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11 Articles in Volume 13, Issue #2
Spinal Cord Stimulation: Fundamentals
Assessment of Psychological Screeners for Spinal Cord Stimulation Success
Educating Patients About Pain Medications
Central Sensitization: Common Etiology In Somatoform Disorders
Demystifying Pain Pathways
Vibroacoustic Harp Therapy in Pain Management
Erythrocyte Sedimentation Rate and C-Reactive Protein: Old But Useful Biomarkers for Pain Treatment
Editor's Memo: Inflammatory Disease—Time to Refine Our Diagnoses
Ask the Expert: Pain Persists in Spite of High-dose Opioids
Ask the Expert: Rectally Administered Morphine
Letters to the Editor: Mistaken Hormone, Lab Values

Editor's Memo: Inflammatory Disease—Time to Refine Our Diagnoses

March 2013

In recent years, I have seen an increasing number of patients present with inflammatory diseases that do not fall into any of the classic rheumatoid diagnoses, such as systemic lupus erythematosus, rheumatoid arthritis, scleroderma, ankylosing spondylitis, or one of the lesser-known conditions such as autoimmune polyglandular syndrome. Make no mistake about it: these patients complain of pain and suffering as much as or more so than patients with other painful conditions. Also, they will complain of any number of systemic symptoms including nausea, exhaustion, depression, insomnia, arthralgia, myalgia, and cognitive impairment. Their pain may be intermittent or constant and may be associated with allodynia and hyperalgesia. Pain can be localized or “all over.”

The National Institute of Arthritis and Musculoskeletal and Skin Diseases has taken a great step in classifying inflammatory disease. It divides the immune system into two components: one is the inborn or “innate” immune system, which causes inflammation for unknown reasons; and the other is the “acquired” immune system, which develops as a person grows. A disease that results from the innate or inborn system is called “autoinflammatory,” and one that results from the “acquired” system is called “autoimmune.” Examples of “autoinflammatory” diseases include familial Mediterranean fever, tumor necrosis factor receptor-associated periodic syndrome, neonatal onset multisystem inflammatory disease, and Behçet’s Disease.1 Autoinflammatory diseases are quite rare. In pain practice, we primarily see patients whose inflammatory conditions involve the “acquired” immune system, as the patient’s condition begins in adulthood and often follows a single event—usually an infection or trauma. In addition, many patients don’t seem to qualify for any standard rheumatologic or autoinflammatory diagnosis.

Since a specific rheumatologic or immunologic diagnosis can’t be assigned to these individuals, they are usually “shown the door” or given a diagnosis of fibromyalgia, psychogenic disease, or myofascial syndrome. For example, I just saw some notes on a patient from a referring physician who stated, “The anti-nuclear antibody isn’t high enough to be called lupus or rheumatoid arthritis, so I’ll treat for fibromyalgia.” In 2010, the American College of Rheumatology published revised criteria for diagnosing fibromyalgia, and these criteria should be met before assigning this diagnosis.2 However, most patients referred to me with the diagnosis of “fibromyalgia” don’t meet these criteria.

I strongly recommend that a scientific description be applied to patients who don’t warrant a classic disease diagnosis but have what I call “autoimmune inflammatory disease” (Table 1). An autoimmune disease is one in which the body produces a disordered immunological response against itself. This process can be genetic and begin in childhood or it can be acquired in adulthood after an infection or severe trauma. There are many examples of autoimmune manifestations following an infection. Some of the better-known examples are infectious mononucleosis, hepatitis C, varicella zoster virus, human immunodeficiency virus, and Lyme disease. There are undoubtedly other infections that can trigger autoimmune disease and pain conditions. Genetic autoimmune inflammatory disease may begin to reveal itself in childhood with frequent infections, missed school, and symptoms of arthralgia, myalgia, headache, and nausea.

The autoimmune process invariably produces inflammation as autoantibodies float through the biologic system and arbitrarily decide to attack a joint, gland, or organ. This process is the historical, clinical tip off that an autoimmune inflammatory disease is present. For example, I just saw a patient who started out with endometriosis, which, soon after, was followed by painful thyroid, gallbladder, and lung symptoms. Pain “all over” came later. When a practitioner receives multi-system complaints over time that seem disconnected, think of autoimmune inflammatory disease, because the apparent and disparate events and complaints may all stem from the underlying autoimmune disease.

To confirm the presence of an autoimmune disease, a number of laboratory tests can help. An autoimmune disease may alter white blood cells, serum proteins, and inflammatory markers. Patients may exhibit high antibody titers to prior infections such as the Epstein-Barr virus. There are now myriad antibodies that can be detected to help establish the diagnosis.

The benefits of refining our diagnostic labels and adopting “autoimmune inflammatory disease” are, in my opinion, many. Patients and their families resent it when no scientific diagnosis and rationale for their condition can be given. This is particularly true for a condition that causes severe pain, suffering, and disability. We owe it to the parties who pay the health bills these days to provide a scientific description of a severe disease process. Don’t forget that autoimmune inflammatory disease may cause severe misery, disability, and a shortened life span. As a first step, let’s upgrade our diagnostic labels and clearly identify patients who have a congenital or acquired autoimmune inflammatory disease so we can deliver more effective and specific treatments, starting with pain relief.

Last updated on: October 28, 2014