenatal factors has not been adequately explored. Data on the timing of menarche among Armenian girls is not available. The present study examines the menarche age among adolescent girls in Yerevan city. Dates regarding gestational age, birth weight and height, chronological age of onset of menarche, anthropometric dates of menarche time were collected. Mean age of onset of menarche was 11.3 ± 0.8 years old for the total group of 450 girls. Age of menarche was negatively correlated with weight at menarche and positively correlated with height. There is a reversal relation between age of menarche and Body Mass Index (BMI) at menarche. All of the analyses show a consistent and significant relationship of infant size at birth to age at menarche. Girls who were relatively long and light at birth attain menarche earlier.","PeriodicalId":11670,"journal":{"name":"Endocrinology and Metabolic Syndrome","volume":"19 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90914562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
T. Young, B. Depczynski, J. Wall, H. Lahooti, G. Wilcsek
{"title":"Sight Threatening Thyroid Eye Disease Complicating HashimotoâÂÂsThyroiditis","authors":"T. Young, B. Depczynski, J. Wall, H. Lahooti, G. Wilcsek","doi":"10.4172/2161-1017.1000274","DOIUrl":"https://doi.org/10.4172/2161-1017.1000274","url":null,"abstract":"A case of sight threatening thyroid eye disease (TED), arising in a 55 year old woman with primary hypothyroidism due to Hashimoto’s thyroiditis (HT), is described. TSH receptor antibody (TSHRab) was positive as were orbital antibodies. Initial management consisted of methylprednisone intravenously followed by prednisone orally in a tapering dose, orbital irradiation and decompressive surgery. Visual acuity improved but 9 months later, there was evidence of relapse with features of compressive optic neuropathy, and exophthalmos had worsened. Prednisone dose was increased. At that time, TSHRab was negative. She underwent total thyroidectomy on the understanding that this was experimental therapy, surgery confirmed that thyroid pathology was solely TH without any evidence of Graves’ disease. Prednisone was successively tapered without further relapse. Rehabilitative ocular muscle surgery is planned. Whether the improvement seen in TED can be attributed to effect of removal of thyroid antigens following thyroidectomy is purely speculative. Our case illustrates that relapsing sight threatening TED is part of spectrum of TED in HT and demonstrates that clinical features can be severe.","PeriodicalId":11670,"journal":{"name":"Endocrinology and Metabolic Syndrome","volume":"25 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82968172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
B. Uçan, M. Kizilgul, M. Ozbek, M. Çalışkan, G. Saylam, E. Çakal
{"title":"Occult Multifocal Thyroid Papillary Carcinoma with Cystic Lymph Nodes Metastases","authors":"B. Uçan, M. Kizilgul, M. Ozbek, M. Çalışkan, G. Saylam, E. Çakal","doi":"10.4172/2161-1017.1000276","DOIUrl":"https://doi.org/10.4172/2161-1017.1000276","url":null,"abstract":"Background: Papillary thyroid microcarcinoma presenting as cystic lymphadenopathy as a first and sole sign has rarely been reported. When the nodal metastasis is cystic, with no apparent suspicious thyroid mass on ultrasound (US) it may be misdiagnosed as benign cystic masses. An accurate pre-operative diagnosis is essential since the management of these two conditions is different. Case report: A 32-year-old woman was referred to our endocrinology outpatient clinic for evaluation of a neck mass. Ultrasonography (USG) showed 3 lymph nodes, the largest one being 6×19×22 mm (conglomerate lymphadenopathy) in size with a cystic component divided by septa, a complex echo, microcalcifications and undistinguishable echogenic hilum, in the right side adjacent to the carotid artery. However, the thyroid USG has not revealed any abnormality. USG-guided fine-needle aspiration cytology of the cystic lymph node was performed, and cytomorphological findings confirmed a papillary carcinoma derived from the thyroid gland. The patient underwent total thyroidectomy with right lateral and central lymph node dissection. Postoperative histopathology evaluation revealed 3 papillary microcarcinomas in the right lobe, the largest one being 0.4 cm in size and 2 metastatic lymph nodes. Conclusion: