Effect of Artemisia annua (Asteraceae) Extracts on Hemolysis in Individuals with G6PD-Deficiency

Individuals with Glucose-6-phosphate dehydrogenase (G6PD) deficiency are susceptible to hemolytic anemia when exposed to pro-oxidant substances. This study investigates the hemolytic impact of Artemisia annua (A. annua) extracts in G6PD-deficient subjects through a mixed experimental approach. In the in vitro phase, red blood cells from G6PD-deficient individuals and rats induced with Dehydroepiandrosterone (DHEA) were exposed to various concentrations of A. annua infusion, with distilled water and physiological saline as positive and negative controls respectively. The in vivo study involved G6PD-deficient Wistar rats divided into three groups receiving A. annua infusion, quinine (positive control), and distilled water (negative control) via gavage. Blood samples were collected for biochemical and hematological analyses. Notably, at a 40% concentration of A. annua infusion, there was a significant increase in the hemolysis rate of G6PD-deficient red blood cells compared to controls (p A. annua exhibited elevated aspartate aminotransferase (129.25 ± 4.55 U/L vs. 80.09 ± 4.03 U/L;p A. annua infusion tested positive for saponins. These findings underscore the risk of hemolysis in G6PD-deficient individuals upon ingesting A. annua.

G6PD Deficiency and COVID-19 in Burkina Faso: A Possible Link?

Burkina Faso is a malaria-endemic country, with a high incidence of G6PD deficiency (G6PDd), which recorded its first case of COVID-19 in March 2020. G6PDd leads to a decrease in the efficiency of erythrocytes to combat oxidative stress, while SARS-CoV-2 infection induces massive production of Reactive Oxygen Species (ROS) in patients. In the present review, we discuss a possible link between G6PDd and SARS-CoV-2 infection. The mean prevalence of G6PDd in Burkina Faso is estimated at 16.6% among males and 6.5% among females. A total of 21,128 cases of COVID-19 have been recorded in Burkina Faso with 387 deaths reported (with a mortality rate of 1.15% among diagnosed cases) as of August 30, 2022. To our knowledge, no association study between G6PDd and SARS-CoV-2 infection has been conducted to date in Burkina Faso. However, several case reports around the world have described elevated risks of hemolysis and thrombosis, and other complications among G6PD-deficient patients infected with SARS-CoV-2. The use of Hydroxychloroquine (HCQ) has also been deemed unsafe by some authors for the treatment of COVID-19 among patients with G6PDd. Although HCQ has been shown to be well tolerated in COVID-19 patients in Burkina Faso, the drug could induce hemolytic crises in people with G6PD deficiency. G6PD is important in regulating ROS and maintaining erythrocyte homeostasis. In view of its high prevalence in Burkina Faso, determination of the G6PD status is required in COVID-19 patients for adequate management such as identifying a subset of COVID-19 patients for whom close monitoring and supportive care may be essential and to restrict treatment with HCQ.

Glucose-6-Phosphate Dehydrogenase Deficiency in Icteric Newborns at the Essos-Yaoundé-Cameroon Hospital

Background: Glucose-6-phosphate dehydrogenase deficiency is an enzymopathy characterized by insufficient production of reduced glutathione (GSH), a molecule known for its antioxidant role. This lack of GSH leads to a deficit in the elimination of peroxide ions from the red blood cells, causing thereby hemolytic accidents, which can be fatal if not properly managed. In neonates, the clinical picture is most often that of neonatal jaundice. Objectives: This study aimed to determine the place of G6PD deficiency as a cause of neonatal jaundice at Essos Hospital Centre. Methods: We conducted a prospective descriptive study over three months. Blood samples taken from newborns aged 0 to 28 days were analyzed in the medical analysis laboratory of the Essos Hospital Centre in Yaoundé. We carried out a determination of the enzymatic activity of G6PD, a blood count and the determination of the bilirubin level. The results obtained were analysed using R statistical software version 4.1.1. Linear regression analyses were used to assess correlations between the variables of interest. Results: Sixty-nine icteric neonates constituted our study population, with a total of 40 boys (58%) and 29 girls (42%) with a sex ratio of 1.37 in favour of boys. The prevalence of G6PD deficiency in icteric children was 50.72%. The mean hemoglobin was 15.3 ± 3.08 g/dL and the mean red blood cell count was 4.52 ± 1.01 × 106/mm3. The mean total bilirubin was 122 ± 48.3 mg/L with a maximum of 308 mg/L and the mean free bilirubin was 104 ± 46.6 mg/L with a maximum of 292 mg/L. Furthermore, after linear regression analysis, we obtained a positive and significant correlation between G6PD enzymatic activity and hemoglobin level (r = 0.33;p ≤ 0.001), G6PD red blood cell level (r = 0.26;p Conclusion: Neonatal jaundice in G6PD-deficient children is a real public health problem and the prevention of hemolysis in children requires an early diagnosis of the enzyme disorder and good follow-up of the children.

