Serum Thymidine Kinase and Beta-2 Microglobulin in Monoclonal Gammopathies

Abstract

We evaluated the serum thymidine kinase (TK) and beta-2 microglobulin (beta-2) levels of 22 patients with monoclonal gammopathy of undetermined significance (MGUS) and of 29 patients with multiple myeloma (MM). Both parameters were significantly lower in MGUS than in MM patients and in early (stage I + II) than in advanced (stage III) MM. TK was also lower in MGUS than in stage I MM (p less than 0.025). A seven-fold increase of TK level was documented in one patient who developed a full blown picture of MM 6 years after a diagnosis of MGUS. In 3 patients with stage III MM, a sharp decrease in TK (40-77%) and in beta-2 (29-53%) levels at remission was evident with respect to the levels measured at diagnosis. Patients with high levels of TK or beta-2 had a shorter survival than those with low levels; however, this was statistically significant only for beta-2 levels (p less than 0.02). Serum TK as well as beta-2 levels appear to be of clinical value in monoclonal gammopathies and related to the course of the disease.

The Merlini, Waldenström, Jayakar staging system revisited

“…The need to reconsider routinely used staging systems so as to account for the most recent prognostic factors is widely recognized (15, 16). Several new parameters have recently emerged as possible prognostic factors: plasma cell morphology (17), plasma cell labeling index (5,18,19,20), DNA hypodiploidy (21), RNA index (21), plasma cell antigens (22,23,24), oncogene expression (25), light chain isotype suppression (26), S-LDH (15, 27) S-thymidine kinase (28,29) and S-B-2M (30). With few exceptions (31) most reports have shown that S-P-2M was the most powerful independent prognostic factor (32)(33)(34)(35)(36)(37)(38).…”

Ras oncogene expression and DNA content in plasma cell dyscrasias: a flow cytofluorimetric study

“…The complete clinical, radiological and laboratory evaluation of patients with plasma cell dyscrasias was carried out according to a protocol that also require special examinations, such as P2-microglobulin and thymidine kinase level determination (Ucci et al, 1987) and BMPC proliferative activity evaluation (as the percentage labelled with in vitro BUDR and with the monoclonal antibody Ki-67). In all patients, BMPC% was counted on imprints of BM sample aspirated for FCM and p21 evaluation.…”