Serum adenosine deaminase enzyme and plasma platelet factor 4 activities in active pulmonary tuberculosis, HIV-seropositive subjects and cancer patients

Tarhan, Gülnur; Gümüşlü, Feyzullah; Yılmaz, Neziha; Saka, Dilek; Ceyhan, İsmail; Cesur, Salih

doi:10.1016/j.jinf.2005.06.009

Cited by 21 publications

(14 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…We also did not find any correlation between ADA values and CD4 cell counts in another cohort of South African HIV infected TB pleuritis patients [25]. This may be due to higher immune activation in HIV positive patients with very low CD4 counts [26]. Furthermore, we did not find any correlation between ADA values and pleural fluid lymphocyte numbers or percentage in agreement with the study by Lee et al [ 27 ] , but in contrast to other studies [12], [28].…”

Section: Discussionsupporting

confidence: 87%

Adenosine Deaminase Activity Is a Sensitive Marker for the Diagnosis of Tuberculous Pleuritis in Patients with Very Low CD4 Counts

et al. 2008

View full text Add to dashboard Cite

BackgroundAdenosine Deaminase Activity (ADA) is a commonly used marker for the diagnosis of tuberculous pleural effusion. There has been concern about its usefulness in immunocompromised patients, especially HIV positive patients with very low CD4 counts. The objective of this study was to evaluate the sensitivity of ADA in pleural fluid in patients with low CD4 counts.Materials and MethodsThis was a retrospective case control study. Medical files of patients with tuberculous pleuritis and non-tuberculous pleuritis were reviewed. Clinical characteristics, CD4 cell counts in blood and biochemical markers in pleural fluid, including ADA were recorded.ResultsOne ninety seven tuberculous pleuritis and 40 non- tuberculous pleuritis patients were evaluated. Using the cut-off value of 30 U/L, the overall sensitivity, specificity, positive likelihood ratio, and negative likelihood ratio of ADA was 94%, 95%, 19, and 0.06 respectively. The mean CD4 cell counts among TB pleuritis patients was 29 and 153 cells/microL in patients with CD4 <50 cells/microL and >50 cells/microL, (p<0.05) respectively. The corresponding mean ADA values for these patients were 76 U/L and 72 U/L respectively (p>0.5). There was no correlation between ADA values and CD4 cell counts (r = −0.120, p = 0.369).ConclusionADA analysis is a sensitive marker of tuberculous pleuritis even in HIV patients with very low CD4 counts in a high TB endemic region. The ADA assay is inexpensive, rapid, and simple to perform and is of great value for the immediate diagnosis of tuberculous pleuritis while waiting for culture result and this has a positive impact on patient outcome.

show abstract

Section: Discussionsupporting

confidence: 87%

Adenosine Deaminase Activity Is a Sensitive Marker for the Diagnosis of Tuberculous Pleuritis in Patients with Very Low CD4 Counts

et al. 2008

View full text Add to dashboard Cite

show abstract

“…Activation of thrombocytopoiesis and platelets in active tuberculosis has been shown by elevated peripheral platelet counts [19], up-regulation of CD62P (unpublished observations), and serum levels of PF4/CXCL4 [20]. As lung endothelial cells constitutively express ICAM-1 and αvβ3 integrins and are prone to tether activated platelets [21], platelets could intimately interact with lung immune cells during M. tuberculosis infection.…”

Section: Discussionmentioning

confidence: 99%

Platelets Direct Monocyte Differentiation Into Epithelioid-Like Multinucleated Giant Foam Cells With Suppressive Capacity Upon Mycobacterial Stimulation

Feng

Dorhoi

Mollenkopf

et al. 2014

The Journal of Infectious Diseases

View full text Add to dashboard Cite

Background. Epithelioid, foam, and multinucleated giant cells (MNGCs) are characteristics of tuberculosis granulomas, yet the precise genesis and functions of these transformed macrophages are unclear. We evaluated the role of platelets as drivers of macrophage transformation in mycobacterial infection.Methods. We employed flow cytometry and microscopy to assess cellular phenotype and phagocytosis. Immune assays allowed quantification of cytokines and chemokines, whereas gene microarray technology was applied to estimate global transcriptome alterations. Immunohistochemical investigations of tuberculosis granulomas substantiated our findings at the site of infection.Results. Monocytes differentiated in presence of platelets (MP-Macs) acquired a foamy, epithelioid appearance and gave rise to MNGCs (MP-MNGCs). MP-Macs up-regulated activation markers, phagocytosed mycobacteria, and released abundant interleukin 10. Upon extended culture, MP-Macs shared transcriptional features with epithelioid cells and M2 macrophages and up-regulated CXCL5 transcripts. In line with this, CXCL5 concentrations were significantly increased in airways of active tuberculosis patients. The platelet-specific CD42b antigen was detected in MP-Macs, likewise in macrophages, MNGCs, and epithelioid cells within tuberculosis granulomas, along with the platelet aggregation-inducing factor PDPN.Conclusions. Platelets drive macrophage differentiation into MNGCs with characteristics of epithelioid, foam, and giant cells observed in tuberculosis granulomas. Our data define platelets as novel participants in tuberculosis pathogenesis.

