Band 50, Heft 2

Fetuin-A (FetA) is a glycoprotein primarily synthesized in hepatocytes, but recent studies have demonstrated that it is also synthesized in adipose tissue, classifying it as both a hepatokine and an adipokine. FetA has been shown to play a role in the regulation of glucose and lipid metabolism, thereby controlling overall body homeostasis. Elevated serum FetA levels have been reported in obesity, and this increase has been associated with insulin resistance (IR) and type 2 diabetes mellitus (T2DM). Therefore, investigating the molecular mechanisms underlying the variations of FetA in obesity and obesity-related metabolic diseases is crucial for the development of preventive strategies. Studies examining the molecular pathways involved in the relationship between FetA, adipose tissue, IR, and T2DM have shown that deviations in the expression of transcription factors such as nuclear factor erythroid-related factor 2 (Nrf2), nuclear factor kappa B (NF-κB), and peroxisome proliferator-activated receptor γ (PPARγ) in pancreatic, adipose, and liver cells contribute to the increase in FetA and the development of IR and/or T2DM. Consequently, future studies aimed at suppressing transcription factors in the signaling pathways that increase FetA expression, and identifying new agents that can regulate FetA secretion, could be therapeutically beneficial in treating obesity and obesity-related complications.

Objectives This systematic review aims to identify common preanalytical errors in pediatric blood sampling. Methods A literature search was conducted in PubMed, Web of Science, and EBSCOhost databases, with March 23, 2024 being the cut-off point. The search was conducted with a variety of keywords, such as ‘preanalytical errors,’ ‘blood sampling,’ ‘child,’ ‘neonatal,’ and ‘infant’, along with ‘AND/OR’ operators. Two researchers independently assessed the quality of the included studies, and the data from the selected studies were presented in tables. Results Nine studies published in English were included in this review, comprising seven descriptive studies and two case reports, involving involved a total of 110,120 pediatric blood samples. Most studies did not use a specific data collection tool; instead, they performed blood analyses using tubes. The most common preanalytical errors identified were inappropriate blood volumes in tubes, non-compliance with blood collection procedures, sample clotting, use of incorrect tubes, and contamination. Conclusions According to the results of this systematic review, systematic theoretical and practical training programs should be implemented, phlebotomy practices should be periodically audited, and quality indicators should be continuously monitored to prevent preanalytical errors in pediatric blood sampling.

Objectives Keloids, characterized by an excessive accumulation of fibrous tissue, remain a significant dermatological challenge. This study elucidates the role of Reticulocalbin 3 (RCN3) in modulating keloid fibroblasts (KFs) in vitro . Methods The RCN3 expression levels in human KFs and normal dermal fibroblast cells were examined using RT-qPCR and Western blot methods. RCN3 expression was knocked down in keloid fibroblasts after cells were transfected with shRNA targeting RCN3. On the other hand, recombinant RCN3 was added to treat the cells. RT-qPCR, Western blot, flow cytometry, CCK8 assays, and wound healing assays were performed to analyze the fibrotic markers (collagen I, III, MMP2, α-SMA) and TGFβ1/Smad2/6/7 pathway, apoptosis, proliferation and migration. Results RCN3 was upregulated in KFs. Its knockdown reduced fibrotic marker expression (collagen I, III, MMP2, α-SMA), cell proliferation, and migration, while increasing apoptosis. Conversely, recombinant RCN3 treatment enhanced the fibrotic responses. Changes in TGFβ1/Smad2 pathway, especially in Smad2 phosphorylation and Smad7, were evident following RCN3 modulation. Conclusions The study reveals RCN3 as a regulator in keloid pathology, affecting fibrosis, cellular behavior through TGFβ1/Smad2/Smad7 signaling.

