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In recent years, our knowledge regarding the physiological role of vitamin K has expanded beyond regulation of coagulation to include many other aspects of human health. In the present review, we aimed to evaluate the existing evidence for beneficial effects of vitamin K on type 2 diabetes and components of the metabolic syndrome as risk factors for cardiovascular disease. Increased dietary intake of vitamin K has been linked to lower incidence of type 2 diabetes mellitus (T2DM), possibly through its enhancement of insulin production and sensitivity. Additionally, higher plasma levels of vitamin K1 have been associated with lower T2DM risk and decreased insulin resistance, and supplementation trials also suggest a positive influence of vitamin K on glucose regulation. Vitamin K might also beneficially affect serum lipids and lipid metabolism. However, the available data remain controversial. Additionally, different studies use different approaches to assess vitamin K status owing to the absence of a generally accepted marker, which further complicates data evaluation. In conclusion, vitamin K possibly improves glucose and lipid metabolism and could be an emerging target in the context of prevention and control of T2DM, insulin resistance, and dyslipidemia.

(1) Background: This study aimed to evaluate hypothalamic–hypophyseal (HH) axis involvement in Primary Sjögren’s syndrome (pSS) using MRI and assess its relationship with hypothalamic–pituitary–adrenal (HPA) axis dysfunction. (2) Methods: A total of 22 postmenopausal women with pSS and 17 healthy controls were enrolled. Midline sagittal T1-weighted MRI was used to measure pituitary gland height (PGH). Dynamic contrast-enhanced imaging assessed hypothalamic–hypophyseal (HH) microcirculation, while diffusion tensor imaging (DTI) evaluated hypothalamic microstructure. Biochemical variables, including cortisol and complement factors, were measured. Linear regression analysis was performed to identify predictors of PGH. (3) Results: Patients had a mean disease duration of 11.5 ± 6.7 years. PGH was significantly different in patients than in controls (3.6 ± 1.1 mm vs. 4.4 ± 0.6 mm, p = 0.004). Cortisol levels were also reduced (8.9 ± 4.6 µg/dL vs. 12.6 ± 4.7 µg/dL, p = 0.040), while ACTH levels were not significantly different. Dynamic imaging demonstrated delayed enhancement of the anterior pituitary lobe. DTI revealed no hypothalamic microstructural abnormalities. PGH was positively associated with C3 (p = 0.029). (4) Conclusions: pSS is associated with pituitary structural and functional alterations consistent with HPA axis hypofunction, likely reflecting immune-mediated pituitary involvement with preserved hypothalamic integrity.

The detection of frequent premature ventricular contractions (PVCs) in an athlete represents one of the most important red flags during pre-participation screening. We report the case of a 6-year-old asymptomatic male athlete practicing basketball and sailing, who was examined for pre-participation screening. His resting electrocardiogram showed very frequent, isolated, monomorphic PVCs. The PVCs exhibited a left bundle branch block morphology with an inferior axis and R/S wave precordial transition in lead V3. The most likely origin of PVCs was considered the left ventricular outflow tract. Resting transthoracic echocardiography revealed reduced left ventricular systolic function, with an ejection fraction of 43%, indicating the possible existence of PVC-induced cardiomyopathy. We detected 43,149 isolated monomorphic PVCs (PVC burden: 40%) on 24-h ambulatory electrocardiographic monitoring. Initiation of treatment with atenolol 12.5 mg twice a day led to inadequate reduction of PVCs, with 29,452 isolated monomorphic PVCs (PVC burden: 29%) still observed on 24-h ambulatory electrocardiographic monitoring. After adding flecainide 25 mg twice daily to atenolol treatment, 24-h ambulatory electrocardiographic monitoring revealed complete resolution of ventricular arrhythmias, with no PVCs detected. Left ventricular systolic function recovered to normal. At 12 years of age, the athlete remained on combination therapy with atenolol and flecainide, continued participating in sports, and remained completely asymptomatic with normal cardiac examinations. The optimization of drug treatment was favored over catheter ablation since the athlete was a child and the probable origin of PVCs was the left ventricular outflow tract. This case report highlights that flecainide at a relatively low dose as an add-on therapy to a beta-blocker was highly effective and safe for treating high-burden PVCs originating from the ventricular outflow tract in a juvenile athlete.

OBJECTIVEThe combination of 32 mg naltrexone and 360 mg bupropion prolonged release (NB32) was recently approved by both the food and drug administration (FDA) and the European medicines agency (EMA) as an adjunct to a comprehensive lifestyle intervention to achieve weight loss.DESIGNRandomized controlled trials with naltrexone/bupropion prolonged release were selected through a search based on PubMed listings using the terms “bupropion AND naltrexone”.RESULTSNB32 treatment resulted in 5.0–9.3% weight loss, while the placebo-subtracted weight loss was 3.2–5.2% during 56 weeks of treatment. The proportion of treated patients with ≥5% weight loss was 45–66%, while the placebo-subtracted proportion was 23–34%. NB32 was associated with a decrease in waist circumference, serum triglycerides and insulin resistance and an increase in high-density lipoprotein-cholesterol (HDL-C). Blood pressure mainly remained stable but there was a small increase in heart rate. The most common side effects were nausea, constipation, headache and vomiting. Serious adverse effects, which were very rare, included suicidal thoughts and seizures. In the majority of patients NB32 treatment was well tolerated.CONCLUSIONSNaltrexone/bupropion combination appears to be an effective adjunct to a comprehensive lifestyle intervention in order to achieve weight loss and treat obesity-related comorbidities.

Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as nonalcoholic fatty liver disease (NAFLD), is the main cause of chronic liver disease in children and adolescents. Indeed, epidemiological studies have shown that MASLD affects up to 40% of children with obesity. Despite the recent approval of medications that target weight loss in adolescents that could have benefits on pediatric MASLD, lifestyle interventions, such as diet and exercise, remain the mainstay of our therapeutic approach. More specifically, studies on diet alone have focused on the possible role of carbohydrate or fat restriction, albeit without a definite answer on the best approach. Weight loss after dietary intervention in children with obesity and MASLD has a beneficial effect, regardless of the diet used. In relation to the role of exercise in MASLD reversal, indirect evidence comes from studies showing that a sedentary lifestyle leading to poor fitness, and low muscle mass is associated with MASLD. However, research on the direct effect of exercise on MASLD in children is scarce. A combination of diet and exercise seems to be beneficial with several studies showing improvement in surrogate markers of MASLD, such as serum alanine aminotransferase and hepatic fat fraction, the latter evaluated with imaging studies. Several dietary supplements, such as vitamin E, probiotics, and omega-3 fatty acid supplements have also been studied in children and adolescents with MASLD, but with equivocal results. This review aims to critically present available data on the effects of lifestyle interventions, including diet, exercise, and dietary supplements, on pediatric MASLD, thus suggesting a frame for future research that could enhance our knowledge on pediatric MASLD management and optimize clinicians’ approach to this vexing medical condition.

Athletes are characterized by distinct haemodynamic adaptations of the cardiovascular system, including descending aorta haemodynamics, that could influence the diagnosis of coarctation of the aorta. This study aims to evaluate the normal range for the maximum velocity of blood flow in the descending aorta (Vmax-AoDesc) and the predictors of Vmax-AoDesc in apparently healthy athletes without coarctation of the aorta. We examined 559 asymptomatic healthy athletes with an age of at least 12 years and a tricuspid aortic valve (420 males, age: 29 ± 14 years). We performed evaluations of athletic history, measurements of brachial systolic and diastolic blood pressure, cardiac and aorta ultrasonography and cardiopulmonary exercise testing. Forty athletes were reassessed after a median follow-up of 3.0 (IQR: 2.1) years. The median Vmax-AoDesc was 1.29 (IQR: 0.28) m/s, with a maximum of 2.00 m/s. The Vmax-AoDesc could be independently predicted by age (β = -0.392, < 0.001), ratio of systole/diastole (β = 0.095, = 0.023), brachial systolic blood pressure (β = 0.251, < 0.001), left ventricular stroke volume (β = 0.256, < 0.001), ascending aorta diameter (β = -0.230, < 0.001), aortic arch diameter (β = -0.111, = 0.044) and descending aorta diameter (β = -0.103, = 0.017). Age accounted for the greatest variability of Vmax-AoDesc (5.8%). Vmax-AoDesc correlated positively with h/week of endurance exercise training (rho = 0.182, < 0.001) and oxygen uptake at second ventilatory threshold (rho = 0.299, = 0.001). Vmax-AoDesc did not change significantly during follow-up ( = 0.438). The median change in Vmax-AoDesc was -0.05 (IQR: 0.18) m/s. However, when Vmax-AoDesc was adjusted for all the above-mentioned independent predictors of Vmax-AoDesc apart from age and systolic blood pressure, there was a reduction in adjusted Vmax-AoDesc during follow-up ( = 0.007), indicating a reduction in Vmax-AoDesc with aging. The upper limit of the normal range for Vmax-AoDesc was 2.00 m/s in athletes without coarctation of the aorta. Young age was the most important predictor for the measurement of high Vmax-AoDesc. There was an upregulation of Vmax-AoDesc in athletes with a greater volume of endurance exercise training.

