Int J Angiol 2016; 25(03): 153-158
DOI: 10.1055/s-0035-1571190
Original Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Investigation of the Etiology of Anemia in Thromboangiitis Obliterans

Mohammad Mehdi Akbarin
1   Inflammation and Inflammatory Diseases Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
,
Hassan Ravari
2   Mashhad Vascular and Endovascular Surgery Research Center, Emamreza Hospital, Mashhad University of Medical Sciences, Mashhad, Iran
,
Ataollah Rajabnejad
3   Student Research Committee, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
,
Narges Valizadeh
1   Inflammation and Inflammatory Diseases Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
,
Bahare Fazeli
1   Inflammation and Inflammatory Diseases Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
› Author Affiliations
Further Information

Publication History

15 July 2015

30 November 2015

Publication Date:
12 January 2016 (online)

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Abstract

During a review of patients admitted with thromboangiitis obliterans (TAO), there was evidence of normochromic normocytic anemia and abrupt changes in hemoglobin (Hgb) levels in patients with several hospital admissions. Therefore, the evidence of hemolytic anemia was evaluated based on 37 banked plasma samples taken from Caucasian male TAO patients during disease exacerbation between 2012 and 2014.

The patients' hospital records, including clinical manifestations and complete blood count, were evaluated. The following tests were performed on all samples: indirect antiglobulin test (IAT), C-reactive protein (CRP), high-sensitivity CRP (hsCRP), lactate dehydrogenase (LDH), haptoglobin, indirect bilirubin, d-aspartate aminotransferase (AST), and d-alanine aminotransferase (ALT).

The mean age of the patients was 40 ± 7 years. Two patients underwent below-knee amputation. The mean hospital-documented Hgb of the patients was 12.9 ± 2.6 g/dL. CRP and IAT were positive in 75.6 and 70.2% of the samples, respectively. The tests and corresponding results were as follows: hsCRP, 14.07 ± 2.37 µg/mL; LDH, 2,552 ± 315 u/L; haptoglobin, 2.27 ± 1.1 g/L; indirect bilirubin, 0.09 ± 0.04 mg/dL; AST, 67 ± 7 u/L; and ALT, 26 ± 3 u/L. There was a significant inverse correlation between hsCRP and hospital-documented Hgb level (p = 0.03).

Anemia with the positive IAT in most of the samples, high LDH and AST, and normal ALT are suggestive of hemolytic anemia. Normal indirect bilirubin is consistent with intravascular hemolysis. The positive CRP and elevated haptoglobin levels could be due to systemic inflammation in TAO. However, it is not known if an autoantigen or an infectious antigen is responsible for TAO systemic inflammation and induction hemolytic anemia. As such, the underlying mechanism of anemia in TAO could be part of the footprint of its main etiology.