呼吸窘迫综合征新生儿肠道菌群的改变

探究呼吸窘迫综合征新生儿肠道菌群的改变,为该类患儿的治疗提供参考。

选取我院2020年4月至2022年4月收治的83例呼吸窘迫综合征新生儿作为试验组,另选我院同期健康新生儿83例作为对照组,收集两组对象粪便标本。对比两组对象肠道菌群的变化情况。

与对照组相比,试验组患儿肠道菌群Chaol指数和Shannon指数显著降低,Ace指数显著升高,差异均有统计学意义（均P＜0.05）。两组对象肠道厚壁菌门、变形菌门、链球菌属相对丰度对比差异均有统计学意义（均P＜0.05）。

呼吸窘迫综合征新生儿肠道菌群改变较大。

     

肠道菌群与腹型过敏性紫癜性肾炎病情严重程度的相关性研究

探究肠道菌群与腹型过敏性紫癜肾炎（HSPN）患儿病情严重程度的相关性。

选取2021年4月至2023年4月在本院收治的腹型过敏性紫癜（HSP）患儿115例作为研究对象,根据患儿是否并发肾炎将患儿分为HSP组（69例）与HSPN组（46例）,根据24 h尿蛋白定量结果,将HSPN患儿分为轻型HSPN组（29例）和重型HSPN组（17例）。选取同期在我院检查健康的115名儿童为对照组,比较各组的肠道菌群数量变化。

对照组、HSP组和HSPN组患儿24 h尿蛋白定量、血清尿素氮（BUN）、血肌酐（SCR）、血清尿酸（SUA）、白细胞计数（WBC）水平依次升高（P＜0.05）。重型HSPN组患儿24 h尿蛋白定量、BUN、SCR、SUA、尿红细胞计数（RBC）、WBC水平比轻型HSPN组患儿高（P＜0.05）。对照组、HSP组和HSPN组患儿双歧杆菌、乳酸杆菌水平逐渐降低（P＜0.05）,大肠杆菌、链球菌水平逐渐升高（P＜0.05）。重型HSPN组患儿双歧杆菌、乳酸杆菌水平比轻型HSPN组低（P＜0.05）,大肠杆菌、链球菌水平比轻型HSPN组高（P＜0.05）。治疗后HSPN患儿双歧杆菌、乳酸杆菌水平比治疗前低（P＜0.05）,大肠杆菌、链球菌水平比治疗前高（P＜0.05）。

随腹型HSPN患儿病情程度加重,肠道菌群失调程度加重,有益菌减少,致病菌增多。

     

双歧杆菌三联活菌散联合熊去氧胆酸对新生儿巨细胞病毒性肝炎的疗效

探讨双歧杆菌三联活菌散联合熊去氧胆酸对新生儿巨细胞病毒性肝炎的疗效,为该类患儿的治疗提供参考。

选取2020年3月至2023年2月我院收治的140例巨细胞病毒性肝炎新生儿为对象,按随机数表法将其随机分为对照组和试验组,各70例。对照组患儿以熊去氧胆酸及更昔洛韦治疗,试验组患儿以双歧杆菌三联活菌散联合熊去氧胆酸及更昔洛韦治疗。比较两组患儿的临床疗效、肝功能指标水平、肠道菌群分布、免疫球蛋白水平、炎症因子水平、不良反应发生率。

治疗后试验组患儿总有效率高于对照组[91.43%（64/70） vs 75.71%（53/70）,χ² = 6.295,P = 0.012]。治疗后试验组患儿的肝功能指标[总胆红素（TBil）、直接胆红素（DBil）、谷丙转氨酶（ALT）]水平均低于对照组（均P＜0.05）。治疗后观察组患儿肠道双歧杆菌、乳杆菌数量高于对照组,而大肠埃希菌、粪肠球菌数量则低于对照组（均P＜0.05）。治疗后试验组患儿免疫球蛋白A（IgA）、免疫球蛋白G（IgG）、免疫球蛋白M（IgM）水平均高于对照组患儿（均P＜0.05）。治疗后试验组患儿干扰素诱导蛋白-10（IP-10）、抗瓜氨酸蛋白抗体（ACPA）、血友病因子（vWF）水平均低于对照组（均P＜0.05）。治疗期间试验组不良反应发生率低于对照组（8.57% vs 12.86%,P＜0.05）。

