Cutaneous Manifestations of Diabetes Mellitus Dr.Hasan İlkova Istanbul University Cerrahpaşa Medical Faculty Division of Endocrinology Metabolism and Diabetes
Cutaneous Manifestations
of Diabetes Mellitus
Dr.Hasan İlkova
Istanbul University
Cerrahpaşa Medical Faculty
Division of Endocrinology Metabolism and Diabetes
Diabetes Mellitus
Cutaneous lesions usually appear after the development of DM, but may be the first presenting sign
According to Perez et al (3) ,approximately 30% of patients with DM develop skin lesions at some point
Overall prevalence of cutaneous disorders does not differ between type I and type II diabetics Type I patients get more autoimmune-type lesions
Type II patients get more cutaneous infections
Skin Infections in DM
Occur in 20-50% of poorly controlled diabetics
More common in Type II
May be related to abnormal microcirculation, hypohidrosis, PVD, neuropathy, decreased phagocytosis and killing activity, impaired leukocyte adherence, and delayed chemotaxis all seen in diabetics
Candidiasis in Diabetics
White, curdlike material adherent to erythematous, fissured oral commisure; angular stomatitis
Skin Infections in DM
Fungal infections- most common
Candida Candidal paronychia
Inframammary candida
Genital candida
Psedudohyphae and spores on KOH prep support dx of Candida
Purulent drainage may indicate secondary bacterial infection
Because maceration and skin breaks can serve as portals of infection, tinea pedis should be treated aggressively in diabetics
Treatment includes drainage of any abscesses, keeping the digits dry, and topical antifungals (clotrimazole)
Candidiasis in Diabetics
Initial pustules on erythematous base that become eroded and confluent
Candidiasis in Diabetics
Skin Infections in DM
Bacterial Infections- can be more severe and widespread in diabetics
Malignant otitis externa
Pseudomonas aeruginosa
Fatal in over 50% patients (13)
Can progress to chondritis, osteomyelitis, and bacterial meningitis
Treat up to 3 months with oral quinolones but may need IV antibiotics
Malignant Otitis Externa in Diabetics
Erythrasma in Diabetics
Skin Infections in DM
Bacterial infections in DM
Erythrasma
Reddish tan scaling patches of the upper inner thighs, axillae, toe web spaces, and inframammary creases
Gram positive Corynebacterium minutissimum
Identified with Wood’s light coral fluorescence
Treat with oral erythromycin for 5 days
Erythrasma in Diabetics
Reddish tan scaling patches of the upper inner thighs, axillae, toe web spaces, and inframammary creases
Dermal Manifestations of Diabetes Mellitus
Diabetic Thick Skin
Yellow Skin
Diabetic thick skin
Knuckle Pebbles. Thickening of the skin on the dorsum of the hand
Scleredema of Diabetes. This patient with Type II diabetes gave an incidental complaint of limitation of motion of his upper extremities. To examination, this appeared to be due to the shield-like involvement of the upper back, neck, and shoulders with marked dermal thickening.
Vascular Manifestations of Diabetes Mellitus
Diabetic Dermopathy
Pigmented Purpura
Red Skin and Rubeosis Facei
Periungual Telangiectasia
Erysipelas-Like Erythema
Diabetic Dermopathy Also known as shin spots, most common cutaneous
finding in diabetics (approximately 50% of diabetics).
Round to oval atrophic hyperpigmented lesions on the pretibial areas of the lower extremities. Early lesions usually raised, then flatten. Brownish hyperpigmentation due to hemosiderin deposits.
Occur bilateral with asymmetrical distribution.
Diabetic Dermopathy Asymptomatic, resolve spontaneously leaving a scar
usually following improved blood glucose control.
Usually occurs in older diabetic patients who have had diabetes >10 years.
Occurs more frequently in diabetic patients with retinopathy, neuropathy, and nephropathy.
Can be indicator of poor control of blood glucose levels.
