open access

Vol 72, No 3 (2021)
Review paper
Published online: 2021-06-21
Submitted: 2021-03-07
Accepted: 2021-03-14
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Changes in complete blood count parameters influenced by endocrine disorders

Ewelina Szczepanek-Parulska, Martyna Adamska, Oliwia Korda, Weronika Kosicka, Dagmara Skowrońska, Anna Świejkowska, Dominika Tuzimek, Daniela Dadej, Aleksandra Krygier, Marek Ruchała
DOI: 10.5603/EP.a2021.0059
·
Pubmed: 34292577
·
Endokrynologia Polska 2021;72(3):261-270.

open access

Vol 72, No 3 (2021)
Review Article
Published online: 2021-06-21
Submitted: 2021-03-07
Accepted: 2021-03-14

Abstract

Complete blood count is one of the most common diagnostic methods used in everyday practice. Hormonal status is known to affect blood count parameters. The aim of this study is to summarize changes in blood count that may indicate endocrine disorders, based on a literature review. Red cell parameters deteriorate in thyroid disorders including autoimmune thyroiditis and tend to resolve with appropriate treatment implementation. The most frequent form of anaemia associated with thyroid dysfunction is normocytic anaemia.

Macrocytic anaemia is more typical of autoimmune thyroiditis-induced hypothyroidism, while microcytic anaemia is more common in hyperthyroidism. Unexplained anaemia or an increase in red cell distribution width should prompt the investigation of thyroid disorders. Cushing’s disease may manifest as an increase in white blood cells and platelets. In the blood smear, neutrophilia is often present, while lymphocytes and eosinophils may be within the lower normal range. Hypercortisolism may induce both hyperaemia and anaemia. In hypopituitarism, a decrease in red blood cell count, haemoglobin, haematocrit, and platelets is observed. Acromegaly may be accompanied by an increase in mean corpuscular volume of erythrocytes.

Testosterone deficiency is manifested by a decrease in red cell parameters,
whereas hyperandrogenism may lead to polycythaemia. In polycystic ovary syndrome an increase in white blood cell count reflects an underlying inflammatory state. Complete blood count analysis is an easily available and cost-effective additional tool in the diagnosis and treatment monitoring of endocrine disorders. 

Abstract

Complete blood count is one of the most common diagnostic methods used in everyday practice. Hormonal status is known to affect blood count parameters. The aim of this study is to summarize changes in blood count that may indicate endocrine disorders, based on a literature review. Red cell parameters deteriorate in thyroid disorders including autoimmune thyroiditis and tend to resolve with appropriate treatment implementation. The most frequent form of anaemia associated with thyroid dysfunction is normocytic anaemia.

Macrocytic anaemia is more typical of autoimmune thyroiditis-induced hypothyroidism, while microcytic anaemia is more common in hyperthyroidism. Unexplained anaemia or an increase in red cell distribution width should prompt the investigation of thyroid disorders. Cushing’s disease may manifest as an increase in white blood cells and platelets. In the blood smear, neutrophilia is often present, while lymphocytes and eosinophils may be within the lower normal range. Hypercortisolism may induce both hyperaemia and anaemia. In hypopituitarism, a decrease in red blood cell count, haemoglobin, haematocrit, and platelets is observed. Acromegaly may be accompanied by an increase in mean corpuscular volume of erythrocytes.

Testosterone deficiency is manifested by a decrease in red cell parameters,
whereas hyperandrogenism may lead to polycythaemia. In polycystic ovary syndrome an increase in white blood cell count reflects an underlying inflammatory state. Complete blood count analysis is an easily available and cost-effective additional tool in the diagnosis and treatment monitoring of endocrine disorders. 

Get Citation

Keywords

complete blood count; endocrine diseases; hyperthyroidism; hypothyroidism; acromegaly; Cushing’s disease

About this article
Title

Changes in complete blood count parameters influenced by endocrine disorders

Journal

Endokrynologia Polska

Issue

Vol 72, No 3 (2021)

Article type

Review paper

Pages

261-270

Published online

2021-06-21

DOI

10.5603/EP.a2021.0059

Pubmed

34292577

Bibliographic record

Endokrynologia Polska 2021;72(3):261-270.

