Volume 131 · Issue 02 · 2018

中风仍然是世界上发病率和死亡率的主要原因。与冠心病不同，脑卒中可因不同病因而发生，其发病机制、治疗和预后各不相同。有不同的病因分类系统：大多数文章使用了Org 10172在急性卒中治疗分类系统中的试验，但也注意到了使用其他分类系统的文章。^[1]尽管分类系统之间的细节存在差异，但大动脉粥样硬化（LAA）、小血管疾病（SVD）和心脏栓塞（CE）是最常分析的亚型，因为它们在患者中的比例很高，已知的风险因素数量很高，并且一些风险因素是可控的。不同地区的亚型比例不同。在一项比较卒中及其亚型流行病学的系统综述中，无论是在医院还是社区研究中，中国人SVD卒中的比例都高于白种人。^[2]此外，由于工业进步和医疗预防，亚型的比例可能会随着时间的推移而变化。分析亚型的趋势对于判断预防程序的效果和为后续步骤提供建议至关重要。

White matter lesions (WMLs) are common findings in brain magnetic resonance imaging (MRI) and are strongly associated with stroke incidence, recurrence, and prognosis. However, the relationship between WMLs and transient ischemic attacks (TIAs) is not well established. This study aimed to determine the clinical significance of WMLs in patients with TIA.

A total of 181 consecutive inpatients with first-ever TIA were enrolled. Brain MRIs within 2 days of symptom onset were used to measure WML volumes. Recurrent vascular events within 1 year of TIA onset were assessed. The relationship between WMLs and recurrent risk of vascular events was determined by a multivariate logistic regression.

WMLs were identified in 104 patients (57.5%). Age and ratio of hypertension were significantly different between patients with and without WMLs. The incidence of vascular events in patients with WMLs significantly increased in comparison to those without WMLs (21.15% vs. 5.19%, 95% confidence interval [CI]: 1.18–15.20, P = 0.027) after controlling for confounders. Furthermore, distributions of WML loads were found to be different between patients who developed vascular events and those who did not. WML volumes were demonstrated to be correlated with recurrent risks, and the fourth quartile of WML volumes led to an 8.5-fold elevation of recurrent risk of vascular events compared with the first quartile (95% CI: 1.52-47.65, P= 0.015) after adjusting for hyperlipidemia.

WMLs occur frequently in patients with TIA and are associated with the high risk of recurrent vascular events, suggesting a predictive neuroimaging marker for TIA outcomes.

Early neurological deterioration (END) is a prominent issue after recanalization treatment. However, few studies have reported the characteristics of END after endovascular treatment (EVT) as so far. This study investigated the incidence, composition, and outcomes of END after intravenous recombinant tissue plasminogen activator (IV rt-PA) and EVT of acute ischemic stroke, and identified risk factors for END.

Medical records of patients who received recanalization treatment between January 1, 2014, and December 31, 2015 were reviewed. Patients were classified into IV rt-PA or EVT group according to the methods of recanalization treatment. The END was defined as an increase in the National Institutes of Health Stroke Scale (NIHSS) ≥4 or an increase in Ia of NIHSS ≥1 within 72 h after recanalization treatment. Clinical data were compared between the END and non-END subgroups within each recanalization group.

Of the 278 patients included in the study, the incidence of END was 34.2%. The incidence rates of END were 29.8% in the IV rt-PA group and 40.2% in the EVT group. Ischemia progression (68.4%) was the main contributor to END followed by vasogenic cerebral edema (21.1%) and symptomatic intracranial hemorrhage (10.5%). Multivariate logistic regression showed that admission systolic blood pressure (SBP) ≥160 mmHg (odds ratio [OR]: 2.312, 95% confidence interval [CI]: 1.105–4.837) and large artery occlusion after IV rt-PA (OR: 3.628, 95% CI: 1.482–8.881) independently predicted END after IV rt-PA; and admission SBP ≥140 mmHg (OR: 5.183, 95% CI: 1.967–13.661), partial recanalization (OR: 4.791, 95% CI: 1.749–13.121), and nonrecanalization (OR: 5.952, 95% CI: 1.841–19.243) independently predicted END after EVT. The mortality rate and grave outcome rate at discharge of all the END patients (26.3% and 55.8%) were higher than those of all the non-END patients (1.1% and 18.6%; P < 0.01).

