Discussion
Infectious infections like tuberculosis have been known to cause polyserositis. Serosal tuberculosis is a common extrapulmonary manifestation, particularly in places with a high tuberculosis burden, whereas polyserositis is a less common form of the disease [7, 8]. In an old case series, 50% of the cases of polyserositis had mycobacterium tuberculosis [9]. Certain case reports have shown that endocrine disorders including hypothyroidism can also be the cause for polyserositis [10]. A diagnostic challenge is faced when both tuberculosis and hypothyroidism are present in a patient who has polyserositis and microbiologic tests, such as GeneXpert, remain the most important tools to confirm tuberculosis as a cause for the polyserositis, like in our case.
The most typical clinical features of hypothyroidism include cold intolerance, fatigue, weight gain, constipation, and dry skin [11, 12]. In patients with primary hypothyroidism, ascites, pericardial effusion, or pleural effusion can all occur alone; however, the occurrence of all three together is highly uncommon and not well recognized [13]. Hypothyroidism-related pericardial and pleural effusions have features that lie in between exudate and transudate and exhibit little sign of inflammation [14]. Different pleural fluid characteristics including transudate, exudative and bloody pleural effusions have been reported from patients with multiple body cavity fluid collections due to hypothyroidism [15 – 18]. Our patient had clinical features and thyroid function tests suggestive of hypothyroidism; however, the polyserositis was most likely due to disseminated tuberculosis evidenced by positive GeneXpert MTB/RIF test from sputum and the exudative nature of the pleural fluid.
In a small study of 50 patients with sputum-positive pulmonary TB who were hospitalized in South Africa, the most prevalent endocrine dysfunction was a low free T3 state, which was present in almost 90% of patients as part of sick euthyroid syndrome. In some hospitalized individuals recovering from nonthyroidal illnesses, temporary spikes in blood TSH values (up to 20 mU/L) may occur [20]. It is typical for patients to have permanent hypothyroidism when their serum TSH levels are over 20 mU/L [21]. Sick euthyroid syndrome might have been considered as one differential diagnosis for the hypothyroidism in our patient; but, the very high TSH level (47 mU/L) was suggestive of permanent hypothyroidism.
Hypothyroidism has been rarely reported to be caused by thyroid tuberculosis (TB), an uncommon disease with an incidence of 0.1-0.4%, even in areas with high rates of pulmonary tuberculosis. Our patient did not have a thyroid mass or nodule, which contrasts with solitary thyroid nodule, which is the most common clinical presentation of thyroid TB [22]. There are also case reports of hypothyroidism following the initiation of second-line anti-TB agents, particularly p-amino salicylic acid and ethionamide, and first-line anti-TB agents such as rifampicin, which have more significant effects on thyroid physiology [23, 24]. Contrary to these findings, our patient did not take any anti-tuberculous medication before the diagnosis of hypothyroidism.