This document discusses various skin manifestations that are associated with diabetes mellitus. It categorizes the dermatological lesions into those that are associated with but not specific to diabetes, skin alterations due to diabetic complications, dermatological changes associated with neurovascular complications, and dermatologic complications of diabetes treatment. Common conditions discussed include necrobiosis lipoidica diabeticorum, granuloma annulare, diabetic dermopathy, acanthosis nigricans, infections, and manifestations of diabetic foot complications. Prevention and treatment approaches are provided.

1. Skin Manifestations of
Diabetes
Presenter: Dr **** ******* (EvilDoctor666)

2. CLASSIFICATION
� Dermatologic lesions associated with but not specific for Diabetes Mellitus
� Skin Alterations due to diabetic complications
� Dermatologic changes associated with neurovascular complications
� Dermatologic complications of diabetes treatment
� Endocrine syndromes with skin alterations and diabetes mellitus
� Dermatoses more common in Diabetes Mellitus.

3. Dermatologic lesions associated but not
specific for Diabetes Mellitus (Disease
Markers)
� Pruritus
� Necrobiosis lipoidica diabeticorum
� Granuloma annulare
� Diabetic dermopathy
� Scleroderma like syndrome
� Diabetic Scleredema
� Acanthosis Nigricans
� Achrochordon
� Diabetic Bullae

4. PRURITUS
� Was previously considered to be typical symptom of diabetes but
frequency is not known.
� Mechanism: Not well understood. Probable cause:
▪ Dry skin due to poor cutaneous circulation.
▪ Diabetic Chronic Renal insufficiency (high blood urea levels)
▪ Diabetic Neuropathy (nerve ending irritations)
▪ Fungal skin infections being more common in diabetics

5. Excoriation Marks of

6. Necrobiosis Lipoidica Diabeticorum
� Age of Onset: 30-40 years, F:M = 4:1
� Etiology:
❑ Not Known
❑ Immunofloresence studies showed C3 and IgM deposits on vessel walls,
suggestive of Immune Complex Vasculitis.
� Clinical Features:
❑ Begins as “indurated, erythematous macules or papules, or nodules.
❑ Old lesion are “discrete, irregularly oval and forms atrophic plaques”
❑ Usually asymptomatic. (Pruritus/Burning ±)
❑ Most common site: Pretibial areas.

7. Complications:
• Spontaneous Ulceration
• Delayed wound healing.
Treatment:
AIM: To prevent ulcerations
Pharmacotherapy:
Control of hyperglycaemia
Although not satisfactory, drugs tried:
• Topical or intralesional steroids
• Cyclosporine (ulcer closure reported in
few cases)
• Aspirin, Clopidogrel and Fibrinolytic
therapy have been tried but without
much success.
• Topical PUVA (50% success rate)
• Etanercept and Infliximab
• Topical platelet rich plasma
Surgical:
• Excision and Grafting (to treat ulcers)

8. Granuloma Annulare
� Benign Necrobiotic Lesion
� Common in children and young adult and females
� Etiology:
� Unknown. Can occur spontaneously, after insect bites, exposure to sun,
photosensitivity reaction
� 10% incidence in diabetics
� Clinical features:
• Reddish pink spots initially.
• Expands outwards in ring like fashion.
• Classic lesion “ring like, flesh coloured, pink, or dusky firm papules, may coalesce
to form plaques”
• Common sites: hands (specially fingers), on dorsal or lateral aspect of hands and
fingers (forearms)

9. Treatment:
• Often resolves spontaneously
• Disappearance of lesion has
been reported after puncture
with needle or skin biopsy.
• Drugs tried:
� Local injection of
Triamcinolone, dapsone,
steroids, chloroquine,
potassium iodide, aspirin,
niacinamide, clofazimine,
PUVA. (Results were variable)
� Chlorpropamide have been
successfully used in some
diabetics.
Prognosis:
Eventual spontaneous clearing
occurs, but may take several
weeks or as long as 3 decades

10. Diabetic Dermopathy
� Also known as “shin spots”
� Most common skin lesions occurring in diabetics
� Pathophysiology:
� Increased vascular permeability due to diabetes predisposes the skin to the
development of these lesions.
� Pigmentation is due to deposition of hemosiderin in histiocytes and extravasated
superficial erythrocytes.
� Histopathology:
o Acute lesion: Oedema of dermis and papillary dermis, extravasated RBCs, sparse
lymphocytic infiltration
o Older lesion: hyperkeratosis, atrophy of rete ridges, variable pigmentation of basal cells.

