Tatjana Peroš-Golubičić

Diffuse pulmonary ossification: an unusual interstitial lung disease

Purpose of review Diffuse pulmonary ossification is a rare disease characterized by diffuse small bone fragments in the lung tissue. It can be idiopathic or associated with underlying chronic pulmonary or heart diseases. The majority of cases had been diagnosed on autopsy. This review collects present knowledge of diffuse pulmonary ossification with the purpose of understanding and considering the entity in the differential diagnosis of interstitial lung diseases better. Recent findings Diffuse pulmonary ossification is the result of multiple factors that interact enhancing each other. Tissue injury is the most important provoking factor that, in an alkaline environment, initiates precipitation of calcium salts, enables alkaline phosphatase activity, and activates profibrogenic cytokines. Alveolar bleeding is responsible for interstitial metallic deposition that attracts calcium salts and multinucleated giant cells. High-resolution computed tomography scan in the mediastinal window facilitates the detection of bone density lesions and provides diagnosis by using low-invasive method. Reports on the efficacy of bisphosphonates and warfarin in the management of heterotopic ossification encourage further investigation. Summary Diffuse pulmonary ossification is still underrecognized during life. Its relevance concerning the increasing age of population and longer survival of patients with chronic diseases is underrated. A timely diagnosis will enable a better understanding of pathogenesis and natural course of disease thus paving the way to new therapeutic strategies.

Transbronchial fine needle aspiration cytology in the diagnosis of mediastinal/hilar sarcoidosis

Objective:  The diagnostic value of transbronchial/transtracheal fine needle aspiration (TBFNA) cytology in the patients with mediastinal and/or hilar lymphadenopathy has been investigated.

Hypereosinophilic syndrome : diagnosis and treatment

Purpose of review Hypereosinophilic syndrome is increasingly recognized as a heterogeneous group of disorders, in some cases with precisely defined pathogenesis, which has led to changes in diagnostic approaches and therapeutic strategies. An update on causes and modern therapy is presented here. Recent findings Clonal eosinophilias belong to the group of myeloid malignancies. Karyotypically occult FIP1L1- platelet-derived growth factor receptor alpha and beta rearranged eosinophilic disorders respond to imatinib mesylate with almost 100% efficacy. If standard therapies fail, the FIP1L1- platelet-derived growth factor receptor-negative cases of hypereosinophilic syndrome should also be considered for treatment with imatinib. The recognition of acquired resistance to imatinib has aroused interest in developing new tyrosine kinase inhibitors. Other subgroups of clonal eosinophilias have been molecularly defined, but the curative verification of pathogenetic relevance has not been certified. Hypereosinophilic syndrome patients with abnormal T-cell populations have benefited from treatment with anti IL-5 monoclonal antibodies. Summary The FIP1L1- platelet-derived growth factor receptor alpha and beta-positive patients, and those with abnormal T-cell populations are currently the only clearly defined treatable subgroups of hypereosinophilic syndrome. The FIP1L1- platelet-derived growth factor receptor alpha-negative responders to imatinib pose a question as to the existence of subentities with unrecognized tyrosine kinases-based mutation. The search for such cases and other treatable subgroups of hypereosinophilic syndrome has already begun.