Clindamycin is a broad spectrum antibiotic used orally, topically and parenterally for bacterial infections due to sensitive organisms. Clindamycin has been linked to rare instances of acute liver injury.


Clindamycin (klin" da mye' sin) is a lincomycin derivative with activity against many aerobic gram-positive cocci as well as many anaerobic gram-negative and gram-positive organisms. It has special activity against Bacteroides fragilis and some activity against Toxoplasma gondii and Pneumocystis jiroveci. Clindamycin acts by its binding to the 50S ribosomal subunit of bacteria, thus inhibiting protein synthesis. Clindamycin was approved for use in the United States in 1970 and is still in wide use with several million prescriptions being filled yearly. Current indications include moderate-to-severe bacterial infections caused by sensitive organisms. It is also used topically for acne and bacterial vaginosis. Clindamycin is available generically in oral and parenteral forms and as gels, foam, lotion and creams for topical use. Oral formulations include capsules of 75, 150 and 300 mg that are available in generic forms and under the commercial name of Cleocin. Clindamycin is also available in suspension for pediatric use. The typical adult dose is 600 to 2700 mg im or iv daily (in two divided doses) or 150 to 450 mg orally every 6 hours for 5 to 14 days, depending upon the type and severity of infection. Common side effects include nausea, diarrhea, headache and skin rash.


Clindamycin has been linked to two forms of hepatotoxicity: transient serum aminotransferase elevations usually occurring after several days of high intravenous doses; and, an acute, idiosyncratic liver injury that arises within 1 to 3 weeks of starting therapy and is typically mild and self-limited.

High doses of intravenous clindamycin can be accompanied by elevations in serum ALT levels in the range of 2 to 10 times the upper limit of normal starting after 5 to 15 days of therapy in a manner similar to what occurs with intravenous oxacillin therapy (Case 1). Symptoms, jaundice, and alkaline phosphatase elevations are mild if they occur at all (Case 2), and aminotransferase levels rapidly fall into the normal range (in 1 to 2 weeks) upon stopping clindamycin or switching to lower doses or to oral formulations with which it rarely occurs.

Clindamycin therapy has also been linked to a clinically apparent, idiosyncratic liver injury that arises between 1 to 3 weeks after starting either oral or parenteral therapy (Case 3). The pattern of serum enzyme elevations is typically hepatocellular or mixed, but can be cholestatic. Allergic manifestations such as rash, fever and eosinophilia are typical, but often are not prominent and are not present in all cases. Autoantibodies are generally not present. The acute liver injury may accompany other signs of hypersensitivity such as Stevens Johnson syndrome or other severe skin reactions. The liver injury is usually mild-to-moderate in severity and resolves rapidly with stopping. However, fatal instances have been reported.

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

Mechanism of Injury

The cause of ALT elevations during high dose clindamycin therapy is not known, but may be due to a direct but mild injury to the liver. Liver biopsy during these episodes generally shows minimal cell injury. The idiosyncratic reaction to clindamycin resembles the immunoallergic types of hepatitis that occur after many types of antibiotics, including the penicillins and cephalosporins.

Outcome and Management

The serum aminotransferase elevations that appear during high dose intravenous therapy with clindamycin are usually benign, minimally symptomatic and resolve rapidly with stopping therapy or switching to oral forms of clindamycin. Acute idiosyncratic hepatitis can occur with either the parenteral or oral forms of clindamycin, but is rare. The liver injury can be symptomatic and prolonged and has been linked to one case of vanishing bile duct syndrome, but not with acute liver failure. Ordinarily, recovery can be expected in 4 to 8 weeks. Prednisone is not recommended. Patients should be told to avoid reexposure to clindamycin and other lincomycin derivatives.

Drug Class: Antiinfective Agents


Case 1. Serum aminotransferase elevations during intravenous therapy with clindamycin.(1)

A 57 year old man with rheumatic heart disease and Staphylococcal endocarditis was treated with clindamycin (300 mg intravenously every 8 hours) and developed elevations in serum aminotransferase levels starting during the first week of therapy. Clindamycin was stopped at day 16 because of continuing elevations in ALT levels, which promptly began to fall when he was switched to cephalothin (Table). While blood cultures became negative on therapy, he subsequently died of E. coli sepsis.

Key Points

Laboratory Values


A typical pattern of serum aminotransferase elevations during intravenous clindamycin therapy that can be seen with several antibiotics, most typically with oxacillin. The liver injury usually arises after 4 to 6 days and is minimally symptomatic, anicteric and resolves rapidly when the antibiotic is stopped. The injury is probably dose related and a direct toxic effect of clindamycin or oxacillin.

