Clinical laboratory最新文献

{"title":"Abundance and Composition of the Meconium Microbiota in Preterm Infants with Infections, Feeding Intolerance, or Necrotizing Enterocolitis.","authors":"YanQiu Jiang, Qiang Yao, YanFeng Zhao, YunWei Kong, Tao Yu, YanFang Wang, Fei Yang, WeiNong Mo","doi":"10.7754/Clin.Lab.2024.240911","DOIUrl":"https://doi.org/10.7754/Clin.Lab.2024.240911","url":null,"abstract":"<p><strong>Background: </strong>The role of the microbial flora of the gut of a newborn is of scientific and practical interest. The aim of this study was to assess the abundance and composition of the meconium microbiota in preterm infants with infections, feeding intolerance, or necrotizing enterocolitis (NEC).</p><p><strong>Methods: </strong>Eighty-four preterm infants born by cesarean section were prospectively enrolled in this study. Out of the 28 diseased infants, 23 developed infections, including 8 cases of sepsis, 10 cases of pneumonia, 1 case of enterocolitis, and 4 cases of NEC. Fifty-six (66.67%) preterm infants without these characteristics served as control group. General clinical information (gender, gestational age, birth weight, presence of preterm rupture of mem-branes, Apgar 1-minute score, and duration of hospitalization) was collected. First-pass meconium samples were collected for 16S rRNA microbiological analysis.</p><p><strong>Results: </strong>Compared with the control group, the diseased infants had a lower gestational age (p < 0.001) and lower body weight (p = 0.014). In addition, the hospitalization time of the diseased infants was longer than that of the control group (p < 0.001). On the α-diversity measure, there was no difference in species abundance and diversity between the two groups; on the β-diversity measure, the differences in the microbial composition of the two groups were subjected to PCoA analyses, which showed that there was a difference between the disease group and the control group. At the phylum level, the dominant phylum in both groups was p_Proteobacteria, with higher abundance of p_Firmicutes in the disease group. At the genus level, the dominant genus in both groups was g_Novosphingobium. Microbiome phenotype prediction by BugBase revealed that microbial phenotypes 'Gram-positive' and 'Anaerobic' were abundantly increased in the disease group; microbial function prediction did not differ between the two groups in terms of significant function.</p><p><strong>Conclusions: </strong>The impact of infections, feeding intolerance, and NEC on a host is complex. Preterm infants delivered by cesarean section have p_Proteobacteria as the dominant phylum, with a higher abundance of p_Firmicutes in the disease group, a difference contributed by g_Peptoniphilus.</p>","PeriodicalId":10384,"journal":{"name":"Clinical laboratory","volume":"71 4","pages":""},"PeriodicalIF":0.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143969899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased Number of Circulating Myeloid Dendritic Cell 1 in Patients with Severe Aplastic Anemia.","authors":"Yingying Sun, Chengcheng Wu, Chunyan Liu, Huaquan Wang, Zonghong Shao","doi":"10.7754/Clin.Lab.2025.250146","DOIUrl":"https://doi.org/10.7754/Clin.Lab.2025.250146","url":null,"abstract":"<p><strong>Background: </strong>A deeper understanding of the immune pathogenesis of severe aplastic anemia (SAA) is required to improve therapeutic effects. Myeloid dendritic cell (mDC) is involved in the initiation of immune disorders in SAA patients. The objective of this study was to characterize the subsets of mDC in patients with SAA.</p><p><strong>Methods: </strong>A total of 136 SAA patients diagnosed in the Hematology Department of Tianjin Medical University General Hospital from December 2020 through November 2024 and 39 healthy controls were enrolled in this study. The percentages of the two main subsets of mDC (mDC1 and mDC2) in SAA patients with different disease status and healthy controls were detected by flow cytometry, and their correlations with the immune status and severity of SAA were analyzed.