diabetes mellitus and its systemic manifestations

1. RHEUMATOLOGICAL
MANIFESTATIONS OF SYSTEMIC
DISEASES
Dr Vinay C
Moderator: Dr Sajjan Shenoy, Rhematologist, KMC

2. Introduction
Rheumatic manifestations of DM are the commonest of all described
endocrine rheumatic manifestations.
 Under-recognized and poorly treated.
These not only involve joints, but also the soft tissues and the bones.
 Closely linked to age, disease duration, vascular complications and
glycemic control.

3. In contrast to various vascular complications of diabetes mellitus
(DM) that are life threatening, rheumatic manifestations lead to
considerable morbidity.

5. Disorder which represents intrinsic complications of diabetes which
include
a. Diabetic muscle infarction (common in type 1 diabetes mellitus).
b. Neuropathic arthropathy which include charcot joint, claw toe, roker
bottom sole.

6. Disorder related to metabolic derangement
i. DISH
ii. Osteopenia
iii. Osteoporosis

7. b. Disorders which share similar aetiological mechanism as with
microvascular disease and change of collagen
i. Limited joint mobility (Chieroarthropathy)
ii. Dupuytren’s contracture
iii. Palmar flexor tenosynovitis (trigger finger)
iv. Adhesive capsulitis of the shoulder
v. Sudeks dystrophy.

8. Other rheumatological disorders which are common in general
population have increased prevalence in diabetic population
a. Carpal tunnel syndrome
b. Gout
c. Osteoarthritis
d. Osteolysis of fore foot
e. Migratory osteolysis of hip and knee

11. Cheiroarthropathy
Also called has stiff hand syndrome/ Limited joints mobility
syndrome.
It is characterized by thick, tight, waxy skin mainly on the
dorsal aspect of the hands, with flexion deformities of the
1. metacarpo-phalangeal and
2. interphalangeal joints
Pathogenesis: Dermal and subcutaneous sclerosis secondary
to non-enzymatic glycation of collagen with decreased
collagen degradation.

12. Limited joint mobility can be shown clinically by the inability
of the two palms to come completely together, with the wrists
maximally flexed, forming the prayer sign .
 In the early stages, paraesthesias and slight pain develop.
The symptoms increase very slowly, and greater pain,
aggravated by movement of the hands.

13. prayer sign

14. Table top sign

15.  Biopsy specimens - thickening of periarticular rather than
articular collagen, due to non-enzymatic glycosylation of
collagen.
Commonly seen in type 1 diabetics and is a marker of other
diabetic vascular complications.
Limited joint mobility and Dupuytren’s contracture are
commonly found in the same patient.
Treatment includes NSAIDS, Physiotherapy and better
glcemic control.

16. DUPUYTREN’S CONTRACTURE
It present with thickening, shortening, fibrosis and nodule formation
of the palmar fascia.
Result in flexion contractures of the fingers.
In patients with diabetes, the ring and middle finger are more
commonly affected, compared with the fifth finger in patients
without diabetes.
 The prevalence of Dupuytren’s contracture in diabetic patients
ranges from 20 to 63%, compared with 13% in the general
population.

17. The contractures are generally milder in diabetics than in patients
with Dupuytren’s contracture who do not have diabetes.
Rx consist of physiotherapy, steroid injections, and Surgical
intervention in some severe cases.

19. Carpel Tunnel Syndrome
Otherwise called as entrapment neuropathy
Characterized by pain and paraesthesia over the median nerve
cutaneous distribution of the thumb, index, middle, and lateral half of
the ring fingers, which is often worse at night.
The symptoms caused by compression of the median nerve within
the carpal tunnel as well as diabetic neuropathy, or a combination of
both
About 20% of patients with CTS have diabetes.

20.  Tinel sign: percussion of nerve triggers pain resembling elecric
shock.
 Phalen sign: palmar flexion for 30 sec causes paraesthesias.
 it is more common in women than in men.
Treatment:
simple analgesics, splints, local steroid injections
Surgery is indicated in those patients who fail the above
conservative measures.

21. Trigger finger
Flexor tenosynovitis (trigger finger or stenosing tenovaginitis) is
caused by fibrous tissue proliferation in the tendon sheath leading to
limitation of the normal movement of the tendon.
Middle and index finger most commonly involved.
Patients complains of a "catching" or "locking" sensation that may be
associated with pain in the affected fingers.
Examination shows a palpable nodule and thickening along the
affected flexor tendon sheath, overlying palmar aspect of the
metacarpophalangeal joint.

22. Flexor tenosynovitis is associated with the duration of diabetes but
not age.
A corticosteroid injection into the symptomatic flexor tendon sheath
is often curative.
other treatment modalities are NSAIDS, splinting, surgical release.

