Table 2: List of similar cases published in literature
The underlying pathophysiology of hyponatremia in pulmonary tuberculosis is likely multifactorial. Firstly, the pulmonary infection can lead to an excessive release of inflammatory cytokines, such as interleukin-6 and tumor necrosis factor-alpha, which may stimulate the secretion of antidiuretic hormone (ADH) from the posterior pituitary gland. The increased ADH levels result in impaired water excretion, leading to dilutional hyponatremia. Secondly, pulmonary tuberculosis can cause systemic inflammation and oxidative stress, which may affect the renal tubules’ ability to regulate sodium and water balance. Additionally, tuberculous involvement of the central nervous system can disrupt the normal regulation of ADH release, further contributing to hyponatremia [13-15]. Patients with PTB who are older and have an increased CRP level are likely to have hyponatremia [16].