Introduction. It is estimated that over 15% of couples of reproductive age face infertility worldwide. In about half of these cases the male factor is involved. To assess the potential of male fertility the spermiogram analysis may not always be an optimal diagnostic tool, but it remains the basic clinical tool. Material and methods. The purpose of the study is to analyze the regional tendencies of the semen quality in male partners of couples facing infertility. A retrospective study of 4625 patients subject to semen analysis between 2012-2018 was conducted. All semen samples were collected after a recommended period of sexual abstinence of three to five days. The spermiogram analysis was performed by the computerized method according to WHO guidelines for Human Semen analysis, 2010. Results. Of the total number of 4625 men examined, 1861 (40.2%) presented normal values of semen-normozoospermia, and 2764 (59.8%) showed abnormal semen parameters. Asthenozoospermia was the most common abnormality profile recorded in 1394 (30.2%) men, followed by oligoasthenozoospermia diagnosed in 973 men (21.0%). Azoospermia was found in 200 men with an estimated prevalence of 4.3%. In 113 men examined, oligozoospermia was found in 2.4%. Oligoasthenoteratozoospermia was diagnosed in 1.5% and necrozoospermia in 0.3%. Conclusion. The study provides the first evidence that semen quality in men in the Republic of Moldova who are facing infertility in couples has deteriorated over the years.
VASCULAR ENDOTHELIAL GROWTH FACTOR: AN IMPORTANT BIOMARKER IN PEDIATRIC ISCHEMIC STROKE
IntroductionEpilepsy (EP) is one of the entities that are developing in children withperinatal brain lesions (PBL). An early and accurate diagnosis of EP is important because EP has major socioeconomic consequences for both the individual patient and society.The purpose of the study:we aimed toelucidate the significance of perinatal brain damage in childhood epilepsy.Research methodologywe performed a longitudinal prospective case-control study of 1036 children with PBL withvarious degrees of severity, followedbetween the age of 1–3 months and 48±12 months. Two hundred and fifty-ninechildren from study group (25%; 95CI23,65–26,35)developed EP. The control group included 334 healthy children. EEG examination and MRI brain imaging was performed. Enzyme-linked Immunosorbent Assay (ELISA) was used to assess the concentrations of brain derived neurotrophic factor (BDNF) and ciliary neurotrophic factor (CNTF) in the serum in all children. Statistical analyses were obtained using Statistics 7.0 software (StatSoftInc) and Excel.Results: Of all cases of EP- 211 (81,47%; 95 CI 79,06–83,88) were generalised forms; 48 (18,5±2,41%; 95CI16,09–20,91)– focalforms. In 89 cases (34,4%; 95CI31,45–37,35) neonatal seizures preceded EP, in the rest 234 cases (90.3% 95 CI 88.47 to 92.13) EP started at infant age, preferentially between 3 and 6 months – 89 (34,4%; 95CI31,45–37,35). We obtained strong correlations between imaging examinations andpharmacoresistant EP (rxy=-0,72)and middle correlations (rxy=-0,53) with controlled EP. EEG changes comprised approximately 9–11 types of routes and have correlated with the type of seizures (rxy=-0,72). Some patterns (isolated slow activity, diffuse slow activity, grouped generalised peaks) werepreceding the epileptiformchanges(rxy=-0,42).The observedcorrelations between low absoluteserum levels of neurotrophic factors(NF) (at 1–3 months) and EEG changes: BDNF (rxy=-0,72) andCNTF (rxy=-0,74), suggestthe development of pharmacoresistant EP and its progress to epileptic encephalopathies with sever neurophysiological processes disturbance.ConclusionsPBL has an important role in child EP. EP is associated withstructural brain abnormalities, variable electroencephalographic changes that strongly correlate with NF deficit, suggesting a reserved prognosis and evolution towards epileptic encephalopathies. NF study allowed the understanding of the pathogeneticaspects of EP, thus forming the basis for the potential neuroprotective strategies and the need for future studies.
BackgroundPaediatric stroke is a neurological injury that can lead to significant morbidity and mortality. Stroke remains among the top 10 causes of death in children and its morecommon causes are cardiac disorders, blood disorders, vasculopathiesand metabolic disorders.AimWe aim to describe two clinical cases of different diseases, wherestroke was the first manifestation.Material and methodswepresenttwo clinical cases: (1) a2-year-old girl diagnosed with MELAS syndrome and (2) a 14-year-old girl of with systemic lupus erythematosus (SLE), both patients with clinical signs of stroke.ResultsThe 2-year-old patientwas admitted in our clinic with status epilepticus, motor deficit, shortage of speech and language, cognitive disorders. The MRI showed multiple areas of cerebral ischemia located in the left hemisphere. The laboratory tests highlightedlactic acidosis, coagulation abnormalities and central nervous system and cardiovascular system damage. The echocardiographic examination revealed cardiomyopathy. Thus the diagnosis of MELAS syndrome was made.The second patient presented the following clinical manifestations: headache, cognitive dysfunction, hemiplegia. The brain MRI showed multiple areas of ischemia.The laboratory analysis revealed anaemia, increased ofacute phase reactants, increased titers of antinuclear antibodies, increased titers of anticardiolipin IgM and IgG antibodies and elevated titer of IgM and IgG antiphospholipid antibodies. The clinical diagnosis of systemic lupus erythematosus (SLE) was established.ConclusionsThese results suggest that stroke may be the initial manifestation of other severe disease (in our case – mitochondrial disorder, MELAS syndrome and autoimmune disease, SLE). In children, multiple brain structures are involved,at the very onset the clinical symptoms are generalised, nonspecific and polymorphous. Nevertheless, in teenagers, brain nonatheroscleroticvasculopathies are more likely to be responsible for developing of stroke and the clinical syndrome correlates with focal neurological deficits.
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