case reports Moxifloxacin
Felix K. Yam and Satish A. Eraly
M
oxifloxacin is a four thgeneration fluoroquinolone widely prescribed for the empirical coverage of pneumococcal and anaerobic infections.1 Adverse events associated with fluoroquinolones include gastrointestinal toxicity central nervous system (CNS) toxicity, less frequently, electrocardiogram abnormalities, hypoglycemia, hepatotoxicity, phototoxicity, tendon and joint disorders, and hypersensitivity reactions.2 While mild CNS toxicities, such as headache and nausea, are common with fluoroquinolone use, severe CNS toxicities are rare. Fluoroquinolone-induced seizures have been reported in patients who are susceptible to and have other risk factors for seizures.3 Rarely, fluoroquinolones have also caused hyponatremia. Two case reports of fluoroquinolone-induced hyponatremia have been published and involved ciprofloxacin and moxifloxacin.4,5 The case report of hyponatremia associated with moxifloxacin, however, was confounded by the concomitant use of thiazide diuretics by the patient.4 Drug-induced syndrome of inappropriate antidiuretic hormone (SIADH) has been associated with a number of different drug classes, including diuretics, antidepressants,
Purpose. A possible case of moxifloxacininduced syndrome of inappropriate antidiuretic hormone (SIADH) is reported. Summary. A 66-year-old Caucasian woman with stage II chronic obstructive pulmonary disease (COPD) arrived at the emergency department from an outpatient clinic complaining of worsening shortness of breath, headache, body aches, and dizziness. Five days before her arrival at the hospital, the patient was seen in an outpatient clinic with symptoms of COPD exacerbation and was given a corticosteroid taper of prednisone 40 mg daily and moxifloxacin 400 mg daily. The patient was hospitalized, and her serum sodium concentration was 110 meq/L. Moxifloxacin was continued on admission, and the patient was admitted to the intensive care unit for frequent neurologic examination, serial serum sodium measurements, and fluid restriction. Her laboratory test results were consistent with SIADH. Fluid restriction at 1 L/day initially corrected her serum sodium concentration to 119 meq/L, but increases in serum
antiepileptics, antipsychotics, chemotherapy agents, nonsteroidal antiinflammatory drugs (NSAIDs), and antimicrobial agents.6 The mechanisms responsible for drug-induced SIADH fall into two categories: (1) drugs that have direct effects on sodium and water homeostasis (e.g., diuretics) and (2) drugs that increase
Felix K. Yam, Pharm.D., is Health Sciences Clinical Assistant Professor, Skaggs School of Pharmacy and Pharmaceutical Sciences; and Satish A. Eraly, M.D., Ph.D., is Associate Adjunct Professor, School of Medicine, University of California San Diego, San Diego. Address correspondence to Dr. Yam at the Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego, 9500 Gilman Drive, MC 0714, La Jolla, CA 92093 (
[email protected]).
sodium plateaued by day 2 of admission (119–122 meq/L). Moxifloxacin was discontinued on hospital day 3. At discharge, on hospital day 5, her serum sodium concentration had increased to 131 meq/L. She was restarted on her home medications and followed up in an outpatient clinic one week later. After multiple etiologies were ruled out, drug-induced SIADH associated with moxifloxacin was the most likely diagnosis for this patient. Clinicians should be aware of this potential adverse drug effect when assessing patients with hyponatremia or SIADH. Conclusion. A 66-year-old woman developed severe hyponatremia after receiving moxifloxacin for five days for treatment of COPD exacerbation. Index terms: Hyponatremia; Inappropriate ADH syndrome; Moxifloxacin; Prednisone; Pulmonary disease; Quinolones; Steroids, cortico-; Toxicity Am J Health-Syst Pharm. 2012; 69:217-20
the central secretion of antidiuretic hormone (ADH)(e.g., antiepileptics, chemotherapy agents, NSAIDs, antimicrobial agents). Agents that act on the CNS have a propensity to cause central release of ADH. We propose that moxifloxacin interactions in the CNS can potentially lead to SIADH and severe hyponatremia.
The authors have declared no potential conflicts of interest. Copyright © 2012, American Society of Health-System Pharmacists, Inc. All rights reserved. 1079-2082/12/0201-0217$06.00. DOI 10.2146/ajhp110201
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Syndrome of inappropriate antidiuretic hormone associated with moxifloxacin
case reports Moxifloxacin
We report a case of SIADH with severe hyponatremia associated with moxifloxacin administration.
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2 and 3. On day 2, the patient’s fluid intake was further restricted to 500 mL daily, but this reduction did not provide any additional benefit. On day 3 of hospital admission, moxifloxacin and fosinopril were discontinued to exclude the possibility of drug-induced causes of SIADH. The patient’s serum sodium concentration increased to 124 meq/L one day after the discontinuation of these medications and eventually increased to 131 meq/L two days after discontinuation, at which time the patient was discharged with instructions to follow up with health care providers within one week. Four days after hospital discharge, the patient’s serum sodium concentration had returned to a near-normal concentration of 134 meq/L. Fosinopril and furosemide were restarted within one week of hospital discharge. One month after discharge, the patient’s serum sodium concentration was 139 meq/L. Discussion Hyponatremia is one of the most common electrolyte disturbances among hospitalized patients and is usually defined as a serum sodium concentration of