Keywords

complete blood count
endocrine diseases
hyperthyroidism
hypothyroidism
acromegaly
Cushing’s disease

Authors

Ewelina Szczepanek-Parulska
Martyna Adamska
Oliwia Korda
Weronika Kosicka
Dagmara Skowrońska
Anna Świejkowska
Dominika Tuzimek
Daniela Dadej
Aleksandra Krygier
Marek Ruchała

References (79)
  1. Hernik A, Szczepanek-Parulska E, Filipowicz D, et al. The hepcidin concentration decreases in hypothyroid patients with Hashimoto's thyroiditis following restoration of euthyroidism. Sci Rep. 2019; 9(1): 16222.
  2. Szczepanek-Parulska E, Hernik A, Ruchała M. Anemia in thyroid diseases. Pol Arch Intern Med. 2017; 127(5): 352–360.
  3. Shakir KM, Turton D, Aprill BS, et al. Anemia: a cause of intolerance to thyroxine sodium. Mayo Clin Proc. 2000; 75(2): 189–192.
  4. Bremner AP, Feddema P, Joske DJ, et al. Significant association between thyroid hormones and erythrocyte indices in euthyroid subjects. Clin Endocrinol (Oxf). 2012; 76(2): 304–311.
  5. Montagnana M, Lippi G, Targher G, et al. The red blood cell distribution width is associated with serum levels of thyroid stimulating hormone in the general population. Int J Lab Hematol. 2009; 31: 581–582.
  6. Aktas G, Sit M, Dikbas O, et al. Could red cell distribution width be a marker in Hashimoto's thyroiditis? Exp Clin Endocrinol Diabetes. 2014; 122: 572–574.
  7. Hernik A, Szczepanek-Parulska E, Filipowicz D, et al. Hepcidin and Iron Homeostasis in Patients with Subacute Thyroiditis and Healthy Subjects. Mediators Inflamm. 2019; 2019: 5764061.
  8. He L, Shen C, Zhang Y, et al. Evaluation of serum ferritin and thyroid function in the second trimester of pregnancy. Endocr J. 2018; 65(1): 75–82.
  9. Keskin H, Kaya Y, Cadirci K, et al. Elevated neutrophil-lymphocyte ratio in patients with euthyroid chronic autoimmune thyreotidis. Endocr Regul. 2016; 50(3): 148–153.
  10. Erikci AA, Karagoz B, Ozturk A, et al. The effect of subclinical hypothyroidism on platelet parameters. Hematology. 2009; 14(2): 115–117.
  11. Kutluturk F, Gul SS, Sahin S, et al. Comparison of Mean Platelet Volume, Platelet Count, Neutrophil/ Lymphocyte Ratio and Platelet/Lymphocyte Ratio in the Euthyroid, Overt Hypothyroid and Subclinical Hyperthyroid Phases of Papillary Thyroid Carcinoma. Endocr Metab Immune Disord Drug Targets. 2019; 19(6): 859–865.
  12. Ford HC, Carter JM. The haematology of hyperthyroidism: abnormalities of erythrocytes, leucocytes, thrombocytes and haemostasis. Postgrad Med J. 1988; 64(756): 735–742.
  13. Garla VV, Abdul Salim S, Yanes-Cardozo LL. Pancytopenia: a rare complication of Graves' disease. BMJ Case Rep. 2018; 2018.
  14. Naji P, Kumar G, Dewani S, et al. Graves' disease causing pancytopenia and autoimmune hemolytic anemia at different time intervals: a case report and a review of the literature. Case Rep Med. 2013; 2013: 194542.
  15. Dorgalaleh A, Mahmoodi M, Varmaghani B, et al. Effect of thyroid dysfunctions on blood cell count and red blood cell indice. Iran J Ped Hematol Oncol. 2013; 3: 73–77.
  16. Krygier A, Szczepanek-Parulska E, Filipowicz D, et al. Changes in serum hepcidin according to thyrometabolic status in patients with Graves’ disease. Endocr Connect. 2020; 9(3): 234–242.
  17. Turan E. Evaluation of neutrophil-to-lymphocyte ratio and hematologic parameters in patients with Graves' disease. Bratisl Lek Listy. 2019; 120(6): 476–480.
  18. Nakamura H, Miyauchi A, Miyawaki N, et al. Analysis of 754 cases of antithyroid drug-induced agranulocytosis over 30 years in Japan. J Clin Endocrinol Metab. 2013; 98(12): 4776–4783.
  19. Ross DS, Burch HB, Cooper DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid. 2016; 26(10): 1343–1421.
