There is an increased incidence of thyroid nodules and cancer. In this article, the reasons for this increase are evaluated and discussed. The factors causing increases in the incidence of nodules are the same as those causing increases in thyroid cancer. There are publications from all over the world regarding the rising incidence of thyroid cancer; it is especially associated with papillary cancer. The literature was reviewed and evaluated with regard to this significant phenomenon. Thyroid-stimulating hormone (TSH) is the main mitotic factor. Any agent that elevates TSH will stimulate nodule formation. Therefore, the incidence of thyroid nodules is high in endemic goiter regions due to iodine deficiency. This paper has described many of the factors causing this higher incidence. Of note, metabolic syndrome and insulin resistance are important factors associated with the increased incidence of nodular goiter and papillary thyroid cancer today. However, these data must be confirmed by other studies in the future.

Context Lipodystrophy syndromes are a heterogeneous group of rare genetic or acquired disorders characterized by generalized or partial loss of adipose tissue. LMNA-related lipodystrophy syndromes are classified based on the severity and distribution of adipose tissue loss. Objective We aimed to annotate all clinical and metabolic features of patients with lipodystrophy syndromes carrying pathogenic LMNA variants and assess potential genotype-phenotype relationships. Methods We retrospectively reviewed and analyzed all our cases (n=115) and all published cases (n=379) curated from 94 studies in the literature. Results The study included 494 patients. The most common variants in our study, R482Q and R482W, were associated with similar metabolic characteristics and complications though those with the R482W variant were younger (33 (24) years vs 44 (25) years, p<0.001), had an earlier diabetes diagnosis, (27 (18) vs 40 (17) years, p<0.001) and had lower BMI levels (24 (5) kg/m2 vs 25 (4) kg/m2, p=0.037). Dyslipidemia was the earliest biochemical evidence described in 83% of all patients at a median age of 26 (10) years, while diabetes was reported in 61% of cases. Among 39 patients with an episode of acute pancreatitis, the median age at acute pancreatitis diagnosis was 20 (17) years. Patients who were reported to have diabetes had 3.2 times, while those with hypertriglyceridemia had 12.0 times, the odds of having pancreatitis compared to those who did not. Conclusion This study reports the largest number of patients with LMNA-related lipodystrophy syndromes to date. Our report helps to quantify the prevalence of the known and rare complications associated with different phenotypes and serves as a comprehensive catalog of all known cases.

Aim: To describe the Turkish generalized lipodystrophy (GL) cohort with the frequency of each complication and the death rate during the period of the follow‐up. Methods: This study reports on 72 patients with GL (47 families) registered at different centres in Turkey that cover all regions of the country. The mean ± SD follow‐up was 86 ± 78 months. Results: The Kaplan–Meier estimate of the median time to diagnosis of diabetes and/or prediabetes was 16 years. Hyperglycaemia was not controlled in 37 of 45 patients (82.2%) with diabetes. Hypertriglyceridaemia developed in 65 patients (90.3%). The Kaplan–Meier estimate of the median time to diagnosis of hypertriglyceridaemia was 14 years. Hypertriglyceridaemia was severe (≥ 500 mg/dl) in 38 patients (52.8%). Seven (9.7%) patients suffered from pancreatitis. The Kaplan–Meier estimate of the median time to diagnosis of hepatic steatosis was 15 years. Liver disease progressed to cirrhosis in nine patients (12.5%). Liver disease was more severe in congenital lipodystrophy type 2 (CGL2). Proteinuric chronic kidney disease (CKD) developed in 32 patients (44.4%) and cardiac disease in 23 patients (31.9%). Kaplan–Meier estimates of the median time to diagnosis of CKD and cardiac disease were 25 and 45 years, respectively. Females appeared to have a more severe metabolic disease, with an earlier onset of metabolic abnormalities. Ten patients died during the follow‐up period. Causes of death were end‐stage renal disease, sepsis (because of recurrent intestinal perforations, coronavirus disease, diabetic foot infection and following coronary artery bypass graft surgery), myocardial infarction, heart failure because of dilated cardiomyopathy, stroke, liver complications and angiosarcoma. Conclusions: Standard treatment approaches have only a limited impact and do not prevent the development of severe metabolic abnormalities and early onset of organ complications in GL.

The purpose of this study is to evaluate the foot care self-efficacy of diabetic foot patients and the effect of an educational intervention for improving it. This study was of a semi-experimental design and was conducted between January and December 2019 in a diabetic foot council of a university hospital. After power analysis to determine sample size, 33 participants meeting the inclusion criteria were included in the study. A Patient Identification Form and Diabetic Foot Care Self-Efficacy Scale (DFCSES) were used to collect data. Of the patients, 51.5% were male and the mean age was 54.91 ± 16.61 years. The mean score of DFCSES was 50.18 ± 20.88 before education and 72.67 ± 20.74 after education. The educational intervention has large effects on self-efficacy (d = 1.233), perceived knowledge level on diabetic foot (d = 1.102), perceived health status (d = 0.859), and perceived quality of life (d = 0.807). Educational intervention was found to be an effective way to improve foot care self-efficacy, perceived knowledge level on diabetic foot, perceived health status, and perceived quality of life.