Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the western blot data shown in Fig. 3B on p. 3428 had already appeared previously in an article written by different authors at different research institutes that was published in the journal BMC Cancer, but which has subsequently been retracted. Upon performing an independent analysis of the data in this paper, it also came to light that other western blot data in Figs. 4B and 5B had appeared in articles in other journals written by different authors at different research institutes, that the Control data panels in Fig. 2A and B were also overlapping within the figure itself, and other data in Fig. 2 had appeared subsequently in an unrelated paper in Oncology Reports. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. fter having been in contact with the authors, they did not accept the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 13: 3423‑3432, 2016; DOI: 10.3892/mmr.2016.4947].

OBJECTIVE:To investigate the association of lipoprotein-associated phospholipase A2 (Lp-PLA2) with large artery atherosclerotic (LAA) stroke and its predictive value for recurrence. METHODS:We consecutively enrolled 412 acute LAA stroke patients. Using a cutoff of 200 ng/mL, patients were divided into high and low Lp-PLA2 groups, and into recurrence and non‑recurrence groups based on 1‑year follow‑up. Baseline characteristics, lipid profiles, National Institutes of Health Stroke Scale (NIHSS) scores, and vascular stenosis degree were compared. Binary logistic regression and Receiver Operating Characteristic (ROC) analysis were used to identify independent risk factors and evaluate predictive value. RESULTS:The high Lp-PLA2 group had significantly higher low-density lipoprotein cholesterol (LDL-C), small dense low-density lipoprotein cholesterol (sdLDL-C), prevalence of severe stenosis (≥70%), and proportion of NIHSS > 15 (all P < 0.05). The recurrence group showed elevated Lp-PLA2, higher LDL‑C and sdLDL-C, more severe neurological deficits, and more severe stenosis (all P < 0.001). Multivariable regression identified elevated Lp-PLA2 (per 10 ng/mL: OR = 1.139, 95% CI: 1.089-1.191), moderate (OR = 3.145) and severe (OR = 11.663) neurological deficits, and severe stenosis (OR = 9.390) as independent risk factors for recurrence (all P < 0.05). The Area Under the Curve (AUC) of Lp-PLA2 was 0.75 (95% CI: 0.69-0.82), with an optimal cutoff of 208.95 ng/mL. CONCLUSION:Elevated Lp-PLA2 is associated with adverse lipid profiles, more severe neurological deficits, and greater vascular stenosis in LAA stroke patients, and independently predicts 1‑year recurrence. Lp-PLA2 shows moderate predictive value, supporting its potential for risk stratification.

Epilepsy is a common neurological disorder resulting from an imbalance between neuronal excitation and inhibition. Synapses play a pivotal role in the pathogenesis of epilepsy. Srchomology 2 (SH2) domain-containing protein 5 (SH2D5) is highly expressed in the brain and is implicated in the regulation of synaptic function. However, its role and mechanism in epilepsy remain unclear. In this study, we found that SH2D5 was predominantly localized to pyramidal neurons in the mouse hippocampus and was upregulated in the hippocampus of epileptic brains. KO of Sh2d5 in the hippocampus alleviated both the susceptibility to and severity of epileptic activity. Mechanistically, SH2D5 regulated N-methyl-D-aspartate receptor-mediated (NMDAR-mediated) excitatory synaptic transmission by altering the protein expression levels of NMDAR subunits. We further demonstrated that SH2D5 modulated the transcription of NMDARs by promoting the autophagic degradation of STAT1. These findings suggest that targeting the SH2D5/STAT1/NMDAR pathway may offer a potential therapeutic strategy for epilepsy.

