Efficacy and Safety of Belimumab Plus Standard Therapy in Patients With Systemic Lupus Erythematosus: A Meta-analysis.

PURPOSE: The treatment of belimumab plus standard therapy in patients with systemic lupus erythematosus (SLE) has been studied extensively in recent years. Our aim was to estimate the efficacy and safety of this therapy compared with placebo plus standard therapy in patients with SLE. METHODS: PubMed, Web of Science, Embase, Chinese Biomedical Literature Database (CBM, Chinese), and Wanfang Database (Chinese) were searched for all randomized clinical trials that mainly studied the efficacy and safety of belimumab plus standard therapy before June 2015. We extracted or calculated the rate of the SLE Response Index and adverse event rate at 52 weeks in all the included studies. The odds ratio (OR) with 95% CI between the 2 groups in this meta-analysis was conducted by using a random-effects model. Sensitivity and publication bias analyses were also performed. All statistical tests were performed by using Stata software version 12.0 (StataCorp., College Station, Texas). FINDINGS: In the overall samples (4 studies, N = 4692 ), a significantly higher SLE Response Index rate at 52 weeks was found in belimumab plus standard therapy group compared with the placebo plus standard therapy group in all studies (OR = 1.49; 95% CI, 1.26-1.77 ; P < 0.001 ). When assessed with the incidence of serious adverse events, the data revealed that there was no significant difference between the 2 groups, with pooled OR = 1.08; 95% CI, 0.83-1.39; P = 0.573; OR = 1.23; 95% CI, 1.02-1.48; P = 0.029; and OR = 1.07; 95% CI, 0.88-1.29; P = 0.506. IMPLICATIONS: The results suggest that treatment with belimumab plus standard therapy is more effective than placebo plus standard therapy in SLE patients, which represents major progress in the treatment of SLE. Regardless of the statistical analyses, further research is necessary to optimize treatment effects.

Surgical strategy for tubercular abscess in the chest wall: experience of 120 cases.

OBJECTIVES: We aim to optimize surgical strategy to decrease relapse of tubercular abscess in the chest wall (TACW). METHODS: The records of 120 patients who underwent surgical treatment for TACW from May 2005 to March 2011 were retrospectively reviewed. We conducted the following surgical treatment as '6C + A' by abbreviating the first alphabet of each step: (i) careful exploration of the abscess; (ii) complete resection; (iii) cavity washing using sodium bicarbonate solution; (iv) coverage using muscle flap; (v) continuous suction and drainage; (vi) compression dressing and (vii) anti-tuberculosis medication. RESULTS: One hundred and thirteen cases were discharged for rehabilitation with the first stage wound healing (113/120). Four cases postoperatively suffered from subcutaneous fistula which was healed after dressing changes for 1-2 months. Three patients with an abscess relapse underwent the second operation 2 months after the first operation. Follow-ups ranged from 2 months to 6 years and demonstrated no recurrence. CONCLUSIONS: We deem the surgical procedures '6C + A' effective to obviate relapse of TACW.

Clinical value of assaying tumor supplied group of factor/tumor specific growth factor in patients with solitary pulmonary nodule.

OBJECTIVE: This pilot study was designed to evaluate the clinical value of assaying tumor supplied group of factor/tumor specific growth factor (TSGF) in solitary pulmonary nodule (SPN). PATIENTS AND METHODS: The study was conducted from March 2007 to September 2010 and included 33 patients with SPN and 28 healthy volunteers. TSGF was assayed in preoperative serum, intraoperative pleural lavage fluid (IPLF), and postoperative serum. RESULTS: At operation, 20 patients were diagnosed with malignancy and 13 patients were diagnosed with nonmalignancy and placed in group A and group B, respectively. In group A, pathologic staging demonstrated 8 patients (group A1) with stage T1N0M0, 7 patients (group A2) with stage T1N1M0 and 53 patients (group A) with stage T1N2M0 disease. In group B, 8 patients were diagnosed with tuberculoma (group B1) and 5 patients were diagnosed with inflammatory pseudotumor (group B2). Before operation, levels of TSGF in peripheral blood were significantly higher in group A compared with group B and the control group (98.8 ± 29.9 vs. 62.1 ± 24.9 and 50.1 ± 17.9, Student-Newman-Keuls test; P < .05). The percentage of patients with positive serum TSGF results was significantly higher in group A than in group B or the control group (90.0% vs. 30.8% and 17.9%, χ(2) test; P < .05). With respect to the diagnostic value of serum TSGF in malignant SPN, we found sensitivity to be 90%, specificity to be 69.2%, positive forecast rate to be 74.5%, negative forecast rate to be 87.4%, and accurate diagnosed rate to be 79.5%. The TSGF level in IPLF in group A was significantly higher than that in group B (132.2 ± 51.9 vs. 84.6 ± 12.6, Student t test, P < .05). Additionally, TSGF in group A2 and group A3 was significantly higher compared with group A1 (162.2 ± 52.3 and 176.4 ± 17.8 vs. 100.2 ± 35.8, Student-Newman-Keuls test; P < .05). Postoperative serum TSGF in the patients diagnosed with lung cancer decreased significantly after operation. TSGF returned to a normal threshold level (71 U/mL) in the sixth month postoperatively. In addition, there was no appreciable change in the patients in group B. CONCLUSION: Serum TSGF is conducive to discriminating between benign and malignant features of SPN. Additionally, investigation of IPLF TSGF can potentially offer a new approach to predict the existence of lymph node metastases.