Objectives Understanding drug resistance in cancer is of importance in treatment. Cancer stem cells are main factor for drug resistance. Therefore, the possible gene/gene interactions/proteins were explored in our study using a cancer stem cell-enriched population (H1299/S) derived from a parental non-small cell lung cancer cell line (H1299/P). Methods Response to cisplatin, which is the main drug for the treatment of lung cancer, was evaluated with the Adenosine triphosphate (ATP) viability test. As a result of the gene expression analysis, while 14 genes were not evaluated, expression profiles were obtained for 37 genes out of 51 genes. By the drug-protein interaction analyses, Topoisomerase I (TOPI), Topoisomerase 2 alpha (TOP2A), Topoisomerase 2 beta (TOP2B), Cyclin-dependent kinases 4 (CDK4), Cyclin-dependent kinases 6 (CDK6), ATP binding cassette subfamily B member 1 (ABCB1), ATP binding cassette subfamily C member 1 (ABCC1), ATP binding cassette subfamily C member 3 (ABCC3), B-cell leukemia/lymphoma 2 (BCL2), Poly (ADP-ribose) polymerase 1 (PARP1), Breast cancer gene 1 ( BRCA1 ) and Cyclin-dependent kinase inhibitor 1A ( CDKN1A ) genes and protein products were statistically significantly found to be in association with drug resistance. Results In bioinformatics analyses, it was observed that 13 pathways were affected due to expression changes and 12 genes related to these pathways were determined to activate multidrug resistance mechanisms. Conclusions Platinum-based drugs, as well as a broad range of other agents including topoisomerase and PARP1 inhibitors, and anthracyclines, have been shown to potentially possess multiple drug resistance.

Objectives Saponins are secondary metabolites naturally found in plants with diverse pharmacological properties such as anticancer. This research aimed to explore the anti-cancer properties of Polygalasaponin XLIV (PS-XLIV) in a human colorectal carcinoma cell line derived from Polygala vulgaris roots. Methods HCT166 cells were treated with different PS-XLIV concentrations and incubated for 24 and 48 h. We used immunocytochemistry to investigate PS-XLIV’s anti-cancer properties, employing antibodies targeting WNT3A, WNT11, STAT3, β-catenin, and Ki-67. The IC50 value of PS-XLIV was 80 μg/mL in HCT116 cells. WNT11, STAT3, β-catenin, and Ki-67. Immunoreactivities significantly decreased in PS-XLIV-treated HCT116 cells than in control group cells. Results After PS-XLIV treatment, the epithelial morphology of cells was protected; however, the number of cells was less than that of the control group cells. While WNT3A immunoreactivity was similar in both groups, WNT11 and β-catenin immunoreactivities were decreased after PS-XLIV application. In addition, the PS-XLIV treated group exhibited significantly weaker Ki-67 immunoreactivity, STAT3 immunoreactivty was moderated after PS-XLIV application. Conclusions For the first time, the anticancer effects of PS-XLIV isolated from P. vulgaris on HCT116 cells were shown. The anticancer effect may involve PS-XLIV reducing WNT11, β-catenin, STAT3, and Ki-67 activation pathways in HCT116 cells.

Objectives β-Thalassemias, caused by mutations in HBB , are hereditary blood disorders that impose a significant global health burden. Detecting these mutations through accurate genetic analysis is essential. This study aimed to create a panel of cell type reference materials for β-thalassemia genetic testing using prime editing (PE), a flexible and precise genomic editing method. Methods PE3 systems were designed to target specific HBB mutations, including single nucleotide variants (SNVs) (−32 (C>A), CD 17 (A>T)), insertions (CD 14/15 (+G), CD 71–72 (+A)), and deletions (CD 31 (−C), CD 41/42 (−TTCT)). HEK293T cells were edited to carry these mutations. Sanger sequencing was performed to confirm the accurate introduction of homozygous and heterozygous mutations. The cell lines were further verified using commercial reverse dot-blot hybridization and melting curve assays. Results We successfully constructed 12 stable HEK293T cell lines carrying the intended homozygous or heterozygous HBB mutations using PE3 systems. No off-target mutations in the HBB were detected by Sanger sequencing in these stable cell lines, even after more than 10 weeks of culturing. Additionally, all target mutations were accurately and consistently detected using two reverse dot-blot hybridization kits and one melting curve assay kit. Conclusions The 12 stable cell lines exhibited accurate and stable HBB mutations, making them valuable reference materials for β-thalassemia genetic testing. PE3 systems show potential for generating a comprehensive panel of HBB mutations, particularly those that are clinically rare.