双歧杆菌三联活菌散联合熊去氧胆酸及更昔洛韦能够改善巨细胞病毒性肝炎新生儿的肝功能指标水平,提升机体免疫水平,抑制炎症因子表达,治疗安全性良好。

     

微生态制剂对慢性支气管炎的临床疗效和对患者免疫功能的影响

探究微生态制剂对慢性支气管炎的临床疗效和对患者免疫功能的影响。

选择2019年6月至2022年6月我院呼吸内科收治的86例慢性支气管炎患者为研究对象,按照随机分配的原则分为对照组和观察组。对照组患者接受常规治疗,包括平喘药物、抗炎药物和止咳药物;观察组患者在常规治疗的基础上使用微生态制剂进行治疗。比较两组患者治疗后的临床疗效、临床症状持续时间以及相关免疫指标（IL-8、TNF-α、CD4⁺细胞、CRP）水平。

与对照组相比,观察组患者的住院时间、喘息、咳嗽、肺部喘鸣音持续时间显著短于对照组（均P＜0.05）。观察组患者的治疗有效率达95.35%,显著高于对照组的81.40%（P＜0.05）。与治疗前相比,治疗后两组患者IL-8、TNF-α、CRP水平均显著降低,且观察组上述指标水平均低于对照组（均P＜0.05）。

微生态制剂可有效治疗慢性支气管炎,提高临床疗效,改善患者的免疫功能。

     

乳酸菌阴道胶囊辅助治疗在行ART反复着床失败患者中的应用

探究行辅助生殖技术（ART）反复着床失败患者应用乳酸菌阴道胶囊辅助治疗对子宫内膜容受性（ER）和阴道微生物的影响。

选取2020年5月至2022年5月本院收治ART反复着床失败患者100例,根据治疗方式分为观察组（n = 50）和对照组（n = 50）。对照组采用常规治疗,观察组采用常规治疗联合乳酸菌阴道胶囊。比较两组的性激素水平（雌二醇、孕酮）,内膜容积、子宫内膜厚度、血管血流指数（VFI）、内膜血流指数（FI）和阻力指数（RI）等子宫内膜容受性指标,阴道pH值、阴道菌群检出率和乳酸菌数量。

两组治疗前后血清雌二醇、孕酮水平比较,差异无统计学意义（P＞0.05）。两组治疗前子宫内膜厚度、内膜容积、血管血流指数、内膜血流指数和阻力指数比较,差异无统计学意义（P＞0.05）。治疗后观察组子宫内膜厚度、内膜容积和血管血流指数均高于治疗前（P＜0.01）和对照组（P＜0.05）。治疗前两组菌群检出率差异无统计学意义（P＞0.05）,治疗后两组菌群检出率均低于治疗前（P＜0.05）,治疗后观察组菌群检出率低于对照组（P＜0.05）。两组阴道pH值均低于治疗前（P＜0.001）,治疗后观察组阴道pH值低于对照组（P＜0.001）。两组阴道乳杆菌正常率均高于治疗前（P＜0.05）,治疗后观察组高于对照组（P＜0.05）。两组胚胎着床率、临床妊娠率、早期流产率和持续妊娠率差异无统计学意义（P＞0.05）。

乳酸菌阴道胶囊治疗ART反复着床失败患者可以改善子宫内膜容受性和阴道菌群。

     

微生态免疫营养剂联合血液净化对脓毒症患者肠道菌群的影响

研究微生态免疫营养剂（microecological immune nutrients,MIN）联合血液净化对脓毒症患者肠道菌群的影响。

选择2020年1月至2022年1月我院收治的120例脓毒症患者,使用随机数表法分为对照组和观察组,每组各60例,对照组患者应用血液净化治疗,观察组应用MIN联合血液净化治疗。分析两组患者治疗前后SOFA评分、APACHE Ⅱ评分、炎症指标水平、免疫功能变化、肠道菌群变化,分析胃肠道不良反应发生率。

