Age: 62.0
Sex: M
Vaccine: FLUX
Symptoms: Blood urea increased, CSF protein normal, Colectomy, Colitis ischaemic, Cytomegalovirus antibody negative
Clinical narrative: This case was reported in a literature article and described the occurrence of Guillain Barre syndrome in a 62-year-old male subject who was vaccinated with Influenza vaccine, manufacturer unspecified) for prophylaxis. The patient has a history of hypertension and alcoholic liver cirrhosis, for which he underwent orthotopic liver transplantation 6 months prior to admission. Since then, he had been on FK506 and a low dose of prednisone without any complications. He denied any precedent episodes of diarrhea, nausea, vomiting, or other gastrointestinal or upper respiratory illness. On an unspecified date the subject received unspecified dose of Influenza vaccine (unknown). Two weeks after vaccination with Influenza vaccine, the subject developed Guillain Barre syndrome. Subsequently he was hospitalized. Neurological examination on admission revealed normal mental status, bilateral facial weakness, dysphagia, hypophonia, quadriplegia (1-2/5 by agency reported scale) throughout, and absence of muscle stretch reflexes in all extremities. Blood chemistry showed blood urea nitrogen 34 mg/dL, creatinine 0.9 mg/dL, albumin 4.5 g/dL, aspartate aminotransferase 78 U/L, alanine aminotransferase 189 U/L, gamma-glutamyl transpeptidase 160 U/L, alkaline phosphatase 146 mg/dL, total bilirubin 1.8 mg/dL, direct bilirubin 0.5 mg/dL, ammonia 47 mol/L, international normalized ratio 0.91, and blood FK506 level 7 mg/mL. Serum immunoglobin G was positive against herpes simplex virus 1, Epstein-Barr virus, and cytomegalovirus (CMV) but negative against herpes simplex virus 2. Immunoglobin M was negative against Epstein-Barr virus and CMV in serum. The testing for Campylobacter jejuni was not performed. Lumbar puncture revealed that the cerebrospinal fluid looked xanthochromic with red blood corpuscles 0/mm3. white blood cells 1/mm3, protein 358 mg/dL, glucose 88 mg/dL, lactic acid 2.7 mEq/L, and opening pressure of 25 cm cerebrospinal fluid. Cerebrospinal fluid venereal disease research laboratory slide test, gram stain, cryptococcal antigen, and cytology were negative. Herpes simplex virus, CMV, and Epstein-Barr virus DNA were not detected by polymerase chain reaction test. Electrodiagnostic studies showed prolonged distal latencies and absence of late responses in all extremities. The component muscle action potentials were reduced throughout with absence of component muscle action potential in the proximal tibial and peroneal nerves bilaterally. The conduction velocities were reduced in the demyelinating range in the median nerves bilaterally. There was a conduction block in medial nerves bilaterally, in right ulnar and in right tibial nerves. These findings were consistent with acute inflammatory demyelinating polyneuropathy. Shortly after admission, the patient was intubated for airway protection and started on intravenous immunoglobulin 0.4 g/kg/day for 3 days without significant improvement. Plasma exchange was not considered because of the patient's unstable hemodynamic status. His hospitalization course was complicated by the development of ischemic colitis secondary to dysautonomia, for which he underwent subtotal colectomy. The patient expired 3 weeks after admission from septic shock and acute renal failure. The author considered that although the temporal relationship between GBS and influenza vaccination was suggestive of causal effect, it does not fully prove it. The cause of GBS in this case might be predominantly humoral dysregulation, triggered by influenza vaccination, although the possibility of the remaining cell-mediated immune reaction could not be completely excluded.