Breast cancer anti-estrogen resistance protein 1 (BCAR1/p130cas) in pulmonary disease tissue and serum.

OBJECTIVE: The purpose of the study was to evaluate clinical presentation of breast cancer anti-estrogen resistance protein 1 (BCAR1, also known as p130cas) expression in pulmonary diseases, and to assess its potential as a molecular marker for diagnosis and prognosis. METHODS: Between March 2008 and August 2010, we enrolled a total of 80 patients (group A) with non-small-cell lung cancer (NSCLC), 48 patients (group B) with pulmonary tuberculosis (including 27 cases of tuberculoma and 21 cases of cavitary pulmonary tuberculosis), and 32 patients (group C) with other benign pulmonary mass (hamartoma in 15 cases, inflammatory pseudotumor in 10 cases, fibroid tumor in 7 cases). Additionally, 160 healthy age- and sex-matched volunteers were recruited as healthy controls. Tissue BCAR1 expression was investigated by using tissue microarray and immunohistochemistry. BCAR1 and tumor markers (carcinoma embryonic antigen [CEA] and the cancer antigens CA19-9 and CA125) in serum were assayed by using ELISA and immunoradiometrics, respectively. RESULTS: BCAR1 expression was detected (either in the nucleus, the cytoplasm, or both) in tumor cells in 79 of the 80 NSCLC cases in group A, and in fibroblasts in 41 of the 48 pulmonary tuberculosis cases in group B. However, it was not detected in the normal adjacent tissue in 70 of the 80 cases in group A and in 47 of the 48 cases in group B. In group C, BCAR1 expression was negative in all 32 cases. Additionally, we investigated adjacent tissue with acute or chronic inflammation in 20 cases from group C, and found no expression of BCAR1. Serum BCAR1 levels were significantly higher in patients with NSCLC than in the control group, increased gradually with the progression of tumor staging, and decreased after removal of the tumors. The levels were significantly lower in bronchioloalveolar carcinoma than in other subtypes of carcinoma (Mann-Whitney U test, Z = -5.089; p < 0.001). Serum BCAR1 levels were significantly higher in patients with pulmonary tuberculosis than in the control group, were positively and significantly correlated with the diameter of the tuberculosis lesion (Spearman's rho, correlation coefficient 0.753; p < 0.001), and decreased after removal of the tuberculosis lesions. The levels were significantly higher in patients with cavitary pulmonary tuberculosis than in those with tuberculoma (517.6 ± 326.5 vs 282.2 ± 137.6; Student's t-test, t = -3.387; p = 0.001). In group C, there was no appreciable difference in serum BCAR1 levels compared with the matched controls (222.8 ± 111.0 vs 201.6 ± 35.7; Dunnett's T3 test, p = 0.993). The discrimination power of combining BCAR1 and tumor markers in NSCLC versus benign lung diseases was higher than that of sole use of BCAR1 as a marker (maximal sum of sensitivity and specificity: 1.538 vs 1.237). CONCLUSION: We conclude that a combined assay of serum BCAR1 and traditional tumor markers is potentially applicable for distinguishing NSCLC from benign lung diseases. However, the clinical utility of serum BCAR1 as a molecular marker for prognosis in NSCLC or pulmonary tuberculosis requires further clarification and verification.