治疗后两组患者SOFA和APACHE Ⅱ评分均显著降低,其中观察组患者SOFA和APACHE Ⅱ评分显著低于对照组（均P＜0.05）。治疗后两组患者Ｃ反应蛋白（CRP）及降钙素原（PCT）水平均显著降低,其中观察组患者CRP和PCT水平显著低于对照组（均P＜0.05）。治疗后两组患者IgG、IgM和IgA水平均显著改善,且观察组患者治疗后IgG、IgM和IgA水平均高于对照组（均P＜0.05）。观察组患者胃肠道不良反应发生率显著低于对照组（P＜0.05）。两组患者肠道双歧杆菌、乳杆菌检出数量均较入院时升高,葡萄球菌检出数量减少,观察组升高或减少幅度均高于对照组（均P＜0.05）。

MIN联合血液净化治疗脓毒症患者可有效改善患者SOFA和APACHE Ⅱ评分,提高免疫因子水平,降低不良反应的发生率,改善患者肠道微生态。

     

注意缺陷多动障碍儿童肠道菌群特点及与行为问题的相关性研究

分析注意缺陷多动障碍（ADHD）儿童肠道菌群特点与行为问题的相关性。

选取2022年1月到2023年5月我院收治的96例ADHD患儿和健康体检的96例儿童,分别作为研究组和对照组。对所有儿童粪便样本进行宏基因组测序并分析肠道菌群特点。采用Conners儿童行为问卷－家长版（PSQ）评估两组儿童的行为。采用Pearson相关性分析肠道菌群分布与行为问题的相关性。

研究组患儿肠道菌群α−多样性低于对照组,肠杆菌属、气味杆菌属和枸橼酸杆菌属相对丰度均高于对照组,韦荣球菌属、拟杆菌属、双歧杆菌属和普氏栖粪杆菌相对丰度均低于对照组,差异均具有统计学意义（P＜0.05）。研究组患儿Conners PSQ问卷评分高于对照组（P＜0.05）。研究组患儿Conners PSQ问卷各因子评分与肠道肠杆菌属、气味杆菌属和枸橼酸杆菌属均呈正相关（P＜0.05）,与韦荣球菌属、拟杆菌属、双歧杆菌属和普氏栖粪杆菌均呈负相关（P＜0.05）。

ADHD儿童肠道菌群构成与健康儿童不同,不同肠道菌群与患儿行为问题有相关性。

     

氨基酸型肠内营养制剂支持后克罗恩病患者肠道微生物和非靶向代谢组学指标的分析

探讨氨基酸型肠内营养制剂支持后克罗恩病患者的肠道微生物和非靶向代谢组学指标的变化,为该类患者的治疗提供参考。

选择我院收治的20例克罗恩病活动期患者作为研究对象,所有患者均采用氨基酸型肠内营养制剂进行支持治疗。比较患者治疗前后肠道菌群结构、菌群多样性以及非靶向代谢组学检测结果的差异。

治疗后,患者肠道乳杆菌属（t=5.200,P＜0.001）、大肠埃希菌（t=11.974,P＜0.001）、克雷伯菌属（t=15.033,P＜0.001）、糖单胞菌（t=12.166,P＜0.001）、恶臭假单胞菌（t=31.063,P＜0.001）、肠球菌属（t=28.867,P＜0.001）数量均显著升高;同时患者肠道菌群OUTs（t=40.435,P＜0.001）、Observed species（t=5.475,P＜0.001）、Chao1指数（t=12.348,P＜0.001）、Simpson指数（t=2.961,P=0.005）、Shannon指数（t=3.330,P=0.002）均显著升高。相比治疗前,治疗后患者血清以及粪便中的氨基酸、多肽、脂肪酸、胆固醇及碳水化合物水平均显著改善。

氨基酸型肠内营养制剂支持后,克罗恩病患者肠道菌群丰度提高,同时患者脂质代谢的改善可能与氧化应激反应通路相关联。

     

妊娠妇女阴道微生态和B族链球菌与胎膜早破及母婴结局的相关性

探讨妊娠妇女阴道微生态状况和B族链球菌（GBS）感染与妊娠晚期胎膜早破及母婴结局的相关性。

回顾性收集2021年1月至2022年12月我院114例临床确诊足月胎膜早破妊娠妇女为研究对象（胎膜早破组）,随机选取同期分娩的129例健康妊娠妇女为对照组。收集两组对象临床资料,比较两组对象阴道微生态变化、GBS感染及不良母婴结局发生情况。

