In this article, an interference caused by hemoglobin H (Hb H), during the measurement of hemoglobin A1c (HbA1c) with ion exchange high pressure liquid chromatography (HPLC) method, was presented in blood sample of a 20-year-old male patient. HbA1c measurement was performed with Agilent 1200 HPLC system using a commercial Recipe HbA1c ion-exchange column. Hemoglobin electrophoresis was performed with Interlab G26 agarose electrophoresis automated compact system. HbA1c level was 18.2% and HbA0 level was 81.5% with ion-exchange HPLC method. Patient's fasting serum glucose was assessed before HbA1c measurement and the result was 165 mg/dL (9.16 mmol/L). On the other hand, the result of HbA0 was 87.9%, Hb H was 10.8% and Hb A2 was 1.3% with electrophoresis. Whole blood test values were within reference ranges except MCV. MCV value was 79.6 fL. It is important to keep in mind that HbA1c level might be considered falsely high with ion-exchange HPLC method because of Hb H containing sample.

We read with great interest the paper by Targońska-Stępniak and Majdan titled "Serum Amyloid A as a Marker of Persistent Inflammation and an Indicator of Cardiovascular and Renal Involvement in Patients with Rheumatoid Arthritis" in which the investigators reported that high serum amyloid A (SAA) concentration was strongly associated with activity of the disease and risk of cardiovascular and renal involvement in patients with rheumatoid arthritis [1]. We thank the authors for their detailed report. However, we wish to make some comments on SAA. SAA is produced in the liver in response to proinflammatory cytokines such as tumor necrosis factor alpha (TNF-𝛼), interleukin-1 (IL-1), and IL-6 [2]. Previous studies suggested that several diseases such as ankylosing spondylitis, autoinflammatory diseases (Hashimoto's thyroiditis, familial Mediterranean fever), major depression, systemic lupus erythematosus, diabetes mellitus, inflammatory bowel diseases, acute pancreatitis, several types of vasculitis, psoriasis, and epilepsy could affect SAA levels [3, 4]. In addition to these diseases, glucocorticoids, statins, disease-modifying antirheumatic drugs, corticosteroids, and nonsteroidal anti-inflammatory drugs could alter SAA levels [5, 6]. Also, dietary food supplements such as antioxidants (ascorbic acid, taurine, and phytic acid), vitamin E, vitamin A, 𝛼 linoleic acid, omega-3 fatty acids, and polyunsaturated fatty acids can influence SAA levels [7, 8]. In this respect, without defining these contributing factors, interpreting the results is problematic.