Dermatologic Manifestations of Eosinophilia-Myalgia Syndrome Clinical Presentation

  • Author: Robert A Schwartz, MD, MPH; Chief Editor: William D James, MD   more...
 
Updated: May 22, 2012
 

History

The case definition of EMS is useful to identify patients with suspected EMS; however, to ensure a more accurate diagnosis, a more stringent set of criteria must be applied. One set of proposed classification criteria includes 4 axes: (1) the presence of a distinct acute episode with the typical signs and symptoms; (2) major physical findings, including typical involvement of organs, such as the skin, the muscles, the lungs, and the nerves; (3) characteristic laboratory values, including an eosinophil count greater than 1.0 X 109 cells/L; and (4) characteristic histopathologic features.

Acute episode

The acute episode is characterized by shortness of breath; cough; fever; debilitating fatigue; arthralgias; paresthesias; severe weakness; muscle cramps; periorbital and peripheral edema; skin hypersensitivity; and a generalized erythematous, maculopapular, or blotchy erythematous rash.

After this acute episode, most patients have more chronic symptoms that involve several organ systems.

Cutaneous involvement

Cutaneous involvement occurs in 60% of patients with EMS. After the initial symptoms, this is the most prominent feature of the disease.

In the acute phase of the disease, patients often have a diffuse eruption with pruritus and swelling.

Later in the disease, patients may experience skin tightening, which reflects sclerodermoid changes. However, unlike scleroderma, the fingers and the toes are almost always spared, and the Raynaud phenomenon is usually absent.

Patients may note an inability to tolerate even light touch. This finding tends to be more pronounced in the lower extremities than elsewhere.

Alopecia is also noted in more than one quarter of patients.

Muscular involvement

By definition, patients must have myalgia. This condition usually begins in the proximal muscle groups, such as those in the shoulders, the buttocks, and the thighs; then, myalgia becomes incapacitating.

Patients may have stiffness and aches in the affected muscles, as well as muscle cramps, particularly during exercise.

Patients also complain of weakness and muscle wasting that limit their ability to walk or lift heavy objects.

Myalgia in the jaw can lead to pain in the facial muscle or the jaw.

Nervous system involvement

Central nervous system and peripheral nervous system involvement is seen in 27% of patients, in whom disorders of these systems are the presenting features.

Patients may have decreased sensation, particularly in the hands, or hyperesthesia in the back and the extremities.

Patients may present with weakness, cognitive deficits, or bladder dysfunction.

Pulmonary involvement

Pulmonary symptoms are the major presenting complaints in the acute phase of EMS.

Patients report rapidly progressive shortness of breath associated with a nonproductive cough and other symptoms related to upper respiratory tract infections.

Patients may have chest tightness, pleuritic chest pain, or dyspnea on exertion.

Cardiac involvement

Most patients do not have heart problems; however, pericarditis, myocarditis, and cardiac arrhythmias are known complications of the disease.

Patients with arrhythmias may have palpitations.

Gastrointestinal involvement

Gastrointestinal problems are not common problems in this disease.

Some patients experience abdominal pain, nausea, vomiting, diarrhea, and weight loss.

Rheumatologic involvement

About 73% of patients have joint pain.

This pain can be located in the wrist, the knees, the ankles, the shoulders, the hips, the spine, or the interphalangeal and metacarpophalangeal joints.

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Physical

Cutaneous manifestations

A diffuse eruption consisting of erythematous macules and papules often develops over the trunk and the extremities. The skin may have a mottled appearance and occasionally appears ecchymotic. No palpable purpura is evident.

Four weeks to 4 months after the onset of myalgias, a progressive peau d'orange–type induration may develop. This process tends to start in the distal part of the lower and upper extremities and gradually moves proximally. The digits are characteristically spared. The skin classically appears firm, shiny, and hide-bound.

Sometimes, venous furrowing of the uplifted arm is observed.

Neuromuscular manifestations

Neuromuscular examination of patients with EMS reveals weakness and paresthesias. Some patients have cutaneous hyperesthesia (the inability to tolerate touch). This finding tends to be more pronounced in the lower extremities.

Muscles are often tender to palpation.

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Causes

Although the consumption of L-tryptophan is not part of the definition of EMS, it is described in more than 96% of patients with EMS. Tryptophan is an essential amino acid that is present in many foods and is part of various remedies. It is used to treat insomnia, anxiety, premenstrual syndrome, and obesity. In fact, prior to 1989, millions of Americans had been ingesting products containing L-tryptophan for many years. Therefore, any hypothesis about the association between L-tryptophan consumption and EMS must address why some individuals had the syndrome while others did not. During the peak of the epidemic, 2 theories emerged: the toxic metabolite hypothesis and the contaminant hypothesis.

Toxic metabolite hypothesis

L-tryptophan is metabolized through 2 separate pathways. In one pathway, L-tryptophan is broken down to serotonin. In the other pathway, L-tryptophan is degraded into kynurenine. In this pathway, kynurenine can be metabolized to quinolinic acid, which is an endogenous neurotoxin implicated in the pathogenesis of several metabolic and neurologic conditions.

Metabolites of both pathways are associated with connective tissue disorders.

Serotonin overproduction by carcinoid tumors is associated with myalgias and arthralgias in addition to sclerodermalike skin changes.

Patients with EMS are noted to have abnormalities in both of these pathways. However, aberrant tryptophan metabolism by itself does not provide an adequate explanation.

Contaminant hypothesis

Because of the epidemic nature of the syndrome, an inherited alteration in tryptophan sensitivity or metabolism is unlikely to be the sole factor responsible for the development of EMS. Rather, a contaminant is implicated as a cause of the syndrome.

In fact, L-tryptophan from different brands of products used by patients with EMS was traced back to one manufacturer in Japan who had altered the manufacturing process of L-tryptophan before the epidemic.

High-performance liquid chromatography of EMS-associated L-tryptophan reveals several peaks that correspond to impurities. One particular peak was consistently found in case-associated lots. This substance was isolated, purified, and shown to be 1,1-ethylidenebis (tryptophan). Although 1,1-ethylidenebis may not be the etiologic agent, it may be a marker for another contaminant.

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Contributor Information and Disclosures
Author

Robert A Schwartz, MD, MPH  Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

Takeji Nishikawa, MD  Emeritus Professor, Department of Dermatology, Keio University School of Medicine; Director, Samoncho Dermatology Clinic; Managing Director, The Waksman Foundation of Japan Inc

Disclosure: Nothing to disclose.

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Lester F Libow, MD  Dermatopathologist, South Texas Dermatopathology Laboratory

Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association

Disclosure: Nothing to disclose.

Glen H Crawford, MD  Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital

Glen H Crawford, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Phi Beta Kappa, and Society of USAF Flight Surgeons

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD  Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology

Disclosure: Elsevier Royalty Other

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, David Arbesfeld, MD, Vinay Arya, MD, and Nicole Quartarolo, MD, to the development and writing of this article.

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