两组妊娠妇女阴道假丝酵母菌菌体及孢子检出情况比较差异均无统计学意义（均P＞0.05）。胎膜早破组患者阴道pH≥4.5、细菌性阴道病、需氧菌性阴道炎的发生率及微生态失衡率高于对照组（均P＜0.05）。胎膜早破组妊娠妇女绒毛膜羊膜炎、产褥感染、胎儿窘迫及新生儿肺炎等不良母婴结局发生率高于对照组（均P＜0.05）。单因素分析结果显示,阴道pH≥4.5、有GBS感染、阴道微生态失调与不良母婴结局有关（均P＜0.05）。

妊娠晚期阴道微生态失衡、GBS感染与妊娠晚期胎膜早破的发生相关,同时会增加不良母婴结局的发生率。加强相关危险因素的干预可降低妊娠晚期女性胎膜早破发生率,改善不良母婴结局。

     

食物过敏患儿肠道菌群特征及其与外周血Treg/Th17的相关性

分析食物过敏患儿肠道菌群分布与外周血免疫细胞Treg/Th17的关系。

选择2020年4月至2022年5月本院儿科收治的86例食物过敏患儿作为观察组,另选择同期80例健康儿童作为健康对照组。采集两组儿童新鲜粪便和外周血样本,分别测定肠道菌群数量以及外周血Treg/Th17细胞、血清相关细胞因子水平,并经Pearson相关性分析肠道菌群与外周血Treg/Th17的相关性。

观察组患儿肠道内乳杆菌、双歧杆菌数量均低于健康对照组（均P＜0.05）;观察组患儿外周血内Treg细胞水平、Treg/Th17比值均低于健康对照组,但Th17细胞水平高于健康对照组（均P＜0.05）;观察组患儿的血清白细胞介素-17（interleukin-17,IL-17）水平高于健康对照组,血清转化生长因子-β1（transforming growth factor-β1,TGF-β1）指标低于健康对照组（均P＜0.05）;Pearson相关性分析结果显示,乳杆菌、双歧杆菌与外周血Treg细胞、TGF-β1水平均呈正相关,而与外周血Th17细胞、IL-17水平均呈负相关（均P＜0.05）。

食物过敏患儿伴显著的肠道菌群紊乱与免疫功能异常状况,肠道内乳杆菌和双歧杆菌水平以及外周血Treg细胞、TGF-β1表达减少,外周血Th17细胞、IL-17表达增多。临床应改善患儿肠道微生态环境,调控肠道菌群结构,促进肠道菌群分布平衡恢复。

     

益生菌预防早产儿坏死性小肠结肠炎的研究进展

新生儿坏死性小肠结肠炎(Neonatal necrotizing enterocolitis,NEC)是早产儿中发病率高、预后差、死亡率高的严重肠道疾病;目前,本病的发病机制尚未明确,缺乏有效的治疗方法。近十几年,大量试验显示,口服益生菌能有效预防早产儿NEC,但其作用机制尚未完全明确,且在益生菌种类选择、给药方式(单药、联合给药)、疗效、安全性等方面,仍存在一些问题。因此,本文就上述问题进行综述。     

Delayed Initiation but Not Gradual Advancement of Enteral Formula Feeding Reduces the Incidence of Necrotizing Enterocolitis (NEC) in Preterm Pigs

