http://repository.usmf.md:80/handle/20.500.12710/10713 2026-04-24T10:28:13Z 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/20.500.12710/28554 Title: Immunohistochemical particularities as prognostic factors in diffuse large B-cell non-Hodgkin lymphoma Authors: Dudnic, Cristina Abstract: Introduction. Diffuse Large B-Cell Lymphoma (DLBCL), the most common type of NonHodgkin Lymphoma (NHL) globally, is classified into two distinct biological categories based on the gene expression profile (GEP): the germinal center B-cell (GCB) subtype and the activated Bcell (ABC) or non-GCB subtype. Aim of study. Identification of Immunohistochemical Particularities as Prognostic Factors in Diffuse Large B-Cell Non-Hodgkin Lymphoma. Methods and materials. Data from medical scientific literature were examined, identified through Google Search and databases such as PubMed, Cochrane, Scopus, along with international clinical guidelines from NCCN and ESMO. Results. Studies have indicated that determining the cell of origin phenotype in DLBCL using gene expression profile (GEP) is significant for establishing the prognosis. Tumors with the GCB phenotype showed a better clinical course compared to those with the ABC/non-GCB phenotype. The classification into GCB and non-GCB subtypes, using the Hans algorithm, suggests a correlation between the expression of CD10 and BCL6 genes in DLBCL GCB and MUM1 in DLBCL non-GCB. In a study led by Patrascu A-M and his team (2017) on a sample of 601 patients, subjects with GCB type DLBCL exhibited a higher overall survival rate and progression-free survival compared to those with non-GCB DLBCL, although the prognosis may vary depending on the specific markers expressed within the same subtype. Studies using fluorescent in situ hybridization (FISH) reported that 7% to 10% of DLBCL cases harbored genetic translocations MYC, BLC2, and/or BCL6 and were termed “double-hit” lymphoma (DHL) or triple-hit lymphoma. More than 90% of patients with DHL present high-risk clinical features, such as leukocytosis, central nervous system (CNS) involvement, lactate dehydrogenase values three times above the upper limit, and an advanced disease stage. The presence of MYC rearrangements in combination with BCL2 and/or BCL6 has been described as a distinct entity with prognostic significance, presenting a poor long-term prognosis, refractoriness to therapy, and an increased risk of relapse. Conclusion. Research and studies emphasize the importance of evaluating the expression of MYC, BCL2, and BCL6 genetic rearrangements, through IHC and FISH, in patients recently diagnosed with DLBCL, for a more accurate assessment of disease progression, prognosis, and progressionfree survival. the gene expression profile (GEP): the germinal center B-ce ll (GCB) subtype and the activated Bcell (ABC) or non-GCB subtype. Aim of study. Identification of Immunohistochemical Particularities as Prognostic Factors in Diffuse Large B-Cell Non-Hodgkin Lymphoma. Methods and materials. Data from medical scientific literature were examined, identified through Google Search and databases such as PubMed, Cochrane, Scopus, along with international clinical guidelines from NCCN and ESMO. Results. Studies have indicated that determining the cell of origi n phenotype in DLBCL using gene expression profile (GEP) is significant for establishing th e prognosis. Tumors with the GCB phenotype showed a better clinical course compared to those wi th the ABC/non-GCB phenotype. The classification into GCB and non-GCB subtypes, using the Hans algorithm, suggests a correlation between the expression of CD10 and BCL6 genes i n DLBCL GCB and MUM1 in DLBCL non-GCB. In a study led by Patrascu A-M and his team ( 2017) on a sample of 601 patients, subjects with GCB type DLBCL exhibited a higher overall surviva l rate and progression-free survival compared to those with non-GCB DLBCL, although the pr ognosis may vary depending on the specific markers expressed within the same subtype . Studies using fluorescent in situ hybridization (FISH) reported that 7% to 10% of DLBCL cases harbored genetic translocations MYC, BLC2, and/or BCL6 and were termed “double-hit ” lymphoma (DHL) or triple-hit lymphoma. More than 90% of patients with DHL present high-r isk clinical features, such as leukocytosis, central nervous system (CNS) involvement, lac tate dehydrogenase values three times above the upper limit, and an advanced disease stage. The pres ence of MYC rearrangements in combination with BCL2 and/or BCL6 has been described as a dis tinct entity with prognostic significance, presenting a poor long-term prognosis, refract oriness to therapy, and an increased risk of relapse. Conclusion. Research and studies emphasize the importance of eval uating the expression of MYC, BCL2, and BCL6 genetic rearrangements, through IHC and FISH, in patients recently diagnosed with DLBCL, for a more accurate assessment of disease progression, prognosis, and progressionfree survival. Description: Universitatea de Stat de Medicină şi Farmacie „Nicolae Testemiţanu”, Chişinău, Republica Moldova 2024-01-01T00:00:00Z http://repository.usmf.md:80/handle/20.500.12710/28500 Title: Genetic aspects of migraine Authors: Morari, Ecaterina Abstract: Introduction. Migraine is a common neurological disorder which affects 15–20% of the population and usually begins at puberty, but has the greatest impact on people aged 35 to 45 years. Migraines present a severe headache with associated symptoms of nausea, vomiting, photo and phonophobia. The pain can localize on one side of