以血小板减少为主要表现的尼曼-匹克病1例

1 病历摘要 患者，女，20岁，农民，因“反复皮肤瘀斑瘀点5年，伴月经量增多，四肢关节疼痛3个月”于2006年4月15日入院。患者于2000年始出现头晕乏力，至当地医院诊治发现血小板减少（具体经过不详），给予输血小板及激素（甲强龙、强的松）治疗后好转出院。但院外反复出现皮肤瘀斑瘀点，月经量增多，无鼻衄、牙龈出血、血尿、黑便、发热等，又多次给予输血及激素治疗后缓解。近3个月来出现四肢骨关节疼痛，以下肢及足趾部为甚，疼痛与饮食、天气无关，活动无受限，为求进一步诊治入院。病程中精神饮食欠佳，二便正常。既往无肝炎、伤寒等相关病史，家族中无类似病史。     

以大量腹腔积液和血小板减少为主要表现的TAFRO综合征1例报告

<正>Castleman病(Castleman disease,CD)又称巨大淋巴结病或血管滤泡性淋巴结增生症,由Castleman等^[1]于1956年首次报道,是一种极为罕见的反应性慢性淋巴组织增殖性疾病。2010年,Takai等^[2]首次将一类以血小板减少、全身水肿、发热、骨髓纤维化、肝脾肿大的多中心型CD患者归为一种新的临床综合征(TAFRO综合征)。TAFRO综合征被认为是CD的一种罕见特殊类型。本文主要报道1例以大量腹水和血小板减少为主要表现的TAFRO综合征患者,旨在提高广大医务工作者对本病的认识,减少误诊和漏诊。     

布鲁氏杆菌病病原学

布鲁氏杆菌属（Brucella）是一类革兰阴性的短小杆菌，牛、羊、猪等动物最易感染，引起母畜传染性流产。人类接触带菌动物或食用病畜及其乳制品，均可被感染，发生波浪热。该菌属早在1886年由Bruce从地中海1名弛张热病人尸体脾脏标本中用显微镜观察到，1887年获得纯培养，为了纪念他，定名为Brucella属。当时虽从病人分出此菌，但传染源仍未解决，该地英军发病率很高。     

新型布尼亚病毒感染致发热伴血小板减少综合征1例报告

2010年郧县人民医院报告的1例发热伴血小板减少综合征病例。流行病学调查显示该病例无啤叮咬史,在其密切接触的村民所养牛和邻居饲养的马身上检出蜱虫,实验室检测该病例血清新型布尼亚病毒核酸阳性。该病例被确诊为新型布尼亚病毒感染致发热伴血小板减少征。     

成人梅毒感染伴极重度血小板减少症1例

<正>患者,男,48岁。因"外阴不适6 d,牙龈出血伴皮肤紫癜5 d"于2013年7月24日入院。患者6 d前出现外阴不适,伴局部红色小片状皮疹,在某医院就诊,查梅毒螺旋体明胶颗粒凝集试验(treponema pallidum particle agglutination,TPPA)和快速血浆反应素试验(rapid plasma reagin,RPR)阳性,诊断"梅毒",给予长效青霉素(具体剂量不详)肌肉注射及     

103例发热待查患者布鲁杆菌病诊断结果分析

发热待查,在临床诊断中最为常见, 发热本身可由多类疾病引起,查清发热的致病原因,是临床医学长期探讨的重要课题之一。布鲁杆菌病（简称布病）是布鲁杆菌引起的急性或慢性传染病,临床上主要表现为病情轻重不一的发热等症状和特有体征。为了解青海省发热待查患者布病诊断情况,于2005 - 2009年作者对103例发热待查患者进行了布病检查,现将结果报道如下。1 对象与方法1.1病例来源：以2005 - 2009年在西宁市各大综合性医院就诊.经全面多项检查未发现病因的发热待查患者103例作为调查对象。     

慢性乙型肝炎合并布鲁氏杆菌病导致肝硬化1例

患者男性,43岁,因腰背部疼痛1 月,眼黄、尿黄2周于2020年9月30日收住入院.于1 月前患者无明显诱因出现腰背部疼痛,伴腰部活动受限,未行诊疗.入院前2周出现眼黄、尿黄,腰背部疼痛加重,腹胀、尿少,24 h尿量约600 mL,无恶心、呕吐、无腹痛、大便正常.遂就诊于当地医院,诊断为乙肝肝硬化失代偿期 细菌性...     

