Alexandra Sima

Dr. Alexandra Sima

Second Department of Internal Medicine, "Victor Babes" University of Medicine and Pharmacy, Timisoara, Romania
orcid

Research Focus & Metrics

Academic Career Length

9Years (2018-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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16 September 2021 in Medicina
Verified
Journal Article
Open access
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AVAdrian Vlad
Adrian Vlad
VSViorel Serban
Viorel Serban
RTRomulus Timar
Romulus Timar
ASAlexandra Sima
Alexandra Sima
VBVeronica Botea
Veronica Botea
MVMihaela Vlad
Mihaela Vlad
Background and Objective: It is known that several viruses are involved in the pathogenesis of type 1 diabetes. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a new worldwide spread virus that may act as a trigger for the autoimmune destruction of the β-cells, as well, and thus lead to an increase in the incidence of type 1 diabetes. Material and Methods: The Romanian National Organization for the Protection of Children and Adolescents with Diabetes (ONROCAD) has collected information regarding new cases of type 1 diabetes in children aged 0 to 14 years from all over the country since 1996 and has computed the incidence of type 1 diabetes in this age group. Results: We observed a marked increase in the incidence of type 1 diabetes in the first year of the COVID-19 pandemic, with 16.9%, from 11.4/100,000 in 2019 to 13.3/100,000 in 2020, much higher compared to previous years (mean yearly increase was 5.1% in the period 1996–2015 and 0.8% in the interval 2015–2019). The proportion of newly diagnosed cases was significantly higher in the second half of 2020 compared to the second half of the previous years (57.8 vs. 51%, p < 0.0001). Conclusions: All these aspects suggest the role that SARS-CoV-2 could have in triggering pancreatic autoimmunity. To confirm this, however, collecting information from larger populations from different geographical regions, monitoring the incidence curves over a period of several years, and gathering background information on COVID-19 and/or data on COVID-19 specific antibodies are needed.

1 December 2019 in Diabetes, Metabolic Syndrome and Obesity
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Journal Article
Open access
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ABAdina Braha
Adina Braha
BTBogdan Timar
Bogdan Timar
LDLaura Diaconu
Laura Diaconu
RLRaluca Lupusoru
Raluca Lupusoru
LVLucian Vasiluta
Lucian Vasiluta
RTRomulus Timar
Romulus Timar
Purpose: The aim of this study was to assess the dynamics of epicardiac adipose tissue (EAT) thickness and total volume as well as that of systolic and diastolic dysfunction in a group of patients with type 2 diabetes (T2D) after initiation of sodium glucose co-transporter 2 (SGLT 2) inhibitors therapy. Patients and methods: This prospective, observational study included 53 patients with T2D who received SGLT-2 inhibitors for 24 weeks. In all patients, echocardiographic screening for EAT, systolic and diastolic dysfunction and non-contrast computed tomography scans were performed, both before and after 24 weeks of SGLT-2 inhibition. Imagistic evaluation was followed by the association’s analysis between the dynamics of EAT and heart function, as well as the patient’s clinical and biological parameters. We considered a decrease or increase of more than 10% in EAT as being clinically significant. Results: The mean volume of EAT decreased significantly after SGLT 2 inhibition (37.8±17.2 vs. 20.7±7 cm3; p<0.001). Median values of EAT thickness also decreased significantly (5.95 vs. 3.01 mm; p<0.001). Most patients, 75.4% (40/53), presented more than 10% decrease in EAT volume, 9.5% (5/53) had stable EAT volume values, while in 15.1% (8/53) the means of EAT volume increased. 73.5% of the patients had diastolic dysfunction type 1 (DD 1) at baseline. No significant change was observed in the left ventricular ejection fraction or diastolic dysfunction after 24 weeks of treatment. Although not statistically significant, an improvement in cardiac function has been noticed throughout the duration of 1 year of treatment with SGLT 2 inhibitors. Conclusion: This study showed the beneficial effect of SGLT 2 inhibitors on EAT after a short period of treatment, but there were no significant changes in the systolic function during the 1st year of study. However, reducing epicardial fat has led to remission of diastolic dysfunction.

1 October 2020 in Diabetes, Metabolic Syndrome and Obesity
Verified
Journal Article
Open access
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OAOana Albai
Oana Albai
BTBogdan Timar
Bogdan Timar
DPDiana Loreta Paun
Diana Loreta Paun
ASAlexandra Sima
Alexandra Sima
Deiana Sorina RomanDeiana Sorina Roman
Deiana Sorina Roman
RTRomulus Timar
Romulus Timar
Introduction: Vitamin B12 (cobalamin) deficiency is a frequent cause of megaloblastic anemia, manifested through various symptoms. Screening for this deficiency can be justified in case of patients with one or more risk factors present from the following: gastric resections, inflammatory bowel disease, use of metformin over a prolonged period of time, administration of proton pump inhibitors or H2 histamine receptor blockers for more than 12 months and in case of adults over 75 years of age. One method of determining vitamin B12 deficiency is measuring its serum levels, as well as performing measurements of serum levels of methylmalonic acid and homocysteine levels, which experience an increase in the early stages of vitamin B12 deficiency. Clinical Case: We bring to your attention, the case of a 62 years old patient diagnosed with Type 2 Diabetes Mellitus in 2015 that presented in the emergency room in October 2019 with an altered general condition, nausea, vomiting, abdominal pain, palpitation, and dyspnea. Treatment with metformin was initiated from the diagnosis of Type 2 Diabetes Mellitus, four years before. Investigations established the diagnosis of megaloblastic anemia by vitamin B12 deficiency. The symptoms disappeared after the injection of vitamin B12. Conclusion: Periodical dosing of vitamin B12 should be performed in the case of patients with Type 2 Diabetes Mellitus treated with metformin, especially if they associate anemia and/or peripheral diabetic polyneuropathy.

