Another thing, I have read research and now have a research article co-written by Drs. XXXX and Michael Carroll, DPMs (published in the Journal of the American Podiatric Medical Association) who have identified a connection to the Hyperparathyroidism I dealt with for countless years, before having the tumored parathyroid removed, and subsequent deposits of calcium crystals (gouty arthritis) in my hands and feet (which have no doubt made the MN (and PF?) difficult to overcome). SEE!!!! I AM NOT CRAZY! And what's really cool?!?!?!? I didn't even know Dr. XXXX then!!!!
Journal of the American Podiatric Medical Association • Vol 97 • No 3 • May/June 2007 245
Celebrating100years of continuous publication:1907–2007
CLINICAL CORRESPONDENCE
Atypical Gout in the Foot and
Ankle Secondary to Primary
Hyperparathyroidism
To the Editor:
It is well established that primary adenomatous hyperparathyroidism
is associated with hyperuricemia
and overt gout.1-5 Awareness and early diagnosis of
primary adenomatous hyperparathyroidism is important
because the condition can lead to a host of problems,
such as kidney stones, diminished bone density,
fracture, gastrointestinal symptoms, mood disturbances,
fatigue, and nonspecific neurologic or musculoskeletal
complaints.6, 7 Furthermore, recent evidence
suggests that hyperuricemia may be a risk
factor for increased morbidity and mortality in cardiovascular
disease,8-11 stroke in the elderly,12 fetal
risk in women with gestational hypertension,13 and insulin
resistance.14-16
Case Report
A 41-year-old, 5 foot 9 inch tall man weighing 225
pounds presented to our Merrillville, Indiana, office
with a 2-year history of diffuse pain and swelling in
his left midfoot, rearfoot, and ankle. The pain worsened
with weightbearing. The patient had previously
been prescribed custom-made foot orthoses by two
podiatric physicians, but these orthoses failed to alleviate
the pain.
The patient’s medical history was significant for
kidney stones, which were treated with lithotripsy,
and gout. He was allergic to penicillin and insect
stings. He denied tobacco or alcohol abuse, and he
was not taking any medications.
The lower-extremity examination revealed nonpitting
edema of the left midfoot, rearfoot, and ankle.
Pain was elicited on palpation of the midfoot and
rearfoot dorsally, the ankle anteriorly, and the plantar
aspect of the heel. Radiographs showed edema and a
possible osteochondral defect of the ankle. Magnetic
resonance imaging and computed tomography scans
of the ankle, rearfoot, and midfoot were ordered. The
radiologist’s report described edema and a large,
well-defined radiolucent lesion involving the medial
talar dome with the possibility of internal calcification.
The report also described subchondral cystic
and erosive changes in the distal tibiofibular articulation
and prominent subchondral radiolucencies involving
the mid–subtalar joint, the anterior aspect of
the calcaneus, the second tarsometatarsal joint, the
second cuneonavicular articulation, and the cuboid.
The joint spaces were described as being relatively
maintained. The findings were consistent with gouty
arthritis or amyloidosis (Figs. 1–4). The results of a
Figure 1. T1-weighted magnetic resonance image
demonstrating lesions in the calcaneus secondary to
severe gouty arthritis.
Figure 2. Sagittal T1-weighted magnetic resonance
image showing lesions in the talar dome and subtalar
joint secondary to severe gouty arthritis.
Figure 3. Frontal T1-weighted magnetic resonance
image displaying lesions in the talar dome and subtalar
joint secondary to severe gouty arthritis.
Figure 4. Frontal T2-weighted magnetic resonance
image showing cystic changes in the talus and calcaneus
secondary to severe gouty arthritis.
246 May/June 2007 • Vol 97 • No 3 • Journal of the American Podiatric Medical Association
Celebrating100years of continuous publication:1907–2007
Bence Jones urinary protein immunofixation test
were negative, and the serum uric acid level was 10.7
mg/dL (reference range, 3.8–8.1 mg/dL). The complete
blood cell count and renal function test results
were within the reference ranges.
On the basis of the atypical gout presentation, tests
for intact parathyroid hormone and calcium were ordered.
The parathyroid hormone level was 637.0
pg/mL (reference range, 12–65 pg/mL), and the calcium
level was 12.0 mg/dL (reference range, 8.7–10.1
mg/dL).
A parathyroid localization scan showed focal moderate
uptake in the right lower neck, consistent with a
parathyroid adenoma. The parathyroid adenoma was
surgically excised by a general surgeon. The patient
was seen in our office 27 days after the adenoma’s excision
and reported that his foot and ankle pain had
resolved.
Conclusion
The foot and ankle may be the first area to show
symptoms of a parathyroid adenoma. Early discovery
of this tumor can limit or prevent the development of
other debilitating medical problems that could ultimately
result in death. This case reveals the importance
of thorough evaluation of patients who have
high serum uric acid levels in order to discover causes
of gout in the foot and ankle. Especially in atypical
presentations of gout, the possibility of a parathyroid
adenoma should be considered.
Financial Disclosures: None reported.
Conflict of Interest: None reported.
MICHAEL S. XXXX, DPM
MICHAEL C. CARROLL, DPM
50 West 94th Pl
Crown Point, IN 46307
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Journal of the American Podiatric Medical Association • Vol 97 • No 3 • May/June 2007 247
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