ORIGINAL ARTICLE

Calcium metabolism disorders simulating rheumatologic diseases

Sule Yasar Bilge • Cengiz Korkmaz

Received: 6 September 2010 / Accepted: 22 January 2011 / Published online: 9 February 2011

� Springer-Verlag 2011

Abstract Hypoparathyroidism and hyperparathyroidism

may lead to spondylarthropathy or spondylarthropathy-like

problems and crystal arthropathy, respectively. In this

report, we present 2 cases with hypoparathyroidism and 1

case with hyperparathyroidism who developed spondy-

larthropathy-like disease, rheumatoid arthritis-like disease,

and chondrocalcinosis, respectively. We briefly discussed

relationship between calcium metabolism disorders and

rheumatologic manifestations. As rheumatologists, we

should be always open to other diagnosis if the treatment

does not work in patients with rheumatologic diseases.

Keywords Hypoparathyroidism �Hyperparathyroidism � Rheumatoid arthritis �Ankylosing spondylitis � Chondrocalcinosis

Introduction

Some endocrine disorders may simulate or be together

rheumatologic diseases [1, 2]. This may result in unwanted

workup and treatments. Calcium metabolism defects are

associated with many skeletal abnormalities and sometimes

cause difficulties in differential diagnosis [3]. In hypo-

parathyroidism, bone structure and turnover are markedly

atypical. Paravertebral and subcutaneous calcifications and

entesopathy can be seen [4]. Hyperparathyroidism is

known to be associated with radiological evidence of

articular chondrocalcinosis. This wide spectrum of

different evidences of calcium metabolism can overlap or

mimic rheumatic diseases. Our aim was to point out the

similarity of the clinical findings of calcium metabolism

disorders and rheumatologic diseases such as rheumatoid

arthritis (RA) and ankylosing spondylitis (AS) by giving

examples from our clinic.

Case 1

A 45-year-old man was referred to our department for

resistant neck, back, and hip pain since 1980s. He was

diagnosed as AS and given sulfasalazine (SZP) 2 g/day,

methotrexate (MTX) 10 mg/week, and indomethasin

75 mg/day. Despite this treatment, there was no change in

his pains. On physical examination, his posture was typical

for AS, cervical and lumbal motions were limited. Roent-

genogram of the cervical spine showed fused osteophytes

anteriorly and ischiatic entesopathy. Computed tomogra-

phy of the sacroiliac joints was normal except minimal

narrowing at left sacroiliac joint. Posterior paraspinal lig-

ament calcifications were found in the spine. Laboratory

findings were as follows: calcium 2.25 mmol/l (4.5–5.5),

phosphate 4.6 mmol/l (1.8–3), parathyroid hormone

\1.20 pg/ml (15–65), and erythrocyte sedimentation rate

(ESR) 38 mm/h, and HLA B27 was found negative. SZP

and MTX were discontinued, and he was treated with

calcitriol 1 mg/day and calcium carbonate 2 g/day. His

pains improved within 2 months.

Case 2

A 68-year-old male patient had admitted to our clinic with

painful joints in his metacarpophalangeal (MCP), proximal

S. Y. Bilge � C. Korkmaz (&)

Division of Rheumatology, Department of Internal Medicine,

Eskisehir Osmangazi Universitesi, Tıp Fak, Ic Hastalıkları,Romatoloji Bolumu, 26480 Eskisehir, Turkey

e-mail: ckorkmaz@ogu.edu.tr

123

Rheumatol Int (2012) 32:1503–1505

DOI 10.1007/s00296-011-1804-3

interphalangeal (PIP), wrists, and elbow. On physical

examination, he had arthritis in the left metacarpophalan-

geal joints and right wrist joints. Both elbow joints had

flexion deformities of 30�. He has been followed up for RA

since 10 years. He has used disease-modifying anti-rheu-

matic drugs (DMARDs) including methotrexate 12.5 mg/

week, prednisolon 10 mg/day, and hydroxychloroquine

200 mg/day but his complaints did not sufficient respond to

this therapy. His laboratory examination revealed a serum

Ca level of 4.8 mg/dl (8.5–10.5 mg/dl), phosphate (P) level

was 6.2 mg/dl (N = 2.7–4.5 mg/dl), magnesium level was

0.75 mmol/L (N = 0.85–1.15 mmol/l), parathormone level

was \3 mg/dl (N = 11–67 pg/ml), erythrocyte sedimen-

tation rate (ESR) was 90 mm/h, and CRP was 5.97 mg/dl,

respectively. Rheumatoid factor was negative and there

were no erosions in his hand X-ray. We thought that the

patient had RA-like disorder associated with hypopara-

thyroidism. His treatment regimen was switched to calcium

acetate and calcitriol 1 lg/day with withdrawal of the

DMARDs. His complaints resolved within 4 weeks after

the beginning of the treatment. His ESR was found to be

40 mm/h in the last control visit.