END was not an uncommon event and associated with death and grave outcome at discharge. High admission SBP and unsatisfactory recanalization of occluded arteries might predict END.

Clinically, it is difficult to differentiate multiple acyl-CoA dehydrogenase deficiency (MADD) from immune-mediated necrotizing myopathy (IMNM) because they display similar symptoms. This study aimed to determine whether muscle magnetic resonance imaging (MRI) could be used for differential diagnosis between MADD and IMNM.

The study evaluated 25 MADD patients, confirmed by muscle biopsy and ETFDH gene testing, and 30 IMNM patients, confirmed by muscle biopsy. Muscles were assessed for edema and fatty replacement using thigh MRI (tMRI). Degrees and distribution patterns of fatty infiltration and edema in gluteus maximus and thigh muscles were compared.

Total fatty infiltration and edema scores (median, [Q1, Q3]) were 4.00 (1.00, 15.00) and 0 (0, 4.00) in MADD and 14.50 (8.00, 20.75) and 22.00 (16.75, 32.00) in IMNM, respectively, which were significantly more severe in IMNM than that in MADD (P = 0.000 and P = 0.004, respectively). Edema scores for gluteus maximus, long head of biceps femoris, and semimembranosus were significantly higher in IMNM than in MADD (all P = 0.000). Fatty infiltration scores for anterior and medial compartments were significantly more severe in IMNM than that in MADD (all P = 0.000).

Different patterns of muscle involvement on tMRI can contribute to differential diagnosis between MADD and IMNM when clinical suspicions alone are insufficient, thereby reducing the need for muscle biopsy.

SH3TC2, PMP2, and BSCL2 genes are related to autosomal recessive (AR) Charcot-Marie-Tooth (CMT) disease type 1, autosomal dominant (AD)-CMT1, and AD-CMT2, respectively. Pathogenic variants in these three genes were not well documented in Chinese CMT patients. Therefore, this study aims to detect SH3TC2, PMP2, and BSCL2 pathogenic variants in a cohort of 315 unrelated Chinese CMT families.

A total of 315 probands from 315 unrelated Chinese CMT families were recruited from the Department of Neurology of Third Xiangya Hospital and Xiangya Hospital. We screened for SH3TC2 pathogenic variants in 84 AR or sporadic CMT probands, PMP2 pathogenic variants in 39 AD or sporadic CMT1 probands, and BSCL2 pathogenic variants in 50 AD or sporadic CMT2 probands, using polymerase chain reaction and Sanger sequencing. All these patients were out of 315 unrelated Chinese CMT families and genetically undiagnosed after exclusion of pathogenic variants of PMP22, MFN2, MPZ, GJB1, GDAP1, HSPB1, HSPB8, EGR2, NEFL, and RAB7. Candidate variants were analyzed based on the standards and guidelines of American College of Medical Genetics and Genomics (ACMG). Clinical features were reevaluated.

We identified three novel heterozygous variants such as p.L95V (c.283C>G), p.L1048P (c.3143T>C), and p.V1105M (c.3313G>A) of SH3TC2 gene and no pathogenic variants of PMP2 and BSCL2 genes. Although evaluation in silico and screening in the healthy control revealed that the three SH3TC2 variants were likely pathogenic, no second allele variants were discovered. According to the standards and guidelines of ACMG, the heterozygous SH3TC2 variants such as p.L95V, p.L1048P, and p.V1105M were considered to be of uncertain significance.

SH3TC2, PMP2, and BSCL2 pathogenic variants might be rare in Chinese CMT patients. Further studies to confirm our findings are needed.

Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is a treatable autoimmune neurologic syndrome that occurs with or without tumor association. However, some severe cases are refractory to systemic immunotherapy. This pilot study aimed to evaluate the utility and safety of intrathecal methotrexate injection for severe patients with anti-NMDAR encephalitis who did not respond to first-line immunotherapy.

Intrathecal injections with methotrexate and dexamethasone were performed weekly in four legible patients within consecutive 4 weeks. Cerebrospinal fluid (CSF) was collected at baseline and each time of intrathecal injection for identification of anti-NMDAR antibody titers.

