CutaneousManifest RC

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Cutaneous Manifestationsof Internal Disease

Residents Conference

Hallie McDonald, MD

August 16, 2005


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Diabetes Mellitus

According to Perez et al (3),approximately30% of patients with DM develop skinlesions at some point

Overall prevalence of cutaneous disordersdoes not differ between type I and type IIdiabetics

Type I patients get more autoimmune-type

lesions

Type II patients get more cutaneous infections


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Diabetes Mellitus

Cutaneous lesions usually appear afterthe development of DM, but may be thefirst presenting sign

Four major groups of skin findings1. Skin diseases associated with DM (necrobiosis

lipoidica and diabetic bullae)

2. Cutaneous infections

3. Cutaneous manifestions of diabeticcomplications (neuropathic ulcers)

4. Skin reactions to diabetic treatment


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Necrobiosis Lipoidica (NL)

NL appears in 0.3-1.6% of diabetics (2,4)

Anywhere from 11-65% of patients withNL have DM at the time of skin dx (2,7,8)

If they do not have DM at time of dx,about 90% will develop diabetes, haveabnormal glucose tolerance, or reportparents with DM (2, 4)

Diabetic control has no effect on thecourse of NL.


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Classically, NL occurs bilaterally on thepretibial 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


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Granuloma Annulare (GA)

Controversy surrounds the association betweenGA and DM.

A case-control study by Nebesio et al. (5) failedto reveal a statistically significant correlationbetween the two.

A retrospective study by Studer et al. (6)suggested that up to 12% of patients presentingwith GA had DM.

Despite conflicting studies, it is reasonable toscreen patients presenting with GA for DM.


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Appearance Ring of small, firm, flesh-colored or red papules

If localized, most frequently found on lateral and dorsalsurfaces of hands and feet

Disease begins with an asymptomatic, flesh-coloredpapule that undergoes central involution

Over months, a ring of papules grows

Can spontaneously regress without scarring

Histology

Focal degeneration of collagen in the upper and mid-dermis, palisaded histiocytes around collagen bundles,and abundant dermal mucin

Pathogenesis unknown


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Treatment

If localized, best left untreated.

Can treat with intralesional steroids, if needed

If generalized, can also use dapsone,isotretinoin, freezing, cyclosporin, or PUVA.


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Histology showing focaldegeneration ofcollagen in the upperand mid-dermis,palisaded histiocytesaround collagenbundles, and abundantdermal mucin


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Diabetic Bullae Approximately 0.5% of diabetics (2)

More common in men with long-standing DM and neuropathy Two types have been described

More frequent, non-scarring lesions with a histologic intraepidermalsplit without acantholysis

Less common, occasionally hemorrhagic bullae that heal with scarring,

slight atrophy, and have a histologic subepidermal split 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 vascularinsufficiency

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


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Diabetic Bullae

Bullae tend to heal spontaneously in 2-5 weeks

Bullosis diabeticorum remains a diagnosis ofexclusion with negative immunofluorescencestudies, porphyrin levels, and cultures DDx: bullous pemphigoid, epidermolysis bullosa

acquisita, porphyria cutanea tarda, bullous impetigo,erythema multiforme, and coma blisters

May recur in the same or new locations

If large and symptomatic, can aspirate the fluidleaving an intact blister roof as a wound covering


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Diabetic Bullae


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Diabetic Bullae


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Diabetic Bullae

Histology showing anoninflammatoryblister with asubepidermal and

focally intraepidermalseparation


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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,

Cushings disease, hypothyroidism) Obesity

Pathogenesis According to Cruz (12), it may be related to insulin

binding insulin-like growth factor receptors onkeratinocytes and dermal fibroblasts, thus stimulatinggrowth.


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Appearance

Hyperpigmented, velvety plaques in bodyfolds, mostly axillae and neck

Can also present on groin, umbilicus, areolae,submammary areas, and on the hands (tripehands)

Treatment- usually asymptomatic

Weight loss Retinoic acid and salicylic acid


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Skin Infections in DM

Occur in 20-50% of poorly controlleddiabetics (2, 4)

More common in Type II

May be related to abnormalmicrocirculation, hypohidrosis, PVD,neuropathy, decreased phagocytosis andkilling activity, impaired leukocyteadherence, and delayed chemotaxis allseen in diabetics (2, 9, 10, 11)


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Fungal infections- most common