Glucose-6-Phosphate Dehydrogenase Deficiency: Difficulties in Diagnosis at the Souro Sanou University Hospital, Burkina Faso

Glucose-6-phosphate dehydrogenase deficiency is the most common enzymopathy worldwide. The precise prevalence of G6PD is unknown in Burkina Faso. The objective of the study was to describe the difficulties to diagnose this disease at the Souro Sanou University hospital (CHUSS) in Bobo-Dioulasso. It involved five patients comprising one child with homozygous SS sickle cell disease, one adolescent screened following a family investigation, and three adults including a man and two women. Blood smear stained with May Grunwald Giemsa was performed to look for specific signs of G6PD-deficient red blood cell and brilliant cresyl Blue for Heinz Bodies. A microscope Olympus BX53 equipped with a Camera (XC10) and connected to a computer was used to read blood smears and capture images. Genes sequencing by Sanger method were performed in a specialized laboratory in molecular genetics. For each analysis, the protocol and instructions of the equipment and reagent manufacturer were applied. Of the five patients, three had anemia and only one had hyperreticulocytosis. Two patients had biological signs of hemolysis and one patient had an elevated CRP. Blood smear stained with MGG and cresyl blue showed specific signs of G6PD-deficient red blood cells and Heinz bodies in all patients. Biochemical analysis and molecular typing confirmed G6PD deficiency. The presence of G6PD-deficient red blood cells in the blood smear guides the diagnosis of G6PD deficiency. The diagnosis is biochemical and is based on the combined measurement of G6PD plus pyruvate kinase and/or hexokinase.

Prevalence of Association of Glucose-6-Phosphate Dehydrogenase Deficiency and Sickle Cell Disease at the National Teaching Hospital of Cotonou in Benin

Background: Glucose-6-phosphate dehydrogenase (G6PD) deficiency and sickle cell disease are common genetic defects of red blood cells that lead to hemolytic anemia. The prevalence of G6PD deficiency in sickle cell patients is unknown in Benin. Objective: This study aimed to determine the prevalence of G6PD deficiency in sickle cell patients at the CNHU-HKM of Cotonou. Methods: This prospective study was conducted from April to November 2022 at the blood-related diseases teaching clinic and included sickle cell patients in the stationary phase. G6PD determination was performed using the enzymatic method on a Mindray BS 200 machine following the Herz method. Hematological parameters were determined using the XT 4000i analyzer and supplemented by a blood smear stained with May Grunwald Giemsa. Data were analyzed using Epi Info 3.5.4 software. Results: One hundred and sixty-four sickle cell patients (80 SS homozygotes and 84 SC heterozygotes) in the intercritical phase, with a mean age of 26.30 ± 10.76 years, were included. The prevalence of G6PD deficiency was 9.1% (15 cases found in 7 SS patients and 8 SC patients). In G6PD-deficient patients, the mean concentration of the enzyme was lower in Hb SC heterozygotes than in Hb SS homozygotes: 3.56 IU/g Hb versus 4.98 IU/g Hb. The mean reticulocyte count was 231.43 G/L in the deficient group, compared to 216.32 G/L in the non-deficient group. Conclusion: The preliminary results of our study reveal a high prevalence of G6PD deficiency in sickle cell patients. The impact of this association on hematologic and biological parameters should be evaluated for better management of sickle cell disease.

