http://repository.usmf.md:80/handle/20.500.12710/27983 The 10th International Medical Congress for Students and Young Doctors, 24-27 April, 2024 2026-06-24T23:24:08Z http://repository.usmf.md:80/handle/20.500.12710/29004 Title: Assessment of the cases of postpartum hemorrhage in multiparous women Authors: Cemortan, Maria; Bubulici, Cristina; Vicol, Maria-Magdalena; Grajdean, Elena; Scripnic, Gabriela; Manic, Milena Abstract: Introduction. Postpartum hemorrhage (PPH) is one of the leading obstetric complications, affecting 5-15% births. Being a major factor in maternal mortality and morbidity, PPH causes about 25% of maternal deaths worldwide. Aim of study. The aim of the study was to assess the cases of PPH in multiparous women, admitted to the Tertiary Perinatal Center. Methods and materials. The retrospective study was performed by assessing 81 clinical cases of PPH in multiparous women. Total blood loss in labor or C-section was performed by using graduated vessels, and all the sterile material used was weighted. For continuous variables, the mean values and standard deviation of the mean were calculated; the median (Me) as well as the interquartile range (Q1;Q3) in the case of a distribution of characteristics that differs from the normal. Results. The average age of women was 31.6±5.5 years (Me 32 (28;35.5)), varying in the limits of 20-42 years. The majority of participants delivered for the second time - 38 cases (46.9% (95% CI 33.3-59.9)), however, 30 women (37.0% (95% CI 25.9-48.2)) gave birth for the third time, and 13 women (16.1% (95% CI 8.5-27.4)) had 4th – 9th delivery. In 41 cases (50.6% (95% CI 40.7- 61.7)) a c-section was performed. The mean blood loss in vaginal delivery was 850±308 (Me 800 (600;1050)) mL, varying in the limits of 500– 1600 mL. Compared to the mean blood loss in Csection – 1752±1093 (Me 1500 (1100;1850)) mL, varying in the limits of 1000 – 5250 mL. In the structure of PPH there were assessed 26 cases (32.1% (95% CI 20.9-47.0)) of the placental defect or placenta adherens, 15 cases (18.5% (95% CI 10.3-30.5)) of lacerations of the birth canal, 11 cases (13.6% (95% CI 7.4-23.4)) of uterine atonia, and 2 cases (2.5% (95% CI 0-7.3)) of uterine rupture. Hence, in 46 women (56.8% (95% CI 44.6-69.1)) it was applied conservative management of the cases. However, in 20 cases (24.6% (95% CI 15.0-38.1)) an operative management was applied, from which 7 cases (8.6% (95% CI 3.7-14.7)) hemostatic sutures were applied. In 13 cases (16.0% (95% CI 8.5-27.4)) hysterectomy was performed, from which 9 cases (69.2% (95% CI 31.6-100)) subtotal hysterectomy without annexes was the elective method for definitive hemostasis. Conclusion. PPH is a major obstetric complication, which occurs more frequently in multiparous women, in association with placental pathology and birth canal trauma, explained by overextension of the uterus and coagulation disorders, requiring extensive surgical management. 2024-01-01T00:00:00Z http://repository.usmf.md:80/handle/20.500.12710/28454 Title: Gluten intolerance. Celiac disease Authors: Volc, Renata Abstract: Introduction. Celiac disease (CD) is an immune-mediated inflammatory condition of the small intestine that occurs in genetically predisposed individuals when they are exposed to gluten (a plant-based protein component found in grains). The disease has a variable incidence, with a worldwide prevalence of approximately 1:100; Statistics have shown that 70% of patients reported with celiac disease are female. Distribution of population groups, reported that HLA DR3 Phenotype occurs in 70-90% of patients. Aim of study. Celiac disease is an autoimmune disorder and an inflammatory disease that manifests itself upon ingestion of gluten in the upper small intestine and is characterized by the gradual deterioration of the intestinal mucosa. Biochemically, it highlights an immune reaction, which is mediated by certain cells of the immune system, which attack the cells of the small intestine. Methods and materials. It has been scientifically proven that the prevalence of celiac disease in the majority of the population ranges from 0.5% to 1%. Medical science researchers have determined that the incidence is higher among people with autoimmune disorders. Patients with type 1 diabetes are prone to celiac disease, and in the last 20 years there has been a considerable increase in cases. Results. Inflammation and nutrient malabsorption, in addition to diarrhea, distention and abdominal pain, lead to damage to many organs and systems such as: iron deficiency leading to anemia, vitamin deficiencies, osteoporosis, dermatitis herpetiformis, tooth enamel defects, chronic fatigue, joint pain, poor growth, delayed puberty, infertility or repeated miscarriages, and other autoimmune disorders. A number of neurological problems have also been associated with celiac disease; these include migraines, depression, attention deficit/hyperactivity disorder and epilepsy. The diagnosis of celiac disease is established: a) upon the histological finding of an increased number of intraepithelial T lymphocytes; of crypt hyperplasia; of the