Candida Candidal paronychia

Inframammary candida

Genital candida

Psedudohyphae and spores on KOH prep support dx ofCandida

Purulent drainage may indicate secondary bacterialinfection

Because maceration and skin breaks can serve as portals of

infection, tinea pedis should be treated aggressively indiabetics

Treatment includes drainage of any abscesses, keeping thedigits dry, and topical antifungals (clotrimazole)


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Candidiasis in Diabetics

White, curdlikematerial adherent toerythematous,fissured oral

commisure; angularstomatitis


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Initial pustuleson erythematousbase thatbecome erodedand confluent


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KOH prep showing pseudohyphae and buddingyeast forms


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Bacterial Infections- can be more severeand widespread in diabetics

Malignant otitis externa

Pseudomonas aeruginosa Fatal in over 50% patients (13)

Can progress to chondritis, osteomyelitis, andbacterial meningitis

Treat up to 3 months with oral quinolones butmay need IV antibiotics


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Malignant Otitis Externa in Diabetics


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Bacterial infections in DM

Erythrasma

Reddish tan scaling patches of the upper inner

thighs, axillae, toe web spaces, andinframammary creases

Gram positive Corynebacterium minutissimum

Identified with Woods light coral fluorescence

Treat with oral erythromycin for 5 days


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Erythrasma in Diabetics

Reddish tan scaling patches of the upperinner thighs, axillae, toe web spaces, andinframammary creases


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W d L i th Di i f


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Woods Lamp in the Diagnosis of

Erythrasma

C t M if t ti f Di b ti


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Cutaneous Manifestations of Diabetic

Complications: Foot Ulcers

Responsible for 70% of annual lower limbamputations in the U.S.(2)

Large economic impact from medical and surgicaltherapy, rehab, loss of work, and mortality

Prevention is key Daily foot inspections, appropriate footwear

Causes for ulcer formation: Peripheral neuropathy (60-70%)

Treatment: aggressive debridement and offloading or witha contact cast

Vascular disease (15-20%) Treatment: surgical re-vascularization

Combination of peripheral neuropathy and vasculardisease (15-20%)

C t R ti t Di b ti


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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 site6-24 months after starting insulin

More common in women and children

Pathogenesis unknown but may be related to lipolytic componentsof the insulin preparation, an immune complex-mediatedinflammatory process with lysosomal enzyme release, cryotraumafrom 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

C t R ti t Di b ti


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Treatment: Lipoatrophy

C t R ti t Di b ti


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Treatment- Insulin

Highly purified or recombinant insulins have areduced allergy prevalence (0.1-0.2%) (4)

Observe the patients technique to make sureit isnt intradermal

Treatment includes substitution of a morepurified insulin, discontinuation ordesensitization for severe systemic rxns

C taneo s Reactions to Diabetic


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Treatment-Oral Hypoglycemics

Most rxns are associated with the first-generationsulfonylureas (chlorpropamide and tolbutamide)

1-5% of patients on these drugs will develop skinrxns during the first 2 months of treatment (2,4)

Most commonly, they present with maculopapulareruptions that resolve despite continuation of thedrug

For patients of chlorpropamide, 10-30% willdevelop a disulfiram-like rxn of flushing,headache, tachycardia, and shortness of break

after ingesting alcohol. This seems to beautosomal dominant. (2,3)

Second-generation sulfonylureas can also beassociated with cutaneous rxns.


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Hyperthyroidism and the Skin

Thyroid hormone plays a pivotal role inthe growth and formation of hair andsebum production.

Thyroid hormone stimulates epidermaloxygen consumption, protein synthesis,mitosis, and determination of epidermalthickness.

There is increased cutaneous blood flowand peripheral vasodilation.


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Hyperthyroidism and the Skin

Skin is usually warm, moist, and smooth

Facial flushing

Palmar erythema

Hyperpigmentation, esp. creases of palms andsoles, gingiva, and buccal mucosa

Hyperhydrosis, particularly of palms and soles

Scalp hair can be soft, fine and sometimes

accompanied by non-scarring alopecia 5% of patients with hyperthyroidism have nail

findings (14)


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Plummers Nail in Hyperthyroidism

Plummers nail: concave contour and distalonycholysis, esp. the ring finger (not specific- alsoseen in hypothyroidism, psoriasis, after trauma, orin allergic contact dermatitis)


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Scleromyxedema in Hyperthyroidism

Numerous firm white, yellow, or pink papules onface, trunk, axillae, and extremities

Lesions result from accumulation of hyaluronic acid inthe dermis, accompanied by large fibrocytes (14, 15)

Can be accompanied by weight loss, esophagealdysmotility, vascular dz, Raynauds phenomenon,monoclonal gammopathy, neurologicmanifestations, joint dz, and myopathy (14)