11. Clinical Presentation:
• Reddish to brownish macules,
irregularly shaped.
• Commonly seen over lower
extremities (anteriorly)
• 3 or more lesions must be present.
• Lesions usually appear in crops and
gradually resolve over 12 to 18
months.
• Asymptomatic
Treatment:
• Spontaneous resolution occurs
• No treatment needed.

12. Scleroderma like syndrome (Waxy Skin
Syndrome)
� Previously called “Diabetic Digital Sclerosis”
� Etiopathology:
� Alteration of collagen
� Due to both Aging and Diabetes Mellitus
� Increased cross-linking of collagen due to non-enzymatic
glycation.
� Postulated that hyperglycemia retards collagen formation,
leading to poor wound healing, while reduced collagen
breakdown results in dermal thickening.

13. Clinical Features
• Thick, tight, waxy skin over dorsum
of hand.
• Pebbling of skin
• Limited joint mobility of fingers
� Loss of mobility is painless
� Initially involves Distal IP joints of 5th
digit and progress proximally
• Clinical sign:
▪ Prayer sign
▪ Inability to extend fingers with
palm placed on table
▪ Restriction of passive movement of
joints
TREATMENT
• Skin may revert to normal with
Strict Glycaemic Control
• Physiotherapy

14. Diabetic Scleredema
� Prevalence of 2.5-14% of Diabetics
� Can also occur as Post Streptococcal respiratory infection (Sceleredema
Adultorum of Buschke) or as Insidious Idiopathic
� Clinical Features:
❑ Increased thickness of dermis (almost twice as thick than normal)
❑ Site: Posterior neck, upper back, deltoids (rare)
❑ Skin is firm, woody, non pitting, peau d’orange appearance.
❑ Pain may be present
❑ Difficulty in movement of upper extremities and neck
� HPE: Thick collagen bundles sperated by unstained spaces in dermis

15. Treatment
• No effective treatment
• Tried with variable
responses:
� Radiotherapy
� Low dose
methotrexate
� Prostaglandin E1
� PUVA
• Strict glycemic control
to slow progression

16. Acanthosis Nigricans
� Two types
� More severe generalized type: Associated with malignancy
� Limited type: Endocrinopathies
� Pathophysiology:
Proliferation of keratinocytes and fibroblasts resulting in AN
Binding and Activation of IGF-1 Receptors
Hyperinsulinemia and Insulin Resistance

17. Clinical Presentations:
� Brown to gray-black papillomatous cutaneous thickening
� Common Sites: Flexural areas including posterolateral neck, axillae, groins
and abdominal folds.
� Rarely can involve: oral, oesophageal, laryngeal, conjunctival and
anogenital mucosa.
Differentials:
• Malignancy
• Other endocrinopathies (Eg. Cushing’s)
• Obesity
• Drugs (Eg. Systemic Steroids, nicotinic acid)
Treatments:
� No satisfactory treatment
� Weight loss in Obese patients
� Keratolytic Agents (Eg. Salicyclic Acid), can improve appearance
cosmetically, if desired.

18. Images of AN

19. Achrochordons
(Skin Tags)
• Incidence upto 66% in diabetics
• Hyperinsulinemia causing
proliferation of keratinocytes and
fibroblasts.
• Benign, soft, fleshy skin coloured
fibromas
• Asymptomatic
• Site: flexural regions, around eyes,
neck, axilla, inframammary areas.
• Marker of impaired glucose
tolerance
• Treatment: For cosmetic concern,
Excision/Electrodessication

20. Diabetic Bullae (Bullous Diabeticorum)
� First described by Kramer in 1930 as “recurrent blisters on extremities of
Diabetics”
� Seen in less then 1% diabetics of middle age.
� Etiopathegenesis:
� Not Known
� In some cases distribution of lesions in light exposed areas was suggestive of
Porphyria Cutenea Tarda, but no abnormality in porphyrin metabolism found.
� Neither trauma nor immune mechanisms has been implicated

