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Open access

Olav Inge Håskjold, Henrik Stenestø Foshaug, Therese Benedikte Iversen, Helga Charlotte Kjøren, and Vegard Heimly Brun

Objective

The basis of thyroid nodule diagnostics is ultrasound-guided fine needle biopsy with cytological evaluation (FNC) if ultrasound appearance is not clearly benign. The aim of this study was to investigate the predictive potential of dedicated, expert high-resolution ultrasound, to see if histopathological entities of thyroid nodules can be diagnosed without invasive FNC biopsies.

Design

Prospective case-cohort study.

Methods

187 patients with 221 thyroid nodules were examined with ultrasound and prospectively assigned to the expected histopathological diagnosis: colloid nodule, adenomatoid colloid nodule, follicular adenoma, follicular carcinoma, follicular variant of papillary thyroid carcinoma, papillary thyroid carcinoma, or other thyroid cancer. In 101 of these, we later obtained histopathological reports for comparison.

Results

Overall accuracy for classification into discrete histopathological categories by expert ultrasound was 71.3% and Cohen’s Kappa was 0.62. The sensitivity and specificity for detecting malignancy were 97.3% and 78.1%. The diagnostic accuracy for malignancy was 85.1%. ACR-TIRADS scores for the same nodules had a sensitivity of 97.3%, specificity of 26.6%, and accuracy of 52.5%.

Conclusion

Dedicated expert high-resolution ultrasound without FNC can reliably distinguish benign vs malignant nodules, but also differentiate between several histopathological entities in thyroid nodules. There is potential for a reduction in the number of invasive FNC biopsies and diagnostic operations.

Open access

Valentina Guarnotta, Silvia Lucchese, Mariagrazia Irene Mineo, Donatella Mangione, Renato Venezia, Piero Luigi Almasio, and Carla Giordano

Objective

The aim of this study is to clarify, in girls with premature pubarche (PP), the influence of premature androgenization on the prevalence of polycystic ovary syndrome (PCOS).

Design and patients

Ninety-nine PP girls, 63 who developed PCOS and 36 who did not develop PCOS, were retrospectively included. Clinical, anthropometric, and metabolic parameters were evaluated at the time of diagnosis of PP and after 10 years from menarche to find predictive factors of PCOS.

Results

Young females with PP showed a PCOS prevalence of 64% and showed a higher prevalence of familial history of diabetes (P = 0.004) and a lower prevalence of underweight (P = 0.025) than PP-NO-PCOS. In addition, girls with PP-PCOS showed higher BMI (P < 0.001), waist circumference (P < 0.001), total testosterone (P = 0.026), visceral adiposity index (VAI) (P = 0.013), total cholesterol (P < 0.001), LDL-cholesterol (P < 0.001), non-HDL cholesterol (P < 0.001) and lower age of menarche (P = 0.015), ISI-Matsuda (P < 0.001), DIo (P = 0.002), HDL cholesterol (P = 0.026) than PP-NO-PCOS. Multivariate analysis showed that WC (P = 0.049), ISI-Matsuda (P < 0.001), oral disposition index (DIo) (P < 0.001), VAI (P < 0.001), total testosterone (P < 0.001) and LDL-cholesterol (P < 0.001) are independent predictive factors for PCOS in girls with PP.

Conclusions

Our study established a strong association between multiple risk factors and development of PCOS in PP girls. These risk factors are predominantly related to the regulation of glucose, lipid, and androgen metabolism. Among these factors, WC, ISI-Matsuda, DIo, VAI, total testosterone, and LDL-cholesterol predict PCOS.

Open access

Chun-feng Lu, Xiao-qin Ge, Yan Wang, Jian-bin Su, Xue-qin Wang, Dong-mei Zhang, Feng Xu, Wang-shu Liu, and Min Su

Background: Prolonged heart rate-corrected QT (QTc) interval may reflect poor prognosis of patients with type 2 diabetes (T2D). Serum adenosine deaminase (ADA) levels are related to hyperglycemia, insulin resistance (IR) and inflammation, which may participate in diabetic complications. We investigated the association of serum ADA levels with prolonged QTc interval in a large-scale sample of patients with T2D.

Methods: In this cross-sectional study, a total of 492 patients with T2D were recruited. Serum ADA levels were determined by venous blood during fasting. QTc interval was estimated from resting 12-lead electrocardiograms, and prolonged QTc interval was defined as QTc > 440 ms.

