Dear Editor:

Guillain-Barré syndrome (GBS), or acute inflammatory demyelinating polyneuropathy (AIDP) is a severe pathology, often fulminating, which in more than two thirds of cases presents as an antecedent infection usually caused by a virus (cytomegalovirus [CMV] or Epstein-Barr virus). We present the case of a 48 year old male, recipient of a renal transplant in January 2007; D/R CMV serology positive; immunosuppression with steroids, mycophenolate and tacrolimus; delayed graft function during initial progress but good subsequent progress (creatinine on discharge, 1.5mg/dL).

During evolution, the patient presented with an acute Banff grade IIB cellular rejection, treated with thymoglobulin, which caused an allergic reaction, and bicytopenia. Treatment was withdrawn, but renal function improved. Four days after receiving thymoglobulin the patient presented with arthromyalgias and febricula, rapidly progressing to weakness of the lower extremities and 4/5 paresis in all four extremities, and severe dysphonia and dysphagia. He remained afebrile and without respiratory compromise. Laboratory tests showed a deterioration of renal function with 2.5mg/dL creatinine. Supplementary tests: cranial CT showed no alterations. Negative cultures. CRP for CMV negative. EMG: alterations compatible with acute motor demyelinating polyneuropathy. On assessment by Neurology, the patient was diagnosed as having symptoms compatible with GBS, starting treatment with polyclonal immunoglobulin IV at a dose of 2g/kg and high doses of steroids. The symptomatology disappeared 24 hours after treatment, although a slight motor deficit persisted for several weeks. Renal function on discharge: Cr: 1.7mg/dL

In an immunodepressed population, it is logical that the most frequently reported issue has been CMV2-4. Immunosuppression in itself constitutes an alteration of immunological equilibrium. This alteration, in keeping T suppressor lymphocytes inhibited, allows lymphocyte clones which are capable of generating an autoaggressive response to remain free. No habitual risk factor associated with the development of this entity was found in our patient. Circumstances exist in which abnormal circulating proteins have been associated with neuropathy (Waldenström’s disease, multiple myeloma, POEMS syndrome). It is possible that the administration of thymoglobulin causes a condition similar to dysproteinemia, through the formation of immune complexes (serum sickness). T cells and neurons possess similar glycolipids in the membrane, with the associated chalcogens against GBS GM1. We have found only one reference5 in the literature to a possible relationship with antilymphocyte polyclonal antibodies. In this instance, the temporal ratio and the symptoms displayed by the patient on administering the ATG, as well as an absence of other causes, cause us to think that there is a possible association between thymoglobulin treatment and subsequent AIDP, possibly related to serum sickness.