Objectives The widespread use of propofol, fentanyl, and midazolam in intensive care units necessitates a thorough understanding of their potential toxic effects. These sedative-hypnotic agents are frequently administered in combination to manage critically ill patients, raising concerns about their cumulative toxicity. To address this, we investigated the cytotoxic and genotoxic effects of these drugs, both individually and in combination, on a human liver epithelial cell line (THLE-2). The liver, as a major organ involved in drug metabolism, is particularly vulnerable to drug-induced toxicity. By evaluating the impact of these agents on liver cells, we aim to gain insights into their potential adverse effects and inform clinical practice. Methods Cells were treated with increasing concentrations of each drug, as well as with their combination, over a 72 h incubation period. Cell viability, oxidative stress, antioxidant defense mechanisms and apoptotic activity and potential genotoxicity were explored using various assays. Results A dose dependent increase in cytotoxicity, intracellular reactive oxygen species production, apoptotic activity, and DNA damage were detected in all treatment groups (p<0.05). Higher concentrations of the study drugs were associated with marked increases in oxidative stress and apoptotic markers. There was a concomitant reduction in intracellular glutathione levels, suggesting a depletion of the cells’ antioxidant defenses. When these drugs were administered in combination, the cytotoxic and genotoxic effects appeared to be mitigated, indicating a potential protective interaction between these agents, particularly involving midazolam. Conclusions The study drugs caused dose-dependent hepatotoxicity, induced DNA damage and apoptosis and consequently decreased cell viability.

Objectives In the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD), hypoxia-associated angiogenesis is increasingly considered a significant mechanism. We aimed to assess serum and urine leucine-rich α-2-glycoprotein 1 (LRG1) levels and their correlation with vascular endothelial growth factor A (VEGF-A), hypoxia-inducible factor 1-alpha (HIF-1α), and disease severity to explore LRG1’s role as a biochemical marker in ADPKD-related angiogenesis. Methods The study involved 67 ADPKD patients and 25 healthy controls. The ADPKD-I group comprised 40 patients with an estimated glomerular filtration rate (eGFR, mL/min/1.73 m 2 ) >60, and the ADPKD-II group comprised 27 patients with an eGFR <60. Height-adjusted total kidney volume (hTKV) was calculated from magnetic resonance (MR) images. Serum levels of LRG1, VEGF-A, HIF-1α, and urine LRG1 levels were assayed by ELISA, and urinary albumin levels were measured by the immunoturbidimetric method. Urine LRG and albumin levels were calculated by normalizing the urine creatinine ratio. Results The levels of serum LRG1 were remarkably higher only in the ADPKD-II group compared to controls (p<0.025). Serum HIF-1α and VEGF-A levels were significantly elevated in both ADPKD-I and ADPKD-II groups compared to controls (p = 0.039, p = 0.029, p<0.001, and p<0.001, respectively); however, there was no notable difference between two groups. Urinary LRG1 and albumin excretion levels were notably higher in both ADPKD groups than in controls but the highest in the ADPKD-II group. In the ADPKD-I group, urine LRG1 correlated positively with urinary albumin excretion (r = 0.338, p = 0.038). Conclusions LRG1 may serve as a mediator in the crosstalk between hypoxia and angiogenesis in patients with ADPKD. Additionally, urinary LRG1 levels could potentially reflect disease severity.

Objectives Physiological changes of trophoblast cells are associated with gestational diabetes mellitus (GDM), and miR-184 involved in the development of GDM can be a potential therapeutic target. Asiaticoside (AS) has potential therapeutic effects on GDM, but its effect on miR-184 in HTR-8/Svneo cells is a relatively unworked area. The present study aimed to explore the effect of AS and miR-184 on physiological changes of HTR-8/Svneo cells. Methods After the cytotoxicity assay of AS, HTR-8/Svneo cells were transfected with miR-184 mimics and/or treated with AS. The mRNA level of miR-184 in different groups was determined by real-time reverse transcription polymerase chain reaction, the cell viability was detected by cell counting kit-8 assay, the cell migration was measured by scratch test, the protein expressions of matrix metalloproteinase-2 (MMP2), MMP9, protein kinase B (AKT) and p-AKT were determined by western blot. Results Eighty μM AS with a treatment time of 48 h had no cytotoxicity and even promoted cell viability of HTR-8/Svneo cells. AS could significantly inhibit the mRNA level of miR-184 in HTR-8/Svneo cells (p<0.05). The overexpression of miR-184 significantly suppressed the cell viability, migration, and protein expressions of MMP2, MMP9 and p-AKT/AKT; however, AS was able to reverse the inhibition effect of miR-184 to increase the cell viability, migration and protein expressions of MMP2, MMP9 and p-AKT/AKT in HTR-8/Svneo cells (p<0.05). Conclusions AS can reverse the inhibition effect of miR-184 on HTR-8/Svneo cells to facilitate cell proliferation, migration and AKT phosphorylation.

