Moxifloxacin is a fourth generation fluoroquinolone with expanded activity against gram-positive bacteria as well as atypical pathogens. Moxifloxacin has been linked to mild ALT elevations during therapy and to rare instances of idiosyncratic acute liver injury with symptoms and jaundice.


Moxifloxacin (mox" i flox' a sin) is a fourth generation fluoroquinolone with expanded activity against gram-positive bacteria including multidrug resistant strains of Streptococcus pneumoniae. Like other fluoroquinolones, moxifloxacin is active against a wide range of aerobic gram-positive and gram-negative organisms. The quinolones are believed to act by inhibition of bacterial DNA gyrase and topoisomerase IV that are required for synthesis of bacterial mRNAs (transcription) and DNA replication. In contrast, DNA gyrases are not present in human [and other eukarotic] cells and the equivalent topoisomerases are not sensitive to fluoroquinolone inhibition. Moxifloxacin was approved for use in the United States in 1999 and is available generically and under the commercial names of Avelox, Moxeza and Vigamox. Current indications include mild-to-moderate bacterial infections such as sinusitis, bronchitis, community acquired pneumonia, skin infections, cellulitis, abscesses and complicated intraabdominal infections due to sensitive organisms. Moxifloxacin is also commonly used as a second line agent for therapy of tuberculosis and atypical mycobacterial infections. Moxifloxacin is available in formulations of 400 mg tablets, the usual dose being 400 mg daily for 5 to 14 days. Intravenous formulations are available for moderate to severe infections, the usual IV dosages being 400 mg daily. Common side effects include gastrointestinal upset, headaches, skin rash and allergic reactions. Less common but more severe side effects of the fluoroquinolones include prolongation of the QT interval, seizures, hallucinations, tendon rupture, severe hypersensitivity syndromes, angioedema, photosensitivity and Stevens Johnson syndrome.


Moxifloxacin, like other fluoroquinolones, is associated with a low rate (1% to 3%) of serum enzyme elevations during therapy. These abnormalities are generally mild, asymptomatic and transient, resolving even with continuation of therapy. Moxifloxacin has been linked to rare but occasionally severe and even fatal cases of acute liver injury. The time to onset is typically short (1 day to 3 weeks) and the presentation is often abrupt with nausea, fatigue, abdominal pain and jaundice. The pattern of serum enzyme elevations can be either hepatocellular or cholestatic, cases with the shorter times to onset usually being more hepatocellular. In addition, the onset of illness may occur a few days after the medication is stopped. Many (but not all) cases have prominent allergic manifestations with fever and rash, and the liver injury may occur in the context of a generalized hypersensitivity reaction (Case 1). Autoantibodies are usually not present. Cases with a cholestatic pattern of enzymes may run a prolonged course but are usually self-limiting, although at least one case of chronic cholestasis and vanishing bile duct syndrome leading to liver failure has been published. Most reported cases have been mild with recovery within 4 to 8 weeks of onset.

Likelihood score: B (rare but likely cause of clinically apparent liver injury).

Mechanism of Injury

The cause of hepatic injury is unknown but is likely to be immune-mediated as many cases occur in the context of a system hypersensitivity reaction. Moxifloxacin is metabolized by sulfate or glucuronide conjugation and has no effect on cytochrome P450 enzymes.

Outcome and Management

Mild-to-moderate hepatic injury due to moxifloxacin should be followed by full recovery within 4 to 8 weeks. Fulminant cases and chronic cholestatic forms with vanishing bile duct syndrome have been described. Cross reactivity of the hepatic injury between different fluoroquinolones has not been demonstrated, but is suspected based upon the similarity of clinical patterns of injury and latency. Thus, patients who develop clinically apparent liver injury from moxifloxacin should be advised to avoid further exposure to other fluoroquinolones.

Drug Class: Antiinfective Agents

Other Drugs in the Subclass, Fluoroquinolones: Ciprofloxacin, Delafloxacin, Gemifloxacin, Levofloxacin, Norfloxacin, Ofloxacin


Case 1. Severe hypersensitivity reaction and hepatitis due to moxifloxacin therapy.(1)

A previously healthy 45 year old man was treated with moxifloxacin for suspected sinusitis and developed severe rash, facial edema and fever one week later. He was admitted with the diagnosis of Stevens Johnson syndrome and was treated with systemic and topical corticosteroids. He had a past medical history of allergic reactions of amoxicillin and erythromycin, but had not received fluoroquinolone antibiotics in the past. He had no history of liver disease, alcohol abuse or risk factors for viral hepatitis. He was taking ranitidine and an antihistamine but denied taking over-the-counter or herbal preparations. On admission, serum aminotransferase values were markedly elevated (~18 fold) and the day after he became jaundiced (Table). There was no eosinophilia or lymphocytosis. Tests for hepatitis A, B and C were negative as were autoantibodies. An abdominal ultrasound was normal except for somewhat echogenic texture of the liver suggesting fatty infiltration. He was treated with methylprednisolone and his skin rash and jaundice improved over three weeks. Ultimately, liver tests returned to normal values.

Key Points

Laboratory Values


This patient developed symptoms of generalized hypersensitivity approximately 9 days after starting moxifloxacin. He had an accompanying hepatitis and jaundice that was not severe. Some degree of hepatic involvement is common with severe hypersensitivity reactions to antibiotics, but usually the allergic manifestations dominate the clinical picture. Notice that the liver injury worsened for a week after stopping the implicated medication before beginning to resolve. The patient should be advised strongly to avoid further exposure to fluoroquinolone antibiotics.



Moxifloxacin – Generic, Avelox®


Antiinfective Agents


Product labeling at DailyMed, National Library of Medicine, NIH



Orman ES, Conjeevaram HS, Vuppalanchi R, Freston JW, Rochon J, Kleiner DE, Hayashi PH., DILIN Research Group. Clinical and histopathologic features of fluoroquinolone-induced liver injury. Clin Gastroenterol Hepatol. 2011;9:517–23.e3. [PMC free article: PMC3718017] [PubMed: 21356330]


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