21. Clinical Features and
Treatment of Diabetic Bullae
Features:
• One or more “clear fluid filled”
bullae
• Appears spontaneously
• Most commonly on lower limbs
• No preceding history of trauma
• Usually asymptomatic
• Resolves spontaneously without
scarring over weeks
• Diagnosis is by exclusion
Treatment:
• Only supportive management
• Sterile Aspiration and compression
bandages

22. Skin alterations due to Diabetic
Complications
� Diabetic Foot
� Cutaneous infections associated with Diabetes
� Bacterial
� Fungal
� Xanthomatosis
� Xanthelesma

23. Diabetic Foot
� “Any infection involving the foot in a diabetic person,
originating from a chronic or acute injury of soft tissues of
the foot, with evidence of pre-existing neuropathy
and/or ischemia”
� 15% of Diabetic individuals suffer from it in their lifetime.
� 20% of patients with such ulcer needs amputation
� Characterized by triad of neuropathy, ischaemia and
infection

24. Pathophysiology of Diabetic foot
� Multifactorial and Complex:
� Neuropathy
� Vasculopathy
� Immune Dysfunction
❖ Prolonged hyperglycaemia contributes to all of the above through different
mechanisms

25. Sensory Neuropathy
Loss of pain sensation
Leading to unnoticed trauma
Progression of lesion
Callous formation and tissue
Necrosis
Diabetic Foot Ulcer
Motor Neuropathy
Weakness and Wasting of
intrinsic foot muscles
Foot Deformities
Abnormal gait leading to injury
Diabetic Foot Ulcer
Autonomic
Neuropathy
Decreased Sweating
Dry and Brittle Skin
Fissures/Cracks that gets
infected
Diabetic Foot Ulcer
Neuropathy Causing Diabetic Foot

26. VASCULOPATHY
� Atherosclerosis leading to skin atrophy.
� Microangiopathy causing poor wound repair capability due to poor tissue
perfusion
IMMUNE DYSFUNCTION
� Impaired defence against infection in diabetics due to:
▪ Decreased PMN migration
▪ Decreased phagocytosis
▪ Decreased Chemotaxis
▪ Decreased Intracellular Killing

27. Classification of Diabetic Foot
Two major types:
� The Neuropathic Foot, (neuropathy dominant)
� The Neuroischaemic Foot (occlusive vascular disease
predominates)
▪ “Differentiation between these entities is essential
because their complications are different and requires
different therapeutic strategies”

28. Clinical Features
Characteristics Neuropathic Foot Neuroischaemic Foot
Skin Temperature Warm Cold
Pain Painless Painful
Skin Colour Not altered Dependent rubor
Callus Thick at Pressure Points Usually absent
Ulcer Usually on tips of toes
and Plantar surfaces and
under metatarsal heads
Often on margins of foot,
tips of toes, heels
Peripheral Pulses Bounding Feeble/Absent
Ankle Brachial Index More than 0.9 Less than 0.9
Complication Charcot Joints Critical Ishaemia

30. Foot examination in Diabetics
� Look for neuropathic changes: dry skin, fissures,
deformities, callous, nail lesions, ulcers
� Loss of hair on dorsum of foot and dependent rubor
suggests significant ischaemia
� Check for temperature, colour changes and peripheral
pulses. Auscultation of femoral arteries for bruits.
� Check for ABI. ABI > 1 rules out ischaemia

31. MANAGEMENT OF DIABETIC FOOT
� Strict Glycaemic Control
� Debridement of Wound
� Antibiotic Coverage
� In Case of Neuroischaemic Diabetic Foot,
revascularization via angioplasty may be carried out.
� In case of severe secondary infection/gangrene, an
amputation may be required

32. Prevention of Diabetic Foot
� Primary Prevention: Regular Screening of high risk feet (neuropathy and/or
ischaemic changes present) and proper advice on preventive footwear.
� Secondary Prevention: Management of trivial foot lesions such as callus
removal, treatment of nail pathologies, deroofing blisters, etc.
� Tertiary Prevention: Prompt referral to a specialist for advanced foot lesions.

