结核病

经纤维支气管镜滴药治疗空洞型肺结核并存糖尿病效果观察，活动性肺结核并发哮喘患吸入糖皮质激素疗效及副作用观察，全程间歇短程板式组合药物治疗初治涂片阳性肺结核的疗效分析，老年肺结核影像特点（附58例分析），耐多药肺结核患机体免疫状况及其治疗研究，对肺结核可疑采用症状查痰法提高患发现率，     

免疫功能低下患者肺结核的影像诊断

目的探讨几种免疫功能低下疾病并发肺结核患者的X线和CT所见。包括糖尿病、肾病综合症、系统性红斑狼疮（SLE）和获得性免疫缺陷综合症（AIDS）合并肺结核。方法回顾分析合并肺结核糖尿病患者68例，肾病综合症患者20例．SLE患者12例，AIDS患者8例X线及胸部CT所见。结果X线和CT表现，糖尿病合并肺结核：大片浸润病灶45例．浸润病灶内多发空洞40例，散在大小不等浸润病灶可不按肺段分布23例，支气管播散病灶21例；部分病例合并胸水10例。肾病综合症或SLE：急性血行播散性肺结核15例，大小不等浸润病灶17例，合并肺门及纵膈淋巴结肿大4例；AIDS合并肺结核；肺内斑片阴影合并有淋巴结肿大5例，急性血行播散性肺结核合并有淋巴结肿大3例。结论免疫功能低下疾病并发肺结核时，肺内结核病灶容易形成大片干酪病灶并合并空洞，结核肺内播散，急性血行播散性肺结核，肺门及纵膈淋巴结肿大及非结核好发部位发生浸润结核灶。     

结核病

肺结核合并肺癌临床分析——刘晓红等（北京北京胸科医院内科100095）：《北京医学》，2006，28（2）：81．83【目的：分析肺结核合并肺癌的临床特征与影像学特点，提高肺结核合并肺癌的诊断率。方法：回顾性分析l18例肺结核合并肺癌患的临床特征和影像学表现，并与同期单纯肺癌96例、单纯肺结核120例进行对照分析。结果：肺结核合并肺癌组胸痛、呼吸困难少于单纯肺癌组，乏力、盗汗多于单纯肺癌组；与单纯肺结核组比较发热少于单纯肺结核组，刺激性咳嗽、持续性胸痛和血性胸水多于单纯肺结核组，有显性差异（P〈0．01）。影像上肺结核合并肺癌组斑片索条影、钙化影多于单纯肺癌组；团块影伴分叶、毛刺、小泡征并肺不张多于单纯肺结核组，小结节影，空洞、空腔影少于单纯肺结核组，有显性差异（P〈0．01）。结论：临床医师在关注肺结核患时，应警惕并发恶性变的可能，并尽早进行多种检查，以提高肺结核合并肺癌的诊断率。】     

肺结核合并呼吸衰竭54例临床分析

目的：探讨肺结核合并呼吸衰竭的发病机制及治疗对策。方法：回顾分析54例肺结核合并呼吸衰竭。结果：54例合并肺部感染40例（74.1％）。I型呼衰35例（64.8％），Ⅱ型呼衰19例（35.2％）。结论：呼吸衰竭是肺结核严重的并发症，需加强营养支持、基础疾病治疗和免疫治疗。     

肺结核患者免疫状态与菌群交替的关系

以免疫功能低下为特征的肺结核患者经试验证明，免疫球蛋白（除ＩｇＡ）Ｅ－ＲＦＣ％，ＬＴＴ％，均明显低于正常人，肺结核患者真菌及细菌合并感染率为３１．７％，证实了以细胞免疫功能低下为特征的肺结核患者易引起细菌和真菌交替感染。     

免疫功能低下疾病患者肺结核的影像分析

目的探讨几种免疫功能低下疾病的肺结核患者的x线和CT所见。方法回顾分析糖尿病患者68例，肾病综合症患者20例，SLE患者12例，8例AIDS患者合并肺结核的x线及胸部cT所见。结果x线和CT表现，糖尿病肺结核：大片浸润病灶45例，浸润病灶内多发空洞40例，散在大小不等浸润病灶可不按肺段分布23例，支气管播散病灶21例；部分病例合并胸水10例。肾病综合症或SLE肺结核：急性血行播散性肺结核15例，大小不等漫润病灶17例，合并肺门及纵膈淋巴结肿大4例；AIDS肺结核：肺内斑片阴影合并有淋巴结肿大5例，急性血行播散性肺结核合并有淋巴结肿大3例。结论免疫功能低下疾病患者的肺结核，肺内结核病灶容易形成大片干酪病灶并合并空洞，结核肺内播散，急性血行播散性肺结核。肺门及纵膈淋巴结肿大及非结核好发部位发生浸润结核灶。     

