RESUMO
The search for biological markers, which allow a relatively accurate assessment of the individual course of pulmonary sarcoidosis at the time of diagnosis, remains one of the research priorities in this field of pulmonary medicine. The aim of our study was to investigate possible prognostic factors for pulmonary sarcoidosis with a special focus on cellular immune inflammation markers. A 2-year follow-up of the study population after the initial prospective and simultaneous analysis of lymphocyte activation markers expression in the blood, as well as bronchoalveolar lavage fluid (BALF) and lung biopsy tissue of patients with newly diagnosed pulmonary sarcoidosis, was performed. We found that some blood and BAL fluid immunological markers and lung computed tomography (CT) patterns have been associated with a different course of sarcoidosis. We revealed five markers that had a significant negative association with the course of sarcoidosis (worsening pulmonary function tests and/or the chest CT changes)-blood CD4+CD31+ and CD4+CD44+ T lymphocytes, BALF CD8+CD31+ and CD8+CD103+ T lymphocytes and a number of lung nodules on chest CT at the time of the diagnosis. Cut-off values, sensitivity, specificity and odds ratio for predictors of sarcoidosis progression were calculated. These markers may be reasonable predictors of sarcoidosis progression.
RESUMO
BACKGROUND: The mechanisms driving the transition from inflammation to fibrosis in sarcoidosis patients are poorly understood; prognostic features are lacking. Immune cell profiling may provide insights into pathogenesis and prognostic factors of the disease. This study aimed to establish associations in simultaneous of lymphocyte subset profiles in the blood, bronchoalveolar lavage fluid (BALF), and lung biopsy tissue in the patients with newly diagnosed sarcoidosis. METHODS: A total of 71 sarcoid patients (SPs) and 20 healthy controls (HCs) were enrolled into the study. CD31, CD38, CD44, CD103 positive T lymphocytes in blood and BALF were analysed. Additionally, the densities of CD4, CD8, CD38, CD44, CD103 positive cells in lung tissue biopsies were estimated by digital image analysis. RESULTS: Main findings: (I) increase of percentage of CD3+CD4+CD38+ in BALF and blood, and increase of percentage of CD3+CD4+CD44+ in BALF in Löfgren syndrome patients comparing with patients without Löfgren syndrome, (II) increase of percentage of CD3+CD4+103+ in BALF and in blood in patients without Löfgren syndrome (comparing with Löfgren syndrome patients) and increase of percentage of CD3+CD4+103+ in BALF and in blood in more advanced sarcoidosis stage. (III) Increasing percentage of BALF CD3+CD4+CD31+ in sarcoidosis patients when comparing with controls independently of presence of Löfgren syndrome, smoking status or stage of sarcoidosis. Several significant correlations were found. CONCLUSIONS: Lymphocyte subpopulations in blood, BALF, and lung tissue were substantially different in SPs at the time of diagnosis compared to HCs. CD3+CD4+CD31+ in BALF might be a potential supporting marker for the diagnosis of sarcoidosis. CD3+CD4+CD38+ in BALF and blood and CD3+CD4+CD44+ in BALF may be markers of the acute immune response in sarcoidosis patients. CD4+CD103+ T-cells in BALF and in blood are markers of the persistent immune response in sarcoidosis patients and are potential prognostic features of the chronic course of this disease.
RESUMO
BACKGROUND: The aim of the present study was to identify specious radiologic and/or physiologic prognostic marker(s), which lead to optimize of the patient follow-up frequency. METHODS: Eighty consecutive patients with newly diagnosed pulmonary sarcoidosis. Patients underwent chest radiography, high-resolution computed tomography (HRCT) examination, pulmonary function tests (PFT), bronchoscopy with bronchoalveolar lavage (BAL) and lung biopsy, and bronchoalveolar lavage fluid (BALF) cell examination. RESULTS: The reduction in PFT values seen in radiological sarcoidosis stage III was greater than that seen in stages I and II. The percentage of neutrophils in the lungs was found to increase in stages II and III. PFT indices were correlated negatively with the consolidation and ground glass opacities CT scores, but not with the micronodule or macronodule scores. The rise in the percentage of BALF lymphocytes was associated with the restriction pattern of PFT. The diagnostic value of BALF for sarcoidosis was higher when the typical radiologic patterns of stage I disease were found and that smoking decreased the diagnostic value of CD4/CD8 ratio. CONCLUSIONS: This study supports the opinion that the staging of the pulmonary sarcoidosis with chest X-rays is still valuable from the prognostic point of view, because significant correlations between the radiologic stages of sarcoidosis and PFT parameters were found. Chest HRCT was significantly superior to chest X-ray in detecting mediastinal and pulmonary parenchymal changes. However, the prognostic role of HRCT needs to be better investigated evaluating serial examinations. Only consolidation and ground glass scores (neither of which are frequently found in sarcoidosis) hold prognostic value, since these were negatively correlated with PFT parameters.
RESUMO
Pneumocystis jirovecii pneumonia has historically been one of the most common opportunistic pneumonias and life-threatening infectious complications in HIV-infected patients. After the introduction of combination antiretroviral therapy, the incidence of Pneumocystis pneumonia and other opportunistic infections has decreased dramatically. Nowadays Pneumocystis pneumonia still occurs in patients unaware of their HIV status, in those not receiving combination antiretroviral therapy, or in those in whom it is ineffective due to resistance. Age factor is the diagnosis delaying one: patients aged more than 50 years are diagnosed with AIDS later than younger persons. Pneumocystis was thought to be a species of protozoa. Over the last 20 years, Pneumocystis has been shown to be a fungus, to be genetically diverse, host species specific, to colonize individuals with minor immunosuppression, and to cause clinical disease by "new" infection in addition to reactivation of latent childhood-acquired infection. Recently, the microorganism Pneumocystis carinii causing disease in humans has been renamed to Pneumocystis jirovecii. This article presents a clinical case of late diagnosis of Pneumocystis jirovecii pneumonia in a 62-year-old patient unaware of her HIV status and a review of literature reflecting epidemiological issues of Pneumocystis jirovecii and latest discoveries related to Pneumocystis as well as the rationale for renaming it.