33. Cutaneous Infections Associated with
Diabetes
� Poorly controlled or undiagnosed diabetics have greater susceptibility of
bacterial and fungal skin infections
� Common infections in Diabetics
o Bacterial
o Fungal Infections

34. Common Bacterial Infections in
Diabetics
� Staphylococcal: Furuncle, Carbuncle, Ecthyma
� Streptococcus Pyogenes: Cellulitis, Erysipelas
� Pseudomonas Sp.:
� Causes Malignant External Otitis
o Common in old aged diabetics
o Characterized by unilateral pain with ear discharge
o Treated by Carbenicillin + Gentamycin, along with complete
excision of infected tissues

35. Common Bacterial Infections in
Diabetics
� Erythrasma
� Causative Organism: Corynebacterium minutissimum
� Characterized by “Chronic, asymptomatic, symmetric, red scaly,
macerated plaques” in axilla or groin
� Wood’s lamp examination: Coral Red Fluorescence
� Treatment: Topical or systemic Erythromycin
� Non Clostridial Gas Gangrene
� Develops in soft tissue near a gangrenous focus
� Caused by: E.Coli, pseudomonas, Bacteriods.

36. Cellulitis
Erythrasma

37. Common Fungal Infections in Diabetics
� Candidiasis
o Oral
o Vaginal/Balonoposthitis
o Paronychia
o Nail Infections
� Dermatophytosis
o Caused by Trichophyton rubrum, T. mentagrophytes and Epidermophyton
Floccosum
� Phycomycetes
o Usually complicates leg ulcers/open wounds of diabetics
o May lead to gangrene formation.
o Treatment: Debridement, i.v. antifungals, correcting of acid-base imbalances,
strict glycemic control

38. Common Fungal Infections in Diabetics
� Rhinocerebral Mucormycosis
o Caused by Zygomycetes (Mucor and Rhizopus Sp.)
o Especially associated with ketosis
o Characterized by black crusting or pus on the turbinates, septum, or ethmoid
and maxillary sinuses
o Cerebral involvement in 2/3rd cases.
o High mortality
o Treatment includes I.V. Amphotericin B, Gylcemic Control, wound debridement,
management of ketosis

39. Xanthomatosis and Xanthelesma
� Eruptive Xanthomas are characteristic but uncommon in diabetics
� Suggestive of sustained hyperlipidaemia
� Decreased “lipoprotein lipase” in IDDM causes accumulation of TGL, high
levels of which can cause eruptive xanthomas
� Features: Appears in crops, reddish yellow nodules upto 0.5 cm in size
� Primarily involves extensor surfaces and buttocks
� Regression occurs on controlling hyperlipidemia
Xanthalesma
� Seen in hyperlipidemia, diabetics and also in people with normal lipid
profile
� Characterized by “yellowish discolouration of skin of palms, soles,
nasolabial folds due to deposition of carotene present in excess in plasma”

40. Eruptive Xanthoma on extensor surface
Xanthalesma

41. Dermatologic Changes Associated
with Neurovascular Complication
� Macroangiopathic manifestations
� Microangiopathic manifestations
� Diabetic Neuropathy

42. Macroangiopathic Dermatological
Manifestations
� Diabetics have slightly higher incidence of large vessel disease
� Dyslipidaemia is a risk factor.
� Atherosclerotic manifestation of skin includes:
▪ Skin atrophy
▪ Loss of hair
▪ Coldness of toe
▪ Pallor on elevation and mottling on dependence
� Treatment to be directed towards management of Dyslipidaemia and
Glycaemic control.

43. Microangiopathic Dermatological
Manifestations
� Microangiopathy precedes over other abnormalities
� Responsible for retinopathy, neuropathy, nephropathy, dermopathy.
� Cutaneous signs associated with Microangiopathy:
❑ Diabetic Dermopathy
❑ Pigmented Purpuras
❑ Erysipelas like erythema
❑ Periungual telangiectasia
❑ Diabetic Foot

44. Diabetic Rubeosis
• Occurs due to
microangiopathy or
decreased vascular tone
• Chronic Flushed
appearance in the face
and neck
• Improved by:
�Glycaemic Control
�Avoidance of Vasodilators
(caffeine and alcohol)

