ISSN: 2538-2462
July 2016
Vol. 1 No. 3 (2016)
Extensive Hematoma in a Patient with HereditaryHypersegmentation of Neutrophils
Journal of Cellular & Molecular Anesthesia,
Vol. 1 No. 3 (2016),
,
Page 109-114
https://doi.org/10.22037/jcma.v1i3.11878
Abstract
Erratum: The correct affiliation of corresponding author of this manuscript has been edited as follows:
"Akbar Dorgalaleh: Department of Hematology and Blood Transfusion, School of Allied Medical Sciences, Iran University of Medical Sciences, Tehran, Iran."
Hypercoagulable states are a group of conditions associated with an enhanced tendency toward blood clotting. Although usual clinical manifestations of hypercoagulable states are thrombotic events such as deep venous thrombosis, hematoma can also occurs as a result of hypercoagulability in some patients. Several inherited or acquired conditions may lead to hypercoagulable states. Some of them include myeloproliferative syndromes, over activity of coagulation factors and methyltetrahydrofolateee reductase (MTHFR) polymorphisms. MTHFR is required for converting
the amino acid homocysteine to methionine. Another significant role of an aptly functioning MTHFR enzyme is nucleic acid biosynthesis. Therefore MTHFR polymorphisms are expected to be associated with hypersegmentation of neutrophils because of a defect in DNA metabolism. Neutrophil hypersegmentation is one of the most sensitive haematological features of cobalamin or folate deficiency with normal serum vitamin B12-folic acid and iron levels. Hypersegmentation of neutrophils and hematoma which both of them suspected to be due to gene variations of MTHFR. Here we report a 37 years old female who simultaneously affected by hereditary hypersegmentation and extensive hematoma. Laboratory analysis revealed normal serum vitamin B12, folic acid and iron levels. Routine and specific coagulation tests were normal in except of factor VIIIc that was high. Results of complete blood cell count (CBC) test were normal. Although this is just an idea, but simultaneous presentations of these two conditions can have a common origin.
- Hematoma
- Neutrophil hyper-segmentation
- Hypercoagulability
How to Cite
References
Ali N, Ayyub M, Khan SA. High prevalence of protein C, protein S, antithrombin deficiency, and Factor V Leiden mutation as a cause of hereditary thrombophilia in patients of venous thromboembolism and cerebrovascular accident. Pakistan journal of medical sciences. 2014;30(6):1323.
Samad F, Ruf W. Inflammation, obesity, and thrombosis. Blood. 2013;122(20):3415-22.
Martinelli I, Passamonti S, Bucciarelli P. Thrombophilic states. Handbook of clinical neurology. 2013;120:1061-71.
Gibson CS, MacLennan AH, Janssen NG, Kist WJ, Hague WM, Haan EA, et al. Associations between fetal inherited thrombophilia and adverse pregnancy outcomes. American journal of obstetrics and gynecology. 2006;194(4):947. e1-. e10.
Den Heijer M, Lewington S, Clarke R. Homocysteine, MTHFR and risk of venous thrombosis: a meta‐analysis of published epidemiological studies. Journal of Thrombosis and Haemostasis. 2005;3(2):292-9.
Fung MM, Salem RM, Lipkowitz MS, Bhatnagar V, Pandey B, Schork NJ, et al. Methylenetetrahydrofolate reductase (MTHFR) polymorphism A1298C (Glu429Ala) predicts decline in renal function over time in the African-American Study of Kidney Disease and Hypertension (AASK) Trial and Veterans Affairs Hypertension Cohort (VAHC). Nephrology Dialysis Transplantation. 2012;27(1):197-205.
Nazki FH, Sameer AS, Ganaie BA. Folate: metabolism, genes, polymorphisms and the associated diseases. Gene. 2014;533(1):11-20.
Yan J, Yin M, Dreyer ZE, Scheurer ME, Kamdar K, Wei Q, et al. A meta‐analysis of MTHFR C677T and A1298C polymorphisms and risk of acute lymphoblastic leukemia in children. Pediatric blood & cancer. 2012;58(4):513-8.
Khaleghparast A, Khaleghparast S, Khaleghparast H. Evaluation of the Association between the C677T Polymorphism of Methylenetetrahydrofolate Reductase Gene and Recurrent Spontaneous Abortion. Iranian Journal of Neonatology IJN. 2014;5(1):7-11.
