Agathoklis Tsatsoulis

Fibroblast growth factors in cardiovascular disease: The emerging role of FGF21

Early detection of risk factors for enhanced primary prevention and novel therapies for treating the chronic consequences of cardiovascular disease are of the utmost importance for reducing morbidity. Recently, fibroblast growth factors (FGFs) have been intensively studied as potential new molecules in the prevention and treatment of cardiovascular disease mainly attributable to metabolic effects and angiogenic actions. Members of the endocrine FGF family have been shown to increase metabolic rate, decrease adiposity, and restore glucose homeostasis, suggesting a multiple metabolic role. Serum levels of FGFs have been associated with established cardiovascular risk factors as well as with the severity and extent of coronary artery disease and could be useful for prediction of cardiovascular death. Furthermore, preclinical investigations and clinical trials have tested FGF administration for therapeutic angiogenesis in ischemic vascular disease, demonstrating a potential role in improving angina and limb function. FGF21 has lately emerged as a potent metabolic regulator with multiple effects that ultimately improve the lipoprotein profile. Early studies show that FGF21 is associated with the presence of atherosclerosis and may play a protective role against plaque formation by improving endothelial function. The present review highlights recent investigations suggesting that FGFs, in particular FGF21, may be useful as markers of cardiovascular risk and may also serve as protective/therapeutic agents in cardiovascular disease.

Rare causes of acute hyperkalemia in the 1st week of life

We describe three neonates with hyperkalemia and renal salt wasting during the 1st week of life. Endocrinological evaluation led to the diagnosis of selective hypoaldosteronism (HA) in two neonates and secondary pseudohypoaldosteronism (PHA) in one. The infant with PHA developed a urinary tract infection, and radiological investigation demonstrated a small dysplastic left kidney with vesicoureteral reflux. The electrolyte and hormonal disturbances in this infant persisted throughout the first months of life. The two infants with selective HA improved rapidly after administration of fludrocortisone orally and the electrolytes and renin values returned to normal. Secondary PHA and selective HA should be considered in the differential diagnosis in salt-losing neonates during the first days of life. Renal ultrasonography, urine culture, and assays of aldosterone and plasma renin activity should be performed in any infant presenting with hyperkalemia and salt wasting after the exclusion of congenital adrenal hyperplasia.

Mosaic Trisomy r(14) Associated With Epilepsy and Mental Retardation

We report a patient with moderate mental retardation, benign clinical course of epilepsy, and type 2 diabetes mellitus. The patient has a mosaic karyotype with 2 cell lines: 1 with a ring chromosome 14 [r(14)], and 1 with an apparently duplicated r(14) chromosome.

Hyperinsulinism and weight loss in obese children

We suggest that due to the intensity of the previous IVIG substitution (resulting in serum IgG trough levels >11 g/l), high amounts of immunoglobulins could have penetrated a damaged blood-brain barrier causing a reduction of viral replication. After initiation of Pleconaril treatment, CSF pleocytosis and the disturbed blood-brain barrier progressively improved and became normal 11 months after treatment. All PCR analyses in CSF and peripheral blood were negative. A local reduction of CSF proin ̄ammatory cytokines (c-interferon) was noted (Fig. 1). Our data suggest successful virus eradication. No new batches of immunoglobulin had been introduced during and after antienteroviral treatment which could have contained high titres of speci®c neutralizing antibodies. However, on rare occasions, PCR results may intermittently be negative during the course of chronic enterovirus encephalitis [1, 2]. Therefore, only further long-term follow up can unequivocally prove sustained virus eradication. In an ongoing study of the European Society of Immunode®ciency, preliminary results with Pleconaril have been promising [5, 6].

Leptin levels are not related to risk factors for coronary heart disease in patients with type 2 diabetes mellitus or normal controls

Abstract This study investigated the relationship between leptin and risk factors for coronary heart disease (CHD) in patients with type 2 diabetes mellitus and nondiabetic controls. A total of 21 patients with diabetes mellitus (group A, 19 men and 2 women) were compared with 10 nondiabetic subjects (group B, 5 men and 5 women). Insulin-treated patients with diabetes mellitus, subjects receiving antihyperlipidemic therapy, and patients with CHD, renal, thyroid, or hepatic disorders were excluded from the study. Body-mass index (BMI), waist-to-hip ratio (WHR), glycosylated hemoglobin A 1c , total cholesterol, triglycerides, apolipoprotein A, apolipoprotein B, apolipoprotein E, fibrinogen, tissue plasminogen activator, and plasminogen inhibitor-1 levels were determined for all patients after an overnight fast. In addition, plasma levels of insulin, proinsulin, and leptin were estimated. The 2 groups were comparable in terms of age (group A, 52.52 ± 4.64 years; group B, 49.50 ± 4.90 years), BMI (group A, 27.50 ± 1.83 kg/m 2 ; group B, 25.79 ± 2.90 kg/m 2 ), and WHR (group A, 0.98 ± 0.07; group B, 0.92 ± 0.09). Plasma leptin levels were significantly higher ( P = 0.038) in nondiabetic subjects than in patients with diabetes mellitus (11.51 ± 8.14 ng/mL vs 5.96 ± 3.85 ng/mL, respectively), possibly because of the higher proportion of women in the nondiabetic group. Leptin levels were significantly correlated with BMI in patients with diabetes mellitus ( r = .51); a tendency toward a positive correlation with insulin levels was noted in this group ( r = .41). No statistically significant correlations were observed regarding leptin with the other risk factors of CHD in either group. Except for the degree of obesity in patients with diabetes mellitus, leptin does not appear to be related to most risk factors for CHD in patients with diabetes or nondiabetic subjects. Additional studies with more patients are needed to help explain the complex interactions of leptin with other CHD risk factors.