Thirty-seven patients with beta-thalassemia major, including 14 adolescents (15.2 +/- 3.0 years) and 23 adults (26.4 +/- 6.9 years), were studied. T2 relaxation time (T2) of the liver, bone marrow, pancreas and pituitary gland was measured in a 1.5-Tesla magnetic resonance (MR) imager, using a multiecho spin-echo sequence (TR/TE 2,000/20, 40, 60, 80, 100, 120, 140, 160 ms). Pituitary gland height was evaluated in a midline sagittal scan of a spin-echo sequence (TR/TE, 500/20 ms). The T2 of the pituitary gland was higher in adolescents (59.4 +/- 15 ms) than in adults (45.3 +/- 10.4 ms), P < 0.05. The T2 of the pancreas was lower in adolescents (43.6 +/- 10.3 ms) than in adults (54.4 +/- 10.4 ms). No difference among groups was found in the T2 of the liver and bone marrow. There was no significant correlation of the T2 among the liver, pancreas, pituitary gland and bone marrow. There was no significant correlation between serum ferritin and T2 of the liver, pancreas and bone marrow. Pituitary T2 showed a significant correlation with pituitary gland height (adolescents: R = 0.63, adults: R = 0.62, P < 0.05) and serum ferritin (adolescents: R = -0.60, adults: R = -0.50, P < 0.05). In conclusion, iron overload evaluated by T2 is organ specific. After adolescence, age-related T2 changes are predominantly associated with pituitary siderosis and fatty degeneration of the pancreas. Pituitary size decreases with progressing siderosis.

Background: Pre-pregnancy overweight and obesity in reproductive-aged women becomes a growing tendency in middle- and high-income populations. This study aimed to evaluate whether maternal excess body mass index (BMI) before gestation is associated with children’s anthropometric characteristics, as well as perinatal and postnatal outcomes. Methods: This was a cross-sectional study performed on 5198 children aged 2–5 years old and their paired mothers, assigned from 9 different areas of Greece. Maternal and childhood anthropometric data, as well as perinatal and postnatal outcomes, were collected from medical history records or validated questionnaires. Results: Prevalences of 24.4% and 30.6% of overweight/obesity were recorded for the enrolled children and their mothers 2–5 years postpartum. Maternal pre-pregnancy overweight/obesity was more frequently observed in older mothers and female children, and was also associated with high childbirth weight, preterm birth, high newborn ponderal index, caesarean section delivery, diabetes type 1, and childhood overweight/obesity at pre-school age. In multivariate analysis, maternal pre-pregnancy overweight/obesity was independently associated with a higher risk of childhood overweight/obesity at pre-school age, as well as with a higher increased incidence of childbirth weight, caesarean section delivery, and diabetes type 1. Conclusions: Maternal overweight/obesity rates before gestation were related with increased childhood weight status at birth and 2–5 years postpartum, highlighting the necessity of encouraging healthy lifestyle promotion, including healthier nutritional habits, and focusing on obesity population policies and nutritional interventions among women of reproductive age.

The most frequent cause of syncope in young athletes is noncardiac etiology. The mechanism of noncardiac syncope (NCS) in young athletes is neurally-mediated (reflex). NCS in athletes usually occurs either as orthostasis-induced, due to a gravity-mediated reduced venous return to the heart, or in the context of exercise. Exercise-related NCS typically occurs after the cessation of an exercise bout, while syncope occurring during exercise is highly indicative of the existence of a cardiac disorder. Postexercise NCS appears to result from hypotension due to impaired postexercise vasoconstriction, as well as from hypocapnia. The mechanisms of postexercise hypotension can be divided into obligatory (which are always present and include sympathoinhibition, histaminergic vasodilation, and downregulation of cardiovagal baroreflex) and situational (which include dehydration, hyperthermia and gravitational stress). Regarding postexercise hypocapnia, both hyperventilation during recovery from exercise and orthostasis-induced hypocapnia when recovery occurs in an upright posture can produce postexercise cerebral vasoconstriction. Athletes have been shown to exhibit differential orthostatic responses compared with nonathletes, involving augmented stroke volume and increased peripheral vasodilation in the former, with possibly lower propensity to orthostatic intolerance.

OBJECTIVE:--The study was to determine whether being the macrosomic offspring of a mother without detected glucose intolerance during pregnancy has an impact on lipid profile, glucose homeostasis, and blood pressure during childhood. RESEARCH DESIGN AND METHODS--Plasma total, HDL, and LDL cholesterol; triglycerides; apolipoprotein (Apo) A-1, -B, and -E; lipoprotein (a); fasting glucose and insulin; homeostasis model assessment of insulin resistance (HOMA-IR) index; blood pressure; BMI; and detailed anthropometry were evaluated in 85 children aged 3-10 years old, born appropriate for gestational age (AGA; n = 48) and large for gestational age (LGA; n = 37) of healthy mothers. RESULTS:--At the time of the assessment, body weight, height, skinfold thickness, BMI, waist circumference, and blood pressure did not differ between the LGA and AGA groups with the exception of head circumference (P < 0.01). There were no significant differences in plasma total or LDL cholesterol; triglycerides; Apo A-1, -B, or -E; lipoprotein (a); Apo B-to-Apo A-1 ratio; or glucose levels between the groups. The LGA group had significantly higher HDL cholesterol levels (P < 0.01), fasting insulin levels (P < 0.01), and HOMA-IR index (P < 0.01) but lower values of the glucose-to-insulin ratio (P < 0.01) as compared with the AGA group. CONCLUSIONS:--Children born LGA of mothers without confirmed impaired glucose tolerance during pregnancy show higher insulin concentrations than AGAs.