Treatment of hyperthyroid state with radioactiveiodine does not improve skin findings (14, 16)


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Firm white, yellow, or pink papules on face, trunk,axillae, and extremities


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Graves Disease

These patients can have all of the other previouslymentioned cutaneous manifestations of hyperthyroidism inaddition to several unique entities

Pretibial myxedema (0.5-4% of patients) Presentation varies from peau dorange appearance to

extensive infiltration that mimics elephantitis vurrucosa nostra

Most often, bilateral, asymmetric, raised, firm plaques ornodules varying from pink to brown, sometimes with woodyinduration

Can appear anywhere (arms, shoulders, head) Can treat with topical steroids, intralesional steroids, IV pulse

steroids, or IVIG

Pathogenesis remains unknown, but one theory suggestspretibial fibroblasts are the target for antithyroid antibodies(14)

In support of this theory, Wu et al. (16)reported the presence ofTSH and TSH receptor antibody binding in fibroblasts as well asthe presence of RNA encoding the extracellular domain of the TSHreceptor.


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Pretibial Myxedema in Graves Disease

Bilateral, asymmetric,raised, firm plaques ornodules varying from pinkto brown, sometimes withwoody induration


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Thyroid Acropachy in Graves Disease

Thyroid acropachy (1% of Graves patients)Triad of digital clubbing, soft tissue swelling of hands and

feet, and periosteal new bone formation


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Graves Disease and Thyroid Acropachy

AP radiograph of the hand demonstratesfeathery periosteal bone proliferation ofthe diaphyses of the metacarpals and

proximal phalanges


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Hypothyroidism and the Skin

Skin changes in hypothyroidism reflect a hypometabolicstate and subsequent reduced core body temperatureresults in cutaneous vasoconstriction. (14)

Skin is cool, dry, and pale. Pallor results from cutaneous vasoconstriction and increased

deposition of water and mucopolysaccharides in the dermis,which alter the refraction of light

Hypohydrosis may lead to palmoplantar keratoderma

Carotenemia (from decreased hepatic conversion of betacarotene to Vit A) gives skin yellowish hue (14, 17)

Hair: dry, brittle, coarse; partial alopecia

Loss of hair from lateral 1/3 of eyebrows

Hypothyroidism Facies with Generalized


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Hypothyroidism Facies with Generalized

Myxedema

Generalizedmyxedema Occurs as a result of

deposition of dermalacid

mucopolysaccharides(esp. hyaluronic acidand chondroitin sulfate)in the skin

Skin is non-pitting

Face: swollen lips,broad nose,macroglossia, and puffyeyelids

Thyroid Disease and Other Cutaneous


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Thyroid Disease and Other Cutaneous

Disease Associations

Autoimmune thyroid disease has been associatedwith other cutaneous diseases

Alopecia areata (18) Bullous disorders

Pemphigus foliaceus Pemphigus vulgaris (19)

Vitiligo (20)

Derived from the Greek vitelius,signifying a calf's whitepatches

Fairly symmetric pattern of white macules with well-

defined borders Connective tissue diseases

Dermatomyositis (21), SLE (22), scleroderma(23)

Alopecia Areata Associated with


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Alopecia Areata Associated with

Autoimmune Thyroid Disease

Rapid onset of total hair loss in a sharplydefined, usually round, area

Regrowth begins in 1 to 3 months and may befollowed by loss in the same or other areas

Pemphigus foliaceus Associated with


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Pemphigus foliaceus Associated with


Pemphigus foliaceus: recurrent shallowerosions, erythema, scaling, and crusting

Pemphigus vulgaris Associated with


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Painful oral erosionsusually precede the onsetof skin blisters by weeksor months



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Nonpruritic flaccid blisters varying in size from 1 to severalcm appear gradually on normal or erythematous skinInvariably generalize if left untreated


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Cutaneous Paraneoplastic Syndromes

In 1976, Helen Ollendorff Curth set criteria thatshould be met before a skin disease can be calleda paraneoplastic dermatosis (24,25): Both conditions start approximately the same time Both conditions follow a parallel course

Neither the onset nor the course of either condition isdependent on the other A specific tumor occurs with a specific skin manifestation The dermatosis is not common in the general population A high percentage of association between the two

conditions is noted

Currently, only the first two criteria should bemet to call a skin disease a paraneoplasticprocess (24, 25).


