Hepatotoxicity of Erythromycin

Braun, Peter

doi:10.1093/infdis/119.3.300

Cited by 88 publications

(21 citation statements)

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“…Of these 539 women, 179, 181, and 179 had been assigned to receive erythromycin estolate, clindamycin hydrochloride, and a placebo, respectively. Table 1 shows the number of participants in each of the groups who had abnormal levels of SGOT in the samples obtained after 3 or 6 weeks of treatment. A total of 45 subjects (18, 13, and 14 from each of the groups) have been excluded because they did not take any of the capsules or because they did not return to the clinic.…”

Section: Resultsmentioning

confidence: 99%

“…Properly designed controlled studies had not been carried out. Some authors of prospective studies attributed hepatic abnormalities to erythromycin estolate; others found no evidence of toxicity (1).…”

Section: Discussionmentioning

confidence: 99%

“…It is not clear whether this represents a subclinical form of the less common clinically apparent syndrome resembling acute cholecystitis, which has been associated with erythromycin estolate (1,11) …”

Section: Discussionmentioning

confidence: 99%

“…As reviewed by Braun (1), there have been reports of individuals who have developed hepatic toxicity in association with the administration of erythromycin estolate (8). Even when the propensity of erythromycin to produce hepatic toxicity has been considered to be established, it has been generally considered that this is an unusual idiosyncratic reaction (1,5). The present report describes a group of pregnant women, over 9% of whom developed subclinical hepatotoxicity while receiving erythromycin estolate. Investigators in this laboratory have associated the genital mycoplasmas Mycoplasma hominis and Ureaplasma urealyticum (T-mycoplasmas) with birth weight.…”

mentioning

confidence: 83%

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Hepatotoxicity of Erythromycin Estolate During Pregnancy

McCormack

George

et al. 1977

Antimicrob Agents Chemother

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Women in the second half of pregnancy, who were infected with genital mycoplasmas and who gave written informed consent, were randomly assigned to receive capsules of identical appearance containing erythromycin estolate, clindamycin hydrochloride, or a placebo for 6 weeks. Levels of serum glutamic oxalacetic transaminase (SGOT) were determined before and during treatment by a fluorometric method. All pretreatment levels of SGOT were normal (<41 units). Participants who received erythromycin estolate had significantly more abnormally elevated levels of SGOT (16/161, 9.9%) than did those who received clindamycin (4/168, 2.4%, P < 0.01) or those who received placebo (3/165, 1.8%, P < 0.01). Elevated levels of SGOT ranged from 44 to 130 U. Serum bilirubin levels were normal. Gamma-glutamyl transpeptidase activity was abnormal in six of six participants who had abnormal levels of SGOT while receiving erythromycin estolate. There were few associated symptoms, and all levels of SGOT returned to normal after cessation of treatment. The treatment of pregnant women with erythromycin estolate may be inadvisable.Erythromycin, a macrolide antibiotic produced by the actinomycete Streptomyces erythreus, has been used extensively in clinical medicine since its introdluction in 1952. Erythromycin base and its salts are not consistently absorbed from the gastrointestinal tract, presumably because they are destroyed by gastric acid. The only preparation of erythromycin that is well absorbed when given orally is the lauryl sulfate salt of the propionyl ester (propionyl erythromycin lauryl sulfate; erythromycin estolate [5]). The estolate is also the only form of erythromycin that has been associated with any reported hepatotoxicity. As reviewed by Braun (1), there have been reports of individuals who have developed hepatic toxicity in association with the administration of erythromycin estolate (8). Even when the propensity of erythromycin to produce hepatic toxicity has been considered to be established, it has been generally considered that this is an unusual idiosyncratic reaction (1, 5). The present report describes a group of pregnant women, over 9% of whom developed subclinical hepatotoxicity while receiving erythromycin estolate. Investigators in this laboratory have associated the genital mycoplasmas Mycoplasma hominis and Ureaplasma urealyticum (T-mycoplasmas) with birth weight. In one study (9), these organisms were found to be more prevalent among low-birth-weight infants than among infants of normal birth weight. In another study (3), women who were colonized with these organisms early in pregnancy gave birth to infants that weighed significantly less than infants whose mothers were not colonized. Earlier studies from this laboratory had found that non-bacteriuric pregnant women who were treated with a broad-spectrum antimicrobial agent gave birth to significantly fewer lowbirth-weight infants than did women who received a placebo (4; H. A. Elder, R. Smith, and E. H. Kass, Program Abstr. Intersci. Conf. Antimicrob. A...

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 83%

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Hepatotoxicity of Erythromycin Estolate During Pregnancy

McCormack

George

et al. 1977

Antimicrob Agents Chemother

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“…Liver abnormalities generally subside within two-five weeks after stopping the drug. 91 In rare cases, cholestasis persists for up to six months.…”

Section: Other Antibioticsmentioning

confidence: 99%

Drug-Induced Liver Injury

Hamilton

Collins‐Yoder

Collins

2016

AACN Advanced Critical Care

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Drug-induced liver injury (DILI) is common and nearly all classes of medications can cause liver disease. Most cases of DILI are benign, and improve after drug withdrawal. It is important to recognize and remove the offending agent as quickly as possible to prevent the progression to chronic liver disease and/or acute liver failure. There are no definite risk factors for DILI, but preexisting liver disease and genetic susceptibility may predispose certain individuals. Although most patients have clinical symptoms that are identical to other liver diseases, some patients may present with symptoms of systemic hypersensitivity. Treatment of drug and herbal-induced liver injury consists of rapid drug discontinuation and supportive care targeted to alleviate unwanted symptoms. KeywordsDrug-induced liver injury (DILI); drug-induced hepatitis; drug-induced cholestasis; acetaminophen; vanishing bile duct syndrome; herbal toxicity Adverse drug reactions are an important cause of liver injury that may require discontinuation of the offending agent, hospitalization, or even liver transplantation. 1 Indeed, drug-induced hepatotoxicity is the most frequent cause of acute liver failure in US. 2 Because the liver is responsible for concentrating and metabolizing a majority of medications, it is a prime target for medication-induced damage. Among hepatotoxic drugs, acetaminophen (paracetamol) is the most often studied. However, a broad range of different pharmacological agents can induce liver damage, including anesthetics, anticancer drugs, antibiotics, antituberculosis agents, antiretrovirals, and cardiac medications. In addition, a plethora of traditional medical therapies and herbal remedies may also be hepatotoxic.Depending on the duration of injury and the histological location of damage, drug-induced liver injury (DILI) is categorized as acute or chronic, and either as hepatitis, cholestatic, or a mixed pattern of injury. The hepatitis pattern is characterized by hepatocyte necrosis and is associated with a poor prognosis. There are three types of acute cholestatic drug-induced injury: bland cholestasis is the result of abnormal biliary secretion, and is not accompanied by significant hepatocellular damage; cholestatic hepatitis (mixed type) refers to cholestasis with concomitant hepatic parenchymal damage; and the third form of acute cholestasis is

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Fulminant Hepatic Failure Associated With Intravenous Erythromycin Lactobionate

Gholson¹

1990

Arch Intern Med

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Hepatotoxicity of Erythromycin

Cited by 88 publications

References 0 publications

Hepatotoxicity of Erythromycin Estolate During Pregnancy

Hepatotoxicity of Erythromycin Estolate During Pregnancy

Drug-Induced Liver Injury

Fulminant Hepatic Failure Associated With Intravenous Erythromycin Lactobionate

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