45. Diabetic Neuropathy
� Distal, symmetric, mixed polyneuropathy involving both motor and sensory
nerves.
� Pathogenesis
Impairment of
Polyol Pathway
Results in increased Sorbitol level in the
cell and thus the intracellular osmotic
pressure
Functional and Structural Abnormalities
Protein Kinase C
Activation
Hyperglycaemia promotes synthesis of
protein kinase C activator, “Diacyl
Glycerol”
Increased Protein Kinase C causes
vasoconstriction and thus Nerve
Hypoxia and damage
Oxidative Stress
Hyperglycaemia enhances NADPH
oxidase expression and also eNOS
reaction, leading to superoxide
production
Excess Superoxide decreases NO by
binding with it, generating ROS which
damages the neurons
• Other mechanisms: Excess PARP activation, Ischaemia,etc

46. Diabetic Neuropathy
� Skin manifestation of Neuropathy:
Autonomic
Neuropathy
Disturbances in Sweating,
Peripheral Hyperaemia
with erythema, oedema
and atrophy
Motor Neuropathy
Gait abnormalities
Recurrent injuries leading
to diabetic foot ulcers
Sensory Neuropathy
Paresthaesia like loss of
temperature and pain
sensation leading to
diabetic foot.

47. Treatment of Diabetic Neuropathy
� FDA approved drugs: Pregabalin or Duloxetine
� Tapentadol, (FDA Approved) centrally acting opiod analgesic, with
modest efficacy.
� Antidepressant for neuropathy:
▪ Desipramine, amitryptiline, Venlafaxine.
▪ Inhibits the membrane pump mechanism for reuptake of neuropeptide
and changes the central perception of pain
▪ Not FDA Approved
� Anticonvulsants for neuropathy: Valproate, Gabapentin,
Carbamazepine
� Capsaisin ointment for local application
� Alpha Lipoic Acid (Efficacious as per SYDNEY 1 and SYDNEY 2 trail)
� “Evidence of effectiveness of chronic pain via strict glycaemic
control is lacking”

48. Dermatologic Complication Due to
Treatment of Diabetes
� Oral Hypoglycaemic Drugs
� Insulin
� Glycaemic Self Monitoring

49. Cutaneous Manifestations due to OHA
First Generation Sulfonylureas (Chlorpropamide, Tolbutamide)
� Most common manifestation: Maculopapular exanthema, disappears on
stopping drugs
� Other skin manifestation: urticaria, erythema multiforme, Erythema nodosum,
phototoxic and photoallergic reaction.
� Chlorpropamide Alcohol Flush
� In patient consuming alcohol who is on this drug
� Starts within 15 minute of ingestion
� Flushing, headache, tachycardia, dyspnea
� Occurs due to inhibition of metabolism of acetaldehyde.
Second Generation Sulfonylureas (Glibenclamide, Glipizide, Gliclazide)
� Photosensitivity, Urticaria, Pruritus
� Skin reaction were infrequent with Glimepride (3rd Gen)

50. Cutaneous Manifestations of Sulfonylureas: Erythema Multiforme (left) and Erythema Nodosum (right)

51. BIGUANIDES
(Metformin)
Common Skin Reactions
• Psoriasiform reactions
• Leukocytoclastic Vasculitis
• Erythema Multiforme
• Lichenoid eruptions
• DRESS Syndrome
❑ Rare
❑ Severe, idiosyncratic and life
threatening
❑ Starts after a latency period of 2-8
weeks
❑ Fever, lymphadenopathy,
eosinophilia, deranged LFT
❑ Skin manifestations: urticaria,
maculopapular eruption, vesicles,
bullae, target lesions
❑ Rx: Stop Offending drug, Start
Systemic Corticosteroids and
emollients.

52. Thiazolidinediones (“Glitazones)
� “Edema” has been reported as a cutaneous side effect of “Rosiglitazone”
and “Pioglitazone”
� Other (rare) skin manifestations: blistering, peeling or red skin, rash and
swelling of hands, ankles or feet.
Alpha Glycosidase Inhibitor
� Rare skin manifestation, cause it is minimally absorbed
� Reported manifestations:
❖ Erythema multiforme
❖ Acute Exanthematous pustulosis