the head. It can be aggravated by physical activity. There are migraines without aura (MO) and migraine with aura (MA) which include many other subtypes. Aim of study. To investigate the molecular and genetic mechanisms of migraine and their impact on the quality of human life. Methods and materials. From a variety of articles from PubMed, NCBI databases, Medlineplus.gov, Americanmigrainefoundation.org we selected and analyzed 25 sources describing the genetic manifestations of migraine in more detail Results. Familial hemiplegic migraine (FHM) is the only known autosomal dominant subtype of migraine with aura. There are mutations in the calcium-channel gene CACNA1A which is present on chromosome 19p13. Four missense mutations were detected in the conserved regions of this gene. This gene usually encodes the pore-forming α1 subunit of the neuronal voltage-gated Cav2.1 channel. The different migraine phenotypes are associated with deletion of the CACNA1A gene. Another involved in increasing the risk of migraines is MTHFR gene which is localized on chromosome 1p36.2 and encodes the enzyme methylenetetrahydrofolate reductase, normally involved in the metabolism of vitamin B9 (folic acid). The MTHFR enzyme catalyses the reduction of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate which is needed for the conversion of homocysteine to methionine. The C677T mutation of the MTHFR gene is quite widespread. For example, it occurs in 35-55% of representatives of the European (Caucasian) race. Missense mutations in this gene lead to protein deficiency or defective protein synthesis. This will lead to an increased level of homocysteine in plasma and a decrease in the amount of methionine. The clinical consequences of elevated plasma homocysteine levels include damage to endothelial cells, spontaneous activation of trigeminal nerve cells, and changes in blood coagulation properties. It is believed that spontaneous activation of trigeminal nerve cells, leading to inflammation of the meninges and blockage of cerebral vessels, is the cause of migraine-related pain. Thus, homocysteine dysfunction can clearly increase the patient's propensity to develop migraines. In this case, the patient is forced to be motionless, since any exposure to light or noise makes the headache unbearable Conclusion. Migraine is a complex brain disorder that occurs when homeostasis is lost, which leads to activation of the trigeminal vascular system and a cascade of events, the manifestation of which depends on mutations in the MTHFR and CACNA1A genes. population and usually begins at puberty, but has the greatest i mpact on people aged 35 to 45 years. Migraines present a severe headache with associated sympt oms of nausea, vomiting, photo and phonophobia. The pain can localize on one side of the he ad. It can be aggravated by physical activity. There are migraines without aura (MO) and migraine with aura (MA) which include many other subtypes. Aim of study. To investigate the molecular and genetic mechanisms of m igraine and their impact on the quality of human life. Methods and materials. From a variety of articles from PubMed, NCBI databases , Medlineplus.gov, Americanmigrainefoundation.org we selected an d analyzed 25 sources describing the genetic manifestations of migraine in more detai l Results. Familial hemiplegic migraine (FHM) is the only known autos omal dominant subtype of migraine with aura. There are mutations in the calcium-c hannel gene CACNA1A which is present on chromosome 19p13. Four missense mutations were detected in the conserved regions of this gene. This gene usually encodes the pore-forming α1 subunit of t he neuronal voltage-gated Cav2.1 channel. The different migraine phenotypes are associated with deletion of the CACNA1A gene. Another involved in increasing the risk of migraines is MTHFR gene which is localized on chromosome 1p36.2 and encodes the enzyme methylenetetrahydrofol ate reductase, normally involved in the metabolism of vitamin B9 (folic acid). The MTHFR enzyme catalyses the reduction of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate whi ch is needed for the conversion of homocysteine to methionine. The C677T mutation of the MT HFR gene is quite widespread. For example, it occurs in 35-55% of representatives of the E uropean (Caucasian) race. Missense mutations in this gene lead to protein deficiency or defectiv e protein synthesis. This will lead to an increased level of homocysteine in plasma and a decr ease in the amount of methionine. The clinical consequences of elevated plasma homocysteine l evels include damage to endothelial cells, spontaneous activation of trigeminal nerve cells, and cha nges in blood coagulation properties. It is believed that spontaneous activation of trigeminal nerve ce lls, leading to inflammation of the meninges and blockage of cerebral vessels, is the cause of migraine-related pain. Thus, homocysteine dysfunction can clearly increase the patie nt's propensity to develop migraines. In this case, the patient is forced to be motionless, since any exposure to light or noise makes the headache unbearable Conclusion. Migraine is a complex brain disorder that occurs when h omeostasis is lost, which leads to activation of the trigeminal vascular system and a cascade of events, the manifestation of which depends on mutations in the MTHFR and CACNA1A genes. Description: Universitatea de Stat de Medicină şi Farmacie „Nicolae Testemiţanu”, Chişinău, Republica Moldova 2024-01-01T00:00:00Z http://repository.usmf.md:80/handle/20.500.12710/28493 Title: Autism spectrum disorder - a comprehensive literary review Authors: Lupașcu, Ecaterina Abstract: Introduction. Autism spectrum disorder (ASD) can be identified from other neurodevelopmental disorders by its distinctive combination of symptoms: difficulties in social interaction and communication, repetitive, stereotyped, and restricted behavior. According to the data provided by the World Health Organization, the worldwide prevalence of ASD is 1:100, while as per Centers for Disease Control and Prevention (CDC), in the USA (2020) 1 in 36 children were diagnosed with autism, in comparison with 2000 when the ratio was 1:150. Aim of study. To elucidate the main key findings within the literature on autism spectrum disorder. Methods and materials. To accomplish the proposed goal, research was performed on scientific and medical databases as HINARI, PubMed, Elsevier. Using the following keywords: “autism spectrum disorder”, “etiology”, “prevalence”, “early prevention” – 14 articles were selected. Results. 1 to 2 percent of the overall population is diagnosed with autism, more commonly in men than in women (ratio 4:1). In ASD “spectrum” emphasizes the broad array of symptoms, the severity and which degree these symptoms manifest in each individual. The complexity of this disease can be explained by its heterogeneous origins. Several family studies have demonstrated that ASD is a highly heritable disorder, with heritability estimates ranging from 40% to 90%, underscoring the influence of genetic factors. Nevertheless, genetic alterations have been detected in only 20-30% of cases. This prompted an exploration of the impact of environmental factors, including drugs, maternal and paternal age, and neonatal hypoxia. These studies revealed that up to 40-50% of the variation in autism susceptibility could be attributed to these variables, and still not all cases of autism can be explained. Hence, an increasing number of studies are centered on exploring the interplay between genetics and the environment, or more precisely, how our surroundings and behavior impact the functioning of our genes - commonly referred to as epigenetics. These factors engage with each other in the prenatal and postnatal period, altering the development of the central nervous system and determining the appearance of the autistic phenotype. The diagnosis can be confirmed by the age of 2, prompting international recommendations to begin screening at 18 months. Conclusion. Since the discovery of ASD, numerous studies have significantly advanced our understanding of the condition, revealing its multifactorial nature. Autism is a lifelong developmental disease for which there is no cure. Therefore, early intervention and diagnosis play a crucial role in influencing the quality of life for individuals with ASD. disorders by its distinctive combination of symptoms: diffi culties in social interaction and communication, repetitive, stereotyped, and restricted beh avior. According to the data provided by the World Health Organization, the worldwide prevalence of ASD is 1:100, while as per Centers for Disease Control and Prevention (CDC), in the USA (2020) 1 in 36 children were diagnosed with autism, in comparison with 2000 when the ratio was 1:150. Aim of study. To elucidate the main key findings within the literature on autism spectrum disorder. Methods and materials. To accomplish the proposed goal, research was performed on scientific and medical databases as HINARI, PubMed, Elsevier. Using the following keywords: “autism spectrum disorder”, “etiology”, “prevalence”, “early preve ntion” – 14 articles were selected. Results. 1 to 2 percent of the overall population is diagnosed with autism, more commonly in men than in women (ratio 4:1). In ASD “spectrum ” emphasizes the broad array of symptoms, the severity and which degree these symptoms manifest in each individual. The complexity of this disease can be explained by its heterogeneous origins. Seve ral family studies have demonstrated that ASD is a highly heritable disorder, with heritability e stimates ranging from 40% to 90%, underscoring the influence of genetic factors. Nevertheless, genetic alterations have been detected in only 20-30% of cases. This prompted an exploration of the impact of environmental factors, including drugs, maternal and paternal age, and neonatal hypoxia. These studies revealed that up to 40-50% of the variation in autism susceptibility could be at tributed to these variables, and still not all cases of autism can be explained. Hence, an inc reasing number of studies are centered on exploring the interplay between genetics and the environment, or more precisely, how our surroundings and behavior impact the functioning of our genes—co mmonly referred to as epigenetics. These factors engage with each other in th e prenatal and postnatal period, altering the development of the central nervous system and determini ng the appearance of the autistic phenotype. The diagnosis can be confirmed by the age of 2, prompting international recommendations to begin screening at 18 months. Conclusion. Since the discovery of ASD, numerous studies have signifi cantly advanced our understanding of the condition, revealing its multifactoria l nature. Autism is a lifelong developmental disease for which there is no cure. There fore, early intervention and diagnosis play a crucial role in influencing the quality of life for indi viduals with ASD. Description: Universitatea de Stat de Medicină şi Farmacie „Nicolae Testemiţanu”, Chişinău, Republica Moldova 2024-01-01T00:00:00Z