The predictive value of cystatin C as a marker of course of the disease has been evaluated. Fifty-two pairs of serum samples of patients with B non-Hodgkin lymphoma have been collected at the time of diagnosis and before fourth cycle of chemotherapy. The levels of cystatin C, CRP, β2M, LDH, and IL-6 in samples have been measured, and clinical parameters of course of the disease (B symptoms, clinical stage, patients’ age, and IPI) have been noted. In total patient’s group cystatin C levels correlated with β2M and IPI. In aggressive lymphomas, the inhibitor levels correlated with clinical stage of disease and were significantly higher in patients with elevated LDH activity. In aggressive nodal lymphomas its levels correlated with β2M, IPI, and clinical stage of disease. The cystatin C level was significantly increased in total group of patients over 60 years old, while in particular types of lymphoma, no statistical significance has been obtained. Our results indicate that cystatin C should be taken into consideration in disease monitoring. However, we expect that the disease-free and overall survival analysis will give the definitive answer about the reliability of cystatin C as an indicator of course of aggressive lymphomas. 1. Introduction Cysteine proteinase inhibitors, cystatins, are involved in mechanisms controlling intracellular and extracellular protein degradation. Under normal physiological conditions, small amounts of catalytically active proteases, released from lysosomes or secreted from infected or dying cells, are effectively blocked by cystatins. A disbalance between proteinases and their natural inhibitors leads to the development of various diseases. Cystatin C, a member of family II of cystatins, is a nonglycosylated 13？kDa protein inhibitor of cysteine proteases, with widespread distribution in almost all extracellular fluids, the highest levels having been determined in cerebrospinal fluid, seminal plasma, and synovial fluid [1]. A broad spectrum of biological roles has been suggested for cystatin C, including control of protein catabolism, regulation of hormone processing and bone resorption, inflammation, antigen presentation, and T-cell dependent immune response [2, 3]. Cystatin C was suggested as a marker of glomerular filtration rate, since it is produced at a constant rate by all nucleated body cells, freely filtered in the renal glomeruli and almost completely reabsorbed and catabolized in the proximal tubules [4]. Cystatin C has also been suggested as playing a role associated with alteration of the proteolytic system in
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