Objectives D-dimer molecules are formed as a result of fibrinolysis and elevation of D-dimer levels are suggestive for thrombosis. The elevation of D-dimer levels and its correspondence with thromboembolism in orthopedic and general surgeries are well studied, but there are only a few studies in literature that investigates this issue in head and neck surgery. We aimed to investigate D-dimer levels and its course throughout the perioperative period in patients who underwent head and neck cancer surgery. Methods We conducted a prospective, observational study in patients who underwent neck dissection along with primary tumor resection in our otorhinolaryngology clinic between January 2022 and June 2023. D-dimer levels were measured from blood samples preoperatively and postoperatively days 0–7 and on postoperative 14th day. D-dimer levels were compared statistically. Results Twenty-one patients were included in the study. D-dimer values peaked on the first day then gradually decreased and reached a level slightly below 2 times of the preoperative values on the 14th day. The change in D-dimer levels between preoperative and postoperative days 1–14 was statistically significant. The difference between D-dimer levels measured on each day of the first week and levels on 14th day was found to be significant. Also, difference of D-Dimer levels between postoperative day 0 and day 7 was statistically significant. Conclusions The trend of D-dimer levels following surgery in head and neck cancer patients may prove useful in clinical practice to rule out thrombotic events, in accordance with other risk factors and symptomatology.

Objectives Evidence from previous documents points to the involvement of the keratin 15 (KRT15) gene in the modulation of signaling networks governing cancer cell death, survival, proliferation, migration, invasion, and metastasis. Nonetheless, its relevance in pan-cancer studies and the precise molecular mechanisms involved in lung cancer remain poorly understood. To comprehensively investigate the clinical relevance of the KRT15 gene in human lung cancer and a diverse array of cancers. Methods A comprehensive investigation of the clinical relevance of the KRT15 gene in a diverse array of human tumors was conducted. In light of this, the study also examined the possible link between the KRT15 gene and tumor immunogenic features. Based on the outcomes of pan-cancer analysis, we selected lung adenocarcinoma (LUAD) as the specific tumor type for an in-depth investigation into KRT15-induced signaling pathways and intercellular communications contributing to tumor progression. Results According to our study, KRT15 may hold significance as a newly identified biomarker, potentially contributing to both prognostic evaluation and immunotherapeutic targeting across various cancer types. Significantly, KRT15 was hypothesized to function as a guiding marker gene, holding potential for clinical prognostication and personalized tumor-specific therapies in LUAD. Suppression of KRT15 significantly impaired lung cancer cells’ growth, migration, invasion, and survival. Conclusions KRT15 possesses the potential to be an innovative biomarker and therapeutic target, playing a role in predicting the prognosis and treatment response of LUAD patients.

Objectives Nitrosative stress is defined as a condition in which oxidative stress accompanies the presence of excess NO and they both may alter the integrity of the red blood cell membrane (RBC). In this study, age- and sex-related effects of nitrosative stress on the membrane osmotic fragility of RBC were investigated using NO and superoxide donors in the RBC isolated from participants. Methods A total of 119 men and women volunteers, both young and old, provided blood samples for the study. The effects of NO precursor L-arginine, Nitric Oxide Synthase (NOS) inhibitor L-NMMA, long-acting NO donor Diethylenetriamine/NO (DETA10 −6 –10 −4 M), short-acting NO donor Diethylamine-NONOate (DEA10 −6 –10 −4  M) and superoxide donor pyrogallol (Pyr) on the fragility of RBC were studied using NaCl-induced osmotic hemolysis. Hemoglobin level, plasma total antioxidant capacity (TAC), and nitrite levels were measured by spectrophotometric methods. Results Although the RBC hemolysis of all groups was not affected by L-arg and L-NMMA, the effect of DETA and DEA varied. The RBC fragility of old and young men was more sensitive to Pyr-induced oxidative stress than old and young women. Human RBC was differentially affected by nitrosative stress induced by Pyr10 −3 M plus varying concentrations of DETA and DEA depending on age and sex. While the plasma TAC values of the young men were higher than those of young women, there was no significant difference in plasma nitrite levels between all groups. Conclusions The findings of this study indicate that the fragility of human red blood cells (RBCs) in response to oxidative and nitrosative stress varies depending on sex and age.

