A 53 years male, known case of type 2 diabetes and hypertension for the last 5 years on regular treatment presented with complaints of backache and stiffness on bending forwards and sideways for the duration of last 6 months. On examination his vital statistics were pulse of 68/min and B.P. of 138/82mmHg right arm supine. His body mass index 2 was 27.9 kg/m . Systemic examination was essentially normal.
Examination of the spine revealed local tenderness
over the lower thoracic and lumbar spine. There was
limitation of movement of forward and lateral
flexion of the spine. The curvature of the spine was
normal and there was no obvious swelling. No
tenderness over the peripheral and sacroiliac joint
was observed.
Investigations revealed that the patient had a
normal haemogram and ESR of 14 mm at the end of
first hour (Westergren). His blood sugar levels were:
fasting-106 mg/dl and postprandial of 165 mg/dL.
He had a glycosylated haemoglobin of 6.7%, urea 28
mg/dL, creatinine 0.9 mg/dL and uric acid of 4.7
mg/dL. His serum calcium and phosphate were 9.2
mg/dL and 3.9 mg/dL, respectively. His alkaline
phosphatase was 44 U/L and lipid profile showed
total cholesterol 230 mg/dL, LDL 157 mg/dL, HDL of
41 mg/dL and triglycerides of 154 mg/dL. TSH levels
were 1.75 U/L. HLA B27 was negative. His
lumbosacral spine X rays are shown in Figure 1.
What are the radiological findings (Figure 1)?
What are the causes of low backache?
Low backache commonly can arise from the muscles
(lumbarsprain/strain), nerves-lumbar
radiculopathy and nerve compression/irritation and
from bone/joint conditions. Various causes of low
backache are enlisted in Table 1 [
1]. At times, the
pain may be referred from the abdominal organs in
which case it is known as a “referred pain”.
How can one differentiate inflammatory from
non-inflammatory backache?
Traditionally, five features distinguish the
inflammatory back pain from non-inflammatory or
mechanical back pain-
1. Age of onset below 40 years
2. Insidious onset
3. Duration > 3 months before medical attention is
sought
4. Morning stiffness
5. Improvement with exercise or activity
Recently, proposed criteria for inflammatory
backache in an adult ≤ 50 years old are-
1. morning stiffness > 30minutes
2. improvement with exercise but not with rest
3. awakening from backache during the second
half of night
4. alternating buttock pain
Ankylosing spondylitis is the classical prototype of
disease with inflammatory backache.
His lumbo-sacral spine radiographs showed large
osteophytes arising from the contiguous surfaces of D11 and D12 vertebrae (pointer arrow A). The lateral
view of dorsolumbar spine showed continuous
flowing ossification (“flowing wax” appearance) on
the anterior surface of L1-4 vertebrae bridging
across the intervertebral spaces (pointer arrows B).
Disc space was well maintained and there were no
findings suggestive of sacroiliac joint sclerosis or
facet joint ankylosis. A diagnosis of Diffuse
Idiopathic Skeletal Hyperostosis (DISH) was made. A
less likely diagnosis could be Degenerative
spondyloarthritis although the age is a factor against
it.
What radiological features distinguish DISH from
ankylosing spondyltitis and spondylosis?
The intervertebral spaces are preserved in DISH visà-
vis spondylosis and the sacroiliac and apophyseal
joints appear normal in DISH unlike ankylosing
spondylitis which has sacroilitis and apophysitis.
What are the characteristics of DISH? What is its
relation to diabetes?
Diffuse idiopathic skeletal hyperostosis (DISH), also
known as “Forestier disease”, is considered to be a
degenerative type of arthritis. It is a disease
characterized by exuberant ossification of
ligaments (enthesopathy) in both axial &
appendicular skeleton. The disease begins early at
around 20 – 40 yrs of age when there is ossification of
tendinous attachments to bony projections like the
calcaneum, patella and olecranon and diagnosis is
often missed. The disease manifests after a couple
of decades when there is involvement of the spine
with florid flowing ossification seen on the
anterolateral aspect of dorsal spine. Pathogenesis is
not clearly understood. Factors implicated in
causation are hyperinsulinemia with or without
diabetes, hypertension, obesity, dyslipidemia &
hyperuricemia[
2,
3,
4]. Most common presentation is
stiffness in back (dorsolumbar region) and localized
back pain. The diagnosis is based on radiological
features (Resnick and Niwayama) which are [
5]:
1. flowing ossification along the anterolateral
aspect of at least 4 contiguous vertebrae;
2. the preserved disk height, with absence of
significant degenerative changes (marginal
sclerosis in vertebrae)
3. absence of any significant facet-joint
ankylosis, sacroiliac erosions, or intra-articular
osseus fusion.