Pigmented Purpura
Periungual Telangiectasia
Large vessel disease (atherosclerosis) may also be present in the lower extremities and result in:
skin atrophy
hair loss
coldness of the toes
nail dystrophy
pallor upon elevation
mottling on dependence
Other Skin Markers of Diabetes Mellitus
Yellow Nails
Diabetic Bullae
Necrobiosis Lipoidica
Eruptive Xanthomas
Acanthosis Nigricans
Kyrle’s Disease
Yellow Nail
Diabetic Bullae
Diabetic Bullae Approximately 0.5% of diabetics (2)
More common in men with long-standing DM and neuropathy
Pathogenesis not well-understood
Could be related to trauma with reduced threshold for blister formation Other theories include immunologic factors, disturbed catabolism of
calcium, magnesium, or carbohydrates, microangiopathy, and vascular insufficiency
Appearance
Painless bullae on non-inflamed base that appear suddenly Most common on the dorsa and sides of lower legs and feet,
sometimes with similar lesions on the hands and forearms Bullae contain clear, sterile fluid
Diabetic Bullae
Bullae tend to heal spontaneously in 2-5 weeks
Bullosis diabeticorum remains a diagnosis of exclusion with negative immunofluorescence studies, porphyrin levels, and cultures
DDx: bullous pemphigoid, epidermolysis bullosa acquisita, porphyria cutanea tarda, bullous impetigo, erythema multiforme, and coma blisters
If large and symptomatic, can aspirate the fluid leaving an intact blister roof as a wound covering
Diabetic Bullae Therapy should be aimed at preventing ulceration and
secondary infection.
Necrobiosis Lipoidica (NL)
Necrobiosis Lipoidica (NL)
NL appears in 0.3-1.6% of diabetics
Anywhere from 11-65% of patients with NL have DM at the time of skin dx
If they do not have DM at time of dx, about 90% will develop diabetes, have abnormal glucose tolerance, or report parents with DM
Diabetic control has no effect on the course ofNL.
According to Jelinek, NL appears earlier (mean age 22) in Type I diabetics than Type II (mean age 49.)
Necrobiosis Lipoidica (NL)
Classically, NL occurs bilaterally on the pretibial or medial malleolar areas.
Not painful.
Spontaneous resolution occurs in 13-19% with residual scarring.
Treatment: potent topical steroids, intralesional steroids at the active border, or rarely systemic steroids
Necrobiosis Lipoidica (NL)
Eruptive Xanthomas Occur in hyperlipidemic/hyperglycemic states:
uncontrolled diabetic patients.
Most common in young men with Type 1 diabetes
Resistance to insulin makes it difficult for the body to clear the fat from the blood.
Acanthosis Nigricans
Acanthosis Nigricans
Seen in situations of insulin resistance Besides in DM, also seen in the following:
Carcinomas, especially of the stomach Secondary to meds (nicotinic acid, estrogen, or
corticosteroids) Pineal tumors Other endocrine syndromes (PCOS, acromegaly,
Cushing’s disease, hypothyroidism) Obesity
Pathogenesis According to Cruz , it may be related to insulin binding
insulin-like growth factor receptors on keratinocytes and dermal fibroblasts, thus stimulating growth.
Acanthosis Nigricans
Appearance
Hyperpigmented, velvety plaques in body folds, mostly axillae and neck
Can also present on groin, umbilicus, areolae, submammary areas, and on the hands (tripe hands)
Treatment- usually asymptomatic
Weight loss
Retinoic acid and salicylic acid
Acanthosis Nigricans
Kyrle’s Disease Primary location: extensor surfaces of the lower
extremity, but can occur on face and trunk.
Seen with DM, CHF, hepatic abnormalities-alcoholic cirrhosis, renal disease
Elimination of collagen and elastin throughout epidermis.
Granuloma Annulare (GA)
Granuloma Annulare (GA)
Controversy surrounds the association between GA and DM.
A case-control study by Nebesio et al. failed to reveal a statistically significant correlation between the two.
A retrospective study by Studer et al. suggested that up to 12% of patients presenting with GA had DM.
Despite conflicting studies, it is reasonable to screen patients presenting with GA for DM.
Granuloma Annulare (GA) Appearance
Ring of small, firm, flesh-colored or red papules
If localized, most frequently found on lateral and dorsal surfaces of hands and feet
Can spontaneously regress without scarring
Pathogenesis unknown
Treatment : If localized, best left untreated.Can treat with intralesional steroids, if needed. If generalized, can also use dapsone, isotretinoin, freezing, cyclosporin, or PUVA.