Garilli B, editor MTHFR mutation: A missing piece in the chronic disease puzzle. Summer; 2012.
Hosseini S, Kalantar E, Hosseini MS, Tabibian S, Shamsizadeh M, Dorgalaleh A. Genetic risk factors in patients with deep venous thrombosis, a retrospective case control study on Iranian population. Thrombosis journal. 2015;13(1):1.
Heller DS, Rush D, Baergen RN. Subchorionic hematoma associated with thrombophilia: report of three cases. Pediatric and Developmental Pathology. 2003;6(3):261-4.
Sharp L, Little J. Polymorphisms in genes involved in folate metabolism and colorectal neoplasia: a HuGE review. American Journal of Epidemiology. 2004;159(5):423-43.
Acharya U, Gau J-T, Horvath W, Ventura P, Hsueh C-T, Carlsen W. Hemolysis and hyperhomocysteinemia caused by cobalamin deficiency: three case reports and review of the literature. J Hematol Oncol. 2008;1:26.
Briani C, Dalla Torre C, Citton V, Manara R, Pompanin S, Binotto G, et al. Cobalamin deficiency: clinical picture and radiological findings. Nutrients. 2013;5(11):4521-39.
Kaferle J, Strzoda CE. Evaluation of macrocytosis. American family physician. 2009;79(3).
Duzgun S, Yildirmak Y, Çetinkaya F. Neutrophil hypersegmentation and thrombocytosis in children with iron deficiency anemia. TURKISH JOURNAL OF PEDIATRICS. 2005;47(3):251.
Westerman D, Evans D, Metz J. Neutrophil hypersegmentation in iron deficiency anaemia: a case-control study. British journal of haematology. 1999;107(3):512-5.
Ozkurt S, Temiz G, Saylisoy S, Soydan M. Cerebral sinovenous thrombosis associated with factor V Leiden and methylenetetrahydrofolate reductase A1298C mutation in adult membranous glomerulonephritis. Renal failure. 2011;33(5):524-7.
Kreidy R. Influence of acquired and genetic risk factors on the prevention, management, and treatment of thromboembolic disease. International journal of vascular medicine. 2014;2014.
Anno M, Yamazaki T, Hara N, Hayakawa K. Recurrent Postoperative Spinal Epidural Hematoma in a Patient with Protein S Deficiency. Case reports in orthopedics. 2015;2015.
Szolnoky G, Nagy N, Kovács R, Dósa-Rácz E, Szabó A, Bársony K, et al. Complex decongestive physiotherapy decreases capillary fragility in lipedema. Lymphology. 2008;41(4):161.
Dharsono F, Phatouros CC. Arterial origin subdural hematoma and associated pial pseudoaneurysm following minor head trauma. Clinical imaging. 2013;37(4):750-2.
Kahraman S, Kayali H, Atabey C, Acar F, Gocmen S. The accuracy of near-infrared spectroscopy in detection of subdural and epidural hematomas. Journal of Trauma and Acute Care Surgery. 2006;61(6):1480-3.
Gadiyaram V, Khan M, Hogan T, Altaha R, Crowell E, Hobbs G, et al., editors. Significance of MTHFR gene mutation with normal homocysteine level in vascular events. ASCO Annual Meeting Proceedings; 2009.
Cappellini MD, Poggiali E. Hypercoagulability and thrombosis. Thalassemia Reports. 2013;3(1s):10.
Smalberg JH, Kruip MJ, Janssen HL, Rijken DC, Leebeek FW, de Maat MP. Hypercoagulability and Hypofibrinolysis and Risk of Deep Vein Thrombosis and Splanchnic Vein Thrombosis Similarities and Differences. Arteriosclerosis, thrombosis, and vascular biology. 2011;31(3):485-93.
Chan MY, Andreotti F, Becker RC. Hypercoagulable states in cardiovascular disease. Circulation. 2008;118(22):2286-97.
Hibbard BM, Hibbard ED. Neutrophil hypersegmentation and defective folate metabolism in pregnancy. BJOG: An International Journal of Obstetrics & Gynaecology. 1971;78(9):776-80.
Leclair SJ. Morphologic and Distributive Leukocyte Disorders. Hematology: Clinical Principles and Applications. 2007:373.
- Abstract Viewed: 673 times
- PDF Downloaded: 402 times