53. Incretins (DPP-4 inhibitors and GLP-1
agonists)Inhibitors of dipeptidyl-peptidase 4 (DPP-4) Glucagon like Peptide 1 (GLP-1) agonist
-Hypersensitivity Reactions (sitagliptin,
saxagliptin, teneligliptin)
-Skin Rash (sitagliptin, linagliptin,
teneligliptin)
-Angioedema (sitagliptin, linagliptin)
-Steven Johnson Syndrome (Sitagliptin)
-Anaphylaxis (Sitagliptin)
-Facial Oedema (Saxagliptin)
-Eczematous Reaction (Teneligliptin)
-Pruritus (Teneligliptin)
-Hyperhidrosis (by Vildagliptin when
associated with Sulphonylureas)
-Bullous Pemphigoid (rarely with
vildagliptin sitagliptin)
-Drugs includes liraglutide, exentanide,
lixisenatide, albiglutide
-Administered subcutaneously
-Cutaneous manifestions
Pruritus
Urticaria
Anaphylaxis
Allergic Reaction at injection site
Post marketing reports of cutaneous
manifestation of Exentanide:
Hyperhidrosis
Alopecia
Angioneurotic Edema
Maculopapular Exanthema

54. Sodium-Glucose Cotransporter 2 inhibitors
� Drugs: Dapagliflozin, Campagliflozin, Empagliflozin
� MOA: Inhibition of Sodium Glucose Cotransporter in PCT
� Cutaneous Manifestation
� Usually Rare
� Reported: Hyperhidrosis, Stomatitis, Herpes Zoster
� In genital area: Erythema, itching, Balnoposthitis, Vaginitis
� Case Report (Vasapollo P et al)
❑ Reported severe pruritus in a 61 year old female on Campagliflozin
❑ No evidence of presence of systemic or skin disease found
❑ Discontinuation of the drug resulted in remission of symptoms

55. Cutaneous Manifestation Of Insulin
Categorized as following:
� Insulin Allergy
� Idiosyncrasy
� Administration Failures: Intraepidermal injections
� Lipodystrophies

56. Insulin Allergy
� Due to impurities in preparation, presence of animal-origin proteins, insulin
molecule itself, preservatives and additives
� Two Types
� Generalized/Systemic
� Localized
� Generalized Reaction such as urticaria, anaphylaxis or angioedema are
rare. Occurs in 0.2% of insulin users

57. Systemic Reaction
� Two types:
❑ Early IgE mediated
❑ Delayed Arthus Reaction
� Features
❖ Circulatory: Pallor, Flushing,
Palpitation, Shock
❖ Gastrointestinal: Nausea, Vomiting,
Abdominal Cramps, Diarrhea
❖ Respiratory: Dyspnea, Stridor
❖ Arthralgia
Localized Reaction
� Two Types
❑ Immediate IgE mediated
❑ Delayed IgG meditated
� Features
❖ Immediate: Erythema, Urticaria
within 30 min of injection, subsides
within an hour
❖ Delayed:
▪ Occurs after 4 hours or more.
▪ Pruritic Nodule develops at injection
site after 2 weeks.
▪ Heals by scarring
� Rx: Shift to more purified insulin.
Antihistaminic and Corticosteriods
have been tried with some success.

58. Idiosyncrasy And Administration Failures
Idiosyncrasy
� Rare
� Manifestations include: Pigmentation and keloid formation
� Skin reaction resembling Acanthosis Nigricans has been reported
Administration Failure
� Due to faulty techniques
� Manifestations: Localized Induration, ulceration, scar formation, cutaneous abscess
and keloid formation

59. Lipodystrophies
� Two Types: Lipoatrophy or lipohypertrophy. May Coexist.
� More common in Obese Children and Woman
� Rare with newer insulin preparation
� Leads to erratic insulin delivery and glycaemic control if injected in those
sites
Lipoatrophy Lipohypertrophy
Proposed Mechanism:
• Lipolytic components of preparation
• Cryotrauma of refrigerated insulin
• Mechanical trauma
• Insulin induced localized TNF-a
production by Macrophages
Feature: Atrophic plaque showing
atrophy of subcutaneous fat at
injection site. Occurs after 6-24 months
of therapy
Rarely shows complete resolution
Most common Cutaneous
manifestation of insulin therapy.
Mechanism: Anabolic action of insulin
over fat metabolism
Feature: Soft dermal nodule with
overlying normal skin

60. Lipoatrophy Lipohypertrophy

61. Glycaemic Self Monitoring
• Seen as post traumatic
lesion by lancets in
fingers of long standing
diabetics
• Preferred method to
reduce lesions:
▪ Use of new lancet in
each test
▪ Rotate the Puncture
site each time.

