Visceral leishmaniasis associated with Ixekizumab therapy
This paper reports the first documented case in the Mediterranean region of visceral leishmaniasis complicated by hemophagocytic lymphohistiocytosis in a patient treated with the IL-17 inhibitor ixekizumab, which was successfully managed with liposomal amphotericin B before the patient was switched to guselkumab.
Original paper licensed under CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). This is an AI-generated explanation of the paper below. It is not written or endorsed by the authors. For technical accuracy, refer to the original paper. Read full disclaimer
Imagine your body is a bustling city with a super-secure police force called the immune system. This force has different squads, and one of them, the "IL-17 Squad," is the special unit responsible for keeping a specific type of invisible stowaway called Leishmania (a tiny parasite) from sneaking in and taking over. Usually, this squad is on high alert, especially in places like the Mediterranean where these parasites hang out in the sand and on dogs.
Now, meet our patient: a 52-year-old woman with a tricky condition called psoriatic arthritis, where her own city walls were attacking her joints. To calm things down, doctors gave her a powerful new tool: ixekizumab. Think of ixekizumab as a "peacekeeper" that tells the IL-17 Squad to stand down and stop fighting. It worked great for her joints and skin at first.
But here's the twist: by telling the IL-17 Squad to stand down, the peacekeeper accidentally left the city gates wide open. In February 2025, her symptoms came back, and she restarted the ixekizumab in April 2025 (starting with a 160 mg loading dose, then 80 mg every four weeks). By July 2025, the invisible stowaways had thrown a massive party inside her.
The parasites, Leishmania infantum, didn't just hang out; they caused a chaotic riot. The woman developed a high fever, extreme tiredness, and a massive spleen (the organ that filters blood) that grew to 15 cm. Her blood work showed a terrifying drop in everything: her hemoglobin was down to 7.4 g/dL, her white blood cells to 3,760/mm³, and her platelets to 54,000/mm³. Her body's inflammation was so high that her ferritin level skyrocketed to 19,525 ng/mL, and her triglycerides hit 272 mg/dL.
This wasn't just an infection; it triggered a condition called Hemophagocytic Lymphohistiocytosis (HLH). You can think of HLH as the city's fire department going haywire and accidentally setting the city on fire while trying to put out a small spark. The doctors calculated she had a 98% probability of having this syndrome.
The paper highlights that this is a first: it's the very first reported case of this specific parasite infection linked to ixekizumab in the Mediterranean region, and only the second time anyone has seen it with this type of drug (an IL-17 inhibitor). The authors suggest that because IL-17 is so important for fighting Leishmania, turning it off with drugs like ixekizumab might wake up a sleeping infection or let a new one in.
The good news? The doctors caught it. They stopped the peacekeeper and gave her liposomal amphotericin B (a strong anti-parasite medicine) for five days, followed by five weekly doses. By October 2025, the fever vanished, her blood numbers went back to normal, and the parasite DNA disappeared from her blood.
However, her arthritis flared up again. So, in November 2025, doctors switched her to a different kind of peacekeeper called guselkumab. This one targets a different squad (IL-23) and is thought to be less likely to let the parasites in. Before starting, they tested her again, and the parasite was gone. She stayed healthy, though her antibody test (the rK39 test) stayed positive until April 2026, showing her body still remembered the battle.
The authors point out that while Europe only has about 2% of the world's leishmaniasis cases, it accounts for nearly 80% of the cases in people with weakened immune systems. They suggest that for patients in these areas, doctors might want to check for this parasite before starting these powerful new drugs, just to make sure the city gates aren't already breached.
What the paper rules out:
The paper makes it clear that this wasn't caused by her previous treatments (corticosteroids and cyclosporine) or by other common viruses like Cytomegalovirus or Epstein–Barr virus, which she had already fought off in the past. It also confirms that the infection wasn't a new, random accident but was likely linked to the specific way ixekizumab works.
How sure are they?
The authors are very sure about the diagnosis because they found the parasite's DNA in her blood using a PCR test and confirmed it with a positive antibody test. They are suggesting (not proving for all time, but strongly hinting) that IL-17 inhibitors are a risk factor for this infection in these areas. They aren't saying this happens to everyone, but that it can happen, and doctors should be aware of it.
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