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Activation of Latent Lyme Disease Following Epidural Steroid Injection: Case Challenge

Immunosuppression secondary to epidural steroid injection (ESI) is a well-documented adverse effect in the medical literature. Reports of systemic effects of immunosuppression resulting from corticosteroid dosages given by ESIs are anecdotal at best. This case report discusses the activation of latent Lyme disease following a lumbar ESI.
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A 32-year-old man presents with a 5-year history of low back pain. He underwent a lumbar laminectomy in 2003, but he began experiencing post-laminectomy syndrome with symptoms including lumbar radiculopathy in June 2009. The patient works as a supervisor for a local school system. He does not drink alcohol or use illicit drugs but reports a 10-pack per year smoking history. The patient noted that he had gone on two “morel mushroom hunting” camping trips around February 2011, in Jasper and Laport counties in Indiana. On the Jasper trip he remembers seeing a lot of deer ticks on his clothes but not on his skin. He does not recall developing any rash or flu-like symptoms.

Photo. Case Challenge: History

His left lower extremity radicular symptoms were consistent with magnetic resonance imaging findings of L4/5 and L5/S1 lesions. His course of treatment consisted of intermittent opioids, non-steroidal anti-inflammatories, muscle relaxants, and six lumbar epidural steroid injections (LESI) given over several years. The LESIs consisted of transforaminal and interlaminar techniques, with final injections performed on May 25, 2011. The injections on this date included a total of 60 mg of methylprednisolone (Depo-Medrol). The patient has never been treated with an oral corticosteroid regimen.

On the morning of May 26, 2011, the patient awoke with severe pain in all major joints in both upper extremities, with the highest intensity in the shoulders and elbows. He was subsequently unable to move for the next 2 hours secondary to intense pain. After taking Percocet (acetaminophen and oxycodone), his visual analog pain scale (VAS) decreased from 9 out of 10 to 5 out of 10, but any joint movement caused severe pain exacerbation. Later the same day, he experienced a fulminant onset of severe right lower extremity joint pain that progressively ascended to include all lower extremity major joints, with the most severe pain in the knees and ankles. The following day, his left lower extremity became affected, following a similar progression.

The patient was tested at his internist’s office and was found to have Lyme disease. The diagnosis was confirmed by Borrelia burgdorferi Western Blot. His sample was reactive in 10/10 critical IgG bands and 2/2 IgM bands. Currently, the patient has moderate to severe pain every day, and on some days he has exacerbations that are debilitating. As of this writing, his lowest pain VAS reported since May 26, 2011 was 5 out of 10, with many days 9 or 10 out of 10. His current medications include Percocet and cyclobenzaprine (Flexeril) as needed.

Lyme disease is the most commonly reported vector-borne illness in the United States, according to the Centers for Disease Control and Prevention. However, the disease does not occur nationwide, but rather is concentrated in the Northeast and Upper Midwest.

There has been some controversy over the terminology describing Lyme disease. For patients with a known tick bite or symptoms (erythema migrans [Figure 1], fever, etc), the diagnosis and treatment (2- to 4-week course of antibiotics) is fairly straightforward. However, approximately 10% to 20% of patients treated for Lyme disease have lingering symptoms of fatigue, pain, or joint and muscle aches. In some cases, these symptoms can last for more than 6 months. These cases now are commonly referred to as post–Lyme disease syndrome (PLDS).

But what about the patient who presents with chronic symptoms who never was formally diagnosed with, or treated for, Lyme disease? It may be natural to consider a chronic Lyme disease (CLD) or PLDS picture. Unfortunately, the non-specific general nature of the symptoms are also consistent with a broad spectrum of illnesses or symptom complexes for which there is no reproducible or convincing scientific evidence of any relationship to B. burgdorferi infection. In many of these types of cases, CLD becomes the default diagnosis, especially when that patient continues to present with persistent pain, neurocognitive symptoms, fatigue, or all of these symptoms, with or without clinical or serologic evidence of previous early or late Lyme disease.

Patients with CLD fall into four predominant categories (Table 1).1-3 The controversy surrounding CLD includes skepticism about whether it is a legitimate diagnosis. Some physicians believe that CLD is a misnomer because there are no controlled trials or carefully conducted laboratory studies supporting the notion that a persistent B. burgdorferi infection, occult or otherwise, causes chronic subjective symptoms. The majority of CLD cases do not warrant antimicrobial therapy because they lack laboratory evidence of B. burgdorferi infection.1,4 Although there is a paucity of support demonstrating the benefit of laboratory testing in the diagnosis of CLD, the following represent the most common techniques used: serum and/or cerebral spinal fluid antibodies; polymerase chain reaction testing for B. burgdorferi DNA; culture in Barbour-Stoenner-Kelly medium; and urinary antigen-capture-inhibition enzyme-linked immunosorbent assay. Unfortunately for patients with chronic disease manifestations, there may be no definitive cure. In these cases, counseling and symptomatic management may be the only viable treatment options.1

Mechanism of Immune Suppression
The immune inhibitory effects of corticosteroids are achieved via a wide variety of mechanisms. These include acquired and innate immune modulation mediated through several pathways, such as antigen presentation, T and B cells, neutrophils, or macrophage activation. Corticosteroids inhibit secretion of cytokines and thus affect downstream immune events.5 They can destabilize the mRNA encoding of interleukins (ILs) 1, 2, 6, and 8; tumor necrosis factor; and granulocyte-macrophage colony-stimulating factor.6 Corticosteroids may suppress leukocytes and endothelium, affecting leukocyte adherence, exit from circulation, and migration to infected tissue sites.7-9 In addition, neutrophil migration to tissue is severely impaired.

Immunosuppression by corticosteroids also causes a dramatic reduction in certain white cells, such as eosinophils, monocytes, and lymphocytes.7 Tissue accumulation of monocytes and macrophages is diminished, not only because of decreased migration from vasculature but also due to modulation of macrophage migration inhibiting factor.10,11 Some macrophage functions, such as cytokine and eicosanoid production, phagocytosis, and microbicidal functions, become attenuated.7,8,12,13 Corticosteroids cause a decrease in circulating and organ-resident dendritic cells.14 Also, a decrease in T-cells can occur via a number of mechanisms, including enhanced circulatory emigration,7 inhibition of IL-2,15,16 impaired release of T-cells from lymphoid tissue,17 and excessive induction of T-cell apoptosis.18 Circulating B-cell populations also have been found to be diminished by corticosteroid use.19

Last updated on: December 20, 2012
First published on: December 1, 2012