Significant clinical improvement was observed in three patients associated with a stepwise decrease of CSF anti-NMDAR antibody titers (maximum: 1/320 to minimum: 1/10). After 2 months of follow-up, they were able to follow simple commands and had appropriate interactions with people (modified Rankin scale [mRS] of 0-2). At 12 months of follow-up, they all had returned to most activities of daily life (mRS of 0), and no relapses were reported. One patient showed no clinical improvement and died of neurologic complications.

Intrathecal treatment may be a potentially useful supplementary therapy in severely affected patients with anti-NMDAR encephalitis. Further large cohort study and animal experiment may help us elaborate the utility of intrathecal injection of methotrexate and its mechanism of action.

Chronic stress contributes to increased risks of atherosclerotic diseases including heart disease, stroke, and transient ischemic attack. However, its underline mechanisms are poorly understood. This study aimed to elucidate the mechanism via which chronic stress exerts its effect on atherosclerosis (AS).

Fifty male New Zealand white rabbits were used. Aortic balloon-injury model was applied. Both social stress and physical stress methods were adopted to establish chronic stress models. The lumen stenotic degree, intimal and medial areas, maximum fibrous cap thickness, and plaque contents were measured with histological sections. Proteomic methods were applied to detect protein changes in abdominal aortas to identify the specialized mediators. Real-time reverse transcription-polymerase chain reaction was used for further verification and investigation.

The stress rabbits exhibited lower body weight, worse fur state, more inactivity behavior, and higher serum cortisol level. Chronic stress was significantly associated with the decreased medial area and increased plaque instability, which was manifested by thinner fibrous caps, larger lipid cores, more macrophages, and new vessels but fewer smooth muscle cells and elastic fibers. After chronic stress, the apoptosis-related genes UBE2K, BAX, FAS, Caspase 3, Caspase 9, and P53 were upregulated, and BCL-2/BAX was down-regulated; the angiogenesis-related genes ANG and VEGF-A were also highly expressed in atherosclerotic arteries.

Rabbit models of chronic stress were successfully established by applying both social stress and physical stress for 8 weeks. Chronic stress can reduce AS tunica media and accelerate plaque instability by promoting apoptosis and neovascularization.

Interleukin (IL)-37, also called IL1F7, is a natural inhibitor of inflammatory and immune responses. It is involved in the pathogenesis of rheumatoid arthritis (RA). This study aimed to investigate the role of IL1F7 gene polymorphism in RA susceptibility in a large cohort of patients.

Five selected single-nucleotide polymorphisms in IL1F7 genes (rs2723186, rs3811046, rs4241122, rs4364030, and rs4392270) were genotyped by TaqMan Allelic Discrimination in Northern Chinese Han population. The allele and the genotype were compared between patients with RA and healthy controls. Association analyses were performed on the entire data set and on different RA subsets based on the status of the anti-cyclic citrullinated peptide antibody and the rheumatoid factor by logistic regression, adjusting for age and gender.

Trend associations were detected between rs2723186, rs4241122, rs4392270, and RA in Stage I (160 patients with RA; 252 healthy controls). Further validation in Stage II comprised 730 unrelated patients with RA (mean age: 54.9 ± 12.6 years; 81.6% females) and 778 unrelated healthy individuals (mean age: 53.5 ± 15.7 years; 79.5% females). No significant differences in the distributions of alleles and genotypes were observed between the case and control groups in both the entire set and the different RA subsets. Disease activity and age of RA onset were also not associated with genotype distributions.

IL1F7 gene polymorphism does not significantly influence RA susceptibility in the Northern Chinese Han population.

Diabetic nephropathy (DN) is the most common and serious microvascular complication of diabetes. To date, the gold standard for identifying DN and nondiabetic renal disease (NDRD) is a renal biopsy; however, there is currently no reliable diagnostic marker to identify DN and NDRD in a noninvasive manner. This study aimed to investigate the different glycopatterns in urine specimens of DN patients and NDRD patients for a differential diagnosis.

In total, 19 DN patients and 18 NDRD patients who underwent renal biopsies between March 2015 and March 2016 at the Chinese People’s Liberation Army General Hospital were enrolled in this study. A lectin microarray was used to investigate the glycopatterns in the urinary protein of the 37 patients. Ratio analysis and one-way analysis of variance were used to screen altered glycopatterns. Then, the altered glycopatterns between the DN and NDRD groups were verified by a urinary protein microarray among another 32 patients (15 with DN and 17 with NDRD), and receiver operating characteristic (ROC) curve analysis was used to determine the diagnostic value of the altered glycopatterns in differentiating DN and NDRD. Finally, lectin blotting was used to evaluate the altered glycosylation in protein level.