</p><p><strong>Results: </strong>The mDC/plasmatoid dendritic cell (pDC) ratio of the untreated SAA group was significantly higher than that of the healthy control group (51.60 ± 122.16 vs. 4.77 ± 5.86, p = 0.015). MDC1 is the primary subset of mDC in all groups. The percentage of mDC1 in the untreated SAA group [(55.39 ± 22.99)%] was significantly higher than that in the partial remission group [(28.22 ± 26.37)%, p = 0.00], complete remission group [(25.55 ± 23.12)%, p = 0.00], and healthy control group [(19.22 ± 22.77), p = 0.00]. The percentage of mDC1 in the non-remission group [(40.25 ± 29.91)%] was significantly higher than that in the healthy control group [(19.22 ± 22.77)%, p = 0.026]. In the untreated SAA group, there was a significant negative correlation between the percentage of mDC1 and the reticulocyte count (r = -0.284, p = 0.048). There was no statistical difference in the percentage of mDC2 among the groups.</p><p><strong>Conclusions: </strong>The activation of mDC1, rather than mDC2, might be involved in the pathogenesis of SAA. MDC1 intervention may have therapeutic potential in treating SAA.</p>","PeriodicalId":10384,"journal":{"name":"Clinical laboratory","volume":"71 4","pages":""},"PeriodicalIF":0.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143955317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic Myeloid Leukemia Progression to Acute Mixed-Lineage Leukemia: a Diagnostic Challenge Complicated by Severe Complications.","authors":"Xu Jing, Luo Shi, Guo Lifu","doi":"10.7754/Clin.Lab.2024.241026","DOIUrl":"https://doi.org/10.7754/Clin.Lab.2024.241026","url":null,"abstract":"<p><strong>Background: </strong>Chronic myeloid leukemia (CML) is a myeloproliferative disorder that can progress to an accelerated or blast phase if left untreated or inadequately managed. Acute transformation of CML, particularly into mixed lineage leukemia, is a rare and challenging complication. This case report describes the clinical course of a 30-year-old male patient with CML progressing to acute mixed lineage leukemia and complicated by gastrointestinal bleeding.</p><p><strong>Methods: </strong>The patient, initially diagnosed with CML in June 2019, was treated with imatinib. However, after discontinuing treatment on his own, the disease progressed to acute myeloid leukemia (AML-M2a) by June 2020, confirmed by bone marrow analysis, flow cytometry, and cytogenetics showing BCR-ABL1 positivity. Despite multiple chemotherapy regimens, including VCLP, VDP with dasatinib, and COP with dasatinib, the patient's condition failed to improve. He developed recurrent gastrointestinal bleeding, which was managed with acid suppression, blood transfusions, and infection control measures.</p><p><strong>Results: </strong>The patient experienced persistent bone marrow failure, characterized by blasts in peripheral blood and bone marrow, as well as refractory gastrointestinal bleeding despite supportive care. During chemotherapy, the patient also developed severe infections and psychiatric symptoms, complicating the treatment course.</p><p><strong>Conclusions: </strong>This case highlights the aggressive progression of CML to acute mixed lineage leukemia and underscores the challenges in managing patients with resistant disease. The patient's gastrointestinal bleeding and recurrent infections further complicated treatment, emphasizing the need for early intervention and close monitoring of high-risk CML patients.</p>","PeriodicalId":10384,"journal":{"name":"Clinical laboratory","volume":"71 4","pages":""},"PeriodicalIF":0.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143955512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"One Case of Abnormal Elevation of PIVKA-II.","authors":"Gangfeng Li, Tao Lu, Qiong Wang","doi":"10.7754/Clin.Lab.2024.241054","DOIUrl":"https://doi.org/10.7754/Clin.Lab.2024.241054","url":null,"abstract":"<p><strong>Background: </strong>Protein Induced by Vitamin K Absence or Antagonist II (PIVKA-II) is a serum biomarker that is specifically elevated in hepatocellular carcinoma (HCC) and has important value in early diagnosis, prognosis evaluation, and recurrence prediction of liver cancer.</p><p><strong>Methods: </strong>We report a case of extreme elevation of serum PIVKA-II due to the use of warfarin.