Aims:This study aims to assess the effects of different exercise types and their specific doses on glycemic control among individuals with prediabetes. Methods:Multiple databases were subjected to a comprehensive search for randomized controlled trials (RCTs) published until 15 July 2024. The study protocol was prospectively registered with PROSPERO (CRD42024573186). The exercise interventions analyzed included aerobic exercise (AE), resistance training (RT), and combined aerobic-resistance training (AE+RT). Outcomes were quantified using standardized mean difference (SMD) with 95% credible intervals (CrIs), employing the confidence in network meta-analysis (CINeMA) framework for network meta-analysis to confirm the outcome reliability. Results:According to the network meta-analysis, irrespective of dose, AE+RT led to the largest decrease in fasting blood glucose (FBG) (-0.44, [-0.62 to -0.26]). AE alone resulted in the largest reductions in 2-hour post-meal blood glucose (2hPG) (-0.71, [-0.97 to -0.45]) and glycosylated hemoglobin A1c (HbA1c) (-0.30, [-0.37 to -0.22]). Dose-response (DR) analysis identified optimal doses for each exercise type: 880 metabolic equivalent of task minutes per week (METs-min/week) for both AE and RT and 800 METs-min/week for AE+RT to reduce FBG. The optimal dose for 2hPG improvement via AE was 1,100 METs-min/week, and for HbA1c reduction via RT, it was 870 METs-min/week. Conclusions:Given the variety of impaired glucose regulation (IGR), we recommend that people with prediabetes engage in RT at 1,100 METs-min/week to improve 2hPG and at 870 METs-min/week to reduce HbA1c. For FBG control, a dose of 800 METs-min/week is optimal for all exercise modalities. These evidence-based recommendations provide practical guidance for designing personalized exercise prescriptions to manage prediabetes.

In clinical practice, cases of drug-induced liver injury (DILI) often occur in renal transplant recipients treated with tacrolimus (Tac) as an immunosuppressive therapy. Numerous studies have confirmed the close relationship between gut microbiota (GM) and DILI. However, systematic studies on the GM and metabolomic characteristics of Tac-associated DILI are lacking, and the role of GM and its metabolites in DILI remains incompletely understood. Renal transplant recipients receiving Tac at the Organ Transplantation Center of Sichuan Provincial People’s Hospital were enrolled. Patients with DILI were assigned to the DILI group, and those with stable liver function to the control group. Stool samples were analyzed by 16 S rRNA gene sequencing and LC-MS non-targeted metabolomics, and blood samples were collected to measure Tac trough concentrations. Seventy-two renal transplant recipients were included, comprising 32 DILI patients and 40 controls. Oscillibacter and Ruminococcus gnavus group were significantly enriched in the DILI group, whereas Bacteroides, Lachnospiraceae NK4A136 group, Anaerostipes, Subdoligranulum, Eubacterium coprostanoligenes group, and Megamonas were significantly decreased in the DILI group. Metabolites such as icosadienoic acid and 1-acyl-sn-glycerol-3-phosphate were significantly elevated in the DILI group, while glycyrrhetinate, S-adenosylmethionine, and other related metabolites were significantly reduced. In renal transplant recipients, distinct GM and enteric metabolic profiles differentiate patients with DILI from those with stable liver function. Key microbial taxa—including Oscillibacter, Bacteroides, Ruminococcus gnavus group, and Lachnospiraceae NK4A136 group—potentially contribute to DILI pathogenesis through modulation of bile acid metabolism and inflammatory signaling pathways.

Drug-induced liver injury is a prevalent severe adverse event in clinical settings, leading to increased medical burdens for patients and presenting challenges for the development and commercialization of novel pharmaceuticals. Research has revealed a close association between gut microbiota and drug-induced liver injury in recent years. However, there has yet to be a consensus on the specific mechanism by which gut microbiota is involved in drug-induced liver injury. Gut microbiota may contribute to drug-induced liver injury by increasing intestinal permeability, disrupting intestinal metabolite homeostasis, and promoting inflammation and oxidative stress. Alterations in gut microbiota were found in drug-induced liver injury caused by antibiotics, psychotropic drugs, acetaminophen, antituberculosis drugs, and antithyroid drugs. Specific gut microbiota and their abundance are associated closely with the severity of drug-induced liver injury. Therefore, gut microbiota is expected to be a new target for the treatment of drug-induced liver injury. This review focuses on the association of gut microbiota with common hepatotoxic drugs and the potential mechanisms by which gut microbiota may contribute to the pathogenesis of drug-induced liver injury, providing a more comprehensive reference for the interaction between drug-induced liver injury and gut microbiota.