18 May 2018 in Journal of Clinical Research in Pediatric Endocrinology
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Journal Article
Open access
AVAdrian Vlad
Adrian Vlad
VSViorel Serban
Viorel Serban
AGAnders Green
Anders Green
Sören MöllerSören Möller
Sören Möller
MVMihaela Vlad
Mihaela Vlad
OGon behalf of the ONROCAD Study Group
on behalf of the ONROCAD Study Group
The incidence of type 1 diabetes mellitus in children is highly variable in the world. The aim of our study was to: 1) analyze the evolution of the incidence of childhood type 1 diabetes in Romania between 1996 and 2015, and: 2) to search for differences amongst age groups, gender, geographic regions and month of diagnosis. Data on all new cases of type 1 diabetes, aged <15 years, obtained from two independent sources, were included in the study. The statistical methods included modeling of the incidence rates, adjusting for age, sex, calendar year, geographic region and seasonality. The study group was composed of 5422 children, with overall completeness of ascertainment estimated at 93.7%. The incidence rate (per 100.000 person-years) rose continuously, from 4.7 [95% confidence interval (CI) 3.9-5.7] in 1996 to 11.0 (95% CI 9.9-12.2) in 2015, by a yearly rate of 5.1%, highest in the youngest and lowest in the oldest children. The mean incidence was significantly higher (p<0.0001) in Transylvania (7.9, 95% CI 7.6-8.3) than in Moldavia (6.5, 95% CI 6.2-6.9) and Muntenia (7.0, 95% CI 6.7-7.3), probably due to differences regarding ethnicity and lifestyle. The monthly incidence showed a sinusoidal pattern, peaking in January and being minimum in June. The incidence of type 1 diabetes mellitus in Romanian children increased continuously during the study period by a rate that, if maintained, would lead to its doubling every 14 years. Important differences were established between geographic regions and seasonality at diagnosis.

28 March 2021 in Life
Verified
Journal Article
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VAVlad Avram
Vlad Avram
ABAnca Mihaela Bina
Anca Mihaela Bina
ASAlexandra Sima
Alexandra Sima
OAOana Maria Aburel
Oana Maria Aburel
ASAdrian Sturza
Adrian Sturza
OCOctavian Marius Cretu
Octavian Marius Cretu
Diabetes mellitus (DM) is the most severe metabolic disease that reached the level of a global pandemic and is associated with high cardiovascular morbidity. Statins are the first–line lipid–lowering therapy in diabetic patients with or without a history of atherosclerotic disease. Although well tolerated, chronic treatment may result in side effects that lead to treatment interruption. Mitochondrial dysfunction has emerged as a central pathomechanism in DM– and statin–induced side effects. Assessment of mitochondrial respiration in peripheral platelets has been increasingly used as a mirror of organ mitochondrial dysfunction. The present study aimed to assess the: (i) changes in mitochondrial respiration elicited by statins in patients with type 2 DM and (ii) the effects of cell–permeable succinate (NV118) on respiratory parameters in platelets harvested from these patients. No significant changes were found in global mitochondrial respiration of intact platelets isolated from diabetic patients treated with either atorvastatin or rosuvastatin. Similarly, no significant changes in mitochondrial respiration of permeabilized platelets were found between diabetic patients treated with atorvastatin and healthy controls. Acute ex vivo administration of NV118 significantly improved respiration in isolated platelets. These results prompt further research on the role of permeable succinate as a therapeutic alternative for improving mitochondrial function in metabolic pathologies and point to the role of peripheral platelets as a potential biomarker of treatment response.

19 May 2025 in Biomedicines
Verified
Journal Article
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Dana Emilia MovilaDana Emilia Movila
Dana Emilia Movila
AMAlexandru Catalin Motofelea
Alexandru Catalin Motofelea
Dragos CozmaDragos Cozma
Dragos Cozma
OAOANA ALBAI
OANA ALBAI
ASAlexandra Sima
Alexandra Sima
Simona DrãganSimona Drãgan
Simona Drãgan
Background/Objectives: Cardiac amyloidosis (CA) is an underdiagnosed and potentially life-threatening infiltrative cardiomyopathy characterized by the extracellular deposition of misfolded amyloid fibrils in cardiac tissue. It is most commonly associated with light-chain (AL) amyloidosis and transthyretin (ATTR) amyloidosis, either hereditary or wild-type. The disease often presents with non-specific symptoms, leading to delayed diagnosis and treatment. This study aims to provide a comprehensive overview of the pathophysiology, diagnostic strategies, and current therapeutic approaches for cardiac amyloidosis, with a focus on improving early detection and clinical outcomes. Methods: A narrative review was conducted using databases such as PubMed and Scopus, covering the period from September 2016 to March 2025. Keywords such as “cardiac amyloidosis”, “cardiac amyloidosis from transthyretin”, “cardiomyopathy”, “transthyretin”, “immunoglobulin light-chain amyloidosis”, and “familial amyloidosis” were used. Relevant clinical trials and guideline-based management recommendations were also included. Results: This review highlights that non-invasive imaging modalities and serum biomarker analyses are key to reducing diagnostic delays. New therapeutic developments, including gene-editing technologies and RNA-based therapies, show promise in early trials. Multidisciplinary management and increased awareness are crucial for timely diagnosis and treatment optimization. Conclusions: The early recognition of cardiac amyloidosis remains a major clinical challenge. Advances in non-invasive diagnostics and emerging disease-modifying therapies are transforming the prognosis of affected patients. Continued research and heightened clinical suspicion are essential to improve outcomes in this complex and heterogeneous disease.