syndrome of inappropriate secretion of antidiuretic hormone ( siadh ) , also known as the syndrome of inappropriate antidiuresis ( siad ) , is one of the most common causes of hyponatremia1 ) . impaired water excretion in the absence of renal insufficiency , glucocorticoid deficiency , hypothyroidism and decreased effective arterial blood volume are the hallmarks of this syndrome . although a growing number of drugs have been reported to produce siadh , most published reports concern vasopressin and its analogues such as thiazide and thiazide - like diuretics , chlorpropamide , carbamazepine , antipsychotics , antidepressants and nonsteroidal anti - inflammatory drugs . old age seems a risk factor of siadh following the use of many of these drugs . a combined use of these drugs , excessive fluid intake , and other underlying conditions which limit free water excretion will increase the risk3 ) . sodium valproic acid ( vpa ) , known as a carboxylic acid , is being used for an anti - epileptic in idiopathic and symptomatic generalized epilepsies and for some symptomatic focal epilepsies as well as trigeminal neuralgia , migraine and bipolar disorders4 ) . its mechanism is unknown ; however it is probably associated with the metabolism of the gaba neurotransmitter . the toxic effect it provokes there are several vpa - related idiosyncrasies ; the most noteworthy are alopecia , bone marrow aplasia , immune - mediated hepatotoxicity and pancreatitis5 ) . here we describe a patient with hyponatremia caused during the treatment with the antiepileptic drug , i.e. , sodium valproic acid ( vpa ) . the clinical course indicated that vpa contributed to an siadh6 ) . to our knowledge , this is a rare case of example in the medical literature in english which shows an association between vpa and siadh . he had suffered from generalized tonic clonic epilepsy that occurred after a craniectomy due to right epidural hematoma . the patient was treated with sodium valproate in a dose of 900 mg / day for 9 months . he had been removed a brain tumor 4 years before and he had craniectomy for an epidural hematoma 10 months ago . he was admitted to our hospital with a reported seizure , dizziness , nausea and vomiting for the day . his vital signs , physical and neurological examination on arrival were within normal limits except drowsy consciousness . significant laboratory findings were : sodium of 111 ( 135 - 145 ) mmol / l , potassium of 2.6(3.5 - 5.0 ) mmol / l , chloride 66 ( 95 - 110 ) mmol / l and serum osmolarity of 245 ( 280 - 300 ) mosm / kg . urine sodium and urine osmolarity were 58 mmol / l and 751 ( 50 - 1,200 ) mosm / kg , respectively . ante meridiem cortisol level , thyroid stimulating hormone , and free thyroxine level were within normal limits . the results of her rapid acth stimulation tests were also within normal ranges ( table 1 ) . valproic acid level was revealed to be within therapeutic range ( 62.76 g / ml ; an optimum therapeutic range 50 to 100 g / ml ) . the diagnosis of siadh was made based on hyponatremia , and low serum and high urine osmolality . no other causes of hyponatremia , including diuretic therapy , tumors and respiratory system disease , were present . the sodium valproate treatment was discontinued , and hypertonic saline was infused because of his symptomatic and profound hyponatremia . his serum sodium concentration increased to 131 the symptoms resolved immediately after the correction of hyponatremia . during the next 48 hours , normal saline infusion was given , and serum sodium level was restored to 134 mmol / l . the patient presented with hyponatremia , hypoosmolality , impaired excretion of water , which are all features of siadh7 ) and of generalized tonic clonic convulsions . we consider these seizures to be caused by hyponatremia due to siadh ; because other symptoms differed from those of the initial convulsive episode and serum vpa level which was useful to assess the patient compliance was within the target therapeutic range . other causes of hyponatremia such as volume depletion , hypothyroidism , renal or adrenal insufficiency and diuretic abuse , and vomiting were excluded . the correction of the patient 's hyponatremia , combined with the discontinuation of sodium valproate , resulted in the resolution of his hyponatremia . this is the first report in korea on such an adverse reaction to this medication . use of vpa could lead to gastrointestinal discomfort , weight gain , hair loss , tremor and sedation , but these side effects seems rather uncommon , mild , and transient during vpa monotherapy8 ) . potentially hazardous reactions such as hepatitis and pancreatitis have occurred in a few patients on vpa , generally in multidrug therapy8 ) . ( consider including this in the introduction before noting side effects are quoted ) , we could find only a few patients who reported hyponatremia at different times after sodium valproate use9 - 13 ) . the mechanism by which valproic acid could cause hyponatremia or siadh has not been fully elucidated . most cases of drug - induced hyponatremia involve the elderly , and could be related to an altered antidiuretic hormone ( adh ) regulation or action of adh on kidneys12 ) . we speculate that dopaminergic , serotonergic and noradrenergic systems may play a role in siadh due to sodium valproate14 ) . another hypothesis is that valproic acid has a direct effect on tubular cell function , because a few cases of tubular dysfunction in association with valproic acid with a positive dechallenge have been described5 ) . thus , we consider this episode of siadh to be due to a combination of factors including serotonergic stimulation of adh , reduced sensitivity of the hypothalamic osmoreceptors , and reduced renal ability to conserve salt and water . hyponatremia accompanied by cns disorders has shown to increase delayed cerebral ischemia and mortality rates15 ) . therefore , we suggest that patients who have high risk of hyponatremia are recommended to measure the baseline electrolyte levels before starting therapy with sodium valproate16 ) , and to monitor for electrolyte levels throughout the full course of treatment .
we report a rare case of the concurrent manifestation of central diabetes insipidus ( cdi ) and type 2 diabetes mellitus ( dm ) . 
 a 56 year - old man was diagnosed as a type 2 dm on the basis of hyperglycemia with polyuria and polydipsia at a local clinic two months ago and started an oral hypoglycemic medication , but resulted in no symptomatic improvement at all . upon admission to the university hospital , 
 the patient 's initial fasting blood sugar level was 140 mg / dl , and he showed polydipsic and polyuric conditions more than 8 l urine / day . despite the hyperglycemia controlled with metformin and diet , his symptoms persisted . 
 further investigations including water deprivation test confirmed the coexisting cdi of unknown origin , and the patient 's symptoms including an intense thirst were markedly improved by desmopressin nasal spray ( 10 g / day ) . 
 the possibility of a common origin of cdi and type 2 dm is raised in a review of the few relevant adult cases in the literature .