Enteral formula feeding is a risk factor for necrotizing enterocolitis (NEC) in premature infants, yet studies are conflicting regarding the safest timing for introduction and advancement of feeds. Our aim was to test the effects of early vs. late initiation and abrupt vs. gradual advancement of enteral feeding of an intact vs. hydrolyzed protein formula on NEC incidence and severity in preterm pigs. In Experiment 1, preterm pigs received total parenteral nutrition (TPN) at birth with abrupt initiation of enteral formula feeds (50% full intake) on d of life (DOL) 2 (EA) or 5 (LA) while PN continued. Pigs were also fed formula containing either intact or hydrolyzed protein. In Experiment 2, preterm pigs received TPN at birth with enteral, hydrolyzed-protein formula feeds introduced on DOL 2 either abruptly (EA; 50% full feeds) or gradually (EG; 10–50% full feeds over 5 d) while PN continued. NEC incidence and severity were assessed based on macroscopic and histological scoring. In Experiment 1, NEC incidence (41% vs. 70%, P<0.05) and severity were reduced in LA vs. EA groups and LA was associated with a higher survival rate, daily weight gain and jejunum villus height. Piglets fed hydrolyzed vs. intact protein formula had lower stomach content weights and similar NEC incidence. In Experiment 2, NEC incidence and severity were not different between pigs the EG vs. EA group. Proinflammatory gene expression (IL-1β, IL-6 and S100A9) in the ileum was lower in both LA and EG vs. EA groups. In conclusion, delayed initiation but not gradual advancement of enteral feeding is protective against NEC in preterm pigs. Feeding hydrolyzed vs. intact protein formula improved gastric transit without affecting the NEC incidence.     

Probiotics and neonatal necrotizing enterocolitis

Neonatal necrotizing enterocolitis (NEC) is one of few diseases for which probiotics have appeared to have clear benefit in clinical trials, however safety concerns persist. Clinical trials of probiotics have preceded our understanding of the effect of probiotics on the developing gut and microbial colonization patterns of the preterm infant. Colonization of the preterm intestine begins with the birthing process and is then influenced by the neonatal intensive care unit and iatrogenic manipulations. Resulting altered microbiota may have significant implications for the immature preterm gut and susceptibility to NEC.     

Hypothesis: inappropriate colonization of the premature intestine can cause neonatal necrotizing enterocolitis.

Neonatal necrotizing enterocolitis (NEC) is a major cause of morbidity in preterm infants. We hypothesize that the intestinal injury in this disease is a consequence of synergy among three of the major risk factors for NEC: prematurity, enteral feeding, and bacterial colonization. Together these factors result in an exaggerated inflammatory response, leading to ischemic bowel necrosis. Human milk may decrease the incidence of NEC by decreasing pathogenic bacterial colonization, promoting growth of nonpathogenic flora, promoting maturation of the intestinal barrier, and ameliorating the proinflammatory response.     

Antibiotics Increase Gut Metabolism and Antioxidant Proteins and Decrease Acute Phase Response and Necrotizing Enterocolitis in Preterm Neonates

Background

The appropriate use of antibiotics for preterm infants, which are highly susceptible to develop necrotizing enterocolitis (NEC), is not clear. While antibiotic therapy is commonly used in neonates with NEC symptoms and sepsis, it remains unknown how antibiotics may affect the intestine and NEC sensitivity. We hypothesized that broad-spectrum antibiotics, given immediately after preterm birth, would reduce NEC sensitivity and support intestinal protective mechanisms.

Methodology/Principal Findings

Preterm pigs were treated with antibiotics for 5 d (oral and systemic doses of gentamycin, ampicillin and metrodinazole; AB group) and compared with untreated pigs. Only the untreated pigs showed evidence of NEC lesions and reduced digestive function, as indicated by lowered villus height and activity of brush border enzymes. In addition, 53 intestinal and 22 plasma proteins differed in expression between AB and untreated pigs. AB treatment increased the abundance of intestinal proteins related to carbohydrate and protein metabolism, actin filaments, iron homeostasis and antioxidants. Further, heat shock proteins and the complement system were affected suggesting that all these proteins were involved in the colonization-dependent early onset of NEC. In plasma, acute phase proteins (haptoglobin, complement proteins) decreased, while albumin, cleaved C3, ficolin and transferrin increased.

Conclusions/Significance

Depressed bacterial colonization following AB treatment increases mucosal integrity and reduces bacteria-associated inflammatory responses in preterm neonates. The plasma proteins C3, ficolin, and transferrin are potential biomarkers of the colonization-dependent NEC progression in preterm neonates.     

