血源播散性肺结核继发噬血细胞综合征1例

Hemophagocytic lymphohistiocytosis (HLH) was a life-threatening syndrome due to the uncontrolled immune activation of cytotoxic T lymphocytes, natural killer (NK) cells, and macrophages. HLH is characterized by primary and secondary causes, the early diagnosis and treatment of patients are closely related to the prognosis and clinical outcome of patients. The clinical presentation is variable but mostly includes prolonged fever, splenomegaly, coagulopathy, hypertriglyceridemia, and hemophagocytosis, none of them is specific and particular for HLH. Tuberculosis (TB) infection is one of the causes of HLH. HLH caused by TB is very rare clinically, but it has a high mortality. For patients with fever of unknown origin, HLH-related clinical manifestations sometimes present before the final diagnosis of TB, and HLH is associated with the most significant mortality rate. This article is mainly about a 28-year-old patient with HLH who suffered from severe TB infection. The patient attended a hospital with a history of 2 months of prolonged fever, 10 days booger and subcutaneous hemorrhage in lower limbs. Before this, he was in good health and denied any history of tuberculosis exposure. Combined with relevant laboratory test results (such as splenomegaly, hemoglobin, platelet count, and hypertriglyceridemia) and clinical manifestations (e.g. fever), the patient was diagnosed with hemophagocytic lymphohistiocytosis, but the etiology of HLH remained to be determined. To confirm the etiology, the patient was asked about the relevant medical history (intermittent low back pain) and was performed chest CT scan, bone marrow biopsy, and fundus photography. Finally, he was diagnosed with hemophagocytic lymphohistiocytosis caused by hematogenous disseminated pulmonary tuberculosis. In response to this, intravenous methylprednisolone and anti-tuberculosis treatment (isoniazid, pyrazinamide, moxifloxacin, and amikacin) were administered to the patient. After more than a month of treatment, the patient recovered from HLH caused by severe TB infection. Therefore, this case suggests that we should be vigilant to the patient who admitted to the hospital with fever for unknown reasons, to diagnose HLH as early as possible and clarify its cause, then perform interventions and treatment, especially HLH secondary to tuberculosis. Also, cases of atypical TB and severe TB should be carefully monitored to achieve early diagnosis and early intervention.     

基于刺突蛋白靶点的抗新型冠状病毒药物研究进展

重症急性呼吸综合征冠状病毒2(SARS-CoV-2)引起的新型冠状病毒肺炎(COVID-19)目前仍在不断蔓延,但针对该病毒的特效治疗药物尚在研发当中。本文基于冠状病毒生物学特点和病毒复制过程中的关键蛋白——刺突蛋白,介绍了相关药物作用位点及研究进展,为抗SARS-CoV-2药物的临床应用提供信息依据,为治疗COVID-19药物研发提供思路。     

肾移植术后感染新型冠状病毒1例

The novel coronavirus is a newly discovered pathogen in late December 2019, and its source is currently unknown, which can lead to asymptomatic infection, new coronavirus pneumonia or serious complications, such as acute respiratory failure. Corona virus disease 2019 (COVID-19) is a new type of respiratory disease that is currently spreading all over the world and caused by this coronavirus. Its common symptoms are highly similar to those of other viruses, such as fever, cough and dyspnea. There is currently no vaccine or treatment for COVID-19. Everyone is susceptible to infection with this disease, and owing to the long-term use of immunosuppressants, the immunity of kidney transplant recipients is suppressed, and it is more likely to be infected with the disease. At present, its impact on kidney transplant recipients is unclear. This article reports the clinical features and therapeutic course of novel coronavirus infection in a patient after renal transplantation. A 37-year-old female patient who received a kidney transplant 6 months before was diagnosed with novel coronavirus pneumonia. The patient’s symptoms (such as fever, chills, dry cough, muscle aches), laboratory tests (such as decreased white blood cell count, elevated liver enzymes and D-dimer, positive viral nucleic acid test), and chest CT (multiple left lower lung plaque ground glass shadow) were similar to those of non-transplanted novel coronavirus pneumonia patients. In terms of treatment, because the immunity of kidney transplant recipients has been suppressed for a long time, it is a very common strategy to suspend the use of immunosuppressive agents. Therefore, the patient immediately discontinued the immunosuppressive agent after admission, so that she could restore immunity against infection in a short time. At the same time, the use of glucocorticoids was also very important. Its immunosuppressive and anti-inflammatory effects played a large role in the treatment process.In addition, prophylactic antibiotics was needed, and nephrotoxic drugs should be used with caution. Finally, following discounting the use of immunosuppressant and a low-dose glucocorticoid-based treatment regimen, COVID-19 in this renal transplant recipient was successfully cured. The cure of this case was of great significance, and this adjuvant nonspecific antiviral therapy could provide a template for the treatment of other such patients.     