Prevalence of Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency in India: A Systematic Review

Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is the most common enzyme deficiency of human erythrocyte affecting more than 400 million people worldwide. In India, G6PD deficiency was first reported in 1963 and since then various investigations have been conducted across country. The objective of this work was to study the prevalence of G6PD deficiency in different ethnic, caste and linguistic groups of Indian population. A systematic search of published literature was undertaken and the wide variability of G6PD deficiency has been observed ranging from 0% - 30.7% among the different caste, ethnic, and linguistic groups of India. It was observed that the incidence of G6PD deficiency was found to be considerably higher among the tribes (9.86%) as compared to other ethnic groups (7.34%) and significantly higher in males as compared to females.

Epidemiological analysis on the incidence of thalassemia and G6PD deficiency in the population of childbearing age in Hengxian county in Guangxi

Objective:We investigated the incidence of thalassemia and glucose-6-phosphate dehydrogenase(G6PD)deficiency in people of childbearing age of Hengxian in Guangxi,to further provide scientific data for the diagnosis,treatment and prepotency consultation for thalassemia.Methods:A total of 12,489subjects at childbearing age who were undergoing a routine prenatal check-up in Hengxian family planning service stations were recruited in this study between January 2014and December 2014.They were screened for thalassemia by mean corpuscular volume(MCV)and mean corpuscular hemoglobin(MCH).The people with positive results then underwent thalassemia gene test.The G6PD activities were measured by enzyme kinetic method.Results:The incidence of thalassemia was 20.26%(2,530/12,489)in Hengxian,among which the incidences ofα-thalassemia,β-thalassemia,andα-thalassemia co-inheritance ofβ-thalassemia were13.20%,6.13%and 0.93%respectively.The incidence of G6PD deficiency was 5.39%(617/12,489),and the ratio between male and female is 4.27∶1.25types ofα-thalassemia genotype and 8types ofβ-thalassemia genotype were identified.The genotypes ofSEA/ααand the genotypes of41-42Mβ/Nβwere the most common genetic types forα-thalassemia andβ-thalassemia respectively.Conclusion:Hengxian is a high prevalence area of thalassemia and G6PD deficiency.SEAmutation type is the most common type inα-thalassemia,and the CD 41-42mutation is the most common type inβ-thalassemia in Hengxian.

2380例新生儿G-6-PD检测结果分析

目的 :探讨新生儿 G- 6 - PD缺乏与性别和高胆红素血症的关系。方法 :采用 G- 6 - PD试纸法对 1999年 1月～ 2 0 0 2年 12月在我院产科出生的新生儿 2 380例进行 G- 6 - PD筛查并跟踪观察。结果 :男性新生儿 G- 6 - PD缺乏显著多于女性 (P <0 .0 1) ;男性 G- 6 - PD缺乏的新生儿高胆红素血症的发病率显著多于女性 (P <0 .0 1)。男女 G- 6 - PD缺乏的新生儿其父母籍贯以广西籍为主 (93% )。结论 :新生儿 G- 6 - PD缺乏存在性别差异 。

地中海贫血和G-6PD缺乏联合检测在产前筛查中的价值

目的了解产检孕妇地中海贫血和G-6PD缺乏发生率,探讨产前筛查地中海贫血和G-6PD的临床价值。方法孕12～20周孕妇3417例,应用全自动血红蛋白电泳仪筛查、生化仪直接测定G-6PD活性,筛查其地中海贫血及G-6PD缺乏症发生率。结果3417例产检孕妇中,G-6PD缺乏105例,占3.07%;检出轻型β-地中海贫血215例,占6.29%,中间型α-地中海贫血16例占0.47%,另外检出异常血红蛋白HbE12例,异常血红蛋白HbK组区带4例,血红蛋白A2减少180例。结论在地中海贫血高发区进行产前地中海贫血和G-6PD缺乏的筛查,是避免重型地贫患儿的出生和新生儿溶血的有效措施。

