Polymyxin B has a reputation. Doctors who reach for it against drug-resistant bacteria expect to watch the kidneys and the nerves, because those are the toxicities the drug is known for. Muscle damage is not on the usual list.
A case published August 24 in the peer-reviewed journal Infection and Drug Resistance describes a 63-year-old woman in whom it appears to have been. The way the injury showed up in her bloodwork is the part clinicians are likely to remember.
One Marker Soared, the Other Barely Moved
The patient had been through a punishing sequence. In October 2025, she suffered a cerebral embolism, underwent mechanical thrombectomy, and then developed a brain hemorrhage that required decompressive surgery. A worsening lung infection followed, along with a tracheotomy. Cultures grew drug-resistant Acinetobacter baumannii extensively in her sputum and Bacillus cereus in her blood.
She was treated with polymyxin B, given both intravenously and by inhalation, combined with tigecycline and vancomycin. Her infection markers improved. Her muscle markers did not.
By hospital day 15, her myoglobin had climbed to 9,002 micrograms per liter against a reference ceiling of 70, roughly 128 times the upper limit of normal. Creatine kinase, the enzyme physicians most often use to flag muscle breakdown, was only 332 units per liter, with a normal range topping out at 200. Her creatinine had risen from 70 to 178 micromoles per liter, signaling acute kidney injury.
The authors explain the gap in terms of molecular size. Myoglobin is a small protein of about 17.8 kilodaltons; creatine kinase is a much larger enzyme at roughly 82 kilodaltons. In reversible membrane injury that stops short of full cell death, small proteins can slip through transient pores, while larger ones remain in place.
How the Team Landed on Polymyxin B
Pinning harm on one drug in a critically ill patient taking several is difficult, and the authors are candid about it.
They ruled out trauma and worsening infection, noting that infection markers were improving while myoglobin continued to rise. They then applied the Naranjo adverse drug reaction probability scale and the World Health Organization Uppsala Monitoring Center causality criteria, both of which pointed to polymyxin B as the most likely agent.
Polymyxin B, tigecycline, and vancomycin were all stopped on November 7 and replaced with meropenem. Supportive care included aggressive fluid resuscitation and urine alkalinization. Eight days later, myoglobin had fallen to 1,550 and creatine kinase to 101. About two weeks after the drugs were withdrawn, myoglobin levels had fallen to 171, and kidney function had returned to near baseline.
Other contributors were plausible. Prolonged immobility after brain surgery could have driven background muscle breakdown. Vancomycin carries well-documented kidney toxicity that may have compounded the injury, and impaired kidneys clear myoglobin more slowly. A drop in fibrinogen was attributed to tigecycline, a pattern the authors say is commonly seen with that drug.
Their conclusion is deliberately hedged: the muscle injury was multifactorial, with polymyxin B as a modifiable trigger rather than the sole cause.
A Drug Pulled Back Off the Shelf
Polymyxins reached clinical use in the late 1950s and were largely set aside in the decades that followed, pushed out by newer antibiotics that were easier on the kidneys and nerves. They came back because bacteria left prescribers with fewer options.
The Centers for Disease Control and Prevention classifies carbapenem-resistant Acinetobacter as an urgent threat. Its 2019 threats report estimated 8,500 infections among hospitalized U.S. patients and 700 deaths in 2017, and the agency has said updated burden estimates covering at least 19 resistance threats are due to be released in 2026.
Trouble from this drug class is not unprecedented. A 2020 report in the journal Medicine described rhabdomyolysis in a woman given polymyxin B after valve replacement surgery. Her creatine kinase and myoglobin both rose, then fell once the drug was stopped. Separately, Chinese clinicians reported in Frontiers in Pharmacology this year on what they describe as the first documented case of drug fever caused by polymyxin B. What distinguishes the new report is the striking mismatch between the two muscle markers.
What This Single Case Cannot Settle
The limitations are substantial, and the authors list them plainly. One patient. Multiple concurrent medications. Serious infection. Other causes of muscle injury could not be fully excluded.
Therapeutic drug monitoring was not performed, so it is unknown whether the injury occurred at standard blood levels or because the drug accumulated. The patient's impaired consciousness meant she could not report muscle pain or weakness, symptoms that might otherwise have prompted earlier testing.
The clinical suggestion the authors draw is narrow. In critically ill patients receiving polymyxin B, particularly those with existing kidney impairment, those on other nephrotoxic drugs such as vancomycin, or those receiving the antibiotic by both intravenous and inhaled routes, checking myoglobin alongside creatine kinase and kidney function may detect injury that creatine kinase alone would understate.
For patients and families, nothing here suggests avoiding a necessary antibiotic. Polymyxin B is used when alternatives have been exhausted. Anyone with questions about a hospitalized relative's medications should raise them with the treating team rather than acting on a single published case.
Key Questions Answered
What is polymyxin B used for?
It is a last-line antibiotic reserved for serious infections caused by gram-negative bacteria that are resistant to other drugs, including carbapenem-resistant Acinetobacter baumannii.
Why is the myoglobin result surprising?
Creatine kinase is the standard screening test for muscle damage. In this patient, it rose only modestly while myoglobin reached about 128 times the upper limit of normal, meaning a creatine kinase check alone could have understated the injury.
Did the drug definitely cause the muscle damage?
No. Two standard causality assessment tools rated polymyxin B the probable cause, but the authors stress that these tools have limits in complex cases and that the injury was likely multifactorial.
Did she recover?
Yes. After the antibiotics were stopped and supportive care was given, her muscle and kidney markers normalized over about two weeks, her infection was controlled, and no kidney failure or arrhythmia developed.
Is this a common side effect?
No. The authors describe muscle injury from polymyxin B as rarely reported and note that the exact incidence is unknown. Kidney and nerve toxicity remain the recognized limitations of the drug.
What should patients take from this?
Nothing about their own prescriptions. This is a single case report from a hospital setting involving a drug given almost exclusively to critically ill inpatients. Questions about a hospitalized family member's treatment belong with the medical team.
