Endocrine Abstracts

Introduction: Thyroid diseases have been known to cause haemostatic changes, either tendency to bleeding or thrombosis. We report a case of a patient with primary hypothyroidism presenting with spontaneous bleeding and jugular thrombosis.

Case report: An 85-year old patient with no medical history was admitted to the endocrinology department with primary auto-immune hypothyroidism. Hypothyroidism was suspected because of severe loss of weight and appetite, constipation and an extreme fatigue and lethargy. Initial TSH levels were>180 µUI/ml, FT4 was at 0pmol/l and morning serum cortisol was at 81ng/ml. Thyroid Peroxydase antibodies were at 643.2 UI/ml (Normal range <9UI/ml). Upon admission, patient was lethargic, had macroglossia and normal blood pressure. No bruising or spontaneous bleeding were noted or reported by the patient. The patient was started on 20 mg of hydrocortisone, and L-thyroxin was progressively initiated at the dosage of 12.5µg daily. Further work-up found megaloblastic anemia at 6,9g/dl along with moderately low level of Platelets at 111 000/µl. Prothrombin time (PT) was normal. On the sixth day of in-hospital stay, the patient presented a mild traumatic bruising on the right arm. Platelets count was normal (170 000/µl) and PT was normal again. CT scan showed an abdominal and pleural effusion, thrombosis of the left jugular vein and an aneurysm on the right iliac artery with partial thrombosis. The patient was started on low dose aspirin. However, the bruising extended to the right shoulder and thorax thus aspirin was discontinued after 2 days. The patient quickly developed unexplained neurological distress, hypoxemia and was started on large spectrum antibiotic. However, death occurred on the 21^st day after admission.

Discussion: The association of bleeding state and thrombosis in our patient is remarkable. Overt hypothyroidism usually leads to tendency de bleeding due to a hypocoaguable state. This can be related to a decreased platelets count, an alteration of their aggregation and agglutination, and decreased levels of von Willebrand factor antigen and several multiple coagulation factors. Subclinical hypothyroidism, autoimmune thyroid disorders and hyperthyroidism are on the other hand associated to increased levels of fibrinogen thus a tendency to hypercoaguablity. These disorders are usually corrected after hormonal therapy. However in our case, spontaneous bleeding manifested and extended after initiation of L-Thyroxin. The use of aspirin was short in duration and could not explain its extension. No other cause for these haemostatic disorders was identified in our case. Prospective studies of thromboembolic states in auto-immune hypothyroidism are warranted.