The result of lectin microarrays revealed that the relative abundance of the (β-1,4)-linked N-acetyl-D-glucosamine (GlcNAc) recognized by lectin Datura stramonium agglutinin (DSA) was significantly higher in urinary protein in DN patients than that in NDRD patients (fold change >1.50, P < 0.001). Subsequently, the results of urinary protein microarrays were consistent with lectin microarrays (P < 0.05). Furthermore, the ROC curve showed that glycopatterns could effectively distinguish DN from NDRD patients (area under the ROC curve = 0.94, P < 0.001). DSA lectin blotting showed that glycoproteins, with a molecular weight of approximately 50,000, demonstrated a difference in urine samples between DN patients and NDRD patients.

The relative abundance of (β-1,4)-linked GlcNAc recognized by lectin DSA and urinary glycoprotein with a molecular weight of approximately 50,000 are significantly different between DN and NDRD patients, indicating that the glycopatterns could be used as potential biomarkers for a differential diagnosis.

Tat-interacting protein 30 (TIP30) has been reported to be a tumor suppressor, with reduced or absent expression in various tumors. However, its role in bladder urothelial cancer (BUC) has not been investigated. Therefore, herein, we investigated the expression of TIP30 protein in BUC and normal bladder mucosa and the clinical significance of TIP30 expression in the prognosis of BUC.

We reviewed data from 79 cases of BUC and 15 adjacent tissue samples from 79 patients treated at our institution between 2004 and 2007. TIP30 expression was examined by immunohistochemistry. The relationship between TIP30 expression and tumor stage, histological grade, and survival was analyzed. Differences between groups were evaluated using the t-test or matched-pairs test, and differences in the survival rates were analyzed with the log-rank test.

TIP30 protein expression was significantly reduced in BUC tissue (t= −6.91, P < 0.05) compared with normal tissue samples, and in invasive bladder cancer (t = 10.89, P < 0.05) compared with superficial bladder cancer. TIP30 protein expression differed significantly among different differentiated groups classified either according to the World Health Organization (2004, F = 17.48, P < 0.01) or World Health Organization (1973, F = 10.68, P < 0.01). TIP30 protein expression was significantly reduced in high-grade papillary urothelial carcinoma compared with papillary urothelial neoplasm of low malignant potential (P < 0.05) and low-grade papillary urothelial carcinoma (P < 0.05). Meanwhile, TIP30 protein expression was significantly reduced in Grade III BUC, compared with Grade I (P < 0.05) and Grade II (P < 0.05). Patients with low TIP30 expression showed a higher incidence of disease progression than those with high TIP30 expression (t = 2.63, P < 0.05). Kaplan-Meier survival analysis showed a strong positive relationship between TIP30 expression and overall survival (OS) (χ² = 17.29, P < 0.05).

TIP30 expression was associated with clinical tumor stage in BUC, suggesting that it might play an important role in disease progression. Furthermore, TIP30 might predict postoperative OS. Thus, its evaluation might be useful for predicting prognosis.

The quality of the lateral compartment cartilage is important to preoperative evaluation and prognostic prediction of unicompartmental knee arthroplasty (UKA). Delayed gadolinium-enhanced magnetic resonance imaging of cartilage (dGEMRIC) enables noninvasive assessment of glycosaminoglycan (GAG) content in cartilage. This study aimed to determine the GAG content of the lateral compartment cartilage in knees scheduled to undergo Oxford medial UKA.

From December 2016 to May 2017, twenty patients (20 osteoarthritic knees) conforming to the indications for Oxford medial UKA were included as the osteoarthritis (OA) group, and 20 healthy volunteers (20 knees) paired by sex, knee side, age (±3 years), and body mass index (BMI) (±3 kg/m²) were included as the control group. The GAG contents of the weight-bearing femoral cartilage (wbFC), the posterior non-weight-bearing femoral cartilage (pFC), the lateral femoral cartilage (FC), and tibial cartilage (TC) were detected using dGEMRIC. The dGEMRIC indices (T1Gd) were calculated in the middle three consecutive slices of the lateral compartment. Paired t-tests were used to compare the T1Gd in each region of interest between the OA group and control group.