show abstract

“…It is known that T-lymphocytes play an important role in the pathogenesis of HIV and that the specific activity of ADA is high in T-lymphocytes [43]. In a study by Baba et al [42], the sensitivity of ADA was not affected by low CD4 counts, nor was there a significant difference in the mean ADA value in patients with lower CD4 counts.…”

Section: Adenosine Deaminasementioning

confidence: 94%

Tuberculous Pleural Effusion

Cohen

Light

2015

Tur Toraks Der

View full text Add to dashboard Cite

When a patient presents with new pleural effusion, the diagnosis of tuberculous (TB) pleuritis should be considered. The patient is at risk for developing pulmonary or extrapulmonary TB if the diagnosis is not made. Between 3% and 25% of patients with TB will have TB pleuritis. The incidence of TB pleuritis is higher in patients who are human immunodeficiency virus (HIV)-positive. Pleural fluid is an exudate that usually has a predominance of lymphocytes. The easiest way to diagnose TB pleuritis in a patient with lymphocytic pleural effusion is to demonstrate a pleural fluid adenosine deaminase level above 40 IU/L. The treatment for TB pleuritis is the same as that for pulmonary TB. Tuberculous empyema is a rare occurrence, and the treatment is difficult. KEY WORDS:Tuberculosis, pleural effusions, adenosine deaminase, gamma interferon, pleural biopsy, empyema INTRODUCTION Tuberculosis (TB) remains a major public health problem in developing countries. Most patients with TB have pulmonary TB; however, 25% of adults can present with extrapulmonary TB, which mainly involves the lymph nodes and pleura but can affect any organ system, including the central nervous system (CNS), cardiovascular system, and gastrointestinal (GI) tract [1]. The most common form of extrapulmonary TB is infection of the pleura. In a patient who presents with undiagnosed pleural effusion, the diagnosis of TB pleuritis should be considered. Pleural effusion, as an isolated manifestation of TB, may be selflimited and of little immediate concern, but untreated, it can lead to serious disease many years later. Pathogenesis and Pathologic FeaturesTuberculous pleural effusion may occur in the absence of radiologically apparent TB [2]. The effusion may result as a sequela to a primary infection from 6-12 weeks earlier, or it may represent the reactivation of TB [2]. In developed countries, TB pleural effusions present more often in older patients. The median age in one North American study was 56, suggesting reactivation of the disease [3]. However, a study from 2004 in San Francisco showed that pleural TB cases were 2 times more likely to be clustered (when assessed by genotyping of the mycobacterial organisms) than pulmonary TB and 3 times more likely to be clustered than nonrespiratory TB cases [4]. The observations made in the San Francisco study suggest that the majority of patients has a postprimary infection [4]. This was not confirmed in studies performed in both Houston [5] and Baltimore [6] or in a study in sub-Saharan Africa, in which the prevalence of pleural TB was 63.2% in patients with a primary TB infection [7].The pathogenesis of TB pleural effusion is thought to be related to the rupture of a subpleural caseous focus in the lung into the pleural space [8]. The basis for this was the observation that a caseous TB focus could be demonstrated in the lung, contiguous with the diseased pleural, in 12 to 15 patients with TB pleuritis [9]. The 3 other patients in this study had parenchymal disease but did not have caseous foci adjacent...

show abstract

Serum adenosine deaminase enzyme and plasma platelet factor 4 activities in active pulmonary tuberculosis, HIV-seropositive subjects and cancer patients

Cited by 21 publications

References 24 publications

Adenosine Deaminase Activity Is a Sensitive Marker for the Diagnosis of Tuberculous Pleuritis in Patients with Very Low CD4 Counts

Adenosine Deaminase Activity Is a Sensitive Marker for the Diagnosis of Tuberculous Pleuritis in Patients with Very Low CD4 Counts

Platelets Direct Monocyte Differentiation Into Epithelioid-Like Multinucleated Giant Foam Cells With Suppressive Capacity Upon Mycobacterial Stimulation

Tuberculous Pleural Effusion

Contact Info

Product

Resources

About