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ORIGINAL ARTICLE
Year : 2021  |  Volume : 12  |  Issue : 4  |  Page : 181-188

Platelet function in overt hypothyroidism


1 Department of Physiology, The Coagulation Research Laboratory, College of Medicine and King Saud University Medical City, King Saud University, Riyadh, Saudi Arabia
2 Department of Medicine, College of Medicine and King Saud University Medical City, King Saud University, Riyadh, Saudi Arabia

Correspondence Address:
Dr. Abeer Khalid Al-Ghumlas
Department of Physiology, The Coagulation Research Laboratory,College of Medicine and King Saud University Medical City, King Saud University, Riyadh
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/joah.joah_8_21

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BACKGROUND: Hypothyroidism is associated with a shift of the hemostatic system to a hypocoagulable state and inhibited platelet function. However, previous studies did not consider the different degrees of response to thyroxine treatment and its effect on platelet function. This raises the need for further studies to clarify the effect of different degrees of responses to treatment on platelet function in hypothyroid disease. OBJECTIVES: To characterize the abnormalities in the primary hemostasis (platelet adhesion and aggregation) in patients with overt hypothyroidism on L-thyroxine therapy and to study the effect of variation of the responses to treatment on platelet function. MATERIALS AND METHODS: This cross-sectional study includes 64 patients with overt hypothyroidism on L-Thyroxine treatment. The patients were divided into three groups according to their response to treatment. Group-I: euthyroid patients (ET) (n = 25): (normal thyroid-stimulating hormone [TSH] and free T4), Group II: subclinical hypothyroid (SH) (n = 22): (high TSH and normal free T4), and Group III: inadequately treated hypothyroid (IH) (n = 17) (high TSH and low T4). Platelet function was assessed by light transmissiom aggregation response to adenosine diphosphate (ADP), arachidonic acid (AA), epinephrine (EPN), collagen, and ristocetin and by the platelet function analyzer (PFA-100) closure times (CTs). RESULTS: Platelet aggregation responses showed a significant reduction to ADP in ET patients (42.9 ± 20.7), SH patients (41.8 ± 24.2), and IH patients (46.9 ± 20.1) and to risocetin in ET patients (62.9 ± 22.8), SH patients (62.6 ± 21.2), and IH patients (61.3 ± 14.6) as compared to the controls (59.1 ± 9.5) and (75.3 ± 6.9), respectively. There is a significant prolongation of C/EPN: (175.6 ± 82.5) in the IH patients as compared to the controls (141.6 ± 26.8). Significant prolongation of C/ADP CT (132.2 ± 72.5) in IH patients as compared to the controls (100.7 ± 24.1) was found with normalization of both CT in ET patients. CONCLUSIONS: In overt hypothyroidism using two different tests of platelet function, we confirmed that the existence of a hypocoagulable state is due in part to a defect in primary hemostasis. Moreover, the defect varies according to the degree of response to L-Thyroxine treatment; it is more pronounced in inadequately treated hypothyroid patients and less in the subclinical hypothyroid.


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