The average age and BMI in the two groups were similar. In the OA group, T1Gd of FC and TC was 386.7 ± 50.7 ms and 429.6 ± 59.9 ms, respectively. In the control group, T1Gd of FC and TC was 397.5 ± 52.3 ms and 448.6 ± 62.5 ms, respectively. The respective T1Gd of wbFC and pFC was 380.0 ± 47.8 ms and 391.0 ± 66.3 ms in the OA group and 400.3 ± 51.5 ms and 393.6 ± 57.9 ms in the control group. Although the T1Gd of wbFC and TC tended to be lower in the OA group than the control group, there was no significant difference between groups in the T1Gd in any of the analyzed cartilage regions (P value of wbFC, pFC, FC, and TC was 0.236, 0.857, 0.465, and 0.324, respectively).

The GAG content of the lateral compartment cartilage in knees conforming to indications for Oxford medial UKA is similar with those of age- and BMI-matched participants without OA.

Advances in genomics and molecular biology have led to the discovery of a large group of uncharacterized long noncoding RNAs (lncRNAs). Emerging evidence indicated that many lncRNAs function in multiple biological processes and its dysregulation often causes diseases. Recent studies suggested that almost all regulatory lncRNAs interact with biological macromolecules such as DNA, RNA, and protein. LncRNAs regulate gene expression mainly on three levels, including epigenetic modification, transcription, and posttranscription, through DNA methylation, histone modification, and chromatin remodeling. LncRNAs can also affect the development of diseases and therefore be used to diagnose and treat diseases. With new sequencing and microarray techniques, hundreds of lncRNAs involved in reproductive disorders have been identified, but their functions in these disorders are undefined.

This review was based on articles published in PubMed databases up to July 10, 2017, with the following keywords: "long noncoding RNAs", "LncRNA", "placentation", and "reproductive diseases".

Original articles and reviews on the topics were selected.

LncRNAs widely participate in various physiological and pathological processes as a new class of important regulatory factors. In spermatogenesis, spermatocytes divide and differentiate into mature spermatozoa. The whole process is elaborately regulated by the expression of phase-specific genes that involve many strains of lncRNAs. Literature showed that lncRNA in reproductive cumulus cells may contribute to the regulation of oocyte maturation, fertilization, and embryo development.

LncRNA has been found to play a role in the development of reproduction. Meanwhile, we reviewed the studies on how lncRNAs participate in reproductive disorders, which provides a basis for the study of lncRNA in reproduction regulation.

Gastrointestinal stromal tumors (GISTs) are rare mesenchymal tumors of the gastrointestinal tract, which frequently cause intraabdominal metastases. The current standard of care is surgery for localized cases, and adjuvant imatinib is recommended for tumors with a high risk of recurrence. To date, radiotherapy has not been commonly accepted as a part of multimodality treatment approach other than palliation. However, recently published case reports and some small series suggest that radiotherapy is a valuable option for controlling locally progressive, drug-resistant disease. The aim of this review is to provide a viewpoint from a radiation oncologist concerning the management of GISTs, especially rectal GIST, and clarify the role and technical aspects of radiotherapy in the treatment approach.

A comprehensive search in PubMed using the keywords "radiotherapy for rectal GIST" and "rectal GIST" was undertaken. The literature search included the related articles after 1995.

The main articles including rectal GIST case reports and GIST series containing rectal cases were the primary references.

Surgery is the mainstay of treatment. However, to date, radiotherapy is included in the multidisciplinary treatment strategy of rectal GISTs in some circumstances with palliative, adjuvant, or definitive intent using different treatment doses and fields.

Recently reported long-term local control rates indicate that GIST is a radiosensitive disease. This makes radiotherapy a valuable alternative in GIST management with curative intent, especially in patients who (1) cannot tolerate or are resistant to chemotherapy agents, (2) have an unresectable disease, (3) have a gross or microscopic residual disease after surgery, and (4) have a recurrent disease.