Results: In this study, the prevalence of prolonged QTc interval was 22.8%. Serum ADA levels were positively associated with QTc interval (r = 0.324, p < 0.0001). The proportion of participants with prolonged QTc interval increased significantly from 9.2% in the first tertile (T1) to 24.7% in the second tertile (T2) and 39.0% in the third tertile (T3) of ADA (p for trend <0.001). After adjusting for other possible risk factors by multiple linear regression analysis, serum ADA level was still significantly associated with QTc interval (β = 0.217, t = 3.400, p < 0.01). Multivariate logistic regression analysis showed that female (OR 5.084, CI 2.379-10.864, p < 0.001), insulin-sensitizers treatment (OR 4.229, CI 1.290-13.860, p = 0.017) and ADA (OR 1.212, CI 1.094-1.343, p < 0.001) were independent contributors to prolonged QTc interval.

Conclusions: Serum ADA levels were independently associated with prolonged QTc interval in patients with T2D.

Open access

Hong Wang, Jie Cao, Jian-bin Su, Xue-qin Wang, Dong-mei Zhang, and Xiao-hua Wang

Background

Antithrombin 3 (AT3) is a physiological inhibitor of thrombin, and serum AT3 activity was found to decrease at the status of type 2 diabetes (T2D). T2D was presented with an increased risk of thrombotic complications at the background of impaired insulin sensitivity. The aim of this study was to investigate the relationship between insulin sensitivity indices and serum AT3 activity in patients with T2D.

Methods

We conducted a cross-sectional study in patients with T2D who consented to participate in the study at the Endocrinology Department of Affiliated 2 Hospital of Nantong University from January 2015 to June 2018. All patients received serum AT3 activity test and 75 g oral glucose tolerance test (OGTT). Basal and systemic insulin sensitivity were assessed by homeostasis model assessment of insulin resistance (HOMA-IR) and Matsuda index (ISIMatsuda), respectively, from the OGTT. And other relevant clinical data were also collected.

Results

Total of 1612 patients with T2D were enrolled in the study, with a mean age of 58.67 ± 13.09 years and a median diabetes duration of 6 years (interquartile range, 1–10 years). Across ascending quartiles of serum AT3 activity, HOMA-IR progressively decreased, while ISIMatsuda progressively increased (all P for trend < 0.001). Moreover, serum AT3 activity was negatively correlated with HOMA-IR (r = −0.189, P < 0.001) and positively correlated with ISIMatsuda (r = 0.221, P < 0.001). After adjusting for other metabolic risk factors, hemostatic parameters and glucose-lowering therapies by multivariate linear regression analysis, HOMA-IR (β = −0.185, t = −5.960, P < 0.001) and ISIMatsuda (β = 0.197, t = 6.632, P < 0.001) remained independently associated with the serum AT3 activity in patients with T2D, respectively.

Conclusions

Reduced basal and systemic insulin sensitivity are associated with decreased serum AT3 activity in patients with T2D.

Open access

Milena Kloter, Claudia Gregoriano, Ellen Haag, Alexander Kutz, Beat Mueller, and Philipp Schuetz

Objective: Systemic infections and sepsis lead to a strong activation of the vasopressin system, which is pivotal for stimulation of the endocrine stress response and in addition has vasoconstrictive and immunomodulatory effects. Our aim was to assess the significance of the vasopressor system through measurement of C-terminal proAVP (copeptin) regarding mortality prediction in a large prospective cohort of patients with systemic infection.

Design and Methods: This secondary analysis of the observational cohort TRIAGE study included consecutive, adult, medical patients with an initial diagnosis of infection seeking emergency department care. We used multivariable regression analysis to assess associations of copeptin levels in addition to the sequential organ failure assessment (SOFA) score with 30-day mortality. Discrimination was assessed by calculation of the area under the curve (AUC).

Results: Overall, 45 of 609 (7.4%) patients with infection died within 30 days. Non-survivors had a marked upregulation of the vasopressin system with a more than 4-fold increase in admission copeptin-levels compared to non-survivors (199.9 ± 204.7 vs. 46.6 ± 77.2 pmol/L). In a statistical model copeptin was significantly associated with mortality (adjusted odds ratio of 1.04, 95% CI 1.01 to 1.07, p=0.002). Regarding discrimination, copeptin alone showed an AUC of 0.82, while adding copeptin to the SOFA score significantly improved its prognostic ability (AUC 0.83 vs. 0.86, p=0.027).

