You will be presented with the full text of a biomedical research paper. Please write an abstract for this paper. Your response should include the abstract and no additional text.

Paper text:
, the syndrome of inappropriate antidiuretic hormone secretion ( siadh ) is the most common cause of euvolemic hyponatremia3 ) .
siadh is characterized by either the sustained release of antidiuretic hormone ( adh ) in the absence of stimuli , or by the enhanced action of adh on the kidney4 ) .
causes of siadh include malignant disease , pulmonary disorders , central nervous system disorders , and a number of medications1 ) .
several drugs are known to cause this syndrome ; however , there are only few reported cases in which siadh was induced by pregabalin .
a chest computed tomography ( ct ) revealed consolidation in both lower lobes of the lungs , and he was diagnosed with pneumonia .
the patient had been treated with numerous drugs , including an angiotensin - converting enzyme inhibitor , metformin , a dpp - iv inhibitor , and thioctacid , for management of type 2 diabetes mellitus and hypertension .
several weeks prior to hospital admission , he had a severe ulcer on his right heel caused by arteriosclerosis obliterans . shortly before admission , he initiated pregabalin therapy to relieve the pain of the right heel . on admission ,
the patient 's blood pressure was 128/58 mmhg , and his pulse rate was 76 beats per minute .
his body temperature was 37.8 , and crackles were heard on both sides of the lung field .
physical examination did not reveal any neurologic dysfunctions or other symptoms , except mild dyspnea .
hematological analysis demonstrated a white blood cell count of 11,150/mm ( reference range , 400 - 10,000/mm ) , and a hemoglobin level of 9.6 g / dl ( reference range , 13 - 17.5 g / dl ) .
meq / l ( reference range , 136 - 145 meq / l ) and a potassium level of 5.0
there was no abnormality in the results of the liver function tests or renal function tests .
as previously stated , the patient was diagnosed with pneumonia ; thus , we initiated administration of ceftriaxone and clarithromycin to treat the pneumonia . the patient 's condition improved , and antibiotic therapy was ceased after 2 weeks of administration . at the point of termination of pneumonia treatment , the patient was found to be hyponatremic , with a sodium level of 122 meq / l .
additionally , the patient 's random spot urine sodium and osmolality levels were 91 meq / l ( reference range , 40 - 220 meq / l ) , and 451 mosm / kg ( reference range , 300 - 900 mosm / kg ) , respectively . based on the patient 's clinical euvolemia and the biochemical data ,
he was then placed on fluid restriction , but it was unsuccessful for correction of the serum sodium level .
subsequently , 3% saline was supplied ; however , laboratory findings indicated a serum sodium level of 116 meq / l .
therefore , he was referred to the nephrology clinic for the treatment and evaluation of siadh .
. therefore , we presumed that siadh might be induced by pregabalin , and decided to stop its administration .
the serum sodium and urine osmolality were again evaluated , followed by administration of 0.9% isotonic saline .
two days later , the serum sodium level of the patient increased to a near - normal level of 130 meq / l ( table 1 ) . to determine whether an adverse drug reaction was caused by pregabalin , we used the naranjo algorithm(table 2 ) .
the total score was 6 , which equates to  probable  as the probability that an adverse event was related to the drug therapy .
the patient remained asymptomatic , even when his sodium level was decreased to 116 meq / l .
drug - induced siadh can occur owing to an increased sensitivity to adh in the nephron or an increase in adh production4 ) . increased adh activity impairs the ability of the kidney to dilute urine , resulting in decreased excretion of ingested water and a highly concentrated and decreased urine volume56 ) .
patients with siadh present with a euvolemic status because the excess water distributes evenly throughout the body 's fluid compartments5 ) .
selective serotonin reuptake inhibitors ( ssris ) , various chemotherapeutic agents ( e.g. , cyclophosphamide , cisplatin , and vinca alkaloids ) , carbamazepine , and antipsychotics appear to be most strongly associated with drug - induced siadh56 ) .
pregabalin is an analog of the neurotransmitter gamma - aminobutyric acid ( gaba ) that has analgesic , anticonvulsant , and anxiolytic properties7 ) .
it is now widely used in the management of diabetic peripheral neuropathy , post - herpetic neuralgia , generalized anxiety disorder , and social anxiety disorder .
the most common adverse events associated with pregabalin include dizziness and somnolence , followed by peripheral edema and weight gain8 ) .
several articles have reported decompensation of patients with chronic heart failure , edema , and weight gain , all caused by pregabalin78 ) .
although the mechanism of pregabalin is not well known , the calcium channel relationship may cause these side effects .
they potently bind to the subunit , resulting in modulation of calcium channels and reduction in the release of several neurotransmitters9 ) .
the effect of alpha2-delta type 1 and 2 subunits on calcium channel functions and conventional calcium channel subtypes are not clear10 ) .
this calcium channel relationship , however , may lead to peripheral edema with peripheral vasodilation and fluid leakage into the interstitial space .
it is thought that unexplained weight gain may be a sign of fluid retention , which may exacerbate congestive heart failure11 ) .
in addition , it is inferred that siadh can develop as a result of this fluid leakage into the interstitial space and fluid retention .
although a large number of drugs are known to potentially induce siadh , pregabalin - induced siadh has rarely been reported .
a patient without underlying disease was administered pregabalin 75 mg once daily for neuropathic pain secondary to l4-l5 radiculopathy ; hyponatremia developed two weeks later12 ) . in another case ,
a patient with type ii diabetes mellitus , nephropathy , neuropathy , and ischemic cardiomyopathy with congestive heart failure ( left ventricular function , 27% ) was given pregabalin for neuropathic pain .
one week later , he presented with disorientation secondary to hyponatremia13 ) . in both cases ,
the patients were treated with pregabalin to alleviate neuropathic pain , and the hyponatremia improved after discontinuation of pregabalin .
pregabalin is considered among the first - line treatments for neuropathic pain , along with tricyclic antidepressants ( tca ) , ssris , and serotonin norepinephrine reuptake inhibitors ( snri ) .
we thought that pregabalin might enhance adh release , or have an effect similar to the aforementioned drugs .
adh secretion results in a concentrated urine , leading to reduced urine volume . in most patients with siadh ,
in addition , the increase in tbw transiently expands the extracellular fluid ( ecf ) volume , and it is thought that this increased ecf volume might cause peripheral edema and weight gain .
increased ecf volume also triggers increased urinary sodium excretion , which both returns the ecf volume towards normal and further lowers the serum sodium concentration .
many medications have been associated with siadh , and the only definitive treatment for drug - induced siadh is the removal of the suspicious agent . here
however , we speculate that pregabalin - induced siadh occurs more frequently than has been reported , because it appears to present with asymptomatic and mild hyponatremia
. therefore , it may be difficult to detect in the absence of laboratory studies . in conclusion
in addition , it is important for clinicians to suspect the drug as a potential cause of hyponatremia , particularly in the absence of another causative explanation , even though the agent is not generally known to induce siadh .
the syndrome of inappropriate antidiuretic hormone secretion ( siadh ) is the most common cause of euvolemic hyponatremia , and many medications have been associated with siadh . 
 pregabalin is a drug used for the treatment of neuropathic pain , though common adverse effects include central nervous system disturbance , peripheral edema , and weight gain . 
 however , hyponatremia caused by pregabalin has been rarely reported . here 
 we report a patient with pregabalin - induced hyponatremia who met the criteria for siadh ; after discontinuation of the drug , his condition rapidly improved . 
 this case can help clinicians diagnose and treat new - onset hyponatremia in patients who recently initiated pregabalin therapy .