Hematologic Abnormalities in Patients with Endocrine and Metabolic Disorders

Orwoll, Eric S.; Orwoll, Rebecca L.

doi:10.1016/s0889-8588(18)30675-0

Cited by 10 publications

(10 citation statements)

References 99 publications

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“…Many factors are responsible for maintaining the haemostatic balance, and, among them, hormones directly influence both primary and secondary haemostasis [1]. A wide variety of endocrine disorders have been associated with both mild abnormalities in laboratory coagulation tests, and clinical thrombotic or bleeding manifestations.…”

Section: Introductionmentioning

confidence: 99%

The coagulation system in endocrine disorders: A narrative review

et al. 2007

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Endocrine disorders can influence the haemostatic balance. Abnormal coagulation test results have been observed in patients with abnormal hormone levels. Also unprovoked bleeding or thrombotic events have been associated with endocrine disease. The aim of the present review is to summarise the available evidence on the influence of common endocrine disorders on the coagulation system, and their possible clinical implications. We focus on thyroid dysfunction, hyper- and hypocortisolism and growth hormone disturbances, while other endocrine disorders are only briefly discussed. In the published literature a clear bleeding diathesis has only been associated with overt hypothyroidism, mainly mediated by an acquired von Willebrand syndrome. A clinically relevant hypercoagulable state may be present in patients with hyperthyroidism, hypercortisolism or abnormal growth hormone levels, but adequate prospective clinical studies are lacking. Also effects of pheochromocytoma, hyperprolactinaemia and hyperaldosteronism on the coagulation system have been described. It is apparent that unprovoked bleeding and thrombotic episodes can be secondary to endocrine disorders.

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Section: Introductionmentioning

confidence: 99%

The coagulation system in endocrine disorders: A narrative review

et al. 2007

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“…However, disturbances in sex steroids contribute to a number of diseases such as anemia. 40 In the chicken, estrogen and GR ligands (Dex) both contribute to long-term self-renewal of erythroid progenitors 41,42 and, consequently, interfere with terminal maturation. 43 These observations prompted us to expand human erythroblasts in the presence of various other hormones besides Dex.…”

mentioning

confidence: 99%

Different steroids co-regulate long-term expansion versus terminal differentiation in primary human erythroid progenitors

Leberbauer

Boulmé

Unfried

et al. 2005

Blood

170

143

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Outgrowth, long-term self-renewal, and terminal maturation of human erythroid progenitors derived from umbilical cord blood in serum-free medium can be modulated by steroid hormones. Homogeneous erythroid cultures, as characterized by flow cytometry and dependence on a specific mixture of physiologic proliferation factors, were obtained within 8 days from a starting population of mature and immature mononuclear cells. Due to previous results in mouse and chicken erythroblasts, the proliferation-promoting effect of glucocorticoids was not unexpected. Surprisingly, however, androgen had a positive effect on the sustained expansion of human female but not male erythroid progenitors. Under optimal conditions, sustained proliferation of erythroid progenitors resulted in a more than 10 9 -fold expansion within 60 days. Terminal erythroid maturation was significantly improved by adding human serum and thyroid hormone ( IntroductionHematopoietic development within the erythroid lineage requires a delicate balance between the opposing effects of proliferationpromoting factors maintaining the renewal capacity of immature erythroid progenitors and differentiation-inducing factors required for successful terminal maturation of erythroid progenitors into red blood cells. 1 In adult humans, erythroid differentiation produces about 2 ϫ 10 11 (roughly 20 g) red cells per day, representing the most vigorous proliferation process in the entire body. Because low numbers of erythrocytes are immediately life-threatening, erythropoiesis needs regulatory mechanisms temporarily altering the balance toward enhanced proliferation to cope with stress situations such as low oxygen levels at elevated altitudes (hypoxia) or massive blood loss.In vivo, both renewal and maturation of human erythroid progenitors proceed in parallel in the bone marrow. It has thus been difficult to assess the contribution of particular signaling pathways and their deregulation during aberrant depletion of these progenitors, or their death on differentiation in anemia, versus unscheduled progenitor proliferation (as occurring in leukemogenesis). Most information was obtained from established cell lines and, more recently, primary animal cell models of chicken and mouse in defined media. [1][2][3] The latter approach even allowed analysis of cells from genetically modified mice. [4][5][6] For sustained proliferation, both avian and murine primary erythroblasts require cooperation between erythropoietin (Epo), stem cell factor (SCF), and glucocorticoids (dexamethasone [Dex]). Involvement of Epo and SCF was expected from their contribution to proliferation and survival of erythroid cells, 7-9 whereas the stress hormone Dex massively prolonged progenitor proliferation (from 10 to 30 days in chickens, 7 to 20 days in mice), at the same time reducing their rate of spontaneous differentiation. Our idea that this might point to specific roles for glucocorticoids in stress erythropoiesis could be verified in vivo using mutant mice carrying a dimerizationdefective glucoco...

