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Transverse myelitis and Guillain Barre Syndrome secondary to reactivation of viral hepatitis B

This case report describes the first documented instance of concurrent transverse myelitis and Guillain-Barré syndrome triggered by hepatitis B virus reactivation in a patient following rituximab-based chemotherapy, highlighting the critical need to consider HBV reactivation in immunosuppressed patients presenting with acute inflammatory neurological syndromes.

Original authors: Wai Kin Su, Saad Shams Bin Shaheen, Jacob George, Natasha Gerbis, Simone I Strasser, Salim Maher, Cameron Gofton

Published 2026-07-10
📖 5 min read🧠 Deep dive

Original authors: Wai Kin Su, Saad Shams Bin Shaheen, Jacob George, Natasha Gerbis, Simone I Strasser, Salim Maher, Cameron Gofton

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's immune system is a highly trained security team, and your liver is a busy factory. Usually, this team keeps the factory running smoothly. But sometimes, a sneaky virus called Hepatitis B (HBV) hides in the shadows of the factory, waiting for the security team to take a nap.

In this story, a 58-year-old man had a history of a blood cancer called lymphoma. To treat it, he received a powerful chemotherapy cocktail called R-CHOP. This treatment is like a heavy-duty vacuum cleaner that sucks up the bad B-cells (a type of white blood cell), but it also accidentally puts the immune security team to sleep. Before the treatment, doctors checked his liver and found he had met the virus in the past but wasn't currently infected. They gave him a shield called Entecavir to keep the virus asleep during the "vacuuming."

Here is the twist: The man stopped taking his shield early. Eight months after finishing his chemotherapy, the virus woke up with a roar. It wasn't just a small nap; it was a full-blown rebellion. His liver enzymes, which act like smoke alarms, screamed into the stratosphere. His Alanine Aminotransferase (ALT) skyrocketed to 2,974 unit/L, and his Aspartate Aminotransferase (AST) hit 1,446 unit/L. The virus was multiplying, and the man's liver was under attack.

But the virus didn't stop at the factory. It decided to throw a chaotic party in the man's nervous system, which is like the body's electrical wiring.

First, the virus seemed to short-circuit the main cable running down his spine. This is called Transverse Myelitis. Imagine a long stretch of electrical wire from his neck down to his lower back suddenly catching fire. The fire started at the C4 level (near the neck) and burned all the way down to T10 (mid-back). On an MRI scan, this looked like a long, bright, glowing line of damage. The result? The man lost feeling in his legs, couldn't move them well, and his bladder and bowels stopped working like a broken faucet. He had a "sensory level" at T4, meaning everything below that point felt like it was underwater.

At the exact same time, the virus attacked the smaller wires branching out to his limbs. This is Guillain-Barré Syndrome (GBS). Think of this as the insulation peeling off the electrical wires, causing the signals to sputter and die. His legs went weak, his reflexes (like the knee-jerk tap) vanished, and he felt tingling sensations.

The doctors had to be detectives. They needed to know: Was the virus itself crawling into the brain and spinal cord? Was it an autoimmune glitch where the body attacked itself? Or was it something else? They took a sample of the fluid surrounding the brain and spine (CSF). The test results were a big "No" to the virus being inside the nervous system directly. The fluid didn't show signs of the virus, and it didn't show the usual markers for other autoimmune diseases. The paper explicitly rules out the idea that the virus was physically invading the central nervous system; instead, it suggests the immune system's reaction to the waking virus caused the damage.

So, what did they do? They launched a two-pronged rescue mission.

  1. The Shield: They immediately restarted the antiviral drug, Entecavir, to put the Hepatitis B virus back to sleep.
  2. The Reset: They gave the man a massive dose of Intravenous Immunoglobulin (IVIG)—125 grams total over five days. Think of this as a "system reboot" for his immune security team, calming them down so they stop attacking the wiring.

The results were like watching a slow-motion movie in reverse. Within three weeks, the glowing fire on the MRI scan of his spine completely vanished. The electrical signals in his legs started to return, and his liver enzymes began to calm down. By three months, the virus was suppressed, his liver was normal, and he had even cleared the virus's surface marker (HBsAg) from his blood.

However, the story isn't a perfect "happily ever after" just yet. While his legs and liver recovered, he still had some trouble with his bladder, which remained a bit like a leaky faucet requiring him to use a catheter.

This case is a first in the medical record books. The authors state that, to their knowledge, this is the first time anyone has reported a patient having both Transverse Myelitis and Guillain-Barré Syndrome at the same time because of a Hepatitis B reactivation. It suggests that when the Hepatitis B virus wakes up after being suppressed by strong medicines, it can cause a double-whammy of nerve damage. The paper doesn't claim this happens often, but it warns doctors: if a patient who recently had strong immune-suppressing treatment suddenly gets weird nerve problems and liver trouble, check for a waking Hepatitis B virus. Early detection and a quick mix of antivirals and immune therapy can turn a disaster into a recovery, even if some small glitches, like the bladder issue, might linger.

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