Ultrasound-guided FNA is a critical step in lymph node metastases. If lymph node FNA cytology and/ or needle wash specimens confirm thyroid cancer metastases, total thyroidectomy with central lymph node dissection would be appropriate even if ultrasound did not detect any lesion in the thyroid gland as in the presented case.","PeriodicalId":11670,"journal":{"name":"Endocrinology and Metabolic Syndrome","volume":"102 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74261780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Thyrotoxic Periodic Paralysis in a 20-Year-Old Nigerian Male","authors":"Anyanwu Ac, M. Ca, Nwazor Eo, Oputa Rn","doi":"10.4172/2161-1017.1000277","DOIUrl":"https://doi.org/10.4172/2161-1017.1000277","url":null,"abstract":"Background: Thyrotoxic Periodic Paralysis (TPP) is a rare complication of hyperthyroidism characterised by hypokalaemia and recurrent episodes of muscle weakness. Increased awareness will promote early diagnosis and prompt treatment of the condition. Objective: To highlight an uncommon case of TPP in a Nigerian male with normokalaemia on presentation. Case: A 20-year-old male patient on treatment for hyperthyroidism (Grave’s disease) who was referred to the endocrine clinic on account of recurrent episodes of acute symmetrical painful lower limb muscle weakness. He had experienced a total of 5 episodes approximately 2-3 months apart with each attack lasting between 10-36 h there was a positive history of strenuous activities preceding each attack. Limb pain was relieved by analgesics and weakness resolved spontaneously without any specific medications after 2-3 days. Investigations revealed elevated T3 and T4 (212.3 ng/ml and 18.3 μg/ml respectively), reduced TSH (<0.1 mIU/ ml), low-normal serum potassium (3.6 mmol/L) on presentation and hypokalaemia (2.5 mmol/L) during an episode and hypocalcaemia (2.0 mmol/L). He was placed on 30 mg of carbimazole, propranolol 120 mg in divided doses and low dose oral potassium chloride. He showed remarkable response to treatment with reduction in the frequency of attacks and eventual resolution of symptoms.","PeriodicalId":11670,"journal":{"name":"Endocrinology and Metabolic Syndrome","volume":"39 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85307062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Carbonic Anhydrase between Aerobic and Anaerobic Glycolysis","authors":"I. Salihu","doi":"10.4172/2161-1017.1000i014","DOIUrl":"https://doi.org/10.4172/2161-1017.1000i014","url":null,"abstract":"Carbonic anhydrase converts CO2 and H2O generated from aerobic oxidation of glucose in the mitochondria to HCO3+ H+, the HCO3 is either transported in the red blood cells for expiration via the lungs, serve as a chemical buffer or is transported into the liver to serve as a substrate for pyruvate carboxylase for gluconeogenesis. Under condition of exclusively anaerobic glycolysis glucose produces lactate as an end product. Lactate is a metabolic dead end and it has to be shuttled out of the cell to prevent intracellular lactate accumulation. Carbonic anhydrase facilitates lactate transport in and out of the cells through monocarboxylate transporters. It facilitates transport of lactate from muscle and red blood cells into the liver where it serves as a substrate for gluconeogenesis. Both exogenous and endogenous glucose metabolism result in the production of this two metabolic dead end products (CO2 and lactate) which must be transported out of the cells to prevent intracellular accumulation, failure of which result in metabolic acidosis. Inhibition of carbonic anhydrase has long been found to cause metabolic acidosis. Salihu’s cycle provides a means of recycling these end products through ‘carbonic anhydrase’ to prevent intracellular accumulation and hence increase the amount of energy needs of the body through continues ATP production (Figure 1). The question is how does this glycolytic metabolic shift affects energy imbalance especially in diabetes and cancer? Endocrinology & Metabolic Syndrome Salihu, Endocrinol Metab Syndr 2016, 6:5 DOI: 10.4172/2161-1017.1000i014","PeriodicalId":11670,"journal":{"name":"Endocrinology and Metabolic Syndrome","volume":"7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73171015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Metabolic Syndrome, Breast Cancer and Exercise","authors":"Nuri R, Akochakian M, Mahmudieh