expansion of regenerative epithelial crypts until the total disappearance of villi; b) positive serological testing (IgA tissue transglutaminase, anti-deamidated gliadin-related peptides IgA and Ig G, IgA antibodies); c) by molecular genetic testing of HLA-DQA1 and HLA-DQB1 which can be determinant or of HLADQ2 and HLA-DQ8) which can be used to exclude celiac disease. Conclusion. Celiac disease (CD) is a very common disorder but in most cases it starts silently. Many of the patients are identified through screening of at-risk groups or after the onset of symptoms of malabsorption, rarely for complications associated with the disease. The diagnosis of CD and its differential diagnosis is made from integrations between typical histological findings and clinical, serological and immunological features. The Corazza-Villanacci system is a useful method to assess mucosal damage and response to gluten-free diet in patient follow-up. intestine that occurs in genetically predisposed individuals when they are exposed to gluten (a plant-based protein component found in grains). The disease has a variable incidence, with a worldwide prevalence of approximately 1:100; Statistics have shown that 70% of patients reported with celiac disease are female. Distribution of populati on groups, reported that HLA DR3 Phenotype occurs in 70-90% of patients. Aim of study. Celiac disease is an autoimmune disorder and an inflammat ory disease that manifests itself upon ingestion of gluten in the upper small i ntestine and is characterized by the gradual deterioration of the intestinal mucosa. Biochemi cally, it highlights an immune reaction, which is mediated by certain cells of the immune system, whi ch attack the cells of the small intestine. Methods and materials. It has been scientifically proven that the prevalence o f celiac disease in the majority of the population ranges from 0.5% to 1%. Medi cal science researchers have determined that the incidence is higher among people with aut oimmune disorders. Patients with type 1 diabetes are prone to celiac disease, and in the l ast 20 years there has been a considerable increase in cases. Results. Inflammation and nutrient malabsorption, in addition to di arrhea, distention and abdominal pain, lead to damage to many organs and systems such as: iron deficiency leading to anemia, vitamin deficiencies, osteoporosis, dermatitis he rpetiformis, tooth enamel defects, chronic fatigue, joint pain, poor growth, delayed puberty, infertility or repeated miscarriages, and other autoimmune disorders. A number of neurological problems ha ve also been associated with celiac disease; these include migraines, depression, attention defi cit/hyperactivity disorder and epilepsy. The diagnosis of celiac disease is established: a) upon the histological finding of an increased number of intraepithelial T lymphocytes; of crypt hyperp lasia; of the expansion of regenerative epithelial crypts until the total disappearance of villi; b) positive serological testing (IgA tissue transglutaminase, anti-deamidated gliadin-related peptides IgA and Ig G, IgA antibodies); c) by molecular genetic testing of HLA-DQA1 and HLA-DQB1 which can be determinant or of HLADQ2 and HLA-DQ8) which can be used to exclude celiac disease. Conclusion. Celiac disease (CD) is a very common disorder but in mos t cases it starts silently. Many of the patients are identified through screening of at- risk groups or after the onset of symptoms of malabsorption, rarely for complications as sociated with the disease. The diagnosis of CD and its differential diagnosis is made from integr ations between typical histological findings and clinical, serological and immunological features. Th e Corazza-Villanacci system is a useful method to assess mucosal damage and response to gluten-free diet in patient follow-up. Description: Universitatea de Stat de Medicină şi Farmacie „Nicolae Testemiţanu”, Chişinău, Republica Moldova 2024-01-01T00:00:00Z http://repository.usmf.md:80/handle/20.500.12710/28463 Title: The influence of type 2 pregestational diabetes mellitus on the fetus Authors: Surlaru, Valeria Abstract: Introduction. The prevalence of type 2 diabetes among women of reproductive age is increasing. According to the latest data from the International Diabetes Federation in 2019, one in six live births is affected by hyperglycemia during pregnancy, that represents a risk for the intrauterine development of the fetus, and despite significant advances in glycemic control of pregnancies with diabetes, adverse outcomes for the fetus are still very common. Aim of study. To elucidate the biochemical mechanisms of influence of type 2 diabetes on the intrauterine development of the fetus with the aim of improving diagnosis, treatment and preventing the occurrence of adverse effects. Methods and materials. To achieve the proposed goal, a bibliographic search was performed using 10 bibliographic sources, between the 2018-2023, including those of the Medical Scientific Library of USMF "Nicolae Testemitanu", data of the electronic libraries such as PubMed, MedScape, Medline, Diabetes Care and