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Hyponatremia after initiation and rechallenge with trimethoprim-sulfamethoxazole in an older adult.

Huntsberry AM, Linnebur SA, Vejar M - Clin Interv Aging (2015)

Bottom Line: The patient's serum sodium concentrations increased to baseline 7 days after completion of the TMP-SMX therapy, and remained normal until she was treated in the emergency department several months later for another presumed urinary tract infection.She was again started on TMP-SMX therapy empirically, and within several days her serum sodium concentrations decreased from 138 mmol/L to a low of 129 mmol/L.The TMP-SMX therapy was discontinued upon negative urine culture results and her serum sodium increased to 134 mmol/L upon discharge.

View Article: PubMed Central - PubMed

Affiliation: University of Colorado Skaggs School of Pharmacy and Pharmaceutical Sciences, Aurora, CO, USA.

ABSTRACT

Purpose: The purpose of this study is to describe a case report of a patient experiencing hyponatremia from trimethoprim-sulfamethoxazole (TMP-SMX) upon initial use and subsequent rechallenge.

Summary: An 82-year-old woman presented to the emergency department with altered mental status thought to be due to complicated cystitis and was treated with TMP-SMX 160 mg/800 mg orally twice daily for 7 days. Her basic metabolic panel prior to initiation of TMP-SMX was within normal limits, with the exception of her serum sodium of 132 mmol/L (range 133-145 mmol/L). The day after completing her 7-day course of TMP-SMX therapy the patient was evaluated by her primary care provider and another basic metabolic panel revealed a reduction in the serum sodium to 121 mmol/L. The patient's serum sodium concentrations increased to baseline 7 days after completion of the TMP-SMX therapy, and remained normal until she was treated in the emergency department several months later for another presumed urinary tract infection. She was again started on TMP-SMX therapy empirically, and within several days her serum sodium concentrations decreased from 138 mmol/L to a low of 129 mmol/L. The TMP-SMX therapy was discontinued upon negative urine culture results and her serum sodium increased to 134 mmol/L upon discharge. Based upon the Naranjo probability scale score of 9, TMP-SMX was the probable cause of the patient's hyponatremia.

Conclusion: Our patient developed hyponatremia from TMP-SMX therapy upon initial use and rechallenge. Although hyponatremia appears to be rare with TMP-SMX therapy, providers should be aware of this potentially life-threatening adverse event.

No MeSH data available.


Related in: MedlinePlus

Serum sodium levels.Note: Index date refers to start date of trimethoprim-sulfamethoxazole prescription.
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f1-cia-10-1091: Serum sodium levels.Note: Index date refers to start date of trimethoprim-sulfamethoxazole prescription.

Mentions: The patient presented to her primary care physician 1 day after completing her course of TMP–SMX. The patient was evaluated for depression and inability to sleep at night. She described some nausea, but denied any signs or symptoms of vomiting. A basic metabolic panel was ordered and the patient was given a prescription for mirtazapine 7.5 mg once daily at bedtime for sleep and depression. The same day, laboratory results from the office visit (Table 1) indicated a low sodium (121 mmol/L) and chloride concentration (92 mmol/L), an increased but normal potassium concentration (4.7 mmol/L), an increased but normal serum creatinine (1.1 mg/dL), and an increased blood urea nitrogen (24 mg/dL). A call was made to the patient to inform her that her sodium concentration was low and to not take the mirtazapine as it can further lower serum sodium. In addition, her lisinopril was held as her potassium had increased from 3.9 to 4.7 mmol/L since the hospitalization. At this point in time the patient had already taken one 7.5 mg tablet of mirtazapine and seemed to have tolerated it well, but she was instructed to hold further doses. The patient did not want to be admitted to the hospital despite the potential seriousness of her low sodium concentrations and was informed of the risks involved. She was instructed to increase her salt intake, but also increase her fluid intake due to her slightly dehydrated state. The patient came back to clinic 2 days later to make sure her sodium concentrations were increasing appropriately. Laboratory work revealed a sodium concentration slightly higher at 123 mmol/L. The patient was monitored closely, and her sodium concentrations increased to, and were maintained, in the normal range as of 8 days after stopping TMP–SMX (Table 1, Figure 1). At the visit where her sodium concentration normalized, the patient restarted mirtazapine and lisinopril, with no further anomalies in her sodium or potassium concentrations for the next 3 months. Her last serum sodium concentration during this time period was 138 mmol/L.


