Treatment Decisions in a Man With Hodgkin Lymphoma and Guillian-Barré Syndrome: A Case Report

Caren L Hughes; Jeffrey T Yorio; Craig Kovitz; Yasuhiro Oki

Disclosures

J Med Case Reports. 2014;8(455) 

In This Article

Discussion

This report describes a young man with simultaneous diagnoses of HL and GBS. Lymphocytes are primary drivers of the immune process, and dysregulation of the immune system can be one outcome of lymphocytic malignancies.[11] In one study of 519 patients with HL, 9% of patients were diagnosed with a lymphoma-associated autoimmune disease. These autoimmune processes are the underlying etiology of many of the paraneoplastic disorders reported for patients with lymphoma.[2] The abnormalities can be hematologic (autoimmune hemolytic anemias, immune thrombocytopenic purpura, blood eosinophelia), dermatologic (Sweet's syndrome, eosinophilic fasciitis), renal (glomerulonephritis) or neurologic.

Neurologic effects experienced by a patient with HL can be the result of the disease itself (infiltration of nerves by tumor, more likely in non-Hodgkin lymphoma (NHL) than HL), chemotherapy adverse events (neuropathy from vinca alkaloids, platinum agents) or paraneoplatic causes.[12] Neurological paraneoplastic syndromes that have been reported with HL include limbic encephalitis, subacute myelopathy, subacute motor neuropathy, GBS, central pontine myelinolysis, and diffuse cerebritis.[13]

GBS is described as an inflammatory immune-regulated neuropathy.[12] Incidence is rare, occurring in one to two in 100,000 people worldwide[4] and it is thought to be related to production of antibodies that can be triggered by infectious agents such as Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, Mycoplasma pneumonia, Haemophilus influenza, and variacella-zoster. However, ganglioside and glycolipid targets for the antibodies exist not only in the invading pathogen's proteins, but also in the tissues of the nervous system. The resulting autoimmune response causes demyelination manifesting as areflexia and ascending motor neuropathy.[2] Similarly, antigens present on the surface of lymphoma cells can also generate production of antibodies that will attack similar proteins in the nervous system.[1,12]

A standard chemotherapy regimen for first-line treatment of classical HL is the four-drug combination containing doxorubicin, bleomycin, vinblastine and dacarbazine (ABVD). Vinblastine can induce numbness and peripheral neuropathy, and patients with preexisting neurologic disorders may be at higher risk of developing neuropathies from vinblastine.[14] This presents a difficult challenge in patients with HL experiencing GBS. In this case, our patient received full-dose vinblastine for four out of 10 doses, and a reduced dose for three doses.

The neurologic abnormalities of GBS can also manifest as respiratory symptoms, seen in 25% of cases.[15] This can complicate decisions to include bleomycin in the treatment regimen, a drug that has resulted in pulmonary interstitial infiltrates in 3 to 5% of patients.[14] Our patient received full doses of bleomycin for seven out of 10 doses, but it was withheld for three doses due to a decline in respiratory status. Certainly, the mechanism of bleomycin-induced lung injury differs from that seen in a neurologic condition such as GBS, but the presence of GBS does make it more difficult to manage a patient like this in an effort to maximally treat the patient without causing underlying damage from chemotherapy agents.

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