</p><p><strong>Results: </strong>The patient's abdominal ultrasound and enhanced CT examinations showed no significant abnormalities. The patient has been taking warfarin for atrial fibrillation, and after supplementing with vitamin K, the PIVKA-II level significantly decreased. Therefore, the PIVKA-II results were extremely elevated, which is believed to be caused by taking warfarin.</p><p><strong>Conclusions: </strong>When patients take warfarin anticoagulant therapy, it may cause an extreme increase in PIVKA-II results. Laboratory staff and clinical doctors should consider the existence of this situation and avoid unnecessary examinations and treatments for patients.</p>","PeriodicalId":10384,"journal":{"name":"Clinical laboratory","volume":"71 4","pages":""},"PeriodicalIF":0.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143977314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Unexpected Finding of a Novel 21.9 kb Deletion (Heyuan deletion, β21.9kb) β-Thalassemia During HbA1c Measurements.","authors":"Hanxian Liao, Liang Liang, Xingyuan Chen, Yu Zheng, Ying Huang, Youqiong Li","doi":"10.7754/Clin.Lab.2024.241035","DOIUrl":"https://doi.org/10.7754/Clin.Lab.2024.241035","url":null,"abstract":"<p><strong>Background: </strong>β-thalassemia is predominantly caused by point mutations in the β-globin gene, whereas large deletions occur less frequently. Here, we described a novel 21.9 kb deletion found in a patient with β-thalassemia dur-ing HbA1c measurements.</p><p><strong>Methods: </strong>The proband was a 25-year-old female who came to the hospital with her husband for routine prenatal examinations. The hemoglobin A1c(HbA1c) was measured by high-performance liquid chromatography (HPLC). Hb analysis was performed by capillary electrophoresis (CE). Routine genetic analysis was carried out by PCR and reverse dot-blot (PCR-RDB) and Gap-PCR. Multiplex ligation-dependent probe amplification (MLPA) was used to screen the deletion in the β-globin chain. Based on the MLPA results, the break location of the deletion was determined by third-generation sequencing (TGS). Sanger sequencing verified the breakpoint in the Gap-PCR amplification products of TGS.</p><p><strong>Results: </strong>HbA1c measurements suggested an elevated HbF value (> 5%) by HPLC, and a retest of the Hb analysis showed an HbF value of 27.9%, and an Hb A2 value of 1.7% using CE. No mutations were detected by Gap-PCR and PCR-RDB. However, MLPA demostrated the presence of large fragment deletion in the β-globin chain. The positions of the deletion were located between 5,225,669 and 5,247,554 on chromosome 11 (chr11: 5,225,669-5,247,554; NG_000007.3:g.50,063-71,947 del) using TGS, spanning the length of 21,886 bp (21.9 kb deletion).</p><p><strong>Conclusions: </strong>This is the first report of the 21.9 kb deletion, so we named it Heyuan deletion for the place of origin of the proband. It presented with normal hematological parameters but an elevated HbF value.</p>","PeriodicalId":10384,"journal":{"name":"Clinical laboratory","volume":"71 4","pages":""},"PeriodicalIF":0.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical and Laboratory Characteristics of Gaucher Disease Caused by Complex Heterozygous Mutation.","authors":"Rui Zhang, Mei Liu, Xin Wei, Zhanxi Gao, Ming Gao, Yukai Guo, Xiaofei Li, Song-Yun Zhang, Min Shi","doi":"10.7754/Clin.Lab.2024.240937","DOIUrl":"https://doi.org/10.7754/Clin.Lab.2024.240937","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to investigate and review the clinical and laboratory characteristics of Gaucher disease type 1 (GD1) caused by the heterozygous mutation of the Glucocerebrosidase (GBA) gene.</p><p><strong>Methods: </strong>In this study, the bone marrow smear and biopsy slice were observed using Wright-Giemsa as well as Hematoxylin and Eosin (HE) stains, respectively. Furthermore, peripheral blood leukocyte lysosomes were monitored by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The patient's and her parents' peripheral blood DNA were extracted, and the mutation sites of the GBA-related genes were sequenced via Sanger sequencing.