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.