抗C反应蛋白自体抗体在系统性红斑狼疮中的研究进展

系统性红斑狼疮(SLE)是一种可累及多脏器系统的慢性自身免疫性疾病,其发病机制尚不明确。有研究表明,免疫炎症反应和细胞凋亡清除受损是SLE发生发展的关键事件,在此过程中,五聚蛋白家族发挥重要作用。本文总结了抗C反应蛋白自体抗体与SLE疾病的相关性研究进展。     

C反应蛋白在慢性阻塞性肺疾病合并骨质疏松中的研究进展

慢性阻塞性肺疾病(COPD)是一组以持续性气流受限和进行性发展为特征的慢性气道阻塞性疾病.COPD患者常合并一种或多种肺外合并症,骨质疏松是COPD最重要的系统性合并症之一.骨保护素/核因子-κB受体活化因子的配体/核因子-κB受体活化因子(OPG/RANKL/RANK)系统在控制和调节骨形成和骨破坏方面发挥重要作用,是骨质疏松发病机制中的关键通路.C反应蛋白(CRP)是机体受到微生物入侵或组织损伤等炎症性刺激时肝细胞合成的急性期蛋白.CRP是COPD的确定性炎症标志物.CRP在体内存在2种构象:循环天然五聚体CRP(nCRP)和单体CRP(mCRP),不同构象CRP的结构和功能有所不同.本文综述了mCRP通过RANKL调节破骨细胞分化的相关机制研究,以期为将来通过免疫分子途径干预或治疗COPD的合并症骨质疏松提供科学依据.     

肾移植术后感染新型冠状病毒1例

The novel coronavirus is a newly discovered pathogen in late December 2019, and its source is currently unknown, which can lead to asymptomatic infection, new coronavirus pneumonia or serious complications, such as acute respiratory failure. Corona virus disease 2019 (COVID-19) is a new type of respiratory disease that is currently spreading all over the world and caused by this coronavirus. Its common symptoms are highly similar to those of other viruses, such as fever, cough and dyspnea. There is currently no vaccine or treatment for COVID-19. Everyone is susceptible to infection with this disease, and owing to the long-term use of immunosuppressants, the immunity of kidney transplant recipients is suppressed, and it is more likely to be infected with the disease. At present, its impact on kidney transplant recipients is unclear. This article reports the clinical features and therapeutic course of novel coronavirus infection in a patient after renal transplantation. A 37-year-old female patient who received a kidney transplant 6 months before was diagnosed with novel coronavirus pneumonia. The patient’s symptoms (such as fever, chills, dry cough, muscle aches), laboratory tests (such as decreased white blood cell count, elevated liver enzymes and D-dimer, positive viral nucleic acid test), and chest CT (multiple left lower lung plaque ground glass shadow) were similar to those of non-transplanted novel coronavirus pneumonia patients. In terms of treatment, because the immunity of kidney transplant recipients has been suppressed for a long time, it is a very common strategy to suspend the use of immunosuppressive agents. Therefore, the patient immediately discontinued the immunosuppressive agent after admission, so that she could restore immunity against infection in a short time. At the same time, the use of glucocorticoids was also very important. Its immunosuppressive and anti-inflammatory effects played a large role in the treatment process.In addition, prophylactic antibiotics was needed, and nephrotoxic drugs should be used with caution. Finally, following discounting the use of immunosuppressant and a low-dose glucocorticoid-based treatment regimen, COVID-19 in this renal transplant recipient was successfully cured. The cure of this case was of great significance, and this adjuvant nonspecific antiviral therapy could provide a template for the treatment of other such patients.     

长五聚体蛋白3与系统性红斑狼疮的相关性研究概况

系统性红斑狼疮(SLE)是一种可累及多脏器系统的慢性自身免疫性疾病。目前,其发病机制尚不明确。有研究表明,免疫炎症反应和细胞凋亡清除受损是SLE发生发展的关键机制。在此过程中,五聚蛋白家族发挥重要作用。本文就长五聚体蛋白3(PTX3)与SLE疾病的相关性研究作一综述。     

中性粒细胞胞质抗体阴性肉芽肿性多血管炎1例

本文报道1例以肺部多发结节伴空洞为主要特征的老年男性病例。患者为73岁老年男性, 主因"干咳伴气短3个月"入院, 胸部CT示双肺多发不规则团块、结节、斑片影, 伴空洞形成, 同时合并贫血、肾功能不全, 经验性抗感染、抗结核治疗后肺部结节进展、空洞增大。多次检测血ANCA均为阴性。支气管镜下对右肺中叶病变行黏膜活检, 可见小片状坏死、局灶肉芽肿结构形成以及血管炎表现, 弹力纤维染色在坏死灶中可见残存的血管壁结构。临床诊断ANCA阴性肉芽肿性多血管炎, 给予糖皮质激素及环磷酰胺治疗后病灶缩小。