Current Issue : October - December Volume : 2018 Issue Number : 4 Articles : 7 Articles
not yet been well documented. This study aimed to establish a practical model for thyroid nodule discrimination.\nMethods: Records for 2984 patients who underwent thyroidectomy were analyzed. Clinical, laboratory, and US\nvariables were assessed retrospectively. Multivariate logistic regression analysis was performed and a mathematical\nmodel was established for malignancy prediction.\nResults: The results showed that the malignant group was younger and had smaller nodules than the benign group\n(43.5 Ã?± 11.6 vs. 48.5 Ã?± 11.5 y, p < 0.001; 1.96 Ã?± 1.16 vs. 2.75 Ã?± 1.70 cm, p < 0.001, respectively). The serum thyrotropin\n(TSH) level (median = 1.63 mIU/L, IQR (0.89ââ?¬â??2.66) vs. 1.19 (0.59ââ?¬â??2.10), p < 0.001) was higher in the malignant group than\nin the benign group. Patients with malignancies tested positive for anti-thyroglobulin antibody (TGAb) and anti-thyroid\nperoxidase antibody (TPOAb) more frequently than those with benign nodules (TGAb, 30.3% vs. 15.0%, p < 0.001;\nTPOAb, 25.6% vs. 18.0%, p = 0.028). The prevalence of ultrasound (US) features (irregular shape, ill-defined margin,\nsolid structure, hypoechogenicity, microcalcifications, macrocalcifications and central intranodular flow) was\nsignificantly higher in the malignant group. Multivariate logistic regression analysis confirmed that age (OR = 0.963, 95%\nCI = 0.934ââ?¬â??0.993, p = 0.017), TGAb (OR = 4.435, 95% CI = 1.902ââ?¬â??10.345, p = 0.001), hypoechogenicity (OR = 2.830, 95%\nCI = 1.113ââ?¬â??7.195, p = 0.029), microcalcifications (OR = 4.624, 95% CI = 2.008ââ?¬â??10.646, p < 0.001), and central intranodular\nflow (OR = 2.155, 95% CI = 1.011ââ?¬â??4.594, p < 0.05) were independent predictors of thyroid malignancy. A predictive\nmodel including four variables (age, TGAb, hypoechogenicity and microcalcification) showed an optimal discriminatory\naccuracy (area under the curve, AUC) of 0.808 (95% CI = 0.761ââ?¬â??0.855). The best cut-off value for prediction was 0.52,\nachieving sensitivity and specificity of 84.6% and 76.3%, respectively.\nConclusion: A predictive model of malignancy that combines clinical, laboratory and sonographic characteristics\nwould aid clinicians in avoiding unnecessary procedures and making better clinical decisions....
Thyroid cancer is the most frequent endocrine malignancy, and its incidence and prevalence are increasing worldwide. Despite its\ngenerally good prognosis, the observedmortality rates are higher in the less-developed regions. This indicates that timely diagnosis\nand appropriate initial management of this disease are important to achieve a positive outcome. We performed an observational\nstudy in order to describe the frequency of the BRAF 1799T>A mutation in Mexican mestizo patients with thyroid nodules, a\nscarcely studied ethnic group with large populations. Competitive allele-specific Taqman PCR was performed in 147 samples\nof thyroid tissue DNA obtained from patients histologically diagnosed with papillary thyroid cancer (PTC), colloid goiters, and\nfollicular adenomas. The BRAF 1799T>A mutation frequency was 61.1% in PTC samples (...
Diabetic chorea (DC) is a rare complication of diabetes. Here we describe two\ncases of DC; patient 1 was an 87-year-old woman with chronic kidney disease\nand was administered with sulphonylurea and dipeptidylpeptodase-4 inhibitor.\nShe showed right side hemiballismus and head magnetic resonance imaging\nT1-weighted images revealed a high intensity area in the putamen and\ncaudate nucleus. Patient 2 was a 51-year-old woman who was diagnosed with\ndiabetic ketoacidosis. She showed right side hemiballism and multiple, small\nhyperintense regions in both the periventricular sides in diffusion weighted\nimages. Based on the hemiballism, we concluded a diagnosis of DC in the diabetic\npatient, although the case presentation is rare or has atypical MRI\nfindings....
Objective: To investigate the relationship between AMPK�±, PGC�±, insulin\nresistance and reproductive function in PCOS mice and to find out the molecular\nmechanisms and potential therapeutic molecular targets of pathogenesis\nof PCOS. Methods: The PCOS mouse model was established by DHEA administering\nwith Balb/c mice. And after AMPK agonist AICAR and inhibitor\nCompound C intervention, Fasting blood glucose, fasting insulin and testosterone\nlevels were observed. The HOMA index was calculated. The changes of\nPGC�± expression in ovarian tissue were observed by western blot and immunohistochemistry\nto determine the relationship between insulin resistance and\nPGC�± in PCOS mice. Results: Western blot and immunohistochemistry\nshowed that PGC1�± protein was expressed in the ovary of mice and the expression\nof PGC1�± was negatively correlated with AMPK�± in our study.\nCompared with the control group, the expression of PGC1�± in the ovaries of\nthe mice in PCOS group was significantly increased (P < 0.05), after intervention\nwith AMPK agonist AICAR, the expression of PGC1�± in PCOS + AICAR\ngroup was lower than that in PCOS group (P < 0.05). It is worth noting that\nthe expression of PGC1�± in PCOS mice exposed to AMPK inhibitor Compound\nC also decreased compared with PCOS group (P < 0.05). Conclusion:\nIn ovarian tissue, the insulin resistance-related AMPK�± pathway in PCOS\nmice may be negatively correlated with PGC�±....
