Emphysema Medical and Health News Headlines

[The first 12 years of history of Hungarian lung transplantations.]

Orv Hetil. 2008 Aug 31;149(35):1635-44

Authors: Czebe K, Csiszér E, Lang G, Jaksch P, Klepetko W

12 years have passed since the first Hungarian patient went through lung transplantation. A small but dedicated group of clinicians work to make lung transplantation an easily accessible, accepted therapy for Hungarian patients. Transplantation is recommended for patients suffering from end stage vascular or parenchymal diseases of the lung after conservative therapies are proven unsuccessful. Lung transplantation as a surgical intervention is currently not available in Hungary. In the past 12 years 64 Hungarian patients were transplanted at the Department of Cardiothoracic Surgery, Medical University of Vienna, in Austria by the Vienna Lung Transplant Group led by Prof. Walter Klepetko. Our patients went through lung transplantation for the following indications: cystic fibrosis (22), idiopathic lung fibrosis (18), primer pulmonary hypertonia (8), lymphangioleimyomatosis (5), emphysema (4) and other (7). The 64 patients altogether went through 68 transplantation procedures. In 4 cases re-transplantation was necessary. The surgery techniques employed were as follows: bilateral lung transplantation (33), bilateral lobar transplantation (18), single lung transplantation (13), heart-lung transplantation (2) and split-lung transplantation (2). Bilateral living-donor lung lobar transplantation was performed in one case. The mean age of patients at the time of surgery was 33.3 years (between age 14 and 58). 48 of the 64 patients are still alive.

PMID: 18713702 [PubMed - in process]

THE POSSIBLE ROLE OF HEMATOPOIETIC CELL KINASE IN THE PATHOPHYSIOLOGY OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE.

Chest. 2008 Aug 21;

Authors: Yanagisawa S, Sugiura H, Yokoyama T, Yamagata T, Ichikawa T, Akamatsu K, Koarai A, Hirano T, Nakanishi M, Matsunaga K, Minakata Y, Ichinose M

Background Hematopoietic-cell-kinase (Hck) is a myeloid cell specific tyrosine kinase, known to induce neutrophil infiltration to the lungs. Although the over-expression of Hck causes emphysema-like histological changes in mouse, its expression and activity in patients with chronic obstructive pulmonary disease (COPD) are unclear. Method The aim of this study is to clarify the expression and activity of Hck in neutrophils from COPD patients, and to investigate the association between the degree of Hck expression and the lung function parameters in COPD. Peripheral blood neutrophils were isolated from 22 patients with COPD and 9 healthy subjects (HS). The protein level of Hck and phosphorylated-Hck (p-Hck) were assessed, and the correlation with various background characteristics was evaluated. Results The Hck protein level was significantly higher in the neutrophils from COPD patients compared with HS (COPD = 1.094, HS = 0.801, p < 0.05). A significant positive correlation was observed between the protein level of Hck and the surface expression of integrin molecule, CD-11b (r = 0.540; p < 0.01), or CXC chemokine receptor-1 (r = 0.432; p < 0.05). In contrast, there was no difference in the phosphorylation of Hck protein between COPD patients and HS. Conclusion The Hck protein level in peripheral blood neutrophils was increased in COPD patients, suggesting that Hck might have an important role in the neutrophil function and play a key role in COPD pathophysiology.

PMID: 18719065 [PubMed - as supplied by publisher]

Identification of a Btk mutation in a dysgammaglobulinemic patient with reduced B cells: XLA diagnosis or not?

