Considering An Autoimmune Etiology In The Differential Diagnosis Of Heel Pain

Pauravi (Po) Raval, DPM, MS

This author provides pearls on diagnosing a tricky case of heel pain in a 55-year-old woman that turned out to be CREST variant scleroderma.

Heel pain is a common complaint in podiatric practices. An initial exam for heel pain includes a past and present medical history, family and social history, medication history, a review of systems, a physical exam including a musculoskeletal exam and history. A differential diagnosis of heel pain is based on local and systemic etiologies. Such causes include arthritic, infectious, mechanical, neuropathic, traumatic, tumorous and vascular etiologies.1 This case study will show why you should add an autoimmune etiology to the differential diagnosis for heel pain.

In December 2015, a 55-year-old Caucasian woman entered my office for routine treatment of an ingrown nail on the lateral side of the left first metatarsal. She also complained of “pain in the bottom of both heels for a few weeks now” and added that she could not put any weight on them at the present time. I had noticed she was limping into the treatment room.

After additional questioning, she revealed she was under the routine care of a rheumatologist for her fibromyalgia, an endocrinologist for her “pre-diabetes” and a cardiologist for precautionary reasons. When I asked her to elaborate on her fibromyalgia, she explained that in the past, she endured spontaneous ruptures of tendons in both her shoulders and in her left elbow as well as other “things” that led her rheumatologist to diagnose her with fibromyalgia after running a few lab tests. The lab test ordered by her rheumatologist showed her immunoglobulin G, immunoglobulin M, rheumatoid factor and hepatitis C antibody were all within normal limits with only a lipid panel abnormality of elevated triglycerides and cholesterol.

The fibromyalgia diagnosis was one of vague physical symptoms but not correlated with a definitive blood test. There is evidence of fibromyalgia presenting as localized heel pain. According a study by Harvey, 85 percent of patients with fibromyalgia complained of heel pain.1

After treating this patient’s ingrown nail, an examination of her heels revealed bilateral 2/5 posterior plantar heel pain, full range of motion (ROM) in the bilateral plantar fascia and Achilles tendon with 0/5 pain, and edema in the entire plantar heel area bilaterally. After obtaining bilateral heel X-rays, I was able to rule out significant heel spurs as the cause of this level of pain, although there was a small plantar in heel spur right foot. The prescription for blood work included a complete blood cell count with differential (CBS with diff), sequential multiple analysis–computer (SMAC 20), urinalysis and arthritic profile. She received a one-week course of Medrol.

When the patient returned to my office a week later, she had no Achilles tendon or plantar fascia pain bilaterally. Plantar fasciitis, the most common mechanical cause for heel pain, was unlikely.

At this time, I also reviewed the patient’s full medical history. Her past and present medical history indicated spontaneous ruptures of tendons in both shoulders as well as her right elbow over 10 years with no history of injury. The latest magnetic resonance imaging (MRI) report of her foot and ankle, done by her orthopedist in March 2016, noted she had sustained several partial thickness tears throughout both her plantar fascia tendons, edema of both ankles, and bilateral Achilles tendinosis despite having no pain upon her first visit for heel pain in at this office. The past medical history also included plantar warts of the feet, on and off cramping and numbness in both feet, anemia, unspecified arthritis, asthma, pre-diabetes, and gastrointestinal ulcers. Her family and social history were negative for genetic issues, smoking and drinking. She was not taking any medication. A review of systems included a history of gastrointestinal upset, cardiac enzyme elevation and noted musculoskeletal spontaneous ruptures.

Her current visit included pinpoint pain in the central left heel of 1/5 (improved) and 0/5 right heel (improved) with visibly less edema bilaterally on the plantar heels with use of the Medrol Dosepak. This patient already wears custom orthotics, which I checked and found to be within normal limits. Her X-rays were positive for a small posterior left heel spur and negative for a left plantar heel spur. Her right heel was positive for small heel spurs, posterior and plantar. She was negative for calcaneal fractures in either foot. Blood tests were still pending.

A Closer Look At The Diagnosis And Initial Treatment

With a small right plantar heel spur, an area of edema and pain in the left foot only, blood tests pending, and improvement of heel pain with a Medrol dose pack, her current diagnosis was heel bursitis greater in the left foot than the right.

To treat her pinpoint pain in the left heel, I gave her an injection of equal parts 1% xylocaine plain and 0.05% Marcaine plain equal parts with 0.25 cc Depo-Medrol (Pfizer) to the area. The patient noted nausea with taking the Medrol Dosepak so I changed her anti-inflammatory to naproxen 500 mg BID, which the patient has had success with on her shoulder pain post-ruptures.

Knowing that 90 percent of heel pain gets better with conservative care and only 10 percent have systemic etiologies for heel pain, I proceeded to treat her with conservative care.

Two days later, this patient’s bloodwork indicated her only abnormality was a positive abnormal antinuclear antibody (ANA) direct test. Her arthritic profile and other autoimmune profiles were normal.

I ordered an ANA titer for her next blood test as recommended if there is a suspicion of autoimmune issues.4 The patient was concurrently discussing this issue with her rheumatologist, cardiologist and endocrinologist, and did forward blood tests to their offices.

After reviewing the blood tests to date, I eliminated the following differential diagnoses.


