[ANEMIA OF CHRONIC DISEASES AS A SYSTEMIC MANIFESTATION OF CHRONIC PULMONARY OBSTRUCTIVE DISEASE].

Anemia of chronic disease (ACD) is one of the most frequent forms of anemia is often observed in patients with infections, cancer and chronic inflammatory or autoimmune diseases. The underlying mechanisms are complex and include dysregulation of iron homeostasis and erythropoietin production, impaired proliferation of erythroid progenitor cells and reduced life span of red blood cells. Moreover, ACD is often superimposed by malnutrition, bleeding and renal failure. ACD is mediated through inflammatory cytokines and characterized by low serum iron (hypoferremia) and often increased reticuloendothelial stores of iron. ACD is usually normocytic, normochromic anemia, but it can become microcytic and hypochromic as the disease progresses. Hepcidin, the main regulator of iron homeostasis and its synthesis, is inhibited by iron deficiency and stimulated by inflammation. In many patients the disease is associated with several extrapulmonary manifestations regarded as the expression of the systemic inflammatory state of chronic obstructive pulmonary disease (COPD). Recent studies showed that anemia in patients with COPD is more frequent than expected, with its prevalence ranging from 8 to 33%. Systemic inflammation may be an important pathogenic factor, but anemia in COPD can also be the result of a number of factors, such as the treatment with certain drugs (angiotensin-converting enzyme inhibitors or theophylline), endocrine disorders, acute exacerbations and oxygen therapy. Anemia in COPD patients is strongly associated with increased functional dyspnea, decreased exercise capacity and is an independent predictor of mortality. Treatment options to correct anemia used in other chronic diseases, such as congestive heart failure, cancer or chronic kidney disease have not been explored in COPD (i.e. erythropoietic agents, iron supplements or combined therapy). It is not known whether treating the underlying inflammation could improve hematological characteristics. It is important to develop basic diagnostic modalities for this group of patients and formulate methods of anemia correction.

[ANEMIC SYNDROME IN PATIENTS WITH COMMUNITY-ACQUIRED PNEUMONIA].

Community-acquired pneumonia remains a most widespread acute infectious disease of socio-economic significance all over the world. Up to 30% of the patients present with anemia responsible for the unfavourable prognosis and elevated mortality. Not infrequently, anemia is not diagnosed during the hospital stay und therefore remains uncorrected. Severe anemia results in enhanced hypercapnia and slowed maturation of red blood cells in the bone marrow which facilitates the development of ischemic syndrome. Hepcidin, a mediator of inflammation and iron-regulatory hormone, plays an important role in the clinical course of community-acquired pneumonia. Hepsidin production increases during inflammation; it suppresses erythtropoiesis and depletes the iron depot leading to so-called anemia of inflammation. Hypoxia and anemia activate erythtropoiesis, and the released erythropoietin inhibits hepsidin production. During pneumonia resolution, hepsidin promotes recovery from anemia by activating iron absorption. The curreni literature contains few data on the use of hepcidin as a diagnostic marker of anemia. The necessity oftreating anemia in patients with pneumonia under hospital conditions is a matter of discussion. Direct involvement of hepcidin in iron metabolism creates a prerequisite for the treatment of anemia. Medicamental suppression of its activity by stimulating erythtropoiesis can facilitate normalization of iron metabolism and restoration of hemoglobin level.