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Cutaneous Paraneoplastic Syndromes

May be initial clue to underlying neoplasm

Can herald the recurrence of a malignancy

Examples

Necrolytic migratory erythema Sign of Leser-Trelat

Hypertichosis lanuginosa acquisita

Bazexs syndrome

Dermatomyositis

Erythroderma


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Necrolytic Migratory Erythema

Glucagonoma syndrome includes glucose intolerance,weight loss, anemia, hair and nail changes,hypoaminoaciduria, psychiatric disturbances, andthromboembolic disease (24, 26)

Skin manifestation of the glucagonoma syndrome Erythematous macules and papules, often annular or arciform,

on central face, lower abdomen, perineum, groin, buttocks,and thighs Progress to erosions secondary to epidermal necrosis Skin disease has waxing and waning course that does not

seem to follow the course of the glucagonoma

Pathophysiology is not known, but it is probably related tocatabolism from increased levels of glucagon

When physician suspects this, be aggressive 75% glucagonomas are metastatic at time of diagnosis(27)

Gold standard for treatment is surgery


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Necrolytic migratory erythema

Erythematous macules and papules, often annular or arciformthan can progress to erosions


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Sign of Leser-Trelat

First described in 1890 as an increase in thenumber of cherry angiomas in patients withcancer (28)

Now refers to an increase in number or size of

seborrheic keratoses in patients with internalmalignancy (24)

Most often found in patients with adenocarcinomaof the stomach or colon (28), but also reportedwith hematopoietic, breast, lung, ovarian, and

uterine cancers (24, 29, 30) Can appear as early as 5 months before the dx of

cancer or as late as 9.8 months after (29)


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Hypertrichosis lanuginosa acquisita

Sudden appearance of downy, soft, nonpigmented hair onthe body

Most common associated malignancy is lung followed bycolorectal cancer (32)

Also has been associated with bladder, ovarian, uterine,

and pancreatic cancer(24, 33)

Typically occurs on face, but also on trunk, limbs, and ears

Palms, soles, and genitals are spared

Can be associated with other signs and symptoms,including glossitis, glossodynia, diarrhea, adeopathy, andacanthosis nigricans

In some cases, the hypertrichosis resolves with treatmentof the tumor (24)


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Bazexs Syndrome

Violaceous, symmetric papulosquamous plaqueson the acral surfaces of ears, nose, hands, andfeet

75% have nail changes including longitudinal orhorizontal ridging, thickening, subungal debris,

and discoloration(24)

Mostly male (93% in one study) (34)

Associated with squamous cell carcinoma of theoropharynx, larynx, lung, or esophagus

In one review, cutaneous changes preceded the

diagnosis of malignancy by an average of 11months in over 60% of patients with Bazexssyndrome (35)


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Bazexs Syndrome

Violaceous, symmetric papulosquamous plaques on the acralsurfaces of ears, nose, hands, and feet

The dermatosis improves with cancer treatment and worsens asthe cancer progresses (24)

Nail changes tend to persist after effective cancer treatment and

resolution of other skin manifestations


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Dermatomyositis

Proximal muscle weakness, elevated CK and aldolase Heliotrope rash, Gottrons papules, and others

Poikiloderma, periungual telangiectasia, scalp pruritis anderythema

Some factors associated with higher incidence of

paraneoplastic dermatomyositis Older age, male gender, patients that are difficult to control

Perform age-appropriate cancer screening fordermatomyositis patients

25% will develop malignancy (24, 35), most commonly

Genital neoplasms in women (24, 36)

Respiratory tract neoplasms in men (24, 36)


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Heliotrope Rash in Dermatomyositis

Heliotrope rash (violaceous erythema) ofperiorbital skin


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Gottrons papules in Dermatomyositis

Flat-topped, violaceous or erythematouspapules on extensor surfaces


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Erythroderma

Exfoliative dermatitis with a dramatic presentation characterizedby widespread erythema and scaling of skin Often have lymphadenopathy, headaches, malaise,

photosensitivity, and chills Pathogenesis is unknown, but may have to do with elevated

cytokines and adhesion molecules causing increased epidermalturnover and exfoliation

Many potential causes, including pre-existing dermatoses, drugrxns, and malignancy. Skin changes most commonly present before the diagnosis of

malignancy is made. According to a study by Nicolis (37) , 20 out of 24 patients with

erythroderma and mycosis fungoides, Hodgkins, or other lymphomasor leukemias had skin changes up to 25 years before the dx of cancer

was made. Most often associated with lymphomas and leukemias (24, 37, 38, 39)

Also been reported with liver, lung, thyroid, and prostate cancer(38)


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Erythroderma

May begin as scattered erythematous pruritic patches thatgeneralize with time

Palms and soles usually spared

Treat the underlying malignancy and use topical steroids.