Case 3

A 63-year-old woman having pain at knees and ankles had

administered to another hospital. A laboratory examination

revealed serum Ca level 10.2 mg/dl (8.5–10.5 mg/dl),

P level 2.93 mg/dl (2.7–4.5 mg/dl), and parathormone

level 197.4 mg/dl (11–67 pg/ml). Parathyroid ultrasound

was performed, and 13 9 9 mm adenoma localized to

parathyroid gland was detected. Then, she had adminis-

tered to our department for her longstanding pains. On

physical examination, crepitation was positive at knees

bilaterally, and there was no finding of acute arthritis. The

roentgenogram of knees showed a continuous band of

dense calcification of articular fibrocartilage. She was

diagnosed as chondrocalcinosis and underwent colchicine

and NSAID therapy. Three months after, she was seen at

policlinic visit and her pains were resolved.

Discussion

In the first case, the presence of hypocalcemia, hyper-

phosphatemia, and low level of parathyroid hormone

confirmed the presence of idiopathic hypoparathyroidism.

Subcutaneous calcifications may be seen in the course of

hypoparathyroidism, especially about the hips and shoul-

ders [3]. The deposits generally are asymptomatic,

although painful calcific periarthritis is reported in this

condition, perhaps due to depression of serum calcium

levels [4]. Goswami et al. [1] reported clinical and radio-

logical profile of spondylarthropathy in patients with

hypoparathyroidism. Three of 40 patients with hypopara-

thyroidism had features suggesting ankylosing spondylitis

in terms of clinically and radiologically. Other 10 patients

had sacroiliitis. The presence of spondyloarthropathy was

related with longer disease duration. HLA-B27 was not

found to be a determining factor for the development of

spondyloarthropathy in course of hypoparathyroidism. In

our case, we could not find sacroiliitis and HLA-B27

positivity.

The second case had been diagnosed before as having

RA and treated with DMARDs. It is interesting to note

that the patient had brisk acute-phase response and his

symptoms significantly resolved after starting calcitriol

and calcium despite discontinuation of DMARDs. How-

ever, ESR and CRP levels decreased more slowly. The

patient met the classification criteria for RA [5], however,

there were no radiographic erosions in his hands and his

RF was negative. Also, peripheral arthritis was associated

with neck stiffness and ischiatical entesopathy without

sacroiliitis. No peripheral arthritis and increased acute-

phase response were reported in patients with hypopar-

athyroidism-related spondylarthropathies by Goswami

et al. [1]. In the literature, it has been reported that

hypoparathyroidism can be associated with other autoim-

mune disorders such as SLE and unspecified polyarthritis

[6]. Salvador et al. [7] reported a case with hypopara-

thyroidism associated with RA. This patient had brisk

acute-phase response, RF positivity, and radiographic

erosions along with osteosclerosis and hyperostosis loca-

ted to pelvis. Edmons et al. [8] reported a case with RA

and Sjogren’s syndrome who developed hypoparathy-

roidism. This patient had also increased acute-phase

response and RF positivity. However, authors did not

report whether the patient had radiographic erosions or

not. We considered our case as having hypoparathyroid-

ism-related RA-like disease. Consequently, we can come

across hypoparathyroidism with spondyloarthropathy-like

findings or RA-like manifestations. Yacoub et al. [9]

reported a case with AS associated with hypoparathy-

roidism. This patient had also oligoarthritis of upper

limbs. In clinical practise, the patients with RA who are

resistant to DMARDs should be evaluated in terms of

mimicking diseases such as hypoparathyroidism.

The third patient had chondrocalcinosis possibly due to

hyperparathyroidism. Chondrocalcinosis is a rare inherited

metabolic disorder, where the chemical calcium pyro-

phosphate dehydrate is deposited in one or more joints in

the body—usually the knee is affected [10]. Hypothy-

roidism, hypo magnesium, hemochromatosis, and Wilson

disease may lead to chondrocalcinosis. These possible

causes were excluded, and the patient’s laboratory

1504 Rheumatol Int (2012) 32:1503–1505

123

findings showed hyperparathyroidism as a cause of

chondrocalcinosis.

In conclusion, parathyroid gland disorders such as

hypoparathyroidism and hyperparathyroidism may result in

some locomotor system manifestations and simulate some

diseases. Therefore, rheumatologist or relevant clinicians

should be aware that resistant patients to appropriate anti-

rheumatic therapy may have parathyroid gland-related

disease. Calcium, phosphate, and parathyroid hormone

levels should be evaluated in these cases. As rheumatolo-

gists, we should be always open to other diagnosis if the

treatment does not work in a patient with rheumatologic

disease.

Conflict of interest We have no conflict of interest.

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