P-119 PRIMARY HYPOTHYROIDISM MISDIAGNOSED AS A CASE OF PROLACTINOMA

Abstract Introduction Primary hypothyroidism is a frequently diagnosed endocrine disorder. Common signs and symptoms include asthenia, lethargy, cold sensitivity, rough voice, dry skin, constipation; however, some patients may present atypical signs and symptoms, which can result in diagnostic confusion. Primary hypothyroidism causes elevated thyrotropin-releasing hormone due to a loss of thyroxin feedback inhibition. Increased thyrotropin-releasing hormone levels can result in lactotroph hyperplasia and increasing prolactin. The degree of hyperprolactinemia is generally modest, and rarely exceeds 100 ng/mL. Clinical Case We report 18 years old female non pregnant patient presented with secondary amenorrhea 8 months ago, breast heaviness, with a presumptive diagnosis of a prolactinoma by her gynecologist based on amenorrhea and hyperprolactinemia. Referred to endocrinology consultation for hyperprolactinemia On clinical examination, her blood pressure was 110/70 mmHg with a pulse rate of 75beats/min. The thyroid gland was enlarged. Her serum prolactin that was 112 ng/mL, thyroid-stimulating hormone (TSH) was 145 mIU/L (0.3-6), FT4 was 0.2ng/dL(0.8-1.7). She was prescribed levothyroxine 100 mcg daily and 6 weeks later the patient presented with improved her general state and decreased breast heaviness. Her repeat blood testing showed normal thyroid stimulating hormone TSH level of 1.6 mIU/ml and normal serum prolactin level of 26ng/ml. Hypothyroidism is an important etiology of hyperprolactinemia. In overt hypothyroidism, the prevalence of hyperprolactinemia has been reported up to 40% Our case is primary hypothyroidism associated with hyperprolactinemia this cannot be only explained by the stimulatory effect of TRH on lactotrophs but also in primary hypothyroidism, pituitary cells also have reduced sensitivity to dopamine’s inhibitory effect. On the other hand, tri-iodothyronine (T3) was shown to decrease PRL mRNA levels in pituitary cells. Therefore, reduced thyroid hormone levels will increase prolactin synthesis. Prolactin clearance from circulation is also reduced in hypothyroidism. Hyperprolactinemia management depends on its etiology. In patients with prolactin-secreting pituitary adenoma, dopamine receptor agonists are used. However, in patients with hypothyroidism, thyroid hormone replacement can lead to the resolution of hyperprolactinemia without the need for additional interventions. Thyroid hormone replacement reversed the condition in our case and no need for treatment with dopaminergic agonists. Conclusion Primary hypothyroidism is known to cause hyperprolactinemia. Clinicians must understand the effect of primary hypothyroidism on prolactin to avoid unnecessary treatment with dopaminergic agonists. Thyroid hormone replacement can reverse the condition.