Granuloma Annulare (GA)
Diabetic Neuropathy and the Skin
Autonomic Neuropathy
Motor Neuropathy
Sensory Neuropathy
Autonomic Neuropathy
Disturbance of sweating (anhydrosis of the feet)
Oversweating (elsewhere)
Abnormally cold feet
Brittle feet and fissures serving as a portal for infection
Sensory Neuropathy The erosion with callus on the tip of the toe is typical of the type of injury which results with sensory neuropathy of diabetes
Cutaneous Reactions to Diabetic
Treatment
Insulin Allergy may be local or systemic and usually occurs within the
first month of therapy Erythematous or urticarial pruritic nodules at the site of injection
Lipoatrophy can also occur Circumscribed depressed areas of skin at the insulin injection site
6-24 months after starting insulin
More common in women and children
Pathogenesis unknown but may be related to lipolytic components of the insulin preparation, an immune complex-mediated inflammatory process with lysosomal enzyme release, cryotrauma from refrigerated insulin, or mechanical trauma from injection
Lipohypertrophy can also occur Soft dermal nodules that resemble lipomas at sites of frequent
injection
May be a response to the lipogenic action of insulin
Treat and prevent by rotating sites of injection
Conclusion Nearly all patients with diabetes eventually develop
cutaneous manifestations of the disease.
It is valuable to recognize for diagnosis, management, and treatment.
Leads to prevention of ulcerations, infections, amputations.
Osteoarthritis Carpal Tunnel Syndrome Bone Health and Osteoporosis Diffuse Idiopathic Skeletal Hyperostosis
(DISH) Crystal-induced Arthritis Charcot Arthropathy Tendinopathy
Although not a true neuroarthropathy, the CTS is a frequent cause of hand pain in patients with diabetes.
Compression of median
nerve in carpal tunnel.
Numbness, tingling, or burning sensations in the thumb and fingers, pain in the hands or wrists , lost gripping strength.
Weakness and atrophy of the thenar muscles
Diagnosis: history taking, physical examination, Electromyogram and nerve conduction velocity.
14 – 30% of patients with diabetes will develop carpal tunnel syndrome.*
10-15% of patients with carpal tunnel syndrome will have diabetes
*Diabetes Care March 2002 vol. 25 no. 3 565-569
More common in women than men (3:1)
Increased incidence in patients with limited joint mobility.
Treatment: Wrist splinting, NSAIDs, Localized corticosteroid injections and Surgery.
Tendinopathies occur frequently in patients with diabetes.
The shoulder and hand are particularly commonly involved.
Painful tendinopathies affect 30-60% of diabetic patients, and cause considerable disability among affected patients
Frozen shoulder, shoulder periarthritis, obliterative bursitis.
Progressive painful loss of motion in all directions, especially external rotation and abduction.
Joint capsule adheres to humeral head
Associated with age(T1 & T2DM) and duration of diabetes(T1DM)*
In diabetics, occurs at younger age, less painful, responds less to treatment
Associated with high morbidity
Treatment: steroid injections in early stages, adequate analgesia, exercise
Resolves over time *Br J Rheumatol 1986:25:147–151.
Shoulder arthrogram showing a contracted and adherent joint capsule in adhesive capsulitis.
Smith L L et al. Br J Sports Med 2003;37:30-35
Cheiropathy, stiff-hand syndrome, diabetic stiff hand, diabetic contractures, or syndrome of limited joint mobility.
Prevalence is 8 – 53% More common in patients with T1DM Risk increases with poor glycemic control
(↑HbA1c ) and duration of diabetes
Mechanism: Deposition of periarticular collagen as seen in
biopsy
Glycosylation of collagen, abnormal cross linking of collagen and increased collagen hydration all contribute
Microangiopathy and neuropathy may lead to contractures via fibrosis and disuse
Diagnosis
“prayer sign”
“table top test”
Treatment: optimizing glycemic control and physiotherapy
Present in 21- 63% of patients with diabetes
Prevalence increases with age
Generally milder in patients with diabetes compared to patients with other conditions
Treatment: Optimize glycemic control, aggressive physiotherapy, NSAIDs, analgesic, Intralesional glucocorticoid injections
Rarely surgery is required
Trigger finger Caused by fibrous tissue proliferation in the
tendon sheath. Limitation of the normal movement of the
tendon. Prevalence 11% in DM patient, < 1% in non-DM Pt.
MSK complications related to diabetes is common and can lead to severe morbidity
Having a long duration of diabetes, especially with poor glycemic control, increases the risk of developing many of these conditions
Health care teams need to be aware of the potential MSK complications in patients with diabetes
Further research is necessary to clearly define the relationship between diabetes and its associated MSK conditions