Table 1- Causes of low backache-
1. Congenital/developmental
a. Spondylolysis and spondylolisthesis
b. Kyphoscoliosis
c. Spina bifida occulta
d. Tethered spinal cord
2. Minor trauma- Strain/Sprain
3. Fractures- ‘Traumatic’ like falls or road
accidents and ‘Atraumatic’ like osteoporotic
and neoplastic infiltration
4. Intervertebral disc herniation
5. Degenerativea.
a. Disk-osteophyte complex
b. Internal disc disruption
c. Spinal stenosis with neurogenic
claudication
d. Uncovertebral joint disease
6. Arthritis- Spondylosis, Facet or sacroiliac
arthropathy, Autoimmune (Ankylosing
spondylitis, Reiter’s syndrome)
7. Neoplasms- Primary bone tumours,
haematologic and metastatic.
8. Infection/inflammation- osteomyelitis,
epidural abscess, arachnoiditis, meningitis
9. Metabolic- osteoporosis, osteosclerosis
10. Vascular- abdominal aortic aneurysm |
It is a less sought for disease and hence
underreported. Complaints are non-specific and
commonly ignored but have a high associated
morbidity. Radiographic images may be confused
with Ankylosing spondylitis but there is no sacroiliac
involvement or facet joint ankylosis. Diagnosis is
mostly late in course of disease when there is florid
ossification of the spinal ligament, hence there is
limited scope of drugs. Large osteophytes may cause
radicular or cord compression and may be
complicated with osteophytic fractures. Often large
osteophytic spurs in cervical spine may be a cause of
difficult intubation during surgery, failed
endoscopic procedures and dysphagia. Therefore,
DISH should be specifically sought for in individuals
presenting with backache and stiffness with
coexistentdiabetes, hypertensionor
atherosclerotic vascular disease not only to limit the
associated morbidity but also because it may
antedate the occurrence of these disorders.
What is the management of DISH?
Although there is no definite cure for DISH, the
primary aim is to provide symptomatic relief, which at times may not even be required (in asymptomatic
individuals). Acetaminophen and non-steroidal antiinflammatory
drugs are of use and may limit
inflammation and further worsening. Corticosteroid
injections can be used for severe pain.
Physiotherapeutic exercises can reduce the
stiffness so very characteristic of DISH. It can also
help improve the range of movements of joints and
improve productivity. Surgical intervention is
restricted to patients who have complications viz.
to remove bony spurs in the enck causing nerve root
compression or dysphagia and to relieve pressure on
the spinal cord caused by DISH.
Patient was advised proper control of weight, life
style modification and physiotherapeutic exercises
along with Naproxen 250 mg BD as an antiinflammatory
analgesic agent.
Key Points
- Microvascularandmacrovascular
complications of diabetes are well-known, the
musculoskeletal manifestations are not reported until very late and are often paid less importance by the health care givers.
- DISH is an important associated
musculoskeletal involvement in diabetes.
Importantly, the morbidity associated with
DISH can be very severe and this limits the implementation of lifestyle modification advices.
- DISH needs to be differentiated from spondylosis and ankylosing spondyllitis.
- A high index of suspicion is required and awareness about this entity (DISH) is required
for an early diagnosis.
|
References
- Engstrom JW. Back and neck pain: Introduction. In: Fauci AS, kasper DL, Longo DL, Braunwald E, Hauser SL, Jameson JL, Loscalzo J (eds). Harrison’s Principles of Internal Medicine. Mc Graw Hill Medical USA 2008 17th edn, pp. 107-17.
- Mader R, Sarzi-Puttini P, Atzeni F, Olivieri I, Pappone N, Verlaan J, et al. Extraspinal manifestations of diffuse idiopathic skeletal hyperostosis. Rheumatology 2009; 48: 1478-81.
- Mader R, Lavi I. Diabetes mellitus and hypertension as risk fators for early diffuse idiopathic skeletal hyperostosis (DISH). Osteoarthritis cartilage 2009; 17: 825-8.
- Littlejohn GO , Smythe HA . Marked hyperinsulinemia after glucose challenge in patients with Diffuse idiopathic skeletal hyperostosis. J Rheumatol. 1981;8:965-8.
- Resnick D, Niwayama G. Diagnosis of bone and joint disorders. 2nd edition. Philadelphia. W. B. Saunders. 1988, 1563-615.