1281例G-6-PD缺乏新生儿高胆红素血症的调查分析

目的了解G-6-PD缺乏的新生儿高胆红素血症的发病情况,为临床防治新生儿高胆红素血症提供科学依据。方法使用高铁血红蛋白还原试验做G-6-PD筛查,阳性者用G6PD/6PGD比值定量法进行确诊。使用重氮法测定总胆红素和直接胆红素。结果1281例G-6-PD缺乏的新生儿高胆红素患者172例,发病率为13.4%,显著高于对照组(!2=98,P<0.005);其中显著缺乏组发病率为21.2%,显著高于中间缺乏组(!2=61.6,P<0.005);男性发病率为18.8%,显著高于女性(!2=35,P<0.005)。结论G-6-PD缺乏是新生儿高胆红素血症的重要原因。

葡萄糖-6-磷酸脱氢酶缺乏症患儿G-6-PDmRNA表达的研究

目的检测葡萄糖-6-磷酸脱氢酶(G-6-PD)缺乏症患者及其家系成员的G-6-PDmRNA表达水平,从转录水平探讨其可能的发病机制。方法提取G-6-PD缺乏症患者及其直系家属(患者父亲和/或母亲等)外周血RNA,采用逆转录方法形成cDNA后,运用逆转录实时定量PCR(QuantitativeReal-TimePCR,QRT-PCR)技术,测定G-6-PDmRNA的表达量。使用SPSS10.0统计分析软件将3组进行组间两两比较。结果G-6-PD缺乏症患儿组mRNA表达量为0.57±0.19,父系组为0.74±0.21,母系组为0.67±0.21,患儿组与父系组比较t=-3.18,(P<0.01);与母系组比较t=-2.54,(P<0.05)。结论G-6-PD缺乏症患者的G-6-PD基因发生突变后其G-6-PDmRNA表达量发生了改变,提示该病的发生与在转录水平上发生变化有关,在G-6-PD缺乏症的发病过程中起到一定的作用。

新生儿G-6-PD缺乏症高未结合胆红素血症的心肌损害

目的 探讨新生儿G-6—PD缺乏症的高未结合胆红素血症对心肌损害。方法 30例G—6-PD缺乏症新生儿分别于入院时(治疗前)和治疗后(显性黄疸消退后)抽血测定心肌酶、肝功能、肾功能等,部分病人同时作心电图检查,并与15例正常新生儿进行比较。结果 30例G—6—PD缺乏症患儿心肌酶及同功酶活性均有不同程度增高,尤以CK—MB活性明显升高,两组比较差异有非常显著意义(P<0.01)。CK—MB升高与黄疸程度呈正相关(r=0.487、P<0.01)。治疗前后,高未结合胆红素心肌酶比较、差异有非常显著意义(P<0.01)。结论 新生儿高未结合肥红素血症可出现心肌损害,与黄道出现程度有关。

新生儿G-6PD缺陷合并高胆红素血症对光疗效果的影响

目的探讨新生儿G-6PD缺陷合并新生儿高胆红素血症对光疗效果的影响。方法184例患高胆红素血症的足月顺产新生儿,除外早产、低体重儿;胎盘、脐带、羊水异常;窒息、肺炎、内脏出血、头颅血肿、败血症;ABO溶血症、红细胞增多症、婴儿肝炎综合征等疾病。根据G-6PD活性分为3组:G-6PD轻度缺陷组45例,重度缺陷组33例,感染组(G-6PD正常组)106例。入选患儿给予蓝光治疗,按常规保护好眼睛和会阴部后,置双面蓝光治疗箱,每天照射12小时,连续5天。光疗前3天,每次给予苯巴比妥片和维生素B2片各5 mg,每日3次,口服。在光疗前、光疗后3天和5天各取静脉血3 m l,测定血常规、红细胞G-6PD活性、高铁血红蛋白还原率、血清总胆红素、直接胆红素、胆汁酸、转氨酶和γ-谷酰转肽酶。结果光疗前总胆红素水平在3组之间无显著性差异(P均>0.05);光疗5天后G-6PD重度缺陷组总胆红素水平显著高于G-6PD轻度缺陷和感染组(P<0.05);G-6PD重度缺陷组血红蛋白水平显著低于G-6PD轻度缺陷组和感染组(P<0.05);γ-谷酰转肽酶的水平在3组之间无显著性差异(P均>0.05)。结论光疗可能会加重G-6PD缺陷患儿溶血的风险,应从严掌握光疗指征。