B","doi":"10.4172/2161-1017.1000256","DOIUrl":"https://doi.org/10.4172/2161-1017.1000256","url":null,"abstract":"Risk of breast cancer and recurrence is increased by Metabolic syndrome. Metabolic syndrome can get improved in patients with breast cancer by regular exercise or physical activity.","PeriodicalId":11670,"journal":{"name":"Endocrinology and Metabolic Syndrome","volume":"37 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2016-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84806704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Godala, I. Materek-Kuśmierkiewicz, D. Moczulski, M. Rutkowski, F. Szatko, E. Gaszyńska, S. Tokarski, J. Kowalski
{"title":"Metabolic Syndrome Increases the Risk of Plasma Vitamin A, C, E and D Deficiency","authors":"M. Godala, I. Materek-Kuśmierkiewicz, D. Moczulski, M. Rutkowski, F. Szatko, E. Gaszyńska, S. Tokarski, J. Kowalski","doi":"10.4172/2161-1017.1000254","DOIUrl":"https://doi.org/10.4172/2161-1017.1000254","url":null,"abstract":"The increasing incidence of metabolic diseases such as obesity or diabetes made them a major public health problem. Increasing oxidative stress induced by reactive oxygen species, which initiate the oxidative adverse changes in the cell, is mentioned, among other risk factors, to underlie these diseases. Vitamin A, C and E are listed among non-enzymatic mechanisms counteracting this phenomenon. Vitamin D deficiency is also associated with cardiovascular diseases. Objectives: The aim of the study was to assess the risk of vitamin A, C, E and D deficit in plasma of metabolic syndrome (MS) patients. Material and methods: The study included 191 patients with MS and 98 subjects without MS. Log-linear analysis was used in the assessment of mutual interactions between the vitamin concentration and the analysis of classification by ROC curves to predict the frequency of vitamin deficiency in MS patients. Results: A correlation was found between the plasma level of vitamins in the group of MS patients. Vitamin A concentration correlated with that of vitamin C (r=0.51, p=0.0000), vitamin D (r=0.49, p=0.0000) and E (r=0.32, p=0.0001). The plasma level of vitamin D correlated with the level of vitamin E (r=0.46, p=0.00000) and vitamin C (r=0.37, p=0.0000). Regression analysis showed a correlation between the concentration of the tested vitamins in patients with MS. Interactions were observed between vitamins C-A and C-D. HDL cholesterol level was lower in patients with vitamin A deficiency compared to patients with its normal level. Conclusions: The plasma levels of vitamin A, C, E and D were significantly lower in patients with MS than in healthy subjects and they mutually correlated with each other. The normalization of glucose and HDL level may contribute to the regulation of the concentration of vitamin A in patients with MS.","PeriodicalId":11670,"journal":{"name":"Endocrinology and Metabolic Syndrome","volume":"33 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2016-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85657795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of Insulin Resistance in Chronic Kidney Disease","authors":"Frank Ah, S. Kazempour-Ardebili","doi":"10.4172/2161-1017.1000255","DOIUrl":"https://doi.org/10.4172/2161-1017.1000255","url":null,"abstract":"Insulin resistance accompanies many well-established cardiovascular risk factors, such as obesity, hypertension, dyslipidaemia and type 2 diabetes. Since cardiovascular disease (CVD) is the leading cause of death in patients with end stage renal disease (ESRD), insulin resistance is thought to play a role in the morbidity and mortality associated with ESRD. This paper reviews the available information on insulin resistance in patients with impaired kidney function as well as those on renal replacement therapy in the form of maintenance hemodialysis. Potential mechanisms for the dynamic changes in insulin resistance, which occur through the different stages of kidney disease, are also discussed. We hypothesize that stabilizing insulin sensitivity may have a positive effect on improving outcome in ESRD subjects.","PeriodicalId":11670,"journal":{"name":"Endocrinology and Metabolic Syndrome","volume":"5 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2016-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76078748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}