ME made worse by Rituximab ? You might actually have seronegative borreliosis and not ME

Was your ME/CFS made worse by Rituximab? Well you might actually have seronegative borreliosis and not ME/CFS


  CASE 1:
  @ PubMed:

  van Dop WA, Kersten MJ, de Wever B, Hovius JW. BMJ Case Rep. 2013 Feb 14;2013. pii: bcr2012007627. doi: 10.1136/bcr-2012-007627. Seronegative lyme neuroborreliosis in a patient using rituximab.

  Abstract
  A 66-year-old woman presented with severe shooting pains throughout her back and legs, followed by progressive deafness, weight loss and headache. She had a history of marginal zone B-cell lymphoma stage IV-B, for which she was successfully treated with immunochemotherapy and rituximab maintenance therapy.

  A relapse was suspected, but chemotherapy was not administered, since, despite elaborate investigations, malignancy could not be proven.

  Because of a history of tick bites she was tested for antibodies against Borrelia burgdorferi in serum and cerebrospinal fluid (CSF), which were negative.

  However, a B burgdorferi PCR on CSF came back positive. The patient was treated for seronegative Lyme neuroborreliosis with ceftriaxone intravenously and dramatically improved.

  This case presentation demonstrates that, in immunocompromised patients, it is important not to solely rely on antibody testing and to use additional diagnostic tests to avoid missing or delaying the diagnosis.

 

  CASE 2:
  @ PubMed:

  Harrer T, Geissdörfer W, Schoerner C, Lang E, Helm G., Infection. 2007 Apr;35(2):110-3. Seronegative Lyme neuroborreliosis in a patient on treatment for chronic lymphatic leukemia.

  Abstract
  We report on a patient who developed seronegative Lyme neuroborreliosis complicating chemotherapy for chronic lymphatic leukemia. After the fifth cycle of chemotherapy (FCR: fludarabine, cyclophosphamide, rituximab and prednisone) the 63-year-old patient developed night sweat, arthralgia in elbows, wrists, proximal interphalangeal joints (PIPs) and strong neuropathic pain in both legs, followed by paresthesia and hypesthesia in the feet, arms and face.

  Laboratory analysis revealed an elevated C-reactive protein (CRP), a slight elevation of liver enzymes and decreased IgG levels. Cerebrospinal fluid (CSF) analysis showed a lymphomononuclear pleocytosis and an elevation of protein.

  A broad diagnostic work-up was negative including a negative Borrelia IgG and IgM ELISA.

  The patient did not remember recent tick bites, but after specific questioning he recollected a transient erythema on his leg developing just before the start of the last cycle of chemotherapy.

  As the combination of neuropathic pain and arthralgia, the transient erythema and the lymphomononuclear pleocytosis raised the suspicion of Lyme neuroborreliosis, the patient was treated for 3 weeks with ceftriaxone. On therapy all symptoms resolved and CRP normalized. Retrospective PCR analysis of a CSF sample confirmed the clinical diagnosis by detecting Borrelia garinii DNA.

  This case demonstrates that in immunosuppressed patients borrelial serology may be negative and that additional diagnostic approaches (including tests for direct Borrelia detection) may be needed to demonstrate borrelial infection.