  • The patient tested negative for spondyloarthropathies and there was no association with back pain.5
  • Testing was negative on gout due to no elevation of uric acid and negative urinalysis. There were also no lesions on X-ray.
  • Negative for rheumatoid arthritis with no deviation of joints noted on exam or X-ray. The patient tested negative for rheumatoid factor as well.


  • Negative for osteomyelitis based on X-ray and MRI
  • Negative for pre-diabetic ulcer based on exam
  • Negative dermatologic exam other than a history of verruca plantaris


  • Negative exam for pain during ROM in the plantar fascia and Achilles tendon


  • Negative for lumbar radiculopathy
  • Negative for history of nerve entrapment in the back and ankle, and there are no symptoms of burning, numbness, tingling to date in the feet and ankles.


  • Negative history


  • Negative history


  • Negative since pulses, capillary return and local temperature gradient were normal

After on and off monthly patient visits managing unilateral or bilateral heel pain, I managed the patient in the long term utilizing local diclofenac (Voltaren gel, GlaxoSmithKline) QID and a diclofenac epolamine topical patch (Flector Patch, Pfizer) on the plantar heel Q12h at full weightbearing with custom orthotics. The custom orthotics have a deep heel cup and ½ medium density foam with PPT heel to end with a Neoprene top cover. The pain on her heels is 1/5 to 3/5 with no association with the level or type of activity and shoegear. The edema is gone. No erythema exists. She has full pain-free range of motion in the plantar fascia and Achilles tendon bilaterally.

Why The Patient Returned For Podiatric Care

One year after ANA testing, the patient suddenly developed burning of the left plantar heel and the entire plantar heel was edematous with no erythema. The plantar fascia and Achilles tendon showed full range of motion with no pain and 0/5 pain on palpation of the heel and ankle.

A new ANA titer showed a definitive positive antiscleroderma-70 antibody elevation. She was positive for CREST variant scleroderma. I referred her to a scleroderma specialist in New York and faxed her results to her local physicians.

Additionally, a new MRI revealed consistent edema of the heels, tendinitis and tendinosis issues. It also revealed a new tear of the left plantar fascia consistent with the burning area of the left heel. With no change in activity, the tear appears spontaneous as the tears in the shoulder and elbows. The patient subsequently utilized a walking cast for six weeks with orthotics and topical Voltaren and Flector Patch use.

Six weeks after stopping use of the walking cast, and following an additional two-week transition to shoes with orthotics, the patient was symptom-free in both heels with no edema, and had full range of motion in the foot and ankle with no pain bilaterally. Her MRI showed no change in status of the plantar fascia tear in the left heel but the patient was symptom-free on both heels to date.

Key Insights On CREST Variant Scleroderma

One would diagnose CREST variant scleroderma with a positive antiscleroderma-70 antibody visible on an ANA titer, which a clinician can order after a positive ANA is apparent on an arthritic profile.CREST variant scleroderma is a limited cutaneous scleroderma consisting of calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly and telangiectasias.6 This patient had some history of gastrointestinal concerns but generally were vague and inconclusive

In the United States, CREST occurs most frequently in women, and involves genetic and environmental triggers. There is much variation in symptoms and onset of this autoimmune disease.6 Ho and Reveille provided a comprehensive review.7

In diagnosing patients who do not show traditional blood test results for arthritis, present with complicated medical histories for ruptures and apparently unrelated medical histories, have heel pain that comes and goes without correlation to level of activity and conservative care, and negative X-rays, blood tests should include a workup of autoimmune diseases, particularly scleroderma. Lastly, in regard to heel pain, once one has diagnosed the patient with an autoimmune disease such as local CREST variant scleroderma, there should be multidisciplinary team management that includes a podiatrist and a rheumatologist at a minimum.8

In Conclusion

Clinicians should add an autoimmune screening test to the basic workup of arthritides to establish a comprehensive differential diagnosis for heel pain.

Dr. Raval is in private practice in Waldwick, NJ. She is on staff at Hackensack University Medical Center, Hackensack UMC at Pascack Valley and New Bridge Medical Center.


1. Tu P, Bytomski JR. Diagnosis of heel pain. Am Acad Fam Phys. 2011; 84(8):909–16.

2. Harvey C. Fibromyalgia part II. Prevalence in the podiatric patient population. J Am Podiatr Med Assoc. 1993; 83(7):416-417.

3. Thomas JL, Christensen JC, Kravitz SR, et al. The diagnosis and treatment of heel pain: a clinical practice guideline-revision 2010. J Foot Ankle Surg. 2010; 49(3 Suppl):S1–19.

4. Lui E. Systemic causes of heel pain. Clinical Podiatr Med Surg. 2010; 27(3):431-441.

5. Akgul O, Ozgocmen S. Classification criteria for spondyloarthropathies. World J Orthop. 2011; 2(12):107-15.

6. Cleveland Clinic. Scleroderma: an overview. Available at . Accessed February 1, 2018.

7. Ho KT, Reveille JD. The clinical relevance of autoantibodies in scleroderma. Arthritis Res Ther. 2003; 5(2):80–93.

8. Bongi SM, Ravenni G, Ciampi B, et al. Biomechanical podiatric evaluation in an Italian cohort of patients with systemic sclerosis: a pilot study. Eur J Rheumatol. 2016; 3(4):169-174.



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