Case 2. Acute hepatitis arising during intravenous therapy with clindamycin.(2)

An 18 year old man with acute bacterial endocarditis related to injection drug use developed elevated serum aminotransferases and then jaundice during intravenous clindamycin therapy. The patient had been treated with high doses of cephalothin and vancomycin for over two months with an inadequate response, during which time his liver tests were normal. Blood cultures revealed Staphylococcus aureus sensitive to clindamycin, and he was started on intravenous clindamycin (3.6 g/day) with a rapid clinical improvement. After a week, however, serum AST levels began to rise. The dose of clindamycin was cut in half, but he subsequently developed urticaria, recurrence of fever, jaundice and rising AST levels (Table). Tests for hepatitis B were negative, and liver biopsy showed acute hepatitis without fibrosis compatible with a drug induced liver injury. Clindamycin was stopped and the rash, fever and jaundice promptly resolved. Follow up blood cultures were negative and serum AST levels were normal when tested one month later.

Key Points

Laboratory Values


A typical pattern of serum aminotransferase elevations arising after a week of intravenous clindamycin therapy. The clindamycin dose was decreased because of the rising AST levels, but fever and urticaria arose, and clindamycin was stopped, whereupon the liver injury resolved rapidly. This example suggests that the asymptomatic elevations in serum aminotransferase levels during intravenous clindamycin therapy can evolve into the immunoallergic and icteric form of liver injury if therapy is continued. This report predated the availability of tests for hepatitis C, which may have been at least partially responsible for the liver injury in this patient.

Case 3. Acute hepatitis with jaundice arising during clindamycin therapy.(3)

A 42 year old woman developed fatigue, nausea, anorexia, pruritus and dark urine followed by jaundice 6 days after starting a course of clindamycin (150 mg four times a day) for a gingival infection. She had received clindamycin for this same problem several times in the past without complications. She had no history of liver disease, alcohol abuse or risk factors for viral hepatitis and was taking no other medications. On presentation, she was jaundiced but without rash or fever. Laboratory testing showed an ALT of 1795 U/L, AST 1337 U/L, alkaline phosphatase 339 U/L, GGT 148 U/L, total bilirubin 4.1 mg/dL (direct 2.9 mg/dL) and INR 1.04. The eosinophil count was normal. Tests for hepatitis A, B and C and for cytomegalovirus and Epstein Barr virus infection were negative. Autoantibodies, including ANA, SMA and anti-LKM, were negative and an abdominal ultrasound showed no evidence of biliary obstruction. A liver biopsy showed cholestatic hepatitis without fibrosis, suggestive of drug induced liver injury. After 3 weeks, she was largely asymptomatic and all liver tests had returned to normal when she was seen 8 weeks after presentation (Table).

Key Points

Laboratory Values


While referred to as “cholestatic” in the title of the publication, the clinical presentation was clearly hepatocellular and acute viral hepatitis-like arising after a week of clindamycin therapy. No other medications were being taken and other causes of liver injury were adequately excluded. The liver injury was clearly idiosyncratic and likely due to hypersensitivity, despite the absence of immunoallergic features (rash, fever and eosinophilia). Previous courses of clindamycin may have sensitized the patient to the antibiotic. Isolated instances of cross sensitivity have been reported between clindamycin and the penicillins and future use of related antibiotics should be done with care.



Clindamycin – Generic, Cleocin®


Antiinfective Agents


Product labeling at DailyMed, National Library of Medicine, NIH



Modified from Case #3: Hinthorn DR, Baker LH, Romig DA, Voth DW, Liu C. Endocarditis treated with clindamycin: relapse and liver dysfunction. South Med J. 1977;70:823–6. [PubMed: 877644]
Elmore M, Rissing JP, Rink L, Brooks GF. Clindamycin-associated hepatotoxicity. Am J Med. 1974;57:627–30. [PubMed: 4432865]
Aygun C, Kocaman O, Gurbuz Y, Senturk O, Hulagu S. Clindamycin-induced acute cholestatic hepatitis. World J Gastroenterol. 2007;13:5408–10. [PMC free article: PMC4171338] [PubMed: 17879418]


References updated: 16 December 2019

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    (42 year old woman developed jaundice and pruritus after 6 days of oral clindamycin [bilirubin 4.1 mg/dL, ALT 1795 U/L, Alk P 339 U/L], resolving within 8 weeks of stopping).
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    (62 year old woman developed liver test abnormalities 5 days after starting clindamycin [bilirubin normal, ALT 423, Alk P 321 U/L] and rose while it was continued [peak ALT 1927 U/L], with improvement on stopping).
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