原发性心脏肿瘤是极其罕见的实体。其中四分之一是恶性的，肉瘤占恶性病例的75%。虽然大多数血管肉瘤起源于头颈部，但只有少数起源于心脏。我们报告了一例罕见的心脏血管肉瘤表现为右心房破裂。

乳头状胶质神经元肿瘤（PGNT）是一种罕见的肿瘤，在世界卫生组织（WHO）2007年分类中被归类为独特的混合胶质神经元肿瘤。^[1]在这里，我们报告了一例老年男性PGNT伴有血管瘤样特征的过度区域。这份报告有助于这种罕见肿瘤实体的多样性。

患者男，14岁，主诉2年进行性劳力性呼吸困难和指尖发绀病史，到广州医科大学附属第一医院就诊。体格检查显示脉搏血氧饱和度显著降低（静息时80%），嘴唇明显发绀。高分辨率计算机断层扫描显示肺野无明显异常[图1a和图1b].肺动脉造影的计算机断层扫描显示肺动脉主干或分支无充盈缺损，无中央肺动脉扩张，无心脏扩大[图1c和图1d].心导管检查显示右心房压平均6 mmHg，肺动脉压平均12 mmHg，肺毛细血管楔压9 mmHg，心输出量6.2 L/min，心脏指数4.10 L·min⁻¹·米⁻²肺血管阻力略有升高，为4.52 wood单位。肺活检显示下叶肺泡间隙充满红细胞或含铁血黄素细胞，肺泡间隔较正常宽。苏木精和伊红染色显示肺泡和细支气管壁内的毛细血管增生在大多数区域可见[图2a,图2b,图2c].肺切片免疫染色CD34强阳性[图2d]、CD31[图2e]，和F8[图2f].临床表现、病理结果和免疫组织化学支持肺毛细血管瘤病（PCH）的明确诊断，肺动脉血压正常，放射学表现正常。由于经济困难，患者放弃了心肺移植，在没有治疗干预的情况下离开了医院。随访近一年，患者在家中使用2 L/min补充鼻插管氧气，病情稳定，无明显缺氧。获得了患者父母的书面知情同意书，以发表本病例报告和任何随附图像。

致编者：随着脓毒症相关器官衰竭评估（SOFA）的重要性日益增加，^[1]临床医生越来越关注其可靠性和准确性。在重症监护室，医生和护士的SOFA评分都不够准确。^[2,3]很少有研究报道急诊科（ED）医生在手动分配SOFA评分方面的表现。因此，我们进行了一项单中心前瞻性研究来检查该问题。

致编辑：儿童脾切除术增加了患者细菌感染的风险。适当的疫苗接种和教育有助于对抗这些疾病；然而，对脾切除术后的病毒感染重视不够。在此，我们报告了一例脾切除术治疗儿童免疫性血小板减少性紫癜（ITP）后由复发性病毒感染引起的冷凝集素病（CAD）。给予抗病毒和免疫刺激剂治疗，导致一般状况改善。

编辑：我们饶有兴趣地阅读了邹和孙关于铁积累与丙型肝炎病毒（HCV）感染相关的综述。^[1]无论超负荷的机制是什么，我们都想强调这种积累的重要医学后果；这些不仅包括较差的慢性肝炎预后，而且包括较高的肝细胞癌(HCC)风险，^[1]2型糖尿病、^[2]和心力衰竭/功能不全。^[3]所有这些并发症现在都在流行病学上证明发生在慢性HCV感染患者中，但它们是铁储存过多的公认后果；正如邹和孙提醒的那样，这反过来可能是几种病毒性疾病的结果。^[1]过量铁沉积的一个非常常见的并发症是几种细菌的感染，包括幽门螺杆菌该病原体在世界范围内存在，并在肝硬化和HCC患者中发现合并感染；这种联系在中国和欧洲非常频繁。^[4,5]幽门螺杆菌被证明加速向肝硬化和HCC的进展，超出了其在胃癌和消化性溃疡和出血中的致病作用。已知肝硬化患者十二指肠溃疡出血的高风险；因此，我们建议谨慎的医生应始终检测是否存在幽门螺杆菌在所有慢性肝炎患者中，无论是由于病毒感染、铁超载、自身免疫性疾病还是酗酒。

我们谨代表题为“丙型肝炎病毒感染和铁超载之间的关系”的文章的作者，感谢Ponzetto教授和Figura教授对我们综述的评论。如信中所述，幽门螺杆菌可能出现在肝硬化和肝细胞癌患者中，并恶化预后，^[1,2]因此，我们同意他们的意见，即测试是否存在幽门螺杆菌应在所有慢性肝炎患者中进行，无论肝炎是如何引起的。