Objectives Urinary incontinence (UI) is defined as any type of involuntary loss of urine. Pathophysiological changes that occur in the urinary system due to aging, especially ischemia, cause functional and structural changes in the urinary system. Oxidative stress is caused by an imbalance between the body’s oxidative radicals and antioxidant defense systems. In this study, we aimed to investigate the link between UI and oxidative stress indicators in older people. Methods Patients were divided into two groups: the group with incontinence and the group without incontinence. A comprehensive geriatric evaluation was performed on all patients, and they were compared according to serum native thiol, disulfide, and ischemia-modified albumin (IMA) levels. Results A total of 145 patients aged 65 years and older were included in the study (44, incontinence; 101, continence). The median age of individuals with UI was 75 (69–83) years. Receiver operating characteristic (ROC) curves were made to determine the cut-off for thiol-disulfide homeostasis and IMA. Disulfide and native thiol divide disulfide values ​​were more significant than other oxidative stress parameters. The area under the curve (AUC) values were 0.65 (95 % CI:0.55–0.74) for disulfide and 0.60 (95 %CI:0.50–0.70) for disulfide divide native thiol (p=0.005, p=0.049, respectively). Conclusions Thiol disulfide homeostasis and IMA molecules, which are indicators of oxidative stress, were found to have significantly higher levels of disulfide and disulfide divide native thiol in patients with incontinence. We think it may be important to look at the possible therapeutic benefits of paying attention to the levels of these molecules in relation to the management of UI in older people.

Objectives Reference change value (RCV) is an objective tool that indicates whether the change between consecutive measurements is clinically significant. This study aimed to determine the instrument-specific RCVs of thyroid-stimulating hormone (TSH), free triiodothyronine (fT3), free thyroxine (fT4), thyroglobulin (Tg), thyroglobulin antibody (Anti-Tg), and thyroperoxidase antibody (Anti-TPO) tests, which are routinely analyzed for the diagnosis, case-finding, and screening of thyroid diseases. Methods This cross-sectional study was conducted between January 1 and December 31, 2018. The twelve-month mean analytical imprecision (CV A ) was calculated from internal quality control data for each test on three different instruments. All tests’ individuality index (II) was calculated using the biological variation data. RCVs were determined by both conventional and logarithmic approaches. Results It was shown that the II of all tests was 0.6 and below. Upward logarithmic RCVs were slightly higher than conventional RCVs, while downward logarithmic RCVs were lower (e.g., conventional RCV for TSH 39 %, whereas upward and downward RCVs 48 and 32 %, respectively). Conclusions Due to high individuality, the results of thyroid-related biomarkers would be more appropriate to evaluate with RCV instead of reference interval. Instrument-specific RCVs should be determined because the analytical imprecision of analyzers may vary. Most presentations to the hospital are not healthy individuals, so logarithmic RCV could provide a more accurate assessment of significant change.

Objectives Serum boron level has not been studied in pregnancies with pre-eclampsia. The aim of this study was to compare the levels of serum boron in pregnancies with early onset severe pre-eclampsia and healthy pregnancies. Methods The study included 43 pregnant patients with early onset severe pre-eclampsia and a control group of 30 healthy pregnant patients. Results The serum boron levels of the patients with severe pre-eclampsia were determined to be significantly higher than those of the control group (28.8 v.s 12.7 μg/L; p<0.05). A statistically significant correlation was determined between the serum boron level and the serum ALT level (r:482, p<0.001), serum AST level (r=554, p<0.001), and platelet count (r=−549, p<0.001). High values of serum boron indicated the presence of pre-eclampsia, with a diagnostic cut-off point of 11.65 μg/L, with 76.7 % sensitivity and 76.7 % specificity (p<0.001, area under curve: 0.832, Confidence interval: 0.736–0.928). Conclusions An increase in serum boron levels without reaching clinically toxic levels may contribute to the development of pre-eclampsia, probably by causing impairment in the placentation process. The current study can be considered of value as the first study in literature to show that serum boron levels were increased in pregnancies with early onset severe pre-eclampsia.