</p><p><strong>Results: </strong>It was revealed that the Gaucher cells in the bone marrow smear and biopsy slice had large volume, were round, ovoid or irregular, occasionally binucleated or multinucleated, with chromatin roughness and occasional nucleoli, rich in the cytoplasm, bluish or grayish-red colored, and with many cytoplasmic onion-skin-like striped structures. Furthermore, the expression of GBA was decreased, while glucosylsphingosine levels were elevated. Moreover, the patient had a heterozygous complex mutation in the GBA gene (GBA NM_001005741.2): c.1604G > Ap.Arg535Hi (R496H) from her mother and c.1448T > Cp. Leu483Pro (L444P) at chromosomal locations chr1:155204793 and chr1:155205043, respectively.</p><p><strong>Conclusions: </strong>The results show that a heterozygous complex mutation of R496H and L444P in the GBA gene causes the development of GD1. Clinical, enzyme activity-based assays, biological markers, and genetic analysis can significantly improve disease diagnosis and are important for early intervention and GD treatment.</p>","PeriodicalId":10384,"journal":{"name":"Clinical laboratory","volume":"71 4","pages":""},"PeriodicalIF":0.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extramedullary Relapse of Acute B-Lymphoblastic Leukemia Leading to Paraplegia in a Child with Down Syndrome.","authors":"Li Yang, Shi Luo, Ping Ye","doi":"10.7754/Clin.Lab.2024.241052","DOIUrl":"https://doi.org/10.7754/Clin.Lab.2024.241052","url":null,"abstract":"<p><strong>Background: </strong>Acute B-lymphoblastic leukemia (B-ALL) is a common malignancy in children. Patients with Trisomy 21 (Down syndrome) are at a higher risk of developing hematologic disorders. Despite advances in treatment, extramedullary relapse remains a challenge, particularly when it manifests as spinal cord compression leading to paraplegia, a rare but severe complication.</p><p><strong>Methods: </strong>We describe the clinical course of an 11-year-old male with Trisomy 21, diagnosed with B-ALL. The patient was treated with standard chemotherapy (VDLP regimen) followed by central nervous system prophylaxis through lumbar puncture and intrathecal chemotherapy. Despite achieving minimal residual disease (MRD)-negative status, the patient developed progressive lower back pain and acute paraplegia. Imaging studies and subsequent spinal surgery were performed to diagnose and manage the spinal cord lesion.</p><p><strong>Results: </strong>The patient's spinal pathology confirmed a relapse of B-ALL with extramedullary involvement. Immunohistochemistry of the tumor showed markers consistent with B-lymphoblastic leukemia/lymphoma. Chemotherapy-induced remission was initially achieved, but the patient experienced bone marrow suppression after each cycle, leading to further hospitalization and supportive treatments. Postsurgical findings showed no CNS involve-ment, and bone marrow MRD remained negative.</p><p><strong>Conclusions: </strong>This case highlights the complexity of managing B-ALL in children with Trisomy 21, who may be prone to extramedullary relapse despite systemic remission. Early recognition of spinal symptoms and prompt surgical intervention are critical in preventing irreversible neurological damage such as paraplegia. This case underscores the need for vigilant monitoring and tailored therapeutic strategies in high-risk populations.</p>","PeriodicalId":10384,"journal":{"name":"Clinical laboratory","volume":"71 4","pages":""},"PeriodicalIF":0.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143957115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Case of Multiple Myeloma with Auer Rod-Like Inclusions in Plasma Cells.","authors":"Qibin Luo, Qingfeng Ma, Sai Zhang","doi":"10.7754/Clin.Lab.2024.241049","DOIUrl":"https://doi.org/10.7754/Clin.Lab.2024.241049","url":null,"abstract":"<p><strong>Background: </strong>Auer rods are considered to be a distinctive feature of acute myeloid leukemia, presenting in the cytoplasm of leukocytes in a purplish-red rod-like, wood-bundles-like, and spindle-like morphology. In this paper, we report a rare presence of wood-bundles-like Auer rods in the plasma cells of patient with multiple myeloma (MM).</p><p><strong>Methods: </strong>Retrospective analysis of the clinical presentation and laboratory diagnosis of patients with multiple myeloma containing Auer rod-like inclusions in plasma cells were reviewed in this study.