糖皮质激素吸入治疗支气管哮喘合并肺结核的安全性探讨

支气管哮喘（简称哮喘）及肺结核都是和免疫功能密切相关的疾病.长期全身应用糖皮质激素（激素）在使哮喘患者获益的同时,可导致机体免疫功能下降,促使肺结核复发或恶化.目前已有报道以吸入激素治疗合并痊愈肺结核的哮喘患者,认为是安全的.Bahceciler等采用激素长期吸入治疗结核菌素试验阳性而无结核活动的哮喘儿童,未发现肺结核的发生.本试验旨在观察合并活动性肺结核的哮喘患者在抗结核治疗期间及疗程结束后,长期吸入激素对肺结核的安全性,现总结如下.     

76例老年肺结核合并糖尿病临床分析

随着人口老龄化,老年人因免疫功能低下,患糖尿病合并肺结核有逐年上升趋势;且并发症多,在治疗肺结核的同时如何治疗糖尿病,是临床医师关注的问题。     

2型糖尿病合并肺结核患者感染新型冠状病毒病例报告

<正>2型糖尿病（type 2diabetes mellitus,T2DM）患者由于免疫功能低下，增加了其罹患肺结核（pulmonary tuberculosis,PTB）的风险，并且与不良治疗结局密切相关。在2型糖尿病合并肺结核（T2DM-PTB）的患者中，合并新型冠状病毒肺炎（简称“新冠肺炎”）的病例很少报告。为此，笔者报道1例成年T2DM-PTB合并重型新冠肺炎患者的临床表现及实验室检查结果，以为临床治疗提供参考。     

93 例老年结核病的临床分析简

目的 探讨老年结核病的临床特点及防治策略.方法对93例确诊老年结核病患者与同期住院的中青年患者进行分析.结果 老年结核病患者中肺结核或肺结核合并胸膜炎发病率较高;其中开放性肺结核16例（17.2%）,初治菌阳14例（15.1%）,复治菌阳2例（2.1%）;肺结核合并其他疾病患者58例（62.4%）;免疫功能低下19例（20.4%）.结论 老年结核病早期诊断及免疫增强剂联合个体化抗结核治疗、同时积极合发症对治愈老年结核患者,控制结核病的蔓延有一定的临床意义.     

Pulmonary tuberculosis in the compromised host--report of the 30th B series of controlled trials of chemotherapy--Cooperative Study Unit of Chemotherapy of Tuberculosis of the National Sanatoria in Japan

The 445 cases of pulmonary tuberculosis in compromised host were investigated. Summary of the analysed results were as follows; (1) The major underlying diseases of compromised hosts with tuberculosis were diabetes mellitus and various types of cancer. (2) The major risk factors for advancement of tuberculosis were malnutrition and iatrogenic suppressions due to long term use of corticosteroids and anticancer agents. (3) The patients with malnutrition in the compromised hosts showed poor prognosis. (4) The chest roentgenogram of tuberculous lesion was difficult to improve in these patients when their clinical stage of tuberculosis had been advanced at admission. (5) The diagnosis and management of pulmonary tuberculosis in compromised host remain as a serious problem in recent years.     

免疫抑制患者并发肺结核临床观察

目的加强对免疫抑制患者并发肺结核的认识,并探讨预防性抗痨的作用。方法对24例免疫抑制患者并发肺结核的临床特点、胸部X线、结核菌素试验、诊断、治疗等进行临床观察。结果24例患者临床表现、胸部X线均不典型,结核菌素试验多为阴性。抗痨治疗16例,好转12例(75.0%),迁延不愈2例(12.5%),死亡2例(12.5%),其中1例死于原发病。结论免疫抑制可导致结核病发病。可以在部分免疫抑制患者中进行预防性抗痨。     

Defective interleukin-2 production and interleukin-2 receptor expression in pulmonary tuberculosis

The evolution of Mycobacterium tuberculosis as an intracellular pathogen has led to a complex relationship between it and its host, the human mononuclear phagocyte. The products of M. tuberculosis-specific T lymphocytes are essential for macrophage activation for intracellular mycobacterial killing. However, dysfunction cell-mediated immune response to infection with M. tuberculosis may contribute to progressive primary infection or reactivation of endogenous foci of mycobacteria. Th1 cells produce IL-2, which is essential for proper cellular immunity. The aim of this study was to identify the variation in IL-2 activity and soluble IL-2 receptor (IL-2 R) in peripheral blood lymphocyte in patients suffering with pulmonary tuberculosis. A significant decrease in IL-2 and IL-2 receptor level was observed in patients with pulmonary tuberculosis when compared to normal controls. Our results suggested that patients with pulmonary tuberculosis had a defect in IL-2 production. Better understanding of these interactions will allow the development of increasingly specific immune-based interventions for prevention and treatment of tuberculosis.     

