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].