BACKGROUND:Mutations in metabolic enzymes and co-administration of drugs may affect the blood concentration of pirfenidone effective in pulmonary fibrosis. To provide a basis for the precise clinical use of pirfenidone, the authors analyzed the correlation between steady-state pirfenidone trough concentration and adverse drug reactions (ADRs) and examined the impact of CYP1A2 *1C (rs2069514) and *1F (rs762551) variants and co-administration on pirfenidone blood concentrations and ADRs. METHODS:Forty-four patients were enrolled. The blood concentration of pirfenidone was determined using high-performance liquid chromatography. CYP1A2 *1C and *1F genotypes were determined using direct SNP sequencing. Additional information related to drug associations was collected to screen factors affecting drug metabolism. RESULTS:The highest predictive value of ADRs was observed when the steady-state trough concentration of pirfenidone was 3.18 mcg·mL -1 and the area under the receiver operating characteristic curve was 0.701 ( P = 0.024). The pirfenidone concentration-to-dose ratio ( C/D ) in CYP1A2 *1F homozygous AA mutants was lower than that in C carriers (CC+AC) (1.28 ± 0.85 vs. 2.03 ± 1.28 mcg·mL -1 ; P = 0.036). Adverse drug reaction (ADR) incidence in the homozygous AA mutant group (28.0%) was significantly lower than that in the C carriers (CC+AC) (63.2%; P = 0.020), and ADR incidence in the A carriers (AC+AA) was considerably lower than that in the CC group (85.7%; P = 0.039). The C/D value of the combined lansoprazole/rabeprazole group was lower than that of the noncombination group ( P < 0.05). CONCLUSIONS:The ADR incidence was positively correlated with pirfenidone blood concentration. The CYP1A2 (rs762551) AA genotype is associated with lower pirfenidone concentrations and fewer ADRs. Lansoprazole/rabeprazole co-administration reduced pirfenidone concentrations. Randomized controlled trials should further explore personalized dosing of pirfenidone and combination therapies.

Intensive care units (ICUs) are specialized environments dedicated to the management of critically ill patients, who are particularly susceptible to drug-resistant bacteria. Among these, carbapenem-resistant Gram-negative bacteria (CR-GNB) pose a significant threat endangering the lives of ICU patients. Carbapenemase production is a key resistance mechanism in CR-GNB, with the transfer of resistance genes contributing to the extensive emergence of antimicrobial resistance (AMR). CR-GNB infections are widespread in ICUs, highlighting an urgent need for prevention and control measures to reduce mortality rates associated with CR-GNB transmission or infection. This review provides an overview of key aspects surrounding CR-GNB within ICUs. We examine the mechanisms of bacterial drug resistance, the resistance genes that frequently occur with CR-GNB infections in ICU, and the therapeutic options against carbapenemase genotypes. Additionally, we highlight crucial preventive measures to impede the transmission and spread of CR-GNB within ICUs, along with reviewing the advances made in the field of clinical predictive modeling research, which hold excellent potential for practical application.

Autoimmune rheumatic diseases are chronic conditions affecting multiple systems and often occurring in young women of childbearing age. The diseases and the physiological characteristics of pregnancy significantly impact maternal-fetal health and pregnancy outcomes. Currently, the integration of big data with healthcare has led to the increasing popularity of using machine learning (ML) to mine clinical data for studying pregnancy complications. In this review, we introduce the basics of ML and the recent advances and trends of ML in different prediction applications for common pregnancy complications by autoimmune rheumatic diseases. Finally, the challenges and future for enhancing the accuracy, reliability, and clinical applicability of ML in prediction have been discussed. This review will provide insights into the utilization of ML in identifying and assisting clinical decision-making for pregnancy complications, while also establishing a foundation for exploring comprehensive management strategies for pregnancy and enhancing maternal and child health.

