it is important that healthcare professionals recognize the imbalance promptly to prevent potential morbidity or mortality , since it is often a marker of underlying disease ( 1 ) . the syndrome of inappropriate secretion of antidiuretic hormone ( siadh ) is the most common cause of hyponatremia in patients suffering from pulmonary diseases . the main causes of siadh are central neurological diseases , malignant diseases , medication - related adverse effects , and pulmonary diseases such as pneumonia and pulmonary tuberculosis ( 2 ) . several cases of pulmonary tuberculosis complicated with siadh have been documented ( 3 - 5 ) . minami et al . summarized eight case reports of tuberculosis - associated siadh and showed that seven of the reports were caused by severe tuberculosis , implying that extensive lung involvement is associated with the development of siadh in patients with pulmonary tuberculosis ( 4 ) . furthering this finding , nishizawa et al . summarized five case reports of tuberculosis with siadh and showed that siadh associated with pulmonary tuberculosis resulted in mild symptoms , including headache , nausea and vertigo ( 5 ) . we herein report a rare case of siadh complicated with status epilepticus that was caused by tuberculosis with mild lung involvement . a 75-year - old woman was admitted to the jikei university hospital due to impaired consciousness and status epilepticus . she was referred to the hospital 's outpatient clinic 24 days before admission to investigate a progressive mass - like lesion with a maximum diameter of 30 mm that was located on her left upper lung . positive results from an interferon - gamma - release assay ( t-spot.tb assay , oxford immunotec ltd . marlborough , ma , usa ) and a tuberculosis polymerase chain reaction ( pcr ) led to a diagnosis of pulmonary tuberculosis 16 days before admission . a sputum culture showed that the patient was positive for tuberculosis , and the diagnosis was later confirmed . the patient was prescribed four anti - tuberculosis medications ( isoniazid , rifampicin , ethambutol , and pyramide ) . she did not start taking full doses of the medications until two days prior to her admission due to anxiety over the side effects . her medical history included hypertension , gastric ulcer and hyperlipidemia , but she had been healthy until admission . on the day of admission , she was found lying on the floor at her home and was transported to the hospital . at the emergency room , she developed generalized seizures five times and was admitted to the intensive care unit to undergo treatment for statue epilepticus . on admission , the patient was unconscious ( glasgow coma scale , e1v1m3 ) with a body temperature of 37 , a heart rate of 108/min , a respiratory rate of 18 breaths / min , a saturation level of 99% on room air and a blood pressure of 160/90 mmhg . biochemical examinations showed hyponatremia ( 120 meq / l ) with low serum osmolality ( 253 mosm / kg ) , high urinary osmolality ( 458 mosm / kg ) , and a normal urinary sodium concentration ( 81 meq / l ) ( table ) . despite the patient 's severe hyponatremia , her serum antidiuretic hormone ( adh ) level was not decreased ( 3.3 pg / ml ) ; it was close to the upper limit of the normal range ( 0.3 - 4.2 pg / ml ) . the fact that her blood urea nitrogen ( bun ) to creatinine ( cr ) ratio was 6.6 and the fact that she did not experience severe diarrhea or vomiting implied that she was clinically euvolemic . based on these laboratory findings , this patient met the criteria for siadh , which were as follows : decreased effective osmolality ; urinary osmolality , > 100 mosm / kg of water ; clinical euvolemia ; urinary sodium concentration , > 40 mmol / l ; and normal thyroid and adrenal functions ( 2 ) . chest radiography and computed tomography ( ct ) showed a wedge - shaped infiltrative shadow with small tree - in - bud satellite lesions in the left upper lobe of the lung ( fig . 1 ) . with the exception of pulmonary tuberculosis , contrast - enhanced ct of the whole body brain magnetic resonance imaging ( mri ) revealed no abnormalities and electroencephalograms , which were taken three times , were all normal . a cerebrospinal fluid examination ( csf ) showed no increase in the cell count ( 0 cells / ul ) or the total protein level ( 47 mg / dl ) , no decrease in the glucose ( 102 mg / dl ) , and was culture - negative for tuberculosis and bacteria . she was not taking any medicines that have previously been reported as a potential cause of siadh . it was therefore concluded the patient 's siadh was caused by pulmonary tuberculosis . among the prescribed medications , only isoniazid has the potential to lead to seizures . however , this possibility was excluded due to a lack of complications during re - administration . accordingly , we concluded that the patient 's status epilepticus could be attributed to hyponatremia , which had caused by pulmonary tuberculosis - associated siadh . pct : procalcitonin , pac : plasma aldosterone concentration , pra : plasma renin activity , crp : c - reactive protein , sil-2r : soluble interleukin-2 receptor a : chest radiography on admission showed mass - like shadow in the left upper lung field . b : ct on admission showed wedge - shaped infiltrative shadow with small tree - in - bud satellite lesions in the left upper lobe . her level of consciousness improved after an infusion of saline to treat her abnormal serum sodium concentration , and she became conscious on the second day after admission ( fig . rhabdomyolysis occurred due to the patient 's status epilepticus , and her creatine kinase ( ck ) levels increased ( 6,630 siadh did not recur after the patient resumed taking the anti - tuberculosis medicines and she was discharged from the hospital on the 22nd day after admission . inh : isoniazid , rfp : rifampicin , eb : ethambutol , pza : pyrazinamide , jcs : japan coma scale , cons : consciousness , p - osmo : plasma osmolality siadh is characterized by the excessive release of adh , which results in dilutional hyponatremia and an increase in the blood volume . this form of hyponatremia is associated with neurological symptoms such as headaches , confusion , weakness , seizures , and coma ( 2 ) . the causes of siadh include , but are not limited to , central nervous system diseases , malignant diseases , drug - induced diseases , and pulmonary diseases . it is estimated that about 2.1% of pulmonary disease - related siadh cases can be attributed to pulmonary tuberculosis ( 3 ) . it has been reported that 10.7% of patients with newly diagnosed active pulmonary tuberculosis have hyponatremia ( 6 ) . although it is not clear what percentage of hyponatremia cases are associated with siadh , nakamata et al . reported that approximately 29% of lung tuberculosis patients had high plasma adh , suggesting the existence of a potential causal relationship between pulmonary tuberculosis and siadh ( 7 ) . adh is released from the posterior pituitary in response to a decrease in the intravascular volume or an increase in the serum osmolality ( 8) ; however the cause of the inappropriate release of adh in patients with pulmonary tuberculosis is not fully understood . first , although our patient was not suffering from tuberculous meningitis , adh production may be triggered by cerebral insults , including infections and malignancies , which suggests that non - specific inflammation may stimulate the release of adh from the posterior pituitary ( 1,9 ) . moreover , recent reports have suggested that interleukin-6 ( il-6 ) has an important role in the release of adh in response to inflammatory diseases such as pneumonia and tuberculosis ( 10 ) . ogawa et al . reported that the monocytes or macrophages of tuberculosis patients showed higher levels of il-6-production than those of healthy subjects ( 11 ) . . however , our patient 's c reactive protein level was only slightly increased , implying that there was low inflammation . secondly , decreased blood flow in the intrathoracic vessels due to the destruction of the lung by extensive pulmonary tuberculosis can be sensed by the mechanoreceptors in the left ventricle , leading to the non - osmotic release of adh ( 12 ) . however , in the present case , the patient 's pulmonary tuberculosis was limited . finally , another intriguing possibility is the direct release of adh from lungs infected with tuberculosis . detected high concentrations of adh in tuberculous lung tissue , suggesting the production of adh in the local lung or that the tuberculous lung tissue had adsorbed an inappropriately released hormone from the posterior pituitary ( 13 ) . moreover , lee et al . reported a case of tuberculosis and proven diabetes insipidus in a patient who had an elevated adh level in the presence of hyponatremia even without using desmopressin , which suggested ectopic adh production ( 14 ) . in our case , siadh occurred two days after the initiation of anti - tuberculosis treatment . the bactericidal property of the medications might have affected the integrity of the tuberculous lung tissue , which may have resulted in the release of adh . thus , although it is still not clear whether adh is produced in tuberculous lung tissue or whether it accumulates there , we hypothesize that the accelerated temporary release of adh from tuberculous lung tissue due to anti - tuberculosis medications may have caused siadh in the present case . however , most of the cases were caused by severe lung tuberculosis or tuberculous meningitis and the symptoms were generally mild ( 5 ) . in contrast , our patient had mild lung tuberculosis complicated with siadh , which caused serious symptoms such as impaired consciousness and status epilepticus . the manifestations of hyponatremia are more prominent when a patient 's serum sodium concentration rapidly decreases ( 15 ) ; we therefore assumed that the severe symptoms in our case occurred due to a rapid decrease in the serum sodium concentration . this rapid decrease in the serum sodium concentration could be explained by a rapid release of adh . we hypothesize that the accelerated and temporary release of adh was from the tuberculous lung tissue , and that it was induced by the bactericidal property of the anti - tuberculosis medicines . we believe that close observation is required to detect symptoms of siadh , even in cases of mild lung tuberculosis , especially when a patient begins to take anti - tuberculosis medications .
a 76-year - old woman was diagnosed with lung tuberculosis . on the second day of anti - tuberculosis treatment 
 , she became unconscious and developed status epilepticus accompanied by hyponatremia . 
 the hyponatremia was caused by the syndrome of inappropriate secretion of antidiuretic hormone ( siadh ) . 
 detailed examinations revealed that the patient 's status epilepticus had occurred due to hyponatremia , which was caused by lung tuberculosis - associated siadh . 
 previous case reports noted that patients with tuberculosis - associated siadh showed mild clinical manifestations . 
 they also reported that extensive lung involvement was associated with siadh development . 
 we herein report a rare case of siadh complicated with status epilepticus that was caused by tuberculosis with mild lung involvement .