Correlation of serum IgE levels with severity of acute pulmonary thromboembolism

We aimed to investigate whether there is a direct correlation of serum IgE concentration with severity of acute pulmonary thromboembolism (PTE). DESIGN: Prospective study. SETTINGS: University medical center. Forty-six patients (27 female, 19 male) who were diagnosed as acute PTE in our clinic between 01 October 2000 and 30 November 2001 comprised the study group. Mean age was 55 (range was 20-82). The study group was divided into three groups according to severity of PTE: Group A, submassive PTE without pulmonary infarction (20 patients); group B, submassive PTE with pulmonary infarction (15 patients); and group C, massive PTE (11 patients). Serum IgE concentrations were measured by ELISA method at 1st, 5th, 15th, 30th, 60th, 90th days, and 120th days, if needed, after the diagnosis. Statistical analysis was made by Post hoc Tukey test. First day serum IgE levels were highest in group B (mean 507.7) followed by group C (mean 324.2), and were lowest in group A (mean 117.2). The differences between group B and group C, between group B and group A, and also between group C and A were all statistically significant (p< 0.5, p< 0.0001, p< 0.015, respectively). 5th day and 15th day results showed statistically significant differences between group B and A, and between group C and A (at 5th day: p<0.0001, p< 0.015 respectively, and at 15th day: p< 0.0001, p< 0.012 respectively). At 30th, 60th, and 90th days of diagnosis serum IgE concentrations were higher in group B than in group A which were statistically significant (p< 0.0001, p< 0.0001, p< 0.019 respectively). Patients with submassive PTE and pulmonary infarction had the highest serum IgE concentrations and the longest duration of high levels of IgE.     

Sequence analysis of rpoB mutations in rifampin-resistant clinical Mycobacterium tuberculosis isolates from Turkey

Drug-resistant tuberculosis is a serious problem throughout the world. Resistance to Rifampicin (RIF) is mainly caused by the mutations in the rpoB gene coding the beta-subunit of RNA polymerase. In this study, we aimed to detect the distribution of rpoB gene mutations in 80 RIF-resistant clinical Mycobacterium tuberculosis (MTB) isolates from Turkey. The rpoB gene was amplified by PCR and mutations leading to RIF resistance were determined by automated sequence analysis. A total of 72 of the 80 isolates (90%) were found to carry mutations in the amplified region, whereas eight isolates (10%) carried no mutations. Overall, 24 different missense mutations affecting 14 codons, and two deletion mutants were identified. Nine new mutations, six in the hot-spot region and three outside this region, were found. The codon numbers of the most frequently encountered mutations were 531 (51.4%), 526 (18.1%), 516 (13.9%), and 513 (12.5%). As a result, 90% of the RIF-resistant MTB isolates from the Turkish patients were found to carry a mutation in the rpoB gene, Ser531Leu being the most frequent one. Although molecular methods identify mutations leading to RIF resistance very quickly, results of the antimycobacterial susceptibility tests must be taken into consideration for the patients carrying no mutations in this region.     

Human Mast Cell Apoptosis Is Regulated Through Bcl-2 and Bcl-XL

It is well established that human mast cell proliferation and maturation are regulated by kit ligand (stem cell factor). Little is known, however, about how these two processes are negatively regulated and thus, how mast cell number is controlled in normal and pathologic conditions. We therefore first hypothesized that SCF-dependent human mast cells would undergo programmed cell death (apoptosis) on removal of SCF as has been shown for growth factor-dependent rodent mast cells. We then examined whether SCF acts as a survival factor through the regulation of the bcl-2 family of apoptosis-regulatory genes. As hypothesized, elimination of SCF from primary peripheral blood-derived human mast cell cultures resulted in a significant apoptotic process. During apoptosis, down-regulation of the two apoptosis-regulatory proteins Bcl-2 and Bcl-X_Lwas observed. Moreover, a deregulated expression of these two proteins was found in two human mast cell lines which are SCF-independent. Thus, SCF functions as a survival factor by repressing apoptosis of human mast cells through Bcl-2 and Bcl-X_L. Deregulated expression of these antiapoptotic proteins may contribute to proliferation and accumulation of mast cells in certain forms of systemic mast cell disorders.     

Diagnostic and prognostic value of Ischemia‐modified albumin in patients with Crimean‐Congo hemorrhagic fever

The aim of this study was to determine the diagnostic and prognostic significance of ischemia modified albumin (IMA) levels in patients with Crimean‐Congo hemorrhagic fever (CCHF). This retrospective study was conducted with patients with CCHF. IMA levels in patients with CCHF were determined using the rapid colorimetric method. IMA levels of CCHF patients were significantly higher compared with the control group (P = 0.0001). At an IMA cut‐off point of 0.555 ABSU (absorbance units), sensitivity was 65.1%, specificity 82.5%, positive predictive values (PPV) 82.5%, and negative predictive values (NPV) 65.1%. IMA levels of patients with hemorrhage were significantly higher compared with patients without hemorrhage (P = 0.005). IMA has been validated as both a new and sensitive ischemia and oxidative stress biomarker. In addition to its diagnostic significance, IMA investigated in CCHF patients at time of arrival may be an important marker with its prognostic role in determining in the early stage whether the disease will follow a hemorrhagic course. J. Med. Virol. 85:684–688, 2013. © 2013 Wiley Periodicals, Inc.     

Early port-site metastasis during neoadjuvant chemotherapy in advanced stage ovarian cancer: report of two cases

Port-site metastases in gynecological malignancies subsequent to laparoscopy have been reported with an incidence of 1.1-16%. These metastases tend to be disappearing after primary debulking surgery and subsequent primary chemotherapy. Local resection, chemotherapy and/or radiotherapy have been defined in the management of these metastases with enhanced clinical success. However, in extremely rare cases these metastases were also defined very early during neoadjuvant chemotherapy. Herein, we present two ovarian cancer cases which are clinically diagnosed with port site metastasis during neoadjuvant chemotherapy following diagnostic laparoscopy. Although neoadjuvant chemotherapy is sometimes needed in cases of fully advanced ovarian cancers, port-site metastasis may be encountered during neoadjuvant chemotherapy. The possible poor prognosis of these patients, especially those who have ascites, should make us careful in performing diagnostic laparoscopy with preventive measures for port-site metastasis and to start the chemotherapy immediately.