Abstract The Parkinson's Progression Marker Initiative (PPMI) aims to identify biomarkers for Parkinson's disease (PD) risk, onset, and progression. This study focuses on the G2019S missense mutation in the LRRK2 gene, which is associated with hereditary and sporadic PD. Utilizing data from the PPMI database, we conducted an analysis of baseline clinical characteristics, as well as serum and cerebrospinal fluid levels in two groups: patients with PD with the G2019S mutation (PD + G2019S) and patients with PD without the mutation (PD‐G2019S). Multiple linear regression and longitudinal analysis were performed, controlling for confounding factors. Compared to the PD‐G2019S group, the PD + G2019S group showed more obvious initial motor dysfunction—higher baseline Movement Disorder Society‐Sponsored Revision of the Unified Parkinson Disease Rating Scale (MDS‐UPDRS) scores (false discovery rate [FDR]‐adjusted p < 0.001), but progressed more slowly. Mechanism of Coordinated Access and activities of daily living (ADL) scores were lower at baseline (FDR‐adjusted p < 0.001), whereas Scales for Outcomes of Parkinson's Disease (SCOPA)‐Thermoregulatory (FDR‐adjusted p = 0.015) scores were higher, emphasizing the increase of non‐motor symptoms associated with LRRK2‐G2019S mutation. During the follow‐up period, the motor and non‐motor symptoms changed dynamically with time, and there were longitudinal differences in the scores of MDS‐UPDRS (FDR‐adjusted PI = 0.013, PII = 0.008, PIV < 0.001), Questionnaire for Impulsive‐Compulsive Disorders in Parkinson's Disease (FDR‐adjusted p = 0.027), SCOPA‐Thermoregulatory (FDR‐adjusted p = 0.021), and ADL (FDR‐adjusted p = 0.027) scale scores. PD associated with the LRRK2 G2019S mutation demonstrated more severe symptoms at baseline but slower progression. Motor complications and thermoregulatory disorders were more pronounced.

CONTEXT:Diabetic kidney disease (DKD) is a prominent complication arising from diabetic microangiopathy, and its prevalence and renal impact have placed it as the primary cause of end-stage renal disease. Traditional Chinese Medicine (TCM) has the distinct advantage of multifaceted and multilevel therapeutic attributes that show efficacy in improving clinical symptoms, reducing proteinuria, protecting renal function, and slowing DKD progression. Over recent decades, extensive research has explored the mechanisms of TCM for preventing and managing DKD, with substantial studies that endorse the therapeutic benefits of TCM compounds and single agents in the medical intervention of DKD.OBJECTIVE:This review lays the foundation for future evidence-based research efforts and provide a reference point for DKD investigation.METHODS:The relevant literature published in Chinese and English up to 30 June 2023, was sourced from PubMed, Cochrane Library, VIP Database for Chinese Technical Periodicals (VIP), Wanfang Data, CNKI, and China Biology Medicine disc (CBM). The process involved examining and summarizing research on TCM laboratory tests and clinical randomized controlled trials for DKD treatment.RESULTS AND CONCLUSIONS:The TCM intervention has shown the potential to inhibit the expression of inflammatory cytokines and various growth factors, lower blood glucose levels, and significantly affect insulin resistance, lipid metabolism, and improved renal function. Furthermore, the efficacy of TCM can be optimized by tailoring personalized treatment regimens based on the unique profiles of individual patients. We anticipate further rigorous and comprehensive clinical and foundational investigations into the mechanisms underlying the role of TCM in treating DKD.