62. Endocrine syndromes with skin
alteration and Diabetes
GLUCAGONOMA
� Most characteristic endocrine syndrome presenting with skin alteration and diabetes
� Syndrome caused by alpha cells, the glucagon secreting cells of pancreas
� Dermatosis is the presenting clue
� Four Components
❑ Hypersecretion of Glucagon
❑ Diabetes
❑ Weight Loss
❑ NECROLYTIC MIGRATORY ERYTHEMA

63. Cutaneous Manifestation in
Glucagonoma (NME)
� Chronic fluctuating Dermatosis characterized by an annular and figurative
erythema that forms bullae and erosion
� Periphery of the lesion extends with Vesiculopustules
� Lesions tends to coalesce before healing starts.
� Common sites: intertriginous area, perioral region and on extremities
� Can be present for 1-6 years before diagnosis of Glucagoma
� Histologically resembles Pustular Psoriasis (intracellular edema in the upper
epidermis, acanthosis and subcorneal pustulosis)
� Somatostatin or its analogue Octreotide improves lesion.
� Complete resolution after extirpation of tumor.

64. Necrolytic Migratory Erythema

65. Dermatoses reported to be more common
in diabetics than in nondiabetics
� Perforating Dermatosis
� Vitiligo
� Lichen Planus
� Yellow Skin and Nails
� Kaposi’s Sarcoma
� Dermatitis Herpetiformis
� Bullous Pemphigoid

66. Perforating Dermatitis
• More common in Diabetic Patients
with Chronic Renal Failure,
particularly those on dialysis
• More common in middle aged
and in men.
• Papules ranging from 2-10 mm in
diameter, often with a keratotic
plaque.
• Itchy with little tendency to resolve
spontaneously
• Site: extensor surface of trunk and
extremities
• Topical Retinoic and UV therapy
found to be useful. Doxycycline
and Allopurinol were also found to
be helpful.

67. Vitiligo
• Diminished or absent function
of melanocytes
• Common in periorifacial
region and extensor aspect of
extremities.
• Usually asymptomatic
• Frequent in diabetics probably
due to the fact both DM and
vitiligo has autoimmune
etiology.
• 4.5-7.7% of Patients with
maturity onset DM develops it.

68. LICHEN PLANUS
� Increased incidence of Diabetes Mellitus and abnormal insulin response to glucose
challenge have been claimed in patients with Lichen Planus
� Especially Erosive Oral Form is more common in Diabetics
� Reason Not Known.
YELLOW SKIN AND NAILS
� Yellow skin usually involves palms and soles
� Usually involves distal hallux
� Earliest sign is yellow/brown colour of distal part of hallux nail plate. Later, a canary-
yellow discolouration occurs
� Also referred to as Carotenemia, but few evidence of carotenoids being the cause
� Discolouration is due to non-enzymatic glycation of dermal collagen, the end
product of which, 2-(2-furoyl)-4[5](2-furanyl)-1H-imidazole, has a yellowish colour.
� No effective treatment available.

69. Yellow Palms (left) and Nails (Right) of Diabetes Mellitus

70. KAPOSI’S SARCOMA
� More in diabetics, but confirmation needed
� Predominant in males
� Oedema in legs may be a prodrome
� Lesion begins in legs as multiple purple macules, nodules or plaques, later
mucous membrane or internal organs may be involved.
Dermatitis Herpatiformis
� HLA association of Dermatitis Herpetiformis and Diabetes may be the reason for
the two appearing together more frequently.
Bullous Pemphigoid
� Very few studies confirming the claim
� Possible explanation: Lower threshold of diabetes for formation of traumatically
induced blisters or on the basis of antigenic changes at the level of lamina lucida
because of enzymatic glycosylation
� Steriods were found useful in treating

71. References
� Sreedevi, Chilukuri & Car, Nikica & Pavliae-Renar, Ivana (2002).
Dermatologic Lesions in Diabetes Mellitus. Diabetologia Croatia.
31.
� IADVL Textbook of Dermatology, 4th Edition, Vol.2, Page 1915-
193, Chapter 39, Cutaneous Manifestation in Diabetes Mellitus.
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