急性甲型肝炎伴血小板减少及溶血性贫血1例报告

急性甲型肝炎是急性感染HAV后导致的以乏力、黄疸、腹部不适、食欲减退、肝功能异常为特征的肝损伤,而免疫介导的肝外表现和血液学并发症在急性甲型肝炎中相对少见,主要见于成人急、慢性乙型肝炎和丙型肝炎[1]。查阅国内外文献发现关于急性甲型肝炎同时并发血小板减少和溶血性贫血非常罕见。本科室近期收治了1例中年男性感染HAV后导致重度血小板减少和溶血性贫血的病例,现报告如下。     

蓬莱市人民医院发热伴血小板减少综合征53例临床分析

目的研究发热伴血小板减少综合征的流行病学和临床特点,以提高对该病的认识。方法对蓬莱市人民医院2011—2013年收治的53例发热伴血小板减少综合征的临床资料进行回顾性分析。结果病例呈高度散发,以农民(94.34%)为主,聚集性发病14例,6—9月为发病高峰。所有患者均发热,主要症状为乏力、全身酸痛、纳差和恶心,主要体征为腹股沟淋巴结肿大和触痛(64.15%)、舌体及肢体震颤(58.49%)。实验室检查结果为发病早期WBC下降(94.34%)、PLT下降(88.68%)和嗜酸性粒细胞比例降低(98.11%),ALT、AST、乳酸脱氢酶、肌酸激酶同工酶和空腹血糖升高以及蛋白尿。治愈39例,死亡14例(26.42%)。年龄偏大、既往有基础疾病、发病后未及时诊治以及有神经系统症状患者病情较重,病死率较高。结论早发现、早诊断、早治疗,同时防止并发症,加强消毒隔离和防护措施,可降低病死率。     

Pazopanib-induced severe acute liver injury: A case report

Rationale:Drug-induced liver injury (DILI) is the most common cause of acute liver failure in the United States. Painkillers and fever antipyretics are the most common cause of DILI. Hepatic injury can be provoked by DILI as hepatocellular or cholestatic type.Patient concerns:A 48-year-old woman presented jaundice accompanied by nausea and vomiting. The patient was an inactive hepatitis B carrier with low viral titer and was diagnosed renal cell carcinoma (RCC) with hepatic metastasis requiring pazopanib treatment. Prior to administration of pazopanib, tenofovir administration was started to prevent exacerbation of hepatitis B. The patient was referred to clinic of gastroenterology department due to sudden elevation of bilirubin after 5 weeks of pazopanib treatment.Diagnoses:Abdominal ultrasound and computed tomography showed non-specific finding other than metastatic nodule in the liver and liver cirrhosis. After then, the patient was performed liver biopsy, and the biopsy result was acute cholestatic hepatitis with centrilobular area necrosis and portal inflammation. Therefore, considering the clinical history and biopsy results, the patient was diagnosed as DILI due to pazopanib.Interventions:After the biopsy, empirical steroid therapy was initiated and after 7 weeks of pazopanib discontinuation.Outcomes:The total bilirubin level returned to normal from peak level of 24.61 to 1.52 mg/dL.Lessons:In patients with renal cell carcinoma, pazopanib treatment requires clinical caution as it causes rare complications such as severe jaundice and acute cholestatic hepatitis.     

Diagnosis of erythropoietic protoporphyria with severe liver injury: A case report

BACKGROUND Porphyria is a rare disease with complex classification. Erythropoietic protoporphyria(EPP) is an autosomal recessively inherited disease, and most are caused by mutations in the FECH gene. EPP combined with liver injury is even rarer.CASE SUMMARY This paper reports a case of EPP which was admitted to the hospital with abnormal liver function and diagnosed by repeated questioning of medical history, screening of common causes of severe liver injury, and second generation sequencing of the whole exon genome. We also summarize the clinical characteristics of EPP with liver injury, and put forward some suggestions on EPP to provide a reference for the diagnosis of such rare disease.CONCLUSION A new mutation locus(c.32_35 dupCCCT) which may be related to the disease was found by detecting the FECH gene in the pedigree of this case.     

甲强龙治疗重型药物性肝损伤合并银屑病1例报告

1病例资料患者男性,31岁,以“全身乏力20余天,尿黄半月,皮肤、巩膜黄染1周”于2018年3月19日住院。患者既往有“银屑病”13余年,无高血压、糖尿病病史;无吸烟、饮酒史;无家族遗传倾向性疾病。于2009年6月至某中医就诊,给予服用“中药”(用药成分不详)治疗3个月,治疗期间出现腹泻,7~8次/d,黄稀便,无腹痛、皮肤黄染、恶心、呕吐等不适,治疗后皮损逐渐缩小接近正常皮肤;后因食“牛肉”诱发皮损,因皮损反复出现,2017年7月再次至当地中医就诊,给予“中药”(具体不详)治疗6个月,治疗期间大便干结,2~3次/d,量少,伴里急后重感,无腹痛、恶心、呕吐,皮损控制不佳。     