Background: Thromboembolic disease is associated with a high rate of disability or death and gravely jeopardizes people’s health and places considerable financial pressure on society. The primary treatment for thromboembolic illness is anticoagulant medication. Fondaparinux, a parenteral anticoagulant medicine, is still used but is confusing due to its disparate domestic and international indications and lack of knowledge about its usage. Its off-label drug usage in therapeutic settings and irrational drug use are also common.Objective: The aim of this guideline is to enhance the judicious clinical application of fondaparinux by consolidating the findings of evidence-based research on the drug and offering superior clinical suggestions.Methods: Seventeen clinical questions were developed by 37 clinical pharmacy experts, and recommendations were formulated under the supervision of three methodologists. Through methodical literature searches and the use of recommendation, assessment, development and evaluation grading techniques, we gathered evidence.Results: This guideline culminated in 17 recommendations, including the use of fondaparinux for venous thromboembolism (VTE) prevention and treatment, perioperative surgical prophylaxis, specific diseases, special populations, bleeding and overdose management. For different types of VTE, we recommend first assessing thrombotic risk in hospitalized patients and then administering the drug according to the patient’s body mass. In surgical patients in the perioperative period, fondaparinux may be used for VTE prophylaxis, but postoperative use usually requires confirmation that adequate hemostasis has been achieved. Fondaparinux may be used for anticoagulation prophylaxis in patients hospitalized for oncological purposes, in patients with atrial fibrillation (AF) after resuscitation, in patients with cirrhosis combined with portal vein thrombosis (PVT), in patients with antiphospholipid syndrome (APS), and in patients with inflammatory bowel disease (IBD). Fondaparinux should be used with caution in special populations, such as pregnant female patients with a history of heparin-induced thrombocytopenia (HIT) or platelet counts less than 50 × 109/L, pregnant patients with a prethrombotic state (PTS) combined with recurrent spontaneous abortion (RSA), and children. For bleeding caused by fondaparinux, dialysis may partially remove the drug.Conclusion: The purpose of this guideline is to provide all healthcare providers with high-quality recommendations for the clinical use of fondaparinux and to improve the rational use of the drug in clinical practice. Currently, there is a lack of a dedicated antidote for the management of fondaparinux. The clinical investigation of activated prothrombin complex concentrate (APCC) or recombinant activated factor VII (rFⅦa) as potential reversal agents is still pending. This critical gap necessitates heightened scrutiny and research emphasis, potentially constituting a novel avenue for future inquiries into fondaparinux sodium. A meticulous examination of adverse events and safety profiles associated with the utilization of fondaparinux sodium will contribute significantly to a more comprehensive understanding of its inherent risks and benefits within the clinical milieu.

Objective: Parkinson's disease (PD) represents the multisystem illness involving immunological and neuro-inflammatory dysfunction. The present work focused on evaluating link of CD33 single nucleotide poly-morphisms (SNPs) with PD vulnerability of the northern Chinese Han people, considering CD33's role as a critical immunoregulatory receptor in neuroinflammatory responses.Methods: The present case-control study included 475 PD cases together with 475 normal controls. A further division of PD patients into two categories was made: 74 patients with early-onset PD (EOPD; onset age = 50 years) and 401 patients with late-onset PD (LOPD; onset age > 50 years). DNA extraction was conducted, fol-lowed by genotyping for 2SNPs of CD33 polymorphisms with polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).Results: Alleles (G vs. A, P = 0.028) and AA genotypes (P = 0.042) of rs12985029 were significantly different between the groups. Distinctions were observed between the two groups in the recessive, co-dominant, and additive models (nominal P = 0.030, nominal P = 0.045, and P = 0.032). AA genotype frequency among male PD was higher compared to corresponding male controls (P = 0.034), and in the male group allele A was a factor causing the disease (P = 0.026). The rs12985029 genotypes and allele frequency were different in EOPD compared with LOPD (P = 0.002, P = 0.002, respectively), and in LOPD group relative to healthy control group (P = 0.020 and P = 0.004, separately). Regarding the rs3826656 polymorphism, the frequency of GA genotype was higher in the control group than in the case group (nominal P = 0.036). Overdominance and co-dominant models were different between these groups (P = 0.026, nominal P = 0.030). Subgroup analysis revealed ge-notype frequency differences between rs3826656 LOPD group and control group (P = 0.018). Furthermore, relationship between rs3826656 and rs12985029 (D' = 0.162, r2 = 0.021) did not reach a complete level of linkage disequilibrium (LD) of northern Chinese Han people.Conclusion: This study establishes an association between CD33 rs12985029 and rs3826656 polymorphisms and PD risk among the selected northern Chinese Han people. The GA genotype, rs3826656, may act as a protective factor against PD, while the A allele, rs12985029,could be genetic risk factor related to PD. Future research should include larger sample sizes and other human populations to further investigate how CD33 polymorphisms contribute to PD.