Background: Here, we report a case of central pontine demyelinization in a type-2 diabetes patient with hyperglycemia\nafter a binge-eating attack in the absence of a relevant hyponatremia.\nCase presentation: A 55-year-old, male type-2 diabetic patient with liver cirrhosis stage Child-Pugh B was admitted due\nto dysmetria of his right arm, gait disturbance, dizziness, vertigo, and polyuria, polydipsia after a binge-eating attack of\nsweets (a whole fruit cake and 2 Liters of soft drinks). A recently initiated insulin therapy had been discontinued for\n8 months. A serum glucose measurement obtained 5 days prior to hospitalisation was 38.5 mmol/l (694 mg/dl). The\npatient graved for sweets since stopping alcohol consumption 8 months earlier. On admission, venous-blood glucose\nwas 29.1 mmol/l (523.8 mg/dl), glycated hemoglobin was 168.0 mmol/mol or 17.6%. No supplementation of sodium\nchloride was reported. Laboratory exams revealed an elevated serum ammonia level (127.1 �¼mol/l), rendering a hepatic\nencephalopathy very likely. After initiation of insulin therapy, capillary glucose normalized, and serum sodium rose from\n133 on admission to 144 mmol/l during the hospital stay. In retrospect, the mild hyponatremia on admission was\nclassified as pseudohyponatremia due to hyperglycemia. The patient had an insulin resistance (HOMA-IR 7.8 (normal\nrange < 2.5)). A T2-weighted magnetic resonance imaging (MRI) of the head and a cranial computed tomography scan\nwere obtained demonstrating a symmetric central pontine demyelinization. After 26 days in hospital, the patient was\ndischarged with an inkretin-mimetic therapy (dulaglutide SC, 1.5 mg/week) and an intensified conventional insulin\ntherapy (insulin aspart: 14 units/d in euglycemia, insulin glargin 20 units/d).\nConclusions: Central pontine and/or cerebellar myelinolysis can be caused by sudden, severe, and sustained\nhyperglycemia, especially when another risk factor (in this case, liver cirrhosis) is present. Functional neurological\ndeficits in the context of hyperglycemia should prompt for the consideration of this differential diagnosis in all\ndiabetes patients....
It is widely accepted that thyroid hormones (THs), secreted from the thyroid, play important roles in energy metabolism. It is\nalso known that THs also alter the functioning of other endocrine glands; however, their effects on pancreatic function have\nnot yet been reviewed. One of the main functions of the pancreas is insulin secretion, which is altered in diabetes. Diabetes,\ntherefore, could be related to thyroid dysfunction. Earlier research on this subject focused on TH regulation of pancreas\nfunction (such as insulin secretion) or on insulin function through TH-mediated increase of energy metabolism.\nAfterwards, epidemiological investigations and animal test research found a link between autoimmune diseases, thyroid\ndysfunction, and pancreas pathology; however, the underlying mechanisms remain unknown. Furthermore, recent studies\nhave shown that THs also play important roles in pancreas development and on islet pathology, both in diabetes and in\npancreatic cancer. Therefore, an overview of the effects of thyroid and THs on pancreas physiology and pathology is\npresented. The topics contained in this review include a summary of the relationship between autoimmune thyroid dysfunction\nand autoimmune pancreas lesions and the effects of THs on pancreas development and pancreas pathology (diabetes and\npancreatic cancer)....
Background: Growth hormone deficiency (GHD) is a potential consequence of traumatic brain injury (TBI),\nincluding sport-related concussion (SRC). GH stimulation testing is required for definitive diagnosis; however, this is\nresource intensive and can be associated with adverse symptoms or risks. Measurement of serum IGF-1 is more\npractical and accessible, and pituitary tumour patients with hypopituitarism and low serum IGF-1 have been shown\nto have a high probability of GHD. We aimed to evaluate IGF-1 measurement for diagnosing GHD in our local TBI\npopulation.\nMethods: We conducted a retrospective chart review of patients evaluated for GHD at the TBI clinic and referred\nfor GH stimulation testing with insulin tolerance test (ITT) or glucagon stimulation test (GST) since December 2013.\nWe obtained demographics, TBI severity, IGF-1, data pertaining to pituitary function, and GH stimulation results.\nIGF-1 values were used to calculate z-scores per age and gender specific reference ranges. Receiver operator curve\nanalysis was performed to evaluate diagnostic threshold of IGF-1 z-score for determining GHD by GST or ITT.\nResults: Sixty four patient charts were reviewed. 48 patients had mild, six had moderate, eight had severe TBI, and\ntwo had non-traumatic brain injuries. 47 patients underwent ITT or GST. 27 were confirmed to have GHD (peak\nhGH < 5 �¼g/L). IGF-1 level was within the age and gender specific reference range for all patients with confirmed\nGHD following GH stimulation testing. Only one patient had a baseline IGF-1 level below the age and gender\nspecific reference range; this patient had a normal response to GH stimulation testing. ROC analysis showed IGF-1\nz-score AUC f, confirming lack of diagnostic utility.\nConclusion: Baseline IGF-1 is not a useful predictor of GHD in our local TBI population, and therefore has no value\nas a screening tool. TBI patients undergoing pituitary evaluation will require a dynamic test of GH reserve....
Loading....