Detection of serum antibody against lipoarabinomannan-B in Mycobacterium tuberculosis (H37Ra)

The serum antibody to lipoarabinomannan-B(LAM-B) purified from mycobacterium tuberculosis (H37Ra) was tested by ELISA in 250 sera, including sera from patients as follows: tuberculosis 96, tubercular pleurisy 11, renal tuberculosis 2, bone and joint tuberculosis 33, tubercular meningitis 16, pulmonary cancer 22, leprosy 20 and normal subjects 50. The positive rate of pulmonary tuberculosis is 69.8%, which is of a similar extent in sera from patients with tuberculosis of miscellaneous organs to be tested except tubercular meningitis, in which only 18.8% positive rate was observed, indicating the blockage of antibody releasing from pathologic foci into blood stream by blood-brain barrier. The positive rates of leprosy and normal subjects are 50.0% and 2.0% respectively. No antibody was found among 22 patients with pulmonary cancer. It is suggested that the existence of an active tubercular lesion in the host might be the basic prerequisite for a positive LAM-B antibody detection. Although LAM-B is a common antigen of both mycobacterium tuberculosis and mycobacterium leprae, the low prevalence of leprosy in China makes little influence of the practicability of using this ELISA in epidemiological study and in clinic as a adjutant tool for tuberculosis diagnosis and differential diagnosis.     

An overwhelming pulmonary fungus ball in a systemic lupus erythematosus patient

Impaired host immunity has been regarded as a predisposing factor in post-primary tuberculosis in adults. Patients with systemic lupus erythematosus (SLE) are usually exposed to high doses of corticosteroids and eventually develop defective cellular immunity that increases the risk for active tuberculosis. SLE-associated pulmonary tuberculosis tends to have a higher incidence of miliary, far-advanced pulmonary disease and therefore establishing the diagnosis can easily be delayed due to generalized, non-specific clinical symptoms such as fever, malaise and weight loss which are also commonly observed in lupus patients. However, cavitary tuberculosis is very rare in patients with SLE. To the best of our knowledge, fungus ball formation in the tuberculosis cavity in a patient with SLE, has not been previously reported. Thus, we present a case of SLE who was found to have a fungus ball within a preexisting tuberculosis cavity. The diagnosis was resolved by computerized tomography of the chest and was confirmed with histopathological examination.     

Effects of HIV co-infection and chemotherapy on the urinary levels of nitric oxide metabolites in patients with pulmonary tuberculosis.

The presence of nitric oxide (NO) and its role as a factor in host defence against intracellular pathogens in human macrophages is controversial. We measured the metabolites of NO (nitrite (NO2-) and nitrate (NO3-)) in urine from Ethiopian patients suffering from tuberculosis. The urinary level of NO2-/NO3- in a group of healthy Ethiopians was 1020+/-471 microM (n = 22). Untreated HIV negative patients with active pulmonary tuberculosis (1574+/-588 microM, p<0.01, n = 12) and household contacts to tuberculosis patients (1949+/-812 microM, p = 0.006, n = 7) had significantly higher levels of urinary NO2-/NO3- than the control group. Untreated HIV positive patients with pulmonary tuberculosis did not have increased levels of urinary NO2-/NO3- (1101+/-614 microM, n = 6). Some of the HIV negative untreated patients with pulmonary tuberculosis (1710+/-519 microM, n = 6) were followed up after treatment and showed a reduction in the levels of urinary NO2-/NO3- 1 week after treatment (945+/-599 microM, p<0.05). We conclude that HIV negative patients with active pulmonary tuberculosis have increased urinary levels of nitric oxide metabolites with a reduction following specific anti-tuberculous chemotherapy.     

Coinfection with Cryptococcus gattii and Mycobacterium tuberculosis in an otherwise healthy 18-year-old woman

A case of Cryptococcus gattii (pulmonary and central nervous system) and Mycobacterium tuberculosis (pulmonary) coinfection in an otherwise healthy young woman is reported. The patient presented with a two-month history of dry cough. She had an unremarkable medical history. Both tuberculosis and cryptococcosis were diagnosed following bronchoscopy, and a subsequent lumbar puncture revealed C gattii in the cerebrospinal fluid. There is evidence that both M tuberculosis and C gattii may have suppressive effects on the host immune system. This suggests a mechanism by which an otherwise healthy individual developed these two infections.     