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References

1. Habif. Clinical Dermatology, 4th

ed. Mosby Inc: 2004.2. Ferringer T, Miller F. Cutaneous manifestations of diabetes mellitus. Dermatol Clin. 2002; 20:483-492.

3. Perez MI, Kohn SR. Cutaneous manifestations of diabetes mellitus. J Am Acad Dermatol 1994;30:519-31.

4. Paron NB, Lambert PW. Cutaneous manifestations of diabetes mellitus. Prim Care 2000; 27:371-83.

5. Nebesio C, Lewis C, Chuang T: Lack of an association between granuloma annulare and type 2diabetes mellitus, Br J Dermatol 2002; 146(1):122.

6. Studer E, Calza A, Saurat J: Precipitating factors and associated diseases in 84 patients with

granuloma annulare: a retrospective study, Dermatology 1996; 193(4):364.

7. Stuart CA, Gilkison CR, Smith MM, et al. Acanthosis nigricans as a risk factor for non-insulindependent diabetes mellitus. Clin Pediatr 1998; 37:73-80.

8. 0-Toole EA, Kennedy U, Nolan JJ, et al. Necrobiosis lipoidica: only a minority of patients havediabetes mellitus. Br J Dermatol 1999;140:283-6.

9. Jelinek JE. Cutaneous manifestations of diabetes mellitus. Int J Dermatol 1994; 33:605-17.10. Sibbald RG, Landolt SJ, Toth D. Skin and diabetes. Endocrinol Metab Clin North Am 1996;25:463-

72.11. Goodfield MJD, Millard LG. The skin in diabetes mellitus. Diabetaologia 1988;31:567-75.12. Cruz PD. Excess insulin binding to insulin-like growth factor receptors: proposed mechanism for

acanthosis nigricans. J Invest Dermatol 1992;89:82S-5S.13. Huntley AC. The cutaneous manifestations of diabetes mellitus. J AM Acad Dermatol 1982;7:427-

55.


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References

14. Leonhardt JM, Heymann WR. Thyroid disease and the skin. 2002; 20: 473-481.15. Lindhoudt V, Schumacher Jr HR, Algeo S, et al. Scleromyxedema with myopathy

and hyperthyroidism. J Rheumatol 1996;23:1299-301.16. Wu SL, Chang TC, Chang TJ, et al. Cloning and sequencing of complete thyrotropin

receptor transcripts in pretibial fibroblast culture cells. J Endocrinol Invest1996;19:365-70.

17. Heymann WR. Cutaneous manifestations of thyroid disease. JAAD 1992;25:885-906.

18. Tosti A, Bardazzi F, Guerra L. Alopecia areata and thyroid function in children.JAAD 1988;19:1118-9.

19. Wolf R, Feuerman EJ. Pemphigus in association with autoimmune thyroid disease.Cutis 1981;27:423-4.

20. Bloch MH, Sowers JR. Vitiligo and polyglandular autoimmune endocrinopathy. Cutis1985;36:417-9.

21. Kato H, Uyeki Y, Kitajama Y, et al. A case of dermatomyositis and Hashimotosthyroiditis. J Dermatol 1988;15:273-5.

22. Goh KL, Wang F. Thyroid disorders in systemic lupus erythematosus. Ann Rheum

Dis 1986;45:579-83.23. Nicholson D, White S, Lipson A, et al. Progressive systemic sclerosis and Graves

disease: report of three cases. Arch Intern Med 1986;146:2350-2.24. Boyce S, Harper J. Paraneoplastic dermatoses. Dermatol Clin. 2002; 20: 523-532.


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References

25. Cohen PR, Kurzrock R. Mucocutaneous paraneoplastic syndromes. Semin Oncol 1997;24:334-59.26. Sheperd M, Raimer S, Tyring SK, Smith E. Treatment of necrolytic migratory erythema inglucagonoma syndrome. J Am Acad Dermatol 1991;25:925-8.

27. Thompson NW, Eckhausser FE. Malignant islet cell tumors of the pancreas. World J Surg1984;30:324-9.

28. Schwartz RA. Sign of Leser-Trelat. J Am Acad Dermatol 1996;35:88-95.29. Holdiness MR. The sign of Leser-Trelat. Int J Dermatol 1986;25:564-72.30. Safai B, Grant J, Good R. Cutaneous manifestation of internal malignancies (II): The sing of

Leser-Trelat. Int J Dermatol 1978;17:494-5.31. Ellis DL