Association between birth weight in preterm neonates and the BclI polymorphism of the glucocorticoid receptor gene

Endogenous and exogenous glucocorticoids influence fetal growth and development, and maternal administration of synthetic glucocorticoids may decrease the risk of perinatal morbidity including lung disease in preterm neonates. Because polymorphisms of the glucocorticoid receptor gene are known to influence the sensitivity to glucocorticoids, in the present study we examined whether any associations could exist among the BclI, N363S and ER22/23EK polymorphisms of the glucocorticoid receptor gene and gestational age, birth weight and/or perinatal morbidity of 125 preterm neonates born at 28-35 weeks' gestation with (n=57) or without maternal dexamethasone treatment (n=68). The prevalence of the three polymorphisms in the whole group of preterm infants was similar to that reported in healthy adult Hungarian population. However, we found that the BclI polymorphism significantly associated with higher birth weight adjusted for the gestational age (p=0.004, ANOVA analysis). None of the three polymorphisms showed an association with perinatal morbidities, including necrotizing enterocolitis, intraventricular hemorrhagia, patent ductus arteriosus, respiratory distress syndrome, bronchopulmonary dysplasia and sepsis in the two groups of preterm neonates with and without maternal dexamethasone treatment. These results suggest that the BclI polymorphism of the glucocorticoid receptor gene may have an impact on gestational age-adjusted birth weight, but it does not influence perinatal morbidities of preterm neonates.     

Elective cesarean delivery affects gut maturation and delays microbial colonization but does not increase necrotizing enterocolitis in preterm pigs

Although preterm birth and formula feeding increase the risk of necrotizing enterocolitis (NEC), the influences of cesarean section (CS) and vaginal delivery (VD) are unknown. Therefore, gut characteristics and NEC incidence and severity were evaluated in preterm pigs (92% gestation) delivered by CS or VD. An initial study showed that newborn CS pigs (n = 6) had decreased gastric acid secretion, absorption of intact proteins, activity of brush-border enzymes and pancreatic hydrolases, plasma cortisol, rectal temperature, and changes in blood chemistry, indicating impaired respiratory function, compared with VD littermates (n = 6). In a second experiment, preterm CS (n = 16) and VD (n = 16) pigs were given total parenteral nutrition (36 h) then fed porcine colostrum (VD-COL, n = 6; CS-COL, n = 6) or infant milk formula (VD-FORM, n = 10; CS-FORM, n = 10) for 2 days. Across delivery, FORM pigs showed significantly higher NEC incidence, tissue proinflammatory cytokines (IFN-gamma and IL-6), Clostridium colonization, and impaired intestinal function, compared with COL pigs. NEC incidence was equal for CS (6/16) and VD (6/16) pigs, CS pigs had decreased bacterial diversity and density, higher villus heights, and increased brush-border enzyme activities (lactase, aminopeptidases) compared with VD pigs. In particular, VD-FORM pigs showed reduced mucosal proportions, reduced lactase and aminopeptidases, and increased proinflammatory cytokine IL-6 compared with CS-FORM (P < 0.06). Despite the initial improvement of intestinal and metabolic functions following VD, gut function, and inflammation were similar, or more negatively affected in VD neonates than CS neonates. Both delivery modes exhibited positive and negative influences on the preterm gut, which may explain the similar NEC incidence.     

Nutritional modulation of the gut microbiota and immune system in preterm neonates susceptible to necrotizing enterocolitis

The gastrointestinal inflammatory disorder, necrotizing enterocolitis (NEC), is among the most serious diseases for preterm neonates. Nutritional, microbiological and immunological dysfunctions all play a role in disease progression but the relationship among these determinants is not understood. The preterm gut is very sensitive to enteral feeding which may either promote gut adaptation and health, or induce gut dysfunction, bacterial overgrowth and inflammation. Uncontrolled inflammatory reactions may be initiated by maldigestion and impaired mucosal protection, leading to bacterial overgrowth and excessive nutrient fermentation. Tumor necrosis factor alpha, toll-like receptors and heat-shock proteins are identified among the immunological components of the early mucosal dysfunction. It remains difficult, however, to distinguish the early initiators of NEC from the later consequences of the disease pathology. To elucidate the mechanisms and identify clinical interventions, animal models showing spontaneous NEC development after preterm birth coupled with different forms of feeding may help. In this review, we summarize the literature and some recent results from studies on preterm pigs on the nutritional, microbial and immunological interactions during the early feeding-induced mucosal dysfunction and later NEC development. We show that introduction of suboptimal enteral formula diets, coupled with parenteral nutrition, predispose to disease, while advancing amounts of mother's milk from birth (particularly colostrum) protects against disease. Hence, the transition from parenteral to enteral nutrition shortly after birth plays a pivotal role to secure gut growth, digestive maturation and an appropriate response to bacterial colonization in the sensitive gut of preterm neonates.     