Microarray analysis of gene expression associated with extrapulmonary dissemination of tuberculosis

OBJECTIVE: Although extrapulmonary organs are involved in 20% of patients with tuberculosis, the host genetic factors associated with the extrapulmonary dissemination of tuberculosis are not yet known. The aim of this study was to identify the host genetic factors associated with the extrapulmonary dissemination of tuberculosis by comparing gene expression profiles of patients who had recovered from extrapulmonary tuberculosis and those who had recovered from pulmonary tuberculosis. METHODS: Five patients from each group were enrolled. Total RNA was extracted from peripheral blood mononuclear cells that had been incubated for 48 h with whole lysate of Mycobacterium tuberculosis (H37Rv, 0.5 microg/mL). Gene expression profiles were acquired using the GeneChip array and its applied systems. Gene expression profiles from five patients with previous extrapulmonary tuberculosis and one pooled control sample from five patients with previous pulmonary tuberculosis were analysed and compared. Genes that were expressed concordantly in more than 80% of arrays and that showed more than twofold changes in at least one array among samples from patients who had recovered from extrapulmonary tuberculosis were identified. RESULTS: Compared with the control sample, the expression of 16 genes, including those for tumour necrosis factor (TNF)-alpha and cathepsin W, was increased, and the expression of 45 genes including that for TNF-receptor superfamily member 7 (TNFRSF7), was decreased in the extrapulmonary tuberculosis patients. The altered expression of the TNF-alpha, cathepsin W and TNFRSF7 genes was confirmed by quantitative RT-PCR. CONCLUSIONS: Altered expression of the genes for TNF-alpha, cathepsin W and TNFRSF7 may be risk factors for the extrapulmonary dissemination of tuberculosis in humans.     

Invasive pulmonary aspergillosis

BACKGROUND: Invasive pulmonary aspergillosis usually occurs in immunocompromised patients. Mild abnormality of host defence is usually present in the chronic necrotising form of the disease. Acute aspergillus pneumonia usually affects patients who are seriously immunocompromised. OBJECTIVES: The purpose of the study was to highlight the possibility of occurrence of invasive pulmonary aspergillosis also in patients with mild abnormality of host defence. METHODS: In a retrospective study 6 patients were analysed. The inclusion criterion was evidence of Aspergillus sp. invasion in lung tissue. Lung tissue was obtained by biopsy or post mortem examination. RESULTS: There were 4 patients with acute aspergillus pneumonia. Two of them were severely immunocompromised - one with dermatomyositis, who was treated with high doses of corticosteroids and methotrexate, and the other with undiscovered miliary tuberculosis, who was treated for myelodysplastic syndrome instead with low doses of corticosteroids. The other 2 had mild immunosuppression: one was suffering from sarcoidosis and was treated with low doses of corticosteroids, the other had dilated cardiomyopathy, renal insufficiency and diabetes mellitus. The two patients with chronic necrotising pulmonary aspergillosis had mild abnormality of host defence: one had reactivation of tuberculosis and diabetes mellitus, the other had inactive tuberculosis and aspergilloma. CONCLUSIONS: Invasive pulmonary aspergillosis must be considered also in patients with mild immunosuppression and pulmonary infiltrates which do not respond to conventional treatment with antibiotic chemotherapy. The key to the diagnosis of invasive pulmonary aspergillosis is the histopathological demonstration of fungal invasion in lung tissue.     

Interleukin-1 signaling is essential for host defense during murine pulmonary tuberculosis

Interleukin (IL)-1 signaling is required for the containment of infections with intracellular microorganisms, such as Listeria monocytogenes and Leishmania major. To determine the role of IL-1 in the host response to tuberculosis, we infected IL-1 type I receptor-deficient (IL-1R(-/-)) mice, in which IL-1 does not exert effects, with Mycobacterium tuberculosis. IL-1R(-/-) mice were more susceptible to pulmonary tuberculosis, as reflected by an increased mortality and an enhanced mycobacterial outgrowth in lungs and distant organs, which was associated with defective granuloma formation, containing fewer macrophages and fewer lymphocytes, whereas granulocytes were abundant. Lymphocytes were predominantly confined to perivascular areas, suggesting a defective migration of cells into inflamed tissue in the absence of IL-1 signaling. Impaired host defense in IL-1R(-/-) mice was further characterized by a decrease in the ability of splenocytes to produce interferon-gamma. Analysis of these data suggests that IL-1 plays an important role in the immune response to M. tuberculosis.