  20. Bagir GS, Haydardedeoglu FE, Bakiner OS, et al. Mean Platelet Volume in Graves' disease: A Sign of Hypermetabolism Rather than Autoimmunity? Pak J Med Sci. 2017; 33(4): 871–875.
  21. Franchini M, Lippi G, Manzato F, et al. Hemostatic abnormalities in endocrine and metabolic disorders. Eur J Endocrinol. 2010; 162(3): 439–451.
  22. Pincet L, Gorostidi F. Graves Disease Causing Pancytopenia: Case Report and Literature Review. Clin Med Insights Case Rep. 2018; 11: 1179547618781090.
  23. Rafhati AN, See CK, Hoo FK, et al. A report of three cases of untreated Graves' disease associated with pancytopenia in Malaysia. Electron Physician. 2014; 6(3): 877–882.
  24. Baagar KA, Siddique MA, Arroub SA, et al. Atypical Complications of Graves' Disease: A Case Report and Literature Review. Case Rep Endocrinol. 2017; 2017: 6087135.
  25. Artemniak-Wojtowicz D, Witkowska-Sędek E, Borowiec A, et al. Peripheral blood picture and aminotransferase activity in children with newly diagnosed Graves' disease at baseline and after the initiation of antithyroid drug therapy. Cent Eur J Immunol. 2019; 44(2): 132–137.
  26. Bolanowski M, Ruchała M, Zgliczyński W, et al. Diagnostics and treatment of acromegaly — updated recommendations of the Polish Society of Endocrinology. Endokrynol Pol. 2019; 70(1): 2–18.
  27. Giustina A, Barkan A, Beckers A, et al. A Consensus on the Diagnosis and Treatment of Acromegaly Comorbidities: An Update. J Clin Endocrinol Metab. 2020; 105(4).
  28. Bolanowski M, Ruchała M, Zgliczyński W, et al. Acromegaly--a novel view of the patient. Polish proposals for diagnostic and therapeutic procedures in the light of recent reports. Endokrynol Pol. 2014; 65(4): 326–331.
  29. Mazziotti G, Marzullo P, Doga M, et al. Growth hormone deficiency in treated acromegaly. Trends Endocrinol Metab. 2015; 26(1): 11–21.
  30. Colao A, Grasso LFS, Di Somma C, et al. Acromegaly and Heart Failure. Heart Fail Clin. 2019; 15(3): 399–408.
  31. Ucler R, Aslan M, Atmaca M, et al. The effect of disease control on mean platelet volume and red blood cell distribution in patients with acromegaly. Int J Clin Exp Med. 2015; 8: 6060–6066.
  32. Strauch G, Lego A, Therain F, et al. Reversible plasma and red blood cells volumes increases in acromegaly. Acta Endocrinol (Copenh. 1997; 85: 465–478.
  33. Vizioli L, Muscari S, Muscari A. The relationship of mean platelet volume with the risk and prognosis of cardiovascular diseases. Int J Clin Pract. 2009; 63(10): 1509–1515.
  34. Arpaci D, Kuzu F, Unal M, et al. Assessment of Mean Platelet Volume and its Effect on Disease Control in Patients with Acromegaly. Clin Lab. 2016; 62(11): 2167–2171.
  35. Demirpence M, Yasar HY, Colak A, et al. Mean Platelet Volume and Platelet Function Analysis in Acromegalic Patients before and after Treatment. Acta Endocrinol (Buchar). 2016; 12(4): 401–406.
  36. Unübol M, Güney E, Türe M, et al. Mean platelet volume and arterial stiffness in patients with acromegaly. Anadolu Kardiyol Derg. 2014; 14(5): 456–463.
  37. Ersoy R, Gul K, Solaroglu N, et al. Effect of a six-month treatment with octreotide long acting repeatable (LAR) on mean platelet volume in patients with acromegaly. Endocrine Abstr. 2008; 16.
  38. Durmaz S, Carlioglu A, Ayhan E, et al. The effects of octreotide acetate long-acting repeatable on mean platelet volume in acromegaly: octreotidelar may have a detrimental effect on MPV, a new indicator of atherosclerosis. Endocrine Abstr. 2014; 35: 855–855.
  39. Gupta P, Dutta P. Co-Occurrence of Acromegaly and Hematological Disorders: A Myth or Common Pathogenic Mechanism. Integr Med Int. 2017; 4(1–2): 94–100.