24. Complex regional pain syndrome
Formerly called Reflex sympathetic dystrophy or shoulder-hand
syndrome(Sudek’s atrophy).
Characterized by localised or diffuse pain, usually with associated
swelling, trophic changes, and vasomotor disturbances, with impaired
mobility of the affected region.
The condition may occur spontaneously, or after minimal trauma—
following surgery or a fracture.

25.  Concurrent medical conditions may predispose to reflex
sympathetic dystrophy, including :
Diabetes mellitus
 Hyperthyroidism
Hyperparathyroidism
Type IV hyperlipidaemia.

27. Treatment includes corticostroids, muscle relaxants, intavenous
sympathetic blockade
surgical symphathectomy, physiotherapy.

28. Adhesive Capsulitis
Adhesive capsulitis/frozen shoulder, seen twice as common in
diabetic patients.
It refers to a stiffened glenohumeral joint, usually caused by
thickening and contraction of the joint capsule which results in a
substantial decrease in capsular volume capacity.
Patients report shoulder stiffness, along with decreased range of
motion and pain.
The pain of this conditions is less in DM than that of the general
population , also be seen in hyperthyroidism, Addison disease, and
parkinsonism.

30. The decreased range of motion is worst in abduction and external
rotation.
Internal rotation is affected least.
Treatment is mainly conservative involves physiotherapy, use of
analgesic, steroids ,Surgical and arthroscopic capsular release.

31. Diffuse idiopathic skeletal hyperostosis
Commonly seen in Type 2 DM
characterized by excessive bone growth and calcification of
paraspinal ligaments, due to hyperostosis effect of
hyperinsulinaemia (osteoblast stimulation and osteoclast inhibition).
New bone formation,mostly involving thoracolumbar vertebrae, as
well as calcification of spinal ligaments.
Degree of glycemic control does not correlate with incidence or
progression of the symptoms.

32. Usually presents with
contiguous thoracic vertebral segments, typically described as
flowing osteophytes along the anterolateral aspects of those four
vertebrae
preservation of intervertebral disc spaces
absence of apophyseal joint degeneration
absence sacroiliac inflammatory changes.

35.  Ossification of ligaments and tendons elsewhere may occur, such
as the skull, pelvis, heels, or elbows.
 A proposed mechanism of causation is the prolonged and high
levels of insulin or insulin-like growth factors occurring in diabetic
patients, stimulating new bone.
 mild stiffness on arising in the morning, and 16% of affected
persons may develop dysphagia.
Treatment :
analgesics, heat application , physiotheraphy and glycemic control.

36. Charcot neuroarthropathy
 Progressive, non infectious disease seen in persons with sensory
neuropathy
 Diabetes is the most common cause of charcot neuroarthopathy.
 It causes severe destruction of joints, particularly in the feet.
 Theories :
 Neurotraumatic theory proposes that loss of neuroprotection leads
to repetitive micro trauma.

37.  Neurotrophic theory:
sympathetic neuropathy catalyses osteoclast bone resorption and
fragmentation.
Treatment : Early immobilisation, Bisphosphonates,
Splinting/bracing to protect the area from weight bearing to avoid
further damage and good glycemic control.

38. Diabetic muscle infarction
 Also called as Tumoriform focal muscular degeneration
 Common in type 1 DM with mean duration of 15 years.
 Acute onset of muscle pain and swelling. Most commonly
effecting thigh muscles and calf muscles. A palpable mass has been
reported in 34-44%.
 muscle biopsy: muscle fibre necrosis, edema, granulation tissue.
Serum creatine kinase levels elevated
 medical treatment : anti platelet and anti inflammatory drugs.

39. Other rarer associations
Osteopenia
Osteoporosis
Osteoarthritis
Gout

40. conclusion
The identification of characteristic rheumatologic manifestations of
diabetes early may facilitate its management.
 On the other hand, presence of rheumatic manifestations in a
diabetic patient can serve as a marker for poor glycemic control and
presence of micro vascular complications like diabetic retinopathy.

41. References
1)Brawn DL, McCrae FC, Show KM. Musculoskeletal disease in diabetes.
Practical Diabetes International 2001;18(2):62-4.
(2)BJ Van Rensburg, Contextualizing musculoskeletal complications of
Diabetes Mellitus. SARJ Vol1.No4
(3)Behrman: Nelson Textbook of Pediatrics, 17th ed. p1947. Elsevier
2004.
(4) Veijola R, Reijonen H, Vahasalo P, Sabbah E, Kulmala P, Ilonen J,
Akerblom JK, Knim M. The childhood diabetes in Finland study group.
HLADQB1-definined genetic susceptibility, [beta]-cell autoimmunity, and
metabolic characteristics in familial and nonfamilial insulin-dependent
diabetes mellitus. 1996. J Clin Invest 98: 2489-2495.