Escitalopram-induced liver injury: A case report and review of literature

BACKGROUND Depression is a growing public health problem that affects over 350 million people globally and accounts for approximately 7.5% of healthy years lost due to disability. Escitalopram, one of the first-line medications for the treatment of depression, is a selective serotonin reuptake inhibitor and one of the most commonly prescribed antidepressant medications worldwide. Although thought to be generally safe and with minimal drug-drug interactions, we herein present an unusual case of cholestatic liver injury, likely secondary to escitalopram initiation.CASE SUMMARY A 56-year-old Chinese lady presented with fever and cholestatic liver injury two weeks after initiation of escitalopram for the treatment of psychotic depression.Physical examination was unremarkable. Further investigations, including a computed tomography scan of the abdomen and pelvis and tests for hepatitis A,B and C and for autoimmune liver disease were unyielding. Hence, a diagnosis of escitalopram-induced liver injury was made. Upon stopping escitalopram, repeat liver function tests showed downtrending liver enzymes with eventual normalization of serum aspartate aminotransferase and alanine aminotransferase one-week post-discharge.CONCLUSION Clinicians should be aware of the possibility of escitalopram-induced liver injury when initiating depressed patients on antidepressant treatment. This requires extra vigilance as most patients may remain asymptomatic. Measurement of liver function tests could be considered after initiation of antidepressant treatment,especially in patients with pre-existing liver disease.     

自身免疫性肝炎后肝硬化合并原发性免疫性血小板减少1例报告

自身免疫性肝炎(AIH)是一种由针对肝细胞自身免疫反应所介导的肝脏实质炎症[1]。AIH常合并其他器官或系统性自身免疫性疾病如:桥本氏甲状腺炎(10%~23%)、糖尿病(7%~9%)、炎症性肠病(2%~8%)、类风湿性关节炎(2%~5%)、干燥综合征(1%~4%)、银屑病(3%)和系统性红斑狼疮(1%~2%)等[2]。而合并原发性免疫性血小板减少(primary immune thrombocytopenia,IPT)者少见,国内外均罕见报道。     

Early intervention of acute liver injury related to venlafaxine: A case report

Rationale:Drug-induced liver injury (DILI) is the leading cause of acute liver injury (ALI), market withdrawal of a drug, and rejection of applications for marketing licenses. The incidence of DILI is very low, with a value between 1 and 19 per 100,000 patient years. All antidepressants may induce DILI even at low therapeutic doses. In this report, we present a case of ALI after venlafaxine administration.Patient concerns:A 27-year-old Chinese Han woman was admitted for depression. Several serum liver function indices in this patient were abnormal after antidepressant treatment. The Roussel Uclaf Causality Assessment Method (RUCAM) causality assessment score was 8, and the R value was 31.18.Diagnoses:The patient was diagnosed with hepatocellular ALI, which was derived from venlafaxine-related adverse events.Interventions:First, all medications were stopped to block the progression of DILI. Then, a hepatoprotective strategy and proper psychological treatment were performed to recover the impaired hepatic function.Outcomes:Liver function was fully recovered as indicated by liver function indices and ultrasound imaging.Lessons:The possibility of DILI should not be overlooked during the long-term use of antipsychotic drugs. In response, regular liver function monitoring should be performed in a timely manner to avoid missing diagnoses and delayed treatment. Furthermore, the necessary medical treatment needs to be conducted after the occurrence of ALI.     

秋水仙碱致伴有自身免疫现象的药物性肝损伤1例报告

秋水仙碱是一种生物碱,能抑制中性粒细胞的趋化、黏附和吞噬作用及抑制局部细胞产生白介素-6等,可控制关节局部的疼痛、肿胀及炎症反应。临床中广泛应用于痛风性关节炎的治疗,主要通过肝肾代谢。常见的不良反应多表现为胃肠道反应,骨髓抑制等,常规剂量情况下引起严重的药物性肝损伤（DILI）较少见。本例患者因常规剂量口服秋水仙碱片4 d后,     

甲亢重症肝损害报告1例

1病例资料 患者,女,49岁,因间断发热、皮肤巩膜黄染半个月入院。患者入院前半个月无明显诱因出现发热,未测体温,自服维C银翘片（1片/次,3次/d）1.5 d后退热。随后出现皮肤巩膜黄染,伴有乏力、厌食、恶心,无腹痛,无陶土样大便,     

Kratom induced severe cholestatic liver injury histologically mimicking primary biliary cholangitis: A case report

BACKGROUND Kratom is a psychoactive substance that is isolated from the plant Mitragyna speciosa. The leaves can be chewed fresh or dried, smoked, or infused similar to herbal teas. The plant leaves have been used by natives of Southeast Asia for centuries. The substance has been used for its stimulant activity at low doses, and as an opium substitute at higher doses due to a morphine like effect.CASE SUMMARY A 37-year-old female with a history of depression and obesity(body mass index: 32) presented to emergency room with a week-long history of nausea, decreased appetite, fatigue, and two days of jaundice. On admission bilirubin was markedly elevated. Her condition was thought to be due to consumption of Kratom 2 wk before onset of symptoms. Liver biopsy showed changes mimicking primary biliary cholangitis. Patient's symptoms and jaundice improved quickly.CONCLUSION The use of Kratom has been on the rise in recent years across the United States and Europe. Several case reports have associated adverse health impact ofKratom-containing products including death due to its ability to alter levels of consciousness. Only a few case reports have highlighted the hepatotoxic effects of Kratom. Even fewer reports exist describing the detailed histopathological changes.