Hyponatremia after initiation and rechallenge with trimethoprim-sulfamethoxazole in an older adult.

Huntsberry AM, Linnebur SA, Vejar M - Clin Interv Aging (2015)

Serum sodium levels.Note: Index date refers to start date of trimethoprim-sulfamethoxazole prescription.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4494188&req=5

f1-cia-10-1091: Serum sodium levels.Note: Index date refers to start date of trimethoprim-sulfamethoxazole prescription.
Mentions: The patient presented to her primary care physician 1 day after completing her course of TMP–SMX. The patient was evaluated for depression and inability to sleep at night. She described some nausea, but denied any signs or symptoms of vomiting. A basic metabolic panel was ordered and the patient was given a prescription for mirtazapine 7.5 mg once daily at bedtime for sleep and depression. The same day, laboratory results from the office visit (Table 1) indicated a low sodium (121 mmol/L) and chloride concentration (92 mmol/L), an increased but normal potassium concentration (4.7 mmol/L), an increased but normal serum creatinine (1.1 mg/dL), and an increased blood urea nitrogen (24 mg/dL). A call was made to the patient to inform her that her sodium concentration was low and to not take the mirtazapine as it can further lower serum sodium. In addition, her lisinopril was held as her potassium had increased from 3.9 to 4.7 mmol/L since the hospitalization. At this point in time the patient had already taken one 7.5 mg tablet of mirtazapine and seemed to have tolerated it well, but she was instructed to hold further doses. The patient did not want to be admitted to the hospital despite the potential seriousness of her low sodium concentrations and was informed of the risks involved. She was instructed to increase her salt intake, but also increase her fluid intake due to her slightly dehydrated state. The patient came back to clinic 2 days later to make sure her sodium concentrations were increasing appropriately. Laboratory work revealed a sodium concentration slightly higher at 123 mmol/L. The patient was monitored closely, and her sodium concentrations increased to, and were maintained, in the normal range as of 8 days after stopping TMP–SMX (Table 1, Figure 1). At the visit where her sodium concentration normalized, the patient restarted mirtazapine and lisinopril, with no further anomalies in her sodium or potassium concentrations for the next 3 months. Her last serum sodium concentration during this time period was 138 mmol/L.

Bottom Line: The patient's serum sodium concentrations increased to baseline 7 days after completion of the TMP-SMX therapy, and remained normal until she was treated in the emergency department several months later for another presumed urinary tract infection.She was again started on TMP-SMX therapy empirically, and within several days her serum sodium concentrations decreased from 138 mmol/L to a low of 129 mmol/L.The TMP-SMX therapy was discontinued upon negative urine culture results and her serum sodium increased to 134 mmol/L upon discharge.

View Article: PubMed Central - PubMed

Affiliation: University of Colorado Skaggs School of Pharmacy and Pharmaceutical Sciences, Aurora, CO, USA.

ABSTRACT

Purpose: The purpose of this study is to describe a case report of a patient experiencing hyponatremia from trimethoprim-sulfamethoxazole (TMP-SMX) upon initial use and subsequent rechallenge.

Summary: An 82-year-old woman presented to the emergency department with altered mental status thought to be due to complicated cystitis and was treated with TMP-SMX 160 mg/800 mg orally twice daily for 7 days. Her basic metabolic panel prior to initiation of TMP-SMX was within normal limits, with the exception of her serum sodium of 132 mmol/L (range 133-145 mmol/L). The day after completing her 7-day course of TMP-SMX therapy the patient was evaluated by her primary care provider and another basic metabolic panel revealed a reduction in the serum sodium to 121 mmol/L. The patient's serum sodium concentrations increased to baseline 7 days after completion of the TMP-SMX therapy, and remained normal until she was treated in the emergency department several months later for another presumed urinary tract infection. She was again started on TMP-SMX therapy empirically, and within several days her serum sodium concentrations decreased from 138 mmol/L to a low of 129 mmol/L. The TMP-SMX therapy was discontinued upon negative urine culture results and her serum sodium increased to 134 mmol/L upon discharge. Based upon the Naranjo probability scale score of 9, TMP-SMX was the probable cause of the patient's hyponatremia.

Conclusion: Our patient developed hyponatremia from TMP-SMX therapy upon initial use and rechallenge. Although hyponatremia appears to be rare with TMP-SMX therapy, providers should be aware of this potentially life-threatening adverse event.

No MeSH data available.


Related in: MedlinePlus