Diabetologia. Results. Maternal hyperglycemia increases apoptosis in the embryo, which is specifically observed in neuroepithelial cells. An important role also has oxidative stress, which increases the BAX:BCL-2 ratio- indicator of apoptosis level in glioma cells, associated with the increase of cytochrome C in mitochondria and the activation of caspase 3 in embryonic cells. Increased glucose transfer from mother to the fetus induces fetal hyperglycemia, pancreatic β-cell hyperplasia, and consequently fetal hyperinsulinemia (FHI). Insulin influences glucose uptake and lipogenesis via the glucose transporter GLUT-4, expressed in fetal adipose tissue and induces fetal macrosomia. The placenta acts as a passive conduit for maternal glucose to the fetus, especially towards the end of gestation. Therefore, increased glucose transport from diabetic mothers, together with FHI, stimulates fetal triacylglycerol formation and deposition of excess fetal adipose tissue. FHI can delay lung development in the fetus of a diabetic mother. A physiological level of insulin plays a role as a stimulatory hormone in the synthesis of surfactant, but a high level of insulin can inhibit the lipid components of the surfactant: phosphatidylcholine (PC), phosphatidylglycerol (PG) and phosphatidylinositol (PI) and low level of surfactant protein expression.Thus, it decreases the ability of surfactant to reduce alveolar surface tension, increasing the risk of respiratory distress syndrome (RDS). Pregnant women usually have a pathological weight gain, associated with a high production of pro-inflammatory cytokines and adipokines TNF-α, IL-1β, IL-6, responsible for insulin resistance. Conclusion. Maintaining maternal glucose in optimal parameters is essential for the normal development of the fetus by reducing the risk of congenital malformations and preventing postpartum complications. According to the latest data from the International Di abetes Federation in 2019, one in six live births is affected by hyperglycemia during pregnancy, that repr esents a risk for the intrauterine development of the fetus, and despite significant advances in glycemic control of pregnancies with diabetes, adverse outcomes for the fetus are still ver y common. Aim of study. To elucidate the biochemical mechanisms of influence of t ype 2 diabetes on the intrauterine development of the fetus with the aim of improving diagnosis, treatment and preventing the occurrence of adverse effects. Methods and materials. To achieve the proposed goal, a bibliographic search was perfo rmed using 10 bibliographic sources, between the 2018-2023, including those o f the Medical Scientific Library of USMF "Nicolae Testemitanu", data of the electronic libraries such as PubMed, MedScape, Medline, Diabetes Care and Diabetologia. Results. Maternal hyperglycemia increases apoptosis in the embryo, which is specifically observed in neuroepithelial cells. An important role also ha s oxidative stress, which increases the BAX:BCL-2 ratio- indicator of apoptosis level in glioma c ells, associated with the increase of cytochrome C in mitochondria and the activation of ca spase 3 in embryonic cells. Increased glucose transfer from mother to the fetus induces fetal hyperglycemia, pancreatic β-cell hyperplasia, and consequently fetal hyperinsulinemia (FHI). Ins ulin influences glucose uptake and lipogenesis via the glucose transporter GLUT-4, expressed in fetal adipose tissue and induces fetal macrosomia. The placenta acts as a passive conduit for maternal glucose to the fetus, especially towards the end of gestation. Therefore, increased glucose transport from diabetic mothers, together with FHI, stimulates fetal triacylglycerol form ation and deposition of excess fetal adipose tissue. FHI can delay lung development in the fetus of a diabetic mother. A physiological level of insulin plays a role as a stimulatory hormone in the s ynthesis of surfactant, but a high level of insulin can inhibit the lipid components of the surfactant: phosphatidylcholine (PC), phosphatidylglycerol (PG) and phosphatidylinositol (PI) and low level of surfactant protein expression.Thus, it decreases the ability of surfactant to reduce alveolar surface tension, increasing the risk of respiratory distress syndrome (RDS). Pregnant women usually have a pathological weight gain, associated with a high production of pro-inflamm atory cytokines and adipokines TNF-α, IL-1β, IL-6, responsible for insulin resistance. Conclusion. Maintaining maternal glucose in optimal parameters is e ssential for the normal development of the fetus by reducing the risk of congenital malformations and preventing postpartum complications. Description: Universitatea de Stat de Medicină şi Farmacie „Nicolae Testemiţanu”, Chişinău, Republica Moldova 2024-01-01T00:00:00Z http://repository.usmf.md:80/handle/20.500.12710/28466 Title: The role of gut microbiota metabolites in atherosclerosis Authors: Berliba, Marina Abstract: Introduction. Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide. Changes in gut microbiota metabolites(GMM) is linked to the development of CVD, which includes atherosclerosis, hypertension, and heart failure. Some GMM, such as trimethylamine-N-oxide (TMAO), bile acids (BA), short-chain fatty acids (SCFA), coprostanol and others influence the atherosclerosis. Aim of study. To research the biochemical pathways of GMM involved in triggering atherosclerosis, thus proving the possibility to use them as predictive markers in cardiovascular disease diagnosis and as treatment targets. Methods and materials. Research, study and analysis of numerous articles from PubMed, NCBI, HINARI, Google Scholar databases over the last ten years. Results. TMAO has been correlated with an increased risk of atherosclerotic cardiovascular disease. Following ingestion of animal products rich in phosphatidylcholine, carnitine and choline, gut microbiota(GM) can use them as a carbon source. GM enzyme trimethylamine (TMN) lyases cleave C-N bond of these nutrients releasing TMA waste product, which is further processed into TMAO by the liver enzyme flavin-dependent monooxygenase 3. TMAO activates NF-κB in endothelial cells and leads to increased expression of vascular cell adhesion molecule-1 (VCAM1), trigger factor for atherosclerosis. TMAO enhances macrophage migration and adhesion due to VCAM-1, thus forming foam cells in plaque that contain cholesterol. Unbalanced GM, could lead to reduced deconjugation of primary bile acids to secondary bile acids, which can increase primary bile acids such as chenodeoxycholic acid, suppress enzyme cholesterol 7-alpha-hydroxylase, then downregulate bile acid production from cholesterol and so its concentration is elevated. SCFAs can lower serum lipid levels by blocking cholesterol synthesis and redirect them to the liver. SCFAs are a microbial-derived metabolites that are mostly formed by Bacteroidetes phylum fermentation of complex carbohydrates. SCFA-producing bacteria can be reduced in certain CVD, dysbiosis of patients with hypertension determined by atherosclerosis. Besides this, species of gut microbiota, such as Eubacterium coprostanoligenes, Bacteroides dorei, Lactobacillus sp. possess the ability to convert absorbable cholesterol to coprostanol, a reduced non-absorbable sterol, which is excreted in feces. Conclusion. As previously mentioned, there is overwhelming evidence that GMM influences CVD-relevant phenotypes, such as atherosclerosis. Therefore the state of GM must be taken into account during atherosclerosis prevention, diagnosis and treatment. worldwide. Changes in gut microbiota metabolites(GMM) is linke d to the development of CVD, which includes atherosclerosis, hypertension, and heart fail ure. Some GMM, such as trimethylamine-N-oxide (TMAO), bile acids (BA), short-chain fatty acids (SCFA), coprostanol and others influence the atherosclerosis. Aim of study. To research the biochemical pathways of GMM involved in t riggering atherosclerosis, thus proving the possibility to use them a s predictive markers in cardiovascular disease diagnosis and as treatment targets. Methods and materials. Research, study and analysis of numerous articles from PubMed, NCBI, HINARI, Google Scholar databases over the last ten years. Results. TMAO has been correlated with an increased risk of ather osclerotic cardiovascular disease. Following ingestion of animal products rich in pho sphatidylcholine, carnitine and choline, gut microbiota(GM) can use them as a carbon source. GM enz yme trimethylamine (TMN) lyases cleave C-N bond of these nutrients releasing TMA waste produc t, which is further processed into TMAO by the liver enzyme flavin-dependent monooxygenase 3. TMA O activates NF-κB in endothelial cells and leads to increased expression of vascu lar cell adhesion molecule-1 (VCAM1), trigger factor for atherosclerosis. TMAO enhances mac rophage migration and adhesion due to VCAM-1, thus forming foam cells in plaque that contain chole sterol. Unbalanced GM, could lead to reduced deconjugation of primary bile acids to secondary bile a cids, which can increase primary bile acids such as chenodeoxycholic acid, suppress enzyme chol esterol 7-alpha-hydroxylase, then downregulate bile acid production from cholesterol and so it s concentration is elevated. SCFAs can lower serum lipid levels by blocking cholesterol syn thesis and redirect them to the liver. SCFAs are a microbial-derived metabolites that are mostly formed by Bacteroidetes phylum fermentation of complex carbohydrates. SCFA-producing bact eria can be reduced in certain CVD, dysbiosis of patients with hypertension determined by athe rosclerosis. Besides this, species of gut microbiota, such as Eubacterium coprostanoligenes, Bacter oides dorei, Lactobacillus sp. possess the ability to convert absorbable cholesterol to copros tanol, a reduced non-absorbable sterol, which is excreted in feces. Conclusion. As previously mentioned, there is overwhelming evidence that GMM influences CVD-relevant phenotypes, such as atherosclerosis. There fore the state of GM must be taken into account during atherosclerosis prevention, diagnosis and t reatment. Description: Universitatea de Stat de Medicină şi Farmacie „Nicolae Testemiţanu”, Chişinău, Republica Moldova 2024-01-01T00:00:00Z