</p><p><strong>Results: </strong>In 2014, 15% of plasma cells were shown in the patient's bone marrow smear, and the diagnosis of multiple myeloma was considered. The cytosol of plasma cells was medium-sized, the nucleus was deviated, the chromatin was aggregated in clumps, and Auer rod-like inclusions arranged in woody bundles were seen in the cytoplasm. In 2017, the patient's condition relapsed, and an abnormal increase of κ-type free light chains was found in the urine, and the urine Bence-Jones protein was positive. In 2021, the patient's condition aggravated to the point of death.</p><p><strong>Conclusions: </strong>In this uncommon case, the source and mechanism of Auer rod-like inclusions production should be paid more attention to provide rational suggestions for clinical diagnosis.</p>","PeriodicalId":10384,"journal":{"name":"Clinical laboratory","volume":"71 4","pages":""},"PeriodicalIF":0.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143993748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Rare Case of Anti-Kpa Antibody Identification in a Chinese Patient.","authors":"Zengzhen Wei, Xiaohong Wang, Fu Cheng, Li Wang, Jinzhe Tan, Bin Tan","doi":"10.7754/Clin.Lab.2025.250212","DOIUrl":"https://doi.org/10.7754/Clin.Lab.2025.250212","url":null,"abstract":"<p><strong>Background: </strong>Here we present a rare case of anti-Kpa alloantibody identified in a Chinese individual, along with a literature review.</p><p><strong>Methods: </strong>An antibody identification test was conducted to clarify the antibody specificity. To further characterize this antibody, we assessed the reactivity of the patient's serum with relative antigen-positive red blood cells at different test phases. We also investigated the sensitivity of the antigen to DTT and papain. We separated the pa-tient's own RBCs from the transfused ones using capillary centrifugation and performed direct antiglobulin test and Kell blood group antigen detection.</p><p><strong>Results: </strong>The patient's Kell phenotype was Kp(a-b+), and an IgG-specific anti-Kpa antibody was identified, resulting from the transfusion of Kp(a+b+) allogeneic red blood cells (RBCs). The Kpa antigen on RBCs was susceptible to 0.2M DTT but not to papain.</p><p><strong>Conclusions: </strong>This case highlights the presence of an anti-Kpa antibody in the Chinese population, suggesting that a reassessment of the frequency of this antigen in this demographic is warranted.</p>","PeriodicalId":10384,"journal":{"name":"Clinical laboratory","volume":"71 4","pages":""},"PeriodicalIF":0.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Overview of the Incidence, Causes, and Impact of Iron Deficiency Anemia in Saudi Arabia.","authors":"Hassan A Hamali","doi":"10.7754/Clin.Lab.2024.241102","DOIUrl":"https://doi.org/10.7754/Clin.Lab.2024.241102","url":null,"abstract":"<p><strong>Background: </strong>Iron deficiency anemia (IDA) is the most prevalent cause of micronutrient anemia globally, accounting for 50% of all anemia cases. It poses a major health burden, reaching epidemic levels in developing countries compared to developed countries. This review aimed to provide a comprehensive overview of the incidence of IDA among young adults, particularly females, and children in Saudi Arabia, and to identify its most common causes and risk factors.</p><p><strong>Methods: </strong>A systematic search was carried out in electronic databases for publications addressing IDA or iron deficiency in Saudi Arabia.</p><p><strong>Results: </strong>In Saudi Arabia, the incidence of IDA is alarmingly high, reaching 67% in certain cities, predominantly affecting females, teenager, children, and infants. This high prevalence of IDA has been attributed to nutritional, socioeconomic, and genetic factors.</p><p><strong>Conclusions: </strong>IDA is a major health burden in Saudi Arabia that requires urgent attention. The detrimental impact of iron deficiency on health necessitates immediate action to reduce its incidence and long-term complications on quality of life as well as mortality and morbidity related to iron deficiency within the Saudi population.</p>","PeriodicalId":10384,"journal":{"name":"Clinical laboratory","volume":"71 4","pages":""},"PeriodicalIF":0.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143955509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}