  40. Üçler R, Aslan M, Atmaca M, et al. Evaluation of blood neutrophil to lymphocyte and platelet to lymphocyte ratios according to plasma glucose status and serum insulin-like growth factor 1 levels in patients with acromegaly. Hum Exp Toxicol. 2016; 35(6): 608–612.
  41. Kluczyński Ł, Gilis-Januszewska A, Rogoziński D, et al. Hypophysitis — new insights into diagnosis and treatment. Endokrynol Pol. 2019; 70(3): 260–269.
  42. Valerio G, Di Ma, Salerno M, et al. Assessment of red blood cell indices in growth-hormone-treated children. Horm Res. 1997; 47: 62–66.
  43. Ten Have SM, van der Lely AJ, Lamberts SW. Increase in haemoglobin concentrations in growth hormone deficient adults during human recombinant growth hormone replacement therapy. Clin Endocrinol (Oxf). 1997; 47(5): 565–570.
  44. Nishioka H, Haraoka J. Hypopituitarism and anemia: effect of replacement therapy with hydrocortisone and/or levothyroxine. J Endocrinol Invest. 2005; 28(6): 528–533.
  45. Beshyah SA, Markussis V, Harbourne T, et al. Haemostatic mechanisms are normal despite increased vascular mortality in hypopituitary adults. Horm Metab Res. 1993; 25(8): 449–450.
  46. Łebek-Szatańska A, Stelmachowska-Banaś M, Zieliński G, et al. Corticotropinoma as the underlying cause of intermittent Cushing's syndrome in a patient previously diagnosed with primary pigmented nodular adrenocortical disease. Endokrynol Pol. 2020; 71(3): 273–274.
  47. Szczepanek-Parulska E, Cyranska-Chyrek E, Nowaczyk M, et al. Diagnostic Difficulties In a Young Women With Symptoms of Cushing Syndrome. Endocr Pract. 2018; 24(8): 766.
  48. Ambrogio AG, De Martin M, Ascoli P, et al. Gender-dependent changes in haematological parameters in patients with Cushing's disease before and after remission. Eur J Endocrinol. 2014; 170(3): 393–400.
  49. Ellegala DB, Alden TD, Couture DE, et al. Anemia, testosterone, and pituitary adenoma in men. J Neurosurg. 2003; 98(5): 974–977.
  50. Masri-Iraqi H, Robenshtok E, Tzvetov G, et al. Elevated white blood cell counts in Cushing's disease: association with hypercortisolism. Pituitary. 2014; 17(5): 436–440.
  51. Wagner J, Langlois F, Lim DS, et al. Hypercoagulability and Risk of Venous Thromboembolic Events in Endogenous Cushing's Syndrome: A Systematic Meta-Analysis. Front Endocrinol (Lausanne). 2018; 9: 805.
  52. Melmed S, Casanueva FF, Hoffman AR, et al. Endocrine Society. Diagnosis and treatment of hyperprolactinemia: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2011; 96(2): 273–288.
  53. Szczepanek-Parulska E, Filipowicz D, Kuśmierek A, et al. Remarkable remission of an invasive giant prolactinoma under high-dose bromocriptine monotherapy. Pol Arch Intern Med. 2017; 127(7-8): 559–560.
  54. Erem C, Kocak M, Nuhoglu I, et al. Blood coagulation, fibrinolysis and lipid profile in patients with prolactinoma. Clin Endocrinol (Oxf). 2010; 73(4): 502–507.
  55. Anaforoglu I, Ertorer ME, Kozanoglu I, et al. Macroprolactinemia, like hyperprolactinemia, may promote platelet activation. Endocrine. 2010; 37(2): 294–300.
  56. Gerli R, Rambotti P, Nicoletti I, et al. Reduced number of natural killer cells in patients with pathological hyperprolactinemia. Clin Exp Immunol. 1986; 64(2): 399–406.
  57. Spry C. Eosinophilia in Addison's disease. Yale J Biol Med. 1976; 49(4): 411–413.
  58. Malu AO, Sanusi BR, Obineche EN. Addison's disease presenting with marked eosinophilia and psychosis. Trop Geogr Med. 1988; 40(3): 241–243.
  59. Coles AJ, Thompson S, Cox AL, et al. Dehydroepiandrosterone replacement in patients with Addison's disease has a bimodal effect on regulatory (CD4+CD25hi and CD4+FoxP3+) T cells. Eur J Immunol. 2005; 35(12): 3694–3703.