Clin Immunol. 2008 Sep;128(3):322-8

Authors: Graziani S, Di Matteo G, Benini L, Di Cesare S, Chiriaco M, Chini L, Chianca M, De Iorio F, La Rocca M, Iannini R, Corrente S, Rossi P, Moschese V

The identification of a Btk mutation in a male patient with <2% CD19(+) B cells warrants making the diagnosis of X-linked Agammaglobulinemia (XLA). Herein we report the case of a 31 year-old male with a gradual decline of peripheral B lymphocytes and low IgA and IgM but normal IgG levels. His clinical history revealed recurrent respiratory and skin infections, sclerosing cholangitis and chronic obstructive pancreatitis. Molecular studies revealed a novel aminoacidic substitution in Btk protein (T316A). His mother, maternal aunts and a maternal female cousin were heterozygotes for the same Btk mutation and were variably affected with pulmonary emphysema. This is a puzzling case where the patient's clinical history and laboratory findings divorce molecular genetics. Either this case confirms the variable expressivity of XLA disease or the T316A change in Btk SH2 domain is a novel non-pathogenic mutation and another unknown gene alteration is responsible for the disease.

PMID: 18708023 [PubMed - in process]

Airway infiltration of CD4+ CCR6+ Th17 type cells associated with chronic cigarette smoke induced airspace enlargement.

Immunol Lett. 2008 Aug 12;

Authors: Harrison OJ, Foley J, Bolognese BJ, Long E, Podolin PL, Walsh PT

Recently, patients with tobacco smoke induced emphysema have been shown to exhibit classical signs of T cell mediated autoimmunity characterized by autoantibody production and Th1 type responses. As the recently described Th17 type subset has been found to play a role in the pathogenesis of a number of autoimmune diseases previously considered to be Th1 driven, we sought to examine whether a Th17 type response was associated with airspace enlargement in a murine model of emphysema. Six to eight months exposure of mice to inhalation of mainstream cigarette smoke led to progressive airspace enlargement as defined by morphometric analysis. Flow cytometric analysis of the bronchoalveolar lavage (BAL) from these mice demonstrated a significant increase in the overall number of both CD4+ and CD8+ T cells present. These cells were subsequently examined for skewing towards a Th1, Th2 or Th17 phenotype by intracellular cytokine analysis. Distinct populations of BAL CD4+ T cells were found to express IFN-gamma or IL-17 demonstrating the presence of both a Th1 and Th17 type response. No expression of the Th2 associated cytokine IL-4 was detected. Further analysis of this Th17 subset demonstrated that the majority of cells with this effector phenotype express the chemokine receptor CCR6. Together these data identify a novel T cell subset associated with pulmonary inflammation as a result of cigarette smoke exposure. Given the reported roles of CCR6 and IL-17 in promoting pulmonary inflammation, this subset may play an important role in the pathogenesis of cigarette smoke induced autoimmunity.

PMID: 18706444 [PubMed - as supplied by publisher]

A Taxonomy of Medical Comorbidity for Veterans Who are Homeless.

J Health Care Poor Underserved. 2008 Aug;19(3):991-1005

Authors: Goldstein G, Luther JF, Jacoby AM, Haas GL, Gordon AJ

Homeless veterans have numerous medical and behavioral health problems. Grouping homeless people based on comorbidity patterns may assist in determining severity of illness and triaging health care more effectively. We sought to determine if a finite number of profiles could be identified related to demographic characteristics, living situation, length of homelessness, and referral areas using interview data from 2,733 veterans who were presently or recently homeless. We considered 12 disorders: eye problems, hypertension, cardiovascular problems, COPD/emphysema, tuberculosis, gastrointestinal problems, hepatic disease, neurologic disorders, orthopedic problems, skin problems, and trauma. Ratings were evaluated using cluster analysis. Comparison statistics were used to compare intercluster differences in demographics, homeless situation, and referral recommendations. A four-cluster solution is proposed: generalized illness, hepatic disease, lung disease, and neurologic disorder. Medical health problems are common and heterogeneous in homeless individuals. Classifications of these problems may be useful in planning treatment and predicting outcome.

PMID: 18677085 [PubMed - in process]

A 51-year-old man with emphysema and progressive dyspnea.

Chest. 2008 Aug;134(2):430-3

Authors: Morehead RS

PMID: 18682462 [PubMed - in process]