The aim of this study was to investigate the possibility of distinguishing between patients with similarities in clinical presentation, suffering from three frequently occurring interstitial lung diseases, by means of discriminant analysis, using a number of selected variables derived from bronchoalveolar lavage fluid (BALF) analysis. The study involved all 277 patients, who had an initial bronchoalveolar lavage (BAL) in the period 1980-1990. These patients belonged to the following diagnostic groups: sarcoidosis (n = 193), subacute extrinsic allergic alveolitis (EAA) (n = 39) and idiopathic pulmonary fibrosis (IPF) (n = 45). Thirty healthy volunteers were used as controls. Cellular and non-cellular constituents of BALF were evaluated. Variables, which could be used to discriminate among the three diagnostic groups were: yield of recovered BALF, total cell count, and percentages of alveolar macrophages, lymphocytes, polymorphonuclear neutrophils, eosinophils and plasma cells in BALF. When the set of data used to predict the membership of patients to diagnostic groups (test set) was the same as that in which the discriminant analysis was performed (learning set), 93% of the cases were correctly classified. This percentage decreased to 90%, however, when the test set was different from the learning set. It is possible to discriminate among patients with sarcoidosis, EAA or IPF with these selected variables. It appears that bronchoalveolar lavage (BAL) is useful as an adjunct in concert with other diagnostic methods.
Community-acquired pneumonia (CAP) can be caused by a variety of microorganisms but is most frequently associated with Streptococcus pneumoniae and gram-negative bacteria like Haemophilus influenzae. Encapsulated bacteria are able to escape phagocytosis, unless they are bound by immunoglobulin G2 subclass antibodies. These antibodies interact with Fcgamma receptor IIa (Fcgamma-RIIa), thereby facilitating opsonophagocytosis of the encapsulated bacteria. We studied the relationship between the Fcgamma-RIIa-R/H131 polymorphism and the clinical course of CAP and pathogen-specific susceptibility. Regarding methodology, the Fcgamma-RIIa genotype R/H131 was determined in 200 patients with CAP and in 313 healthy controls and was correlated with the clinical course, laboratory parameters, and causative microorganism. The Fcgamma-RIIa-R/R131 genotype was found more frequently in patients with severe sepsis (odds ratio [OR], 2.55; 95% confidence interval [CI], 1.30 to 5.00; P < 0.01). The majority of patients in this group suffered from invasive pneumococcal disease. The duration of hospital stay was longer for patients with the Fcgamma-RIIa-R/R131 genotype. Fcgamma-RIIa genotypes were not associated with an increased risk of CAP in general; however, the Fcgamma-RIIa-R/R131 genotype was found more frequently in patients with CAP caused by H. influenzae than in controls (OR, 3.03; CI, 1.04 to 9.09; P < 0.05). In conclusion, the Fcgamma-RIIa-R/R131 genotype is associated with severity of CAP and is more frequent in CAP caused by H. influenzae.
Antibody replacement therapy has been used in the treatment of primary antibody deficiencies (PADs) for several decades, and an evidence-based guideline for its treatment is currently available. By contrast, the use of antibody replacement therapy in iatrogenic hypogammaglobulinemia (IHG), a condition that is associated with immunosuppressive medication, has hardly any evidence base and no guidelines. As IHG can be equally as severe as PAD and is much more prevalent, evidence-based guidelines are urgently needed. This review will focus on the differences and similarities between PAD and IHG and the use of antibody replacement therapy in both conditions. Suggestions for the development of evidence-based guidelines and future research are given.
Sarcoidosis is generally characterized by a CD4+ lymphocyte predominance in bronchoalveolar lavage fluid (BALF), whereas in extrinsic allergic alveolitis (EAA) a CD8+ lymphocyte predominance is found. However, we have previously demonstrated an increase in CD4+ lymphocytes in BALF obtained from EAA patients as well. The aim of this study was to evaluate whether in sarcoidosis and EAA the BALF cellular profile-even without the help of cytokine detection-might reflect differences in the CD4+ T-lymphocyte subpopulations, i.e. T helper (TH)-1 and TH2 lymphocytes.For this purpose, we analyzed BALF analysis results obtained from 77 nonsmoking patients with histologically proven sarcoidosis and 54 nonsmoking patients suffering from EAA.Patients with EAA showed the highest mean absolute numbers of lymphocytes, CD8+ as well as CD4+ T lymphocytes, whereas the percentage of CD4+ T lymphocytes in BALF was low. In contrast, patients with sarcoidosis showed the lowest absolute and relative number of CD8+ T lymphocytes, the highest percentage of CD4+ T lymphocytes and CD4+/CD8+ ratio. Moreover, patients with Löfgren's syndrome demonstrated an alveolitis suggesting a TH1 lymphocyte-subset-like predominant related profile, characterized by lower numbers of eosinophils and mast cells, whereas sarcoidosis patients with respiratory symptoms formed a more mixed TH1/TH2 pattern. Patients with EAA showed a cellular BALF profile suggesting a functional predominance of TH2 lymphocytes.These preliminary data suggest a different distribution of the CD4+ T lymphocyte subtypes characterized by a functional heterogeneity of CD4+ T lymphocytes between-as well as within-these various pulmonary disorders. The exact role of this imbalance of TH1 and TH2-like activity in the lung with regard to the pathogenesis and prognosis needs to be further elucidated.
Abstract Objectives: To analyse the effects of ranitidine treatment on vaccination induced antibody responses in patients with chronic lymphocytic leukaemia (CLL). Methods: Fifty CLL patients were vaccinated with tetanus conjugated Hib vaccine and a 23‐valent pneumococcal polysaccharide vaccine with ( n = 25) or without ( n = 25) ranitidine treatment in a matched case‐‐control setting. Anti tetanus toxoid (TT), anti‐ Hib and anti‐pneumococcal antibody levels were determined before and after vaccination. Additionally, cytokine levels were assessed in patients treated with ranitidine. Results: Vaccination‐induced increases in anti‐ Hib and anti‐TT antibody levels were higher in the ranitidine group compared with the control group. Anti‐pneumococcal antibody responses were not improved by administration of ranitidine. Higher levels of IL‐18 were found in patients treated with ranitidine compared with healthy controls. Levels of IL‐6, IL‐8, IL‐18, RANTES, IP‐10, sVCAM‐1 and sICAM‐1 were within normal ranges and did not change during ranitidine treatment. Conclusion: Ranitidine treatment improves vaccination‐induced T‐cell dependent antibody responses in patients with CLL but has no beneficial effect on the response to vaccination with unconjugated polysaccharide antigens.