益生菌联合早期微量喂养对早产儿肠道菌群及免疫功能影响的相关性研究

目的 探讨口服益生菌联合早期微量喂养对早产儿肠道菌群、喂养不耐受及免疫功能的影响。方法 本研究以120例早产儿为研究对象,并随机将其分为观察组（60例）和对照组（60例）。对照组在早产儿出生24 h内开始非营养性吸吮、早期微量喂养,使用配方奶喂养,每次0.5~1 mL/kg,2~3 h 1次）,观察组在对照组基础上给予口服益生菌,0.25 g/次,1次/天;观察患儿出生后3 d、7 d、14 d血清胃泌素水平,呕吐、腹胀、胃潴留、排便情况,观察体质量、恢复出生体质量时间,达到完全肠内营养时间;分别在出生后2 d、10 d、20 d检测粪便中乳杆菌和双歧杆菌数量,并比较治疗前后两组患儿的免疫指标。结果 第14 d胃泌素水平观察组高于对照组（53.75±6.50 vs 43.75±5.78）pg/mL,呕吐、腹胀、胃潴留的发生率和排便不畅的例数观察组明显低于对照组（7.55±1.34 vs 14.22±1.78）,第14 d的体质量观察组高于对照组（1 682.34±159.11 vs 1 426.10±141.58）g,恢复出生体质量时间（8.00±1.22 vs 9.80±0.83）d、达到完全肠内营养时间（9.60±1.81 vs 12.00±1.93）d均短于对照组（均P＜0.05）;治疗10 d、20 d 粪便中双歧杆菌和乳杆菌的数量均高于对照组（均P＜0.05）。肠道乳杆菌和双歧杆菌菌群载量与CD4+T细胞百分比和CD4+/CD8+比例存在显著正相关（均P0.05）。两组治疗前CD3+、CD4+、CD8+T淋巴细胞数量、CD4+/CD8+比较差异无统计学意义（均P＞0.05）。观察组患者治疗后CD4+T淋巴细胞水平（39.28±4.09 vs 37.42±3.97）%、CD4+/CD8+（1.61±0.48 vs 1.37±0.49）高于对照组,且比较差异具有统计学意义（均P＜0.05）。结论 口服益生菌联合早期微量喂养对早产儿改善其肠道菌群,提高免疫功能有一定作用。     

早期应用微生态制剂对极低出生体重儿影响的临床观察

目的观察早期应用微生态制剂对极低出生体重儿黄疸、喂养、生长以及免疫功能的影响。方法我院NICU收治的生后24h内极低出生体重儿84例,随机分为观察组46例,对照组38例。观察组生后4h内开始口服或鼻饲胃管服用妈咪爱0.5g,2次/d,连用14d。观察两组达到高胆红素血症标准的人数,以及生后24h、5d总胆红素值;喂养不耐受人数;生后5d生理性体重下降及1个月体重增长情况;生后1个月免疫学指标。并加以对比。结果24h内血清胆红素比较无统计学意义(P0.05),治疗5d后观察组血清总胆红素明显低于对照组(P0.05),观察组出现高胆红素血症人数明显低于对照组(P0.05);观察组喂养不耐受出现例数明显低于对照组(P0.01);观察组生后5d体重下降的克数低于对照组(P0.05),1个月时体重增长克数高于对照组(P0.01);观察组IgA水平较对照组明显增加(P0.05),但IgG及IgM含量与对照组比较差异无统计学意义(P0.05)。结论早期应用微生态制剂能降低血清胆红素水平,对预防极低出生体重儿高胆红素血症有一定作用;能提高喂养的耐受性,有利于患儿生长发育;对极低出生体重儿的肠道功能及免疫功能有明显影响,能增加免疫球蛋白IgA水平,从而促进体液免疫的发展。