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“…The hematopoietic system is affected in hyperthyroidism and changes can be seen in all three blood cell lineages [1], although they are usually not catastrophic [2]. Graves' disease is the most common cause of hyperthyroidism and results from production of autoantibodies that bind to and stimulate the TSH receptors [3].…”

Section: Discussionmentioning

confidence: 99%

“…Anemia can be seen in 10–20% of patients with thyrotoxicosis [2]. Interestingly, hyperthyroidism is associated with increased total number of red blood cells, likely due to increased tissue oxygen demands resulting in increased erythropoietin secretion.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, hyperthyroidism is associated with increased total number of red blood cells, likely due to increased tissue oxygen demands resulting in increased erythropoietin secretion. However, anemia can be seen in hyperthyroid patients because of simultaneous increase in plasma volume, shorter erythrocyte life span, abnormal iron utilization, or deficiency of iron, vitamin B12, or folate [1, 2]. In one study, anemia was present in 33% of GD patients, and an obvious secondary cause could be found only in one-third of the anemic patients [5].…”

Section: Discussionmentioning

confidence: 99%

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Graves’ Disease Causing Pancytopenia and Autoimmune Hemolytic Anemia at Different Time Intervals: A Case Report and a Review of the Literature

Naji

Kumar

Dewani

et al. 2013

Case Reports in Medicine

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Graves' disease (GD) is associated with various hematologic abnormalities but pancytopenia and autoimmune hemolytic anemia (AIHA) are reported very rarely. Herein, we report a patient with GD who had both of these rare complications at different time intervals, along with a review of the related literature. The patient was a 70-year-old man who, during a hospitalization, was also noted to have pancytopenia and elevated thyroid hormone levels. Complete hematologic workup was unremarkable and his pancytopenia was attributed to hyperthyroidism. He was started on methimazole but unfortunately did not return for followup and stopped methimazole after a few weeks. A year later, he presented with fatigue and weight loss. Labs showed hyperthyroidism and isolated anemia (hemoglobin 7 g/dL). He had positive direct Coombs test and elevated reticulocyte index. He was diagnosed with AIHA and started on glucocorticoids. GD was confirmed with elevated levels of thyroid stimulating immunoglobulins and thyroid uptake and scan. He was treated with methimazole and radioactive iodine ablation. His hemoglobin improved to 10.7 g/dL at discharge without blood transfusion. Graves' disease should be considered in the differential diagnosis of hematologic abnormalities. These abnormalities in the setting of GD generally respond well to antithyroid treatment.

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Hematologic Abnormalities in Patients with Endocrine and Metabolic Disorders

Cited by 10 publications

References 99 publications

The coagulation system in endocrine disorders: A narrative review

The coagulation system in endocrine disorders: A narrative review

Different steroids co-regulate long-term expansion versus terminal differentiation in primary human erythroid progenitors

Graves’ Disease Causing Pancytopenia and Autoimmune Hemolytic Anemia at Different Time Intervals: A Case Report and a Review of the Literature

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