Evaluation of sex hormones and sperm parameters in male epileptic patients.

OBJECTIVES: The aim of this study was to investigate the effect of carbamazepine (CBZ) and sodium valproate (VPA) monotherapy on sexual functions, sex hormones, and semen analysis and quality in male patients with epilepsy. METHODS: A total of 59 male patients with epilepsy, of which 30 were on VPA monotherapy and 29 were on CBZ monotherapy, were included in the study between January 2015 and March 2016. A control group was established with 30 healthy males. Luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin (PRL), free testosterone (fT), estradiol (E2), sex hormone-binding globulin (SHBG) levels and bioactive testosterone (BAT)/bioactive estradiol (BAE), and BAT/LH ratio were studied in groups. All groups received semen analysis and International Index of Erectile Function Scale (IIEF-5) test for erectile dysfunction. RESULTS: E2 and DHEAS levels were higher in VPA and CBZ groups compared to control group (P < .001, P = .014). The decrease in fT levels in the VPA group was statistically significant (P = .038). No significant difference was detected in levels of SHBG, LH, and FSH (P > .05). BAT/BAE ratios were low both in VPA and CBZ groups (P < .001; P < .001), while BAT/LH ratios were low only in CBZ group (P = .033). In semen analysis, semen volume and number of normal sperms were found to be significantly lower in patients receiving antiepileptic drugs compared to control group (P < .05). There were no differences between the groups in rates of abnormal sperm morphology. IIEF-5 scores were found to be significantly lower in VPA and CBZ groups (P < .001). CONCLUSION: VPA or CBZ therapy may lead to dysregulation of sex hormones, sexual dysfunction, and alterations in semen analysis in male patients with epilepsy. This must be considered for the selection of antiepileptic drugs in young male patients.

Role of inflammation in sensory neuropathy in prediabetes or diabetes.

OBJECTIVES: Prediabetes includes individuals with impaired glucose metabolism, and it has been associated with various complications of diabetes mellitus (DM), including peripheral neuropathy. We aimed to investigate the associations between pro-inflammatory (TNF-α) and anti-inflammatory (IL-10) cytokines and neuropathy of very distal sensory nerves in patients with prediabetes or type 2 DM. MATERIALS AND METHODS: We included 50 patients with prediabetes, 50 patients with type 2 DM, and 44 controls in the study. Plasma levels of HbA1c, TNF-α, and IL-10 were analyzed. Electrodiagnostic testing was performed on dorsal sural and medial plantar sensory nerves, which are the very distal sensory nerves of the feet. RESULTS: Abnormalities in nerve conduction studies (NCS) of the dorsal sural and medial plantar sensory nerves were substantially higher in patients with prediabetes or type 2 DM. In addition, plasma levels of TNF-α were significantly higher in patients with type 2 DM than in controls, whereas IL-10 levels were significantly lower in patients with both prediabetes and diabetes. However, we found no correlation between the levels of HbA1c, TNF-α, IL-10, and abnormalities in NCS of the dorsal sural or medial plantar sensory nerves in either patient group. CONCLUSIONS: To our knowledge, this is the first study to assess the relationships between TNF-α, IL-10, and NCS of the most distal sensory nerves in patients with prediabetes or type 2 DM. The mechanisms involved in the pathogenesis of DM and diabetic peripheral neuropathy are complex. The pro-inflammatory stage and the high incidence of neuropathy in patients with prediabetes may suggest a possible causative effect; however, the potential role of inflammation in the pathogenesis of peripheral neuropathy needs further clarification.

Leukoencephalopathy, cerebral calcifications, and cysts.

Association of leukoencephalopathy, cerebral calcifications, and cysts (LCC) is a rare disorder that was recently described. To our knowledge, only 2 reports, including 3 patients in each, have been published in the literature to date. Herein, we report a 19-year-old man with LCC who had neurological symptoms beginning in late adolescence. Clinically, he had rare convulsive seizures, slowly progressive pyramidal symptoms, and normal intelligence. On radiological examination, there were progressive calcifications in the basal nuclei and the cerebral white matter, as well as parenchymal cysts and diffuse abnormal signals of the white matter on T2-weighted sequences on MR imaging. On histopathological examination, angiomatous changes and secondary gliosis were demonstrated.

Macrocyclic Cu(ii)-organophosphonate building block with room temperature magnetic ordering.

Engineering a copper coordination sphere with organoimine ligands and tuning the organophosphonate protonation states produced [{Cu(2,2'-bpy)}2(HO3P(CH2)8PO3H2)4] (1) and [{Cu(terpy)}2(2,7-FDA-H2)2]·(2,7-FDA-H4)(2H2O) (2) (2,7-FDA-H4 = 2,7-fluorenonediphosphonic acid) macrocyclic copper-organophosphonate building blocks. 1 exhibits high temperature magnetic ordering, while 2 is paramagnetic. The structures were characterized by single crystal X-ray diffraction.

Late onset muscular dystrophy with cerebral white matter changes due to partial merosin deficiency.

Merosin-deficient congenital muscular dystrophy (CMD) is an autosomal recessive condition usually with onset at birth or within the first months of life. Affected children are severely disabled and usually do not achieve the ability to walk without support. They invariably have white matter abnormalities on brain magnetic resonance imaging (MRI). We report a 29-year-old man with a late childhood onset limb-girdle type muscular dystrophy and cerebral white matter changes on MRI. Immunocyto-chemical studies of the patient's muscle biopsy showed a reduction in expression of the laminin alpha 2 chain of merosin. The patient had three affected siblings, and microsatellite genotyping confirmed linkage to the laminin alpha 2 locus (LAMA2) on chromosome 6q2 in this family. This case probably represents a milder allelic variant of classical merosin-deficient CMD. Merosin status should be assessed in patients with late-onset limb girdle muscular dystrophy.

The effects of interferon-beta on interleukin-10 in multiple sclerosis patients.

The incidence of the neuropathological lesions and the severity of the clinical symptoms in multiple sclerosis (MS) are correlated with the amount of the transferred autoreactive T cells. The balance between the T helper 1 (Th1) and T helper 2 (Th2) cytokine phenotypes may affect the activity of the disease in MS patients. Interleukin-10 (IL-10) is a cytokine secreted by Th2 cells. Thus, it has been thought that inducing IL-10 may have therapeutic effects in the treatment of MS patients. In this study, in order determine whether different types of prophylaxis change the secretion of IL-10, we measured the levels of IL-10 in relapsing-remitting type multiple sclerosis (RRMS) patients receiving interferon-beta 1b (IFN-beta 1b) or azathioprine (AZA). Our study consisted of RRMS patients (n=45) and healthy subjects (n=15) as control group. Patients were categorized into three groups as those receiving either IFN-beta 1b or AZA and those not receiving prophylaxis. Each group was compared with the control group. Serum IL-10 levels were determined using ELISA method. IL-10 levels of those receiving IFN-beta 1b were found to be significantly higher than that of other groups. These results support that the ability of inducing anti-inflammatory cytokine IL-10 plays a role in the clinical advantage of IFN-beta 1b in MS treatment.