30 Sep 2021
30 Sep 2021
Azerbaijan medical journal (ISSN: 0005-2523) - is a scopus indexed journal since 1961. The publisher of the journal is Izdatel'stvo Elm by WHO Office in Azerbaijan. Azerbaijan medical journal (AMJ) is also UGC approved. The journal publishes general medicine, health science, psychological, pharmaceutical journals and so on.
Aim and Scope
Azerbaijan Medical Journal
Azerbaijan Medical Journal (ISSN: 0005-2523) - is a peer-reviewed journal. The journal seeks to publish original research articles that are hypothetical and theoretical in its nature and that provide exploratory insights in the following fields but not limited to.
Azerbaijan Medical Journal
Crouzon syndrome, also called craniofacial dysostosis, is an autosomal dominant disorder with complete penetrance and variable expressivity. Described by a French neurosurgeon in 1912, it is a rare genetic disorder characterized by premature closure of cranial sutures, midfacial hypoplasia, and orbital defects. Here, we report a case of this rare entity. The patient presented with brachycephaly, maxillary hypoplasia, exophthalmos, mandibular prognathism, along with dental and orbital abnormalities.
Histomorphological parameters of the gastric mucosa in patients with gastritis and helicobacteriosis
Gastritis is an inflammatory condition of the gastric mucosa that has several classifications and causes. The persistence of symptoms of the acute state can lead to the atrophic development of the disease, increasing the tissue injury and consequential the development of gastric cancer. The diagnosis is made by clinical and endoscopic information as well as histopathological analysis of samples obtained from biopsy. The purpose of this review is demonstrate the morphological aspects of gastric mucosa and gastric abnormalities found in the histopathological diagnosis of gastritis.
Features of changes in Vitamin D and carbohydrate metabolism in girls with hyperandrogenia syndrome during puberty
Vitamin D status may be associated with insulin resistance and other key features of polycystic ovary syndrome (PCOS), but data from preliminary randomized controlled trials (RCTs) are conflicting. Therefore, we aimed to investigate the effects of vitamin D supplementation on plasma glucose area under the curve (AUCgluc, primary outcome measure) and on other metabolic and endocrine parameters (secondary outcome measures). This study was a single-center, double-blind, randomized placebo-controlled trial conducted between December 2011 and July 2017 at the Medical University of Graz, Austria. One-hundred and eighty women with PCOS and 25-hydroxyvitamin D [25(OH)D] concentrations <75 nmol/L were randomized in a 2:1 ratio to either receive 20,000 IU of cholecalciferol weekly or placebo over 24 weeks. Primary outcome was the between-group difference in AUCgluc at study end while adjusting for baseline values. In total, 123 participants completed the study [age 25.9±4.7 years; BMI 27.5±7.3 kg/m2 baseline 25(OH)D 48.8±16.9 nmol/L, baseline fasting glucose 84±8 mg/dL]. Vitamin D supplementation lead to a significant increase in 25(OH)D [mean treatment effect 33.4 nmol/L 95% confidence interval (CI) 24.5 to 42.2; p<0.001] but had no significant effect on AUCgluc (mean treatment effect −9.19, 95% CI −21.40 to 3.02 p=0.139). Regarding secondary outcome measures, we observed a significant decrease in plasma glucose at 60 min during oral glucose tolerance test (mean treatment effect −10.2 mg/dL 95% CI −20.2 to −0.3 p=0.045). Vitamin D supplementation had no significant effect on metabolic and endocrine parameters in PCOS with the exception of a reduced plasma glucose during OGTT.
Respiratory tract infections (RTIs) represent one of the main health problems in children. Probiotics are viable bacteria that colonize the intestine and affect the host intestinal microbial balance. Accumulating evidence suggests that probiotic consumption may decrease the incidence of or modify RTIs. The authors systematically reviewed data from randomized controlled trials (RCTs) to investigate the effect of probiotic consumption on RTIs in children. MEDLINE/PubMed, Embase, Cochrane Library, and Web of Science were systematically searched for RCTs regarding the effect of probiotics on RTIs in children. The outcomes included number of children experienced with at least 1 RTI episode, duration of illness episodes, days of illness per subject, and school/day care absenteeism due to infection. A random-effects model was used to calculate pooled relative risks, or mean difference (MD) with the corresponding 95% confidence interval (CI). A total of 23 trials involving 6269 children were eligible for inclusion in the systematic review. None of the trials showed a high risk of bias. The quality of the evidence of outcomes was moderate. The age range of subjects was from newborn to 18 years. The results of meta-analysis showed that probiotic consumption significantly decreased the number of subjects having at least 1 RTI episode (17 RCTs, 4513 children, relative risk 0.89, 95% CI 0.82–0.96, P=0.004). Children supplemented with probiotics had fewer numbers of days of RTIs per person compared with children who had taken a placebo (6 RCTs, 2067 children, MD ─0.16, 95% CI ─0.29 to 0.02, P=0.03), and had fewer numbers of days absent from day care/school (8 RCTs, 1499 children, MD ─0.94, 95% CI ─1.72 to ─0.15, P=0.02). However, there was no statistically significant difference of illness episode duration between probiotic intervention group and placebo group (9 RCTs, 2817 children, MD ─0.60, 95% CI ─1.49 to 0.30, P=0.19). Based on the available data and taking into account the safety profile of RCTs, probiotic consumption appears to be a feasible way to decrease the incidence of RTIs in children. CI = confidence interval, IL = interleukin, LRTI = lower respiratory tract infection, MD = mean difference, RCT = randomized controlled trial, RTI = respiratory tract infection, SAE = serious adverse event, SD = standard deviation, URTI = upper respiratory tract infection.
Influence of Perinatal Lesions of the Central Nervous System in Women of Reproductive Age with Hypothalamic Syndrome on the Neuroendocrine Regulation
The hypothalamo-pituitary-adrenocortical (HPA axis) is required for stress adaptation. Activation of the HPA axis causes secretion of glucocorticoids, which act on multiple organ systems to redirect energy resources to meet real or anticipated demand. The HPA stress response is driven primarily by neural mechanisms, invoking corticotrophin releasing hormone (CRH) release from hypothalamic paraventricular nucleus (PVN) neurons. Pathways activating CRH release are stressor dependent: reactive responses to homeostatic disruption frequently involve direct noradrenergic or peptidergic drive of PVN neurons by sensory relays, whereas anticipatory responses use oligosynaptic pathways originating in upstream limbic structures. Anticipatory responses are driven largely by disinhibition, mediated by trans-synaptic silencing of tonic PVN inhibition via GABAergic neurons in the amygdala. Stress responses are inhibited by negative feedback mechanisms, whereby glucocorticoids act to diminish drive (brainstem), promote transsynaptic inhibition by limbic structures (e.g, hippocampus). Glucocorticoids also act at the PVN to rapidly inhibit CRH neuronal activity via membrane glucocorticoid receptors. Chronic stressinduced activation of the HPA axis takes many forms (chronic basal hypersecretion, sensitized stress responses, even adrenal exhaustion), with manifestation dependent upon factors such as stressor chronicity, intensity, frequency and modality. Neural mechanisms driving chronic stress responses can be distinct from those controlling acute reactions, including recruitment of novel limbic, hypothalamic and brainstem circuits. Importantly, an individual’s response to acute or chronic stress is determined by numerous factors, including genetics, early life experience, environmental conditions, sex and age. The context in which stressors occur will determine whether an individual’s acute or chronic stress responses are adaptive or maladaptive (pathological).