Voriconazole (VRZ) is a broad-spectrum antifungal medication widely used to treat invasive fungal infections (IFI). The administration dosage and blood concentration of VRZ are influenced by various factors, posing challenges for standardization and individualization of dose adjustments. On the one hand, VRZ is primarily metabolized by the liver, predominantly mediated by the cytochrome P450 (CYP) 2C19 enzyme. The genetic polymorphism of CYP2C19 significantly impacts the blood concentration of VRZ, particularly the trough concentration (Ctrough), thereby influencing the drug's efficacy and potentially causing adverse drug reactions (ADRs). Recent research has demonstrated that pharmacogenomics-based VRZ dose adjustments offer more accurate and individualized treatment strategies for individuals with hepatic insufficiency, with the possibility to enhance therapeutic outcomes and reduce ADRs. On the other hand, the security, pharmacokinetics, and dosing of VRZ in individuals with hepatic insufficiency remain unclear, making it challenging to attain optimal Ctrough in individuals with both hepatic insufficiency and IFI, resulting in suboptimal drug efficacy and severe ADRs. Therefore, when using VRZ to treat IFI, drug dosage adjustment based on individuals' genotypes and hepatic function is necessary. This review summarizes the research progress on the impact of genetic polymorphisms and hepatic insufficiency on VRZ dosage in IFI individuals, compares current international guidelines, elucidates the current application status of VRZ in individuals with hepatic insufficiency, and discusses the influence of CYP2C19, CYP3A4, CYP2C9, and ABCB1 genetic polymorphisms on VRZ dose adjustments and Ctrough at the pharmacogenomic level. Additionally, a comprehensive summary and analysis of existing studies' recommendations on VRZ dose adjustments based on CYP2C19 genetic polymorphisms and hepatic insufficiency are provided, offering a more comprehensive reference for dose selection and adjustments of VRZ in this patient population.

目的 探讨药学门诊建设的现状和难点,及其对提高医院医疗质量的促进作用.方法 从药学学科角度出发,多维度分析目前开展药学门诊的现状和难点,并结合四川省人民医院药学门诊实践情况,重点探讨药学门诊在促进医院医疗质量提高等方面的作用.结果 药学门诊创新工作,即大病医疗保险(医保)审核门诊在医保控费和健康管理方面发挥重要作用.药学门诊促进医院医疗质量提高的作用主要体现在临床结局、人文结局、经济结局、科研创新、教学等多方面.结论 未来应该致力于克服和解决药学门诊建设的困难,进一步践行和探索药学门诊建设对医院医疗质量的提高作用,推动药学学科建设和医院的共同发展.

