C M Vadikolia

Publications (3)2.53 Total impact

• Article: Proteolytic matrix metallopeptidases and inhibitors in BCR-ABL1-negative myeloproliferative neoplasms: correlation with JAK2 mutation status.

  C M Vadikolia, C Tsatalas, K Anagnostopoulos, G Trypsianis, D Pantelidou, I Bazdiara, A Anastasiadis, E Spanoudakis, I Kotsianidis, D Margaritis, A Kortsaris, G Bourikas
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  ABSTRACT: Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) share the same acquired lesion JAK2(V617F) and may exhibit substantial overlap. Variability in JAK activation and allele burden, complemented by host, genetic and non-genetic modifiers, determine the phenotype. The aim of this study was to investigate the presence of the JAK2 mutation in association with the ratio of metallopeptidases inhibitors (TIMPs) to tissue metallopeptidases (MMPs) in MPNs, where inhibitory rather than proteolytic activity in marrow microenvironment appears to predominate. 94 patients with polycythemia vera, essential thrombocythemia and primary myelofibrosis, and 102 healthy individuals were evaluated. Allele-specific PCR and RFLP were used to detect JAK2 and genomic status. Serum concentrations of MMP and TIMP were measured by ELISA. The parameters were assessed with covariance analysis, and adjusted for gender, age and co-morbidity. Mutation frequency was 81.91%. Abnormal TIMP/MMP ratios were identified in all three diseases. JAK2 mutation was correlated with significant changes in TIMP concentrations. Identification of an abnormal TIMP/MMP ratio in all three diseases, regardless of the JAK2 status, indicates invariable marrow remodeling. In this particular group of patients, presence of a JAK2(V617F) mutation, being associated with even higher ratios, appears to be a concurring participant in bone marrow-reforming processes. Additional research may delineate correlates with the JAK2 allelic burden.
  Acta Haematologica 04/2011; 126(1):54-62. · 1.35 Impact Factor
• Article: Acquired haemophilia masked by warfarin therapy.

  C M Vadikolia, A Riddell, S Brooks, T T Yee, S Brown, C Lee
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  ABSTRACT: Acquired haemophilia is a rare phenomenon and prompt diagnosis is essential for successful treatment. Early laboratory detection could minimize its potentially devastating consequences and reduce mortality but when a masking element such as anticoagulant therapy is present, delay in diagnosis is not uncommon. A prolonged activated partial thromboplastin time (APTT) may be falsely attributed to warfarin alone, particularly when it is associated with oral anticoagulant overdose. We describe two patients on treatment with warfarin who presented with a bleeding diathesis and disproportionately prolonged APTT, which led to the diagnosis of antibodies directed against factor VIII.
  International Journal of Laboratory Hematology 03/2007; 29(1):64-8. · 1.18 Impact Factor
• Article: Proteolytic Matrix Metallopeptidases and Inhibitors in BCR-ABL1-Negative Myeloproliferative Neoplasms: Correlation with JAK2V617F Mutation Status

  C.M. Vadikolia, C. Tsatalas, K. Anagnostopoulos, G. Trypsianis, D. Pantelidou, I. Bazdiara, A. Anastasiadis, E. Spanoudakis, I. Kotsianidis, D. Margaritis, A. Kortsaris, G. Bourikas
  [show abstract] [hide abstract]
  ABSTRACT: Background/Aims: Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) share the same acquired lesion JAK2V617F and may exhibit substantial overlap. Variability in JAK activation and allele burden, complemented by host, genetic and non-genetic modifiers, determine the phenotype. The aim of this study was to investigate the presence of the JAK2 mutation in association with the ratio of metallopeptidases inhibitors (TIMPs) to tissue metallopeptidases (MMPs) in MPNs, where inhibitory rather than proteolytic activity in marrow microenvironment appears to predominate. Methods: 94 patients with polycythemia vera, essential thrombocythemia and primary myelofibrosis, and 102 healthy individuals were evaluated. Allele-specific PCR and RFLP were used to detect JAK2 and genomic status. Serum concentrations of MMP and TIMP were measured by ELISA. The parameters were assessed with covariance analysis, and adjusted for gender, age and co-morbidity. Results: Mutation frequency was 81.91%. Abnormal TIMP/MMP ratios were identified in all three diseases. JAK2 mutation was correlated with significant changes in TIMP concentrations. Conclusions: Identification of an abnormal TIMP/MMP ratio in all three diseases, regardless of the JAK2 status, indicates invariable marrow remodeling. In this particular group of patients, presence of a JAK2V617F mutation, being associated with even higher ratios, appears to be a concurring participant in bone marrow-reforming processes. Additional research may delineate correlates with the JAK2 allelic burden.
  Acta Haematologica. 08/1970; 126(1):54-62.