Objectives Diabetic cardiomyopathy (DCM) is a chronic complication of type 2 diabetes mellitus, leading to heart failure. Addressing DCM requires a comprehensive therapeutic approach. This study examines the protective role of Δ(9)-tetrahydrocannabinol (THC) in DCM by assessing its impact on cardiac function, inflammation, oxidative stress, and mitochondrial health and exploring the involvement of the SIRT3/FOXO1 and TLR4/NF-κB/NLRP3 signaling pathways. Methods Over a four-week period, THC (1.5 mg/kg, administered intraperitoneally) was given to type-2 diabetic Sprague-Dawley rats. Cardiac function was evaluated using a carotid catheter in vivo while mitochondrial integrity was assessed through fluorometric techniques. Moreover, cardiac biochemical biomarkers and the protein expression of key signaling proteins were measured via ELISA and immunoblotting. Results Compared to untreated diabetic rats, THC treatment showed pronounced protective effects, improving cardiac function and reducing markers of DCM. It significantly lowered the expression of NF-κB, NLRP3, IL-1β, and TNF-α while reducing diabetes-induced oxidative stress in the heart, as evidenced by decreased malondialdehyde levels and increased glutathione and catalase levels. THC also prevented mitochondrial membrane depolarization and reactive oxygen species production and substantially suppressed the upregulation of TLR4 and MyD88 while increasing FOXO1 expression in diabetic rats. Inhibition of the SIRT3/FOXO1 pathway using 3-TYP reversed the cardioprotective effects of THC, negating its impact on mitochondrial function and the expression of NF-κB/NLRP3/IL-1β without influencing TLR4/MyD88. Conclusions These results underscore that THC offers significant protection against diabetes-induced cardiac damage by mitigating functional and biochemical changes associated with DCM, primarily through modulation of the TLR4/NF-κB/NLRP3 and SIRT3/FOXO1/mitochondrial pathways.

Objectives In this study, Rosa damascena Mill. essential oil (RDEO) was aimed to evaluate its potential anti-inflammatory and mitochondria-mediated anti-apoptotic effects in vitro and in vivo in acetic acid (AA)-induced ulcerative colitis (UC) rat model. Methods In the UC rat model, RDEO (100 μL/kg, p.o.) or sulfasalazine (100 mg/kg/p.o.) was administered to the treatment groups. After decapitation, the UC activity index, colon mass index, and macroscopic and microscopic damages were determined in rat colon tissue. TNF-α levels and MPO activity were measured to evaluate the effect of the inflammation in the colon. Changes in the expression levels of Bcl-2, Bax, casp-3, and casp-9 proteins, which are indicators of mitochondrial-mediated apoptosis were determined by the Western blot method. Results Our study results revealed that AA-induction caused a significant increase in colitis activity index (CAI), colon mass index (CMI), and macroscopic and microscopic damages in rat colon tissue. It shows that RDEO treatment has an effective curative effect by reducing AA-induced inflammation (TNF-α and MPO activity), CAI, CMI, pro-apoptotic protein (Bcl-2, Bax, Casp-3, and Casp-9), and morphological damages in rat colon tissue. Conclusions All these results suggest that RDEO may have suppressed changes in colon tissue due to its ability to reduce AA-induced inflammation and apoptosis. The results of this study showed that RDEO was beneficial in UC and, like other herbal anti-inflammatory agents, RDEO did not cause gastrointestinal side effects.

Objectives Blood collection, one of the most frequently performed procedures in healthcare settings. The study aimed to develop a scale for phlebotomy procedures based on national phlebotomy guidelines and to assess the tendencies of phlebotomy personnel in certain blood collection practices. Methods The survey included a 5-point likert scale, which consisted of 20 items and multiple-choice questions. The survey was disseminated to the attendees via an online platform (Google Forms ® , Mountain View, CA, USA), and they were requested to complete it, and a total of 1,439 participants were included in the study. Results The data showed that the scale complied with the guidelines and was highly valid and reliable. A significant finding from the study indicates that 47.9 % of the participants (689 individuals) chose the syringe response during the blood collection procedure. The variable of prior phlebotomy training exhibited no statistically significant effect on these responses (χ²=1.893, p=0.093). A statistically significant difference was observed in the frequency of tendencies for using intravenous cannulas/catheters in inpatient settings (p<0.05). Conclusions The standardization of blood collection practices may be enhanced through the implementation of these procedures by specialized medical professionals. It is necessary to audit the quality of current practices and identify the most vulnerable steps in phlebotomy. The implementation of phlebotomy guidelines in healthcare settings should be encouraged. Furthermore, greater commitment is required from relevant authorities to develop educational programs and establish continuous education courses for healthcare phlebotomy personnel.