Parkinson's disease (PD) is a neurodegenerative disease that integrates a series of motor symptoms and non-motor symptoms, making early recognition challenging. The exploration of biomarkers is urgently required. Abnormal eye movements in PD have been reported to appear in a variety of ways since eye tracking technology was developed, such as decreased saccade amplitude, extended saccade latency, and unique saccade patterns. Non-invasive, objective and simple eye tracking has the potential to provide effective biomarkers for the PD diagnosis, progression and cognitive impairment, as well as ideas for research into the occurrence and treatment strategy of motor symptoms. In this review, we introduced the fundamental eye movement patterns and typical eye movement paradigms (such as fixation, pro-saccade, anti-saccade, smooth tracking, and visual search), summarized the symptoms of various ocular motor abnormalities in PD, and discussed the research implications of oculomotor investigation to the pathogenesis of PD and related motor symptoms, as well as the clinical implications as biomarkers and its inspiration on treatment.

中药在妊娠期女性中应用广泛,其应用安全风险大多未知,这给临床决策带来很多困扰.我国尚未根据中医药的特色建立妊娠期中药应用安全性评价体系,随着中医药的不断发展,对妊娠期使用中药的风险进行评估的方法学问题日渐凸显.该文概述妊娠期使用中药的现状,对中药的临床前研究与临床研究进行分析,结合国外妊娠暴露登记研究的策略,探讨妊娠期中药应用安全性评价的思路,以期为孕妇提供风险评估与用药指导,为中药妊娠期安全性评价体系的建立奠定基础.

巨细胞病毒(CMV)是器官移植后最常见的感染源.除感染外,CMV还增加器官移植并发症的风险,导致移植失败率和死亡率升高.CMV感染的预防和治疗对于移植的结局至关重要.最近出现了几种新型抗病毒药物,包括来特莫韦、马立巴韦和布林西多福韦,为移植患者抗CMV感染提供了新的治疗选择.

目的 对免疫相关性妊娠多学科诊疗(MDT)门诊的全程化药学服务模式、流程及成果进行介绍,为提升药物治疗有效性、安全性和患者依从性提供参考.方法 以合并风湿免疫的基础疾病、或者因为免疫异常等因素而存在复发性流产的患者为服务对象,介绍本院免疫相关性妊娠MDT门诊的团队构建、工作模式和临床药师职责.统计分析215例免疫相关性妊娠患者的一般情况、疾病情况、合并用药情况、药学服务内容、患者孕期并发症发生情况及母儿结局.结果 药师为215例MDT门诊就诊患者提供了全程化药学服务,包括用药史回顾、医嘱审核、药物重整、用药教育和生活方式指导,回答家属咨询,解答患者疑问,并就用药方案及治疗方案调整提出意见建议,开展患者随访、药物不良反应监测等,患者满意度达100％.在有效随访且有妊娠结局的53例就诊患者中,活产47例,活产率87.04％;2例自然流产,自然流产率3.78％;2例治疗性流产,治疗性流产率3.78％;2例胎死宫内,胎死宫内发生率3.78％;1例出生缺陷,产检发现胎儿脑积水,母亲选择性终止妊娠(羊膜腔穿刺引产),出生缺陷率为1.86％,相较于我国总人群的出生缺陷发生率(5.6％)明显偏低.18例患者出现并发症;其中妊娠糖尿病最多(6例),发生率为11.32％;妊娠高血压(3例)发生率5.66％.结论 临床药师通过开设MDT门诊,参与特殊患者全程化药物治疗管理,可提高合理用药水平、患者依从性、药物治疗安全性及治疗效果.

2018年10月的一个夜晚,我在互联网医院药物咨询门诊上收到一例较为复杂的用药咨询.患者是一名31岁的孕妇,有乙型肝炎(以下简称乙肝)基础病史,现为"大三阳"状态.原发不孕,试孕8年未成功,中间做了2次输卵管疏通术,最后通过体外胚胎移植术终于成功妊娠,目前妊娠14+2周.但在胚胎植入10+3周时患者因急性血行播散型肺结核住院11天,其间做了胸部CT及X线检查各1次,使用了抗结核药、保肝药等,用结核药后出现了肝功能异常.