  60. Miller RA, Chrisp C. Lifelong treatment with oral DHEA sulfate does not preserve immune function, prevent disease, or improve survival in genetically heterogeneous mice. J Am Geriatr Soc. 1999; 47(8): 960–966.
  61. Vrkljan AM, Pašalić A, Strinović M, et al. Coexistence of Addison's Disease and Pernicious Anemia: Is the New Classification of Autoimmune Polyglandular Syndrome Appropriate? Acta Clin Croat. 2015; 54(2): 232–235.
  62. Benschop RJ, Rodriguez-Feuerhahn M, Schedlowski M. Catecholamine-induced leukocytosis: early observations, current research, and future directions. Brain Behav Immun. 1996; 10(2): 77–91.
  63. Larsson PT, Wallén NH, Hjemdahl P. Norepinephrine-induced human platelet activation in vivo is only partly counteracted by aspirin. Circulation. 1994; 89(5): 1951–1957.
  64. Sukoh N, Hizawa N, Yamamoto H, et al. Increased neutrophils in bronchoalveolar lavage fluids from a patient with pulmonary edema associated with pheochromocytoma. Intern Med. 2004; 43(12): 1194–1197.
  65. Zelinka T, Petrák O, Strauch B, et al. Elevated inflammation markers in pheochromocytoma compared to other forms of hypertension. Neuroimmunomodulation. 2007; 14(1): 57–64.
  66. Heilberg IP, Tótoli C, Calado JT. Adult presentation of Bartter syndrome type IV with erythrocytosis. Einstein (Sao Paulo). 2015; 13(4): 604–606.
  67. Erkelens DW, Statius van Eps LW. Bartter's syndrome and erythrocytosis. Am J Med. 1973; 55(5): 711–719.
  68. Novello L, Speiser PW. Premature Adrenarche. Pediatr Ann. 2018; 47(1): e7–ee11.
  69. Orio F, Manguso F, Di Biase S, et al. Metformin administration improves leukocyte count in women with polycystic ovary syndrome: a 6-month prospective study. Eur J Endocrinol. 2007; 157(1): 69–73.
  70. Dutkowska A, Konieczna A, Breska-Kruszewska J, et al. [Recomendations on non-pharmacological interventions in women with PCOS to reduce body weight and improve metabolic disorders [Zalecenia dotyczące postępowania niefarmakologicznego u kobiet z PCOS celem zmniejszenia masy ciała i poprawy zaburzeń metabolicznych]]. Endokrynol Pol. 2019; 70(2): 198–212.
  71. Milewicz A, Kudła M, Spaczyński RZ, et al. The polycystic ovary syndrome: a position statement from the Polish Society of Endocrinology, the Polish Society of Gynaecologists and Obstetricians, and the Polish Society of Gynaecological Endocrinology. Endokrynol Pol. 2018; 69(4).
  72. Rudnicka E, Kunicki M, Suchta K, et al. Inflammatory Markers in Women with Polycystic Ovary Syndrome. Biomed Res Int. 2020; 2020: 4092470.
  73. Nieschlag E. Late-onset hypogonadism: a concept comes of age. Andrology. 2020; 8(6): 1506–1511.
  74. Lunenfeld B, Mskhalaya G, Zitzmann M, et al. Recommendations on the diagnosis, treatment and monitoring of late-onset hypogonadism in men - a suggested update. Aging Male. 2013; 16(4): 143–150.
  75. Pekkolay Z. Idiopathic hypogonadotropic hypogonadism: erythrocyte indices in naive male patients. Eur J Med Invest. 2018.
  76. Namiki M, Akaza H, Shimazui T, et al. Working Committee on Clinical Practice Guidelines for Late-onset Hypogonadism, Japanese Urological Association/Japanese Society for Study of Aging Male. Clinical practice manual for late-onset hypogonadism syndrome. Int J Urol. 2008; 15(5): 377–388.
  77. Hughes D. The World Anti-Doping Code in sport: Update for 2015. Aust Prescr. 2015; 38(5): 167–170.
  78. Bird SR, Goebel C, Burke LM, et al. Doping in sport and exercise: anabolic, ergogenic, health and clinical issues. Ann Clin Biochem. 2016; 53(Pt 2): 196–221.
  79. Chrostowski K, Kwiatkowska D, Pokrywka A, et al. Renin-angiotensin-aldosterone system in bodybuilders using supraphysiological doses of anabolic-androgenic steroids. Biol Sport. 2011; 28(1): 11–17.

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