新生儿G-6PD酶缺陷致急性溶血1例

目的:探讨G-6PD酶缺陷所致的急性溶血新生儿的临床特点、治疗进展。方法:对已诊断明确的1例G-6PD酶缺陷的急性溶血新生儿,回顾性分析临床特点、治疗经验,并对2005年以来国内外报道的病例进行文献复习。结果:病例为10 min新生儿,出生即皮肤黏膜青紫、呼吸困难、呻吟、对刺激反应差;体格检查,神清,囟门平软,皮肤浅黄染达四肢,进展快,无出血点、瘀斑及皮疹,呼吸略急,可闻及散在干湿啰音,双肺呼吸音粗,三凹征阳性,四肢原始反射引出欠完整,出现血红蛋白尿;出生后2 h辅助检查,总胆红素125.9μmol/L、直接胆红素8.9μmol/L、间接胆红素117.0μmol/L、白细胞220×109/L、血红蛋白84 g/L、红细胞压积20%、血小板205×109/L、血型RH(+);初步诊断为自身免疫性溶血性贫血,予以蓝光照射、丙种球蛋白、白蛋白、甲泼尼龙治疗,输注洗涤红细胞纠正贫血,患儿家长不同意换血治疗,经治疗2周后复查肝功能、血常规恢复正常。经患儿父母同意,抽取患儿及父母静脉血标本行特异性G-6PD基因PCR检测,父母、患儿均为G-6PD酶缺陷Ⅱ型阳性,追踪上一代,患儿、父亲、母亲、外祖母为G-6PD酶缺陷Ⅱ型阳性,外祖父G-6PD酶缺陷Ⅱ型阴性。结论:新生儿G-6PD酶缺陷导致急性溶血具有早发性进展性黄疸、血红蛋白尿、高胆红素血症、发热、肝肿大等临床特征,主要与遗传、感染等因素有关,多发生于早产儿,及时治疗、早期诊断可显著降低新生儿G-6PD酶缺陷导致急性溶血的病死率。

红细胞G-6PD酶缺乏症20例临床分析

目的探讨红细胞G-6PD酶缺乏症的临床特点、治疗及转归。方法对20例病人进行输血、补液治疗及随访。结果20例病人贫血均于1个月恢复正常。结论红细胞G-6PD酶缺乏症急性溶血期输血、硷化尿液及补液治疗可有效促进患儿早期恢复。

光疗对G-6PD缺陷新生儿高胆红素血症的副效应观察

目的 :观察光疗对红细胞葡萄糖 6-磷酸脱氢酶 (G- 6PD)缺陷高胆红素血症 (高胆 )新生儿的不良影响。方法 :对 88例 G-6PD缺陷高胆儿和 2 1 2例非 G- 6PD缺陷高胆儿行光疗的退黄时间、反跳及继续溶血情况作了观察。结果 :G- 6PD缺陷组退黄时间明显长于非 G- 6PD缺陷组 ,反跳现象及光疗后进行性溶血倾向均明显高于非 G- 6PD缺陷患儿 (P<0 .0 1 )。结论 :G- 6PD缺陷患儿对光疗的溶血效应可能更为敏感 。

G-6PD缺陷症溶血危象的抢救

目的 探讨G-6PD缺陷症溶血危象的抢救治疗方法。方法 采用综合抢救措施,包括快速成分输血、静脉滴注多巴胺3～5μg/(kg·min)、吸入高浓度氧、碱化尿液、抗感染等措施抢救G-6PD缺陷症溶血危象15例。结果 15例患者均抢救成功,痊愈出院。结论 G-6PD缺陷症溶血危象的抢救应采取综合措施。

新生儿红细胞G-6PD缺陷并高胆红素血症临床探讨

对６４ 例葡萄糖６ － 磷酸脱氢酶（ Ｇ－ ６ＰＤ） 缺陷并高胆红素血症（ 高胆） 新生儿进行总结，讨论Ｇ－ ６ＰＤ 缺陷在高胆中的地位、发病诱因、临床特点和预防问题。强调早诊断、早治疗对改善预后有重要意义。