Conclusion: Activation of vasopressin system mirrored by an increase in copeptin levels provided significant information regarding mortality risk and improved the SOFA score for prediction of sepsis mortality.

Trial registration: ClinicalTrials.gov NCT01768494. Registered January 9, 2013

Open access

Rossella Cannarella, Andrea Crafa, Sandro La Vignera, Rosita A. Condorelli, and Aldo E. Calogero

BACKGROUND. Animal studies suggest that insulin-like growth factor 1 (IGF1) may influence the function of the hypothalamus-pituitary-testicular axis, especially in childhood, but the evidence in humans is scanty. Laron syndrome, a human model of IGF1 deficiency, may help to solve this issue.

PURPOSE. This systematic review aims to analyze puberty onset and progression, testicular volume, gonadotropin, and total testosterone serum levels, sperm parameters and fertility, and penile length in patients with Laron syndrome.

METHODS. Specific key-words were used. All data on male patients with Laron syndrome were included.

RESULTS. Seventeen articles matched the inclusion criteria and entered in the analysis, for a total of 125 male patients. Puberty was absent in 8.9% and delayed in 35.6% of untreated patients of pubertal age. After onset, the duration of the pubertal process was prolonged in 76.9% of untreated patients. The growth spurt was absent in 52.6% and delayed in 31.6% of untreated patients. The testicular volume was small in the two patients who did not receive any treatment. Treatment with IGF1 increased gonadotropin and testosterone serum levels in 5 out of 5 patients of pubertal age. No effect was found in 4 out of 4 patients younger than 5 years. No study reported data on sperm parameters and fertility. Micropenis occurred in 67.2% of patients.

CONCLUSION AND FUTURE PERSPECTIVES. Delayed puberty is common in patients with Laron syndrome. The growth hormone-IGF1 axis may influence the time of puberty onset. Serum levels of IGF1 should be investigated in children with delayed puberty, scarce progression of testicular growth, and/or micropenis.IGF1 levels might be measured in children with delayed puberty, poor testicular growth, and/or micropenis.

Open access

Beibei Zhu, Yan Han, Fen Deng, Kun Huang, Shuangqin Yan, Jiahu Hao, Peng Zhu, and Fangbiao Tao

Objectives

Compared with other thyroid markers, fewer studies have explored the associations between triiodothyronine (T3), T3/free thyroxine (fT4) and glucose abnormality during pregnancy. Thus, we aimed to: (i) examine the associations of T3 and T3/fT4 with glucose metabolism indicators and (ii) evaluate, in the first trimester, the performance of the two markers as predictors of gestational diabetes mellitus (GDM) risk.

Methods

Longitudinal data from 2723 individuals, consisting of three repeated measurements of T3 and fT4, from the Man’anshan birth cohort study (MABC), China, were analyzed using a time-specific generalized estimating equation (GEE). The receiver operating characteristic curve (ROC) – area under the curve (AUC) and Hosmer–Lemeshow goodness of fit test was used to assess the discrimination and calibration of prediction models.

Results

T3 and T3/fT4 presented stable associations with the level of fasting glucose, glucose at 1h/2 h during pregnancy. T3 and T3/fT4 in both the first and second trimesters were positively associated with the risk of GDM, with the larger magnitude of association observed in the second trimester (odds ratio (OR) = 2.50, 95% CI = 1.95, 3.21 for T3; OR = 1.09, 95% CI = 1.07, 1.12 for T3/fT4). T3 ((AUC) = 0.726, 95% CI = 0.698, 0.754) and T3/fT4 (AUC = 0.724, 95% CI = 0.696, 0.753) in the first trimester could improve the performance of the prediction model; however, the overall performance is not good.

Conclusion

Significant and stable associations of T3, T3/fT4 and glucose metabolism indicators were documented. Both T3 and T3/fT4 improve the performance of the GDM predictive model.

Open access

Chun-feng Lu, Wang-shu Liu, Xiao-qin Ge, and Feng Xu

The aim of the present study was to evaluate the association between adenosine deaminase (ADA) levels and diabetic kidney disease (DKD) in patients with type 2 diabetes (T2D). In this study, patients with T2D who had been screened for DKD were recruited. Patients with an estimated glomerular filtration rate (eGFR) < 60 ml/min/1.73 m2 or a urinary albumin-to-creatinine ratio (UACR) ≥ 30 mg/g for 3 months were identified as having DKD. The prevalence of DKD was 13.3%, and the range of serum ADA levels was 4-37 U/L. Serum ADA levels were positively associated with cystatin C levels and UACR (r = 0.295 and r = 0.302, respectively, both p < 0.05) and negatively associated with eGFR (r = -0.342, p < 0.05). The proportion of participants with DKD increased significantly from 3.8% in the first tertile (T1) to 13.6% in the second tertile (T2) and 25.9% in the third tertile (T3) of ADA (p for trend < 0.001). After adjusting for clinical risk factors for DKD via multiple logistic regression, the corresponding odds ratios (ORs) of DKD for the participants in T2 and T3 versus those in T1 of ADA were 5.123 (1.282–20.474) and 10.098 (1.660–61.431), respectively. Receiver operating characteristic (ROC) analysis revealed that the optimal cutoff value of ADA to indicate DKD was 10 U/L. Its corresponding sensitivity and specificity were 75.5% and 56.4%, respectively. Our results demonstrated that serum ADA levels were closely associated with DKD and partly reflect the risk of DKD in patients with T2D.

Open access

Wenrui Wang and Chuan Zhang

The most distinctive pathological characteristics of diabetes mellitus induced by various stressors or immune-mediated injuries are reductions of pancreatic islet β-cell populations and activity. Existing treatment strategies cannot slow disease progression; consequently, research to genetically engineer β-cell-mimetics through bi-directional plasticity is ongoing. The current consensus implicates β cell dedifferentiation as the primary etiology of reduced β-cell mass and activity. This review aims to summarize the etiology and proposed mechanisms of β-cell dedifferentiation, and to explore the possibility that there might be a time interval from the onset of β-cell dysfunction caused by dedifferentiation to the development of diabetes, which may offer a therapeutic window to reduce β-cell injury and to stabilize functionality. In addition, to investigate β-cell plasticity, we review strategies for β-cell regeneration utilizing genetic programming, small molecules, cytokines, and bioengineering to transdifferentiate other cell types into β-cells; and the development of biomimetic acellular constructs to generate fully functional β-cell mimetics. However, the maturation of regenerated β-cells is currently limited. Further studies are needed to develop simple and efficient reprogramming methods for assembling perfectly functional β-cells. Future investigations are necessary to transform diabetes into a potentially curable disease.

Open access

Po-Chung Cheng and Chia-Hung Kao

Objective

Coronary heart disease (CHD) is a prevalent complication of type 2 diabetes mellitus (T2DM). The proatherogenic low-density lipoprotein (LDL) cholesterol is an established risk factor of cardiovascular disease, and evidence also suggests that postprandial plasma glucose (PPG) levels closely delineate CHD mortality in diabetes. The investigators hypothesized that the addition of telehealth consultation to standard antidiabetic therapy may help to reduce postprandial glucose variability and plasma LDL cholesterol levels in patients with T2DM.

Methods

This cross-sectional study enrolled patients with newly diagnosed T2DM who received standard antidiabetic therapy with or without additional telehealth consultation. Participants received blood tests for plasma lipid profile and glucose levels at the diagnosis of diabetes and after 1 month of therapeutic intervention. Laboratory results were compared between treatment groups to determine the efficacy of complementary telehealth consultation.

Results

In this study, 375 participants were enrolled. The standard treatment group had considerably greater levels of plasma LDL cholesterol than recipients of telehealth consultation (110 mg/dL vs 93.1 mg/dL, P < 0.001). Moreover, patients receiving standard treatment had greater levels of fasting plasma glucose (104 mg/dL vs 98.5 mg/dL, P = 0.027), 2-h PPG (169 mg/dL vs 111 mg/dL, P < 0.001), and postprandial glucose variability (65.4 mg/dL vs 12.8 mg/dL, P < 0.001) than participants under telehealth consultation.

Conclusions

Telemedicine in addition to standard antidiabetic therapy helped to reduce plasma LDL cholesterol levels and postprandial glucose variability in patients with newly diagnosed T2DM. Therefore, telehealth consultation is a suitable complement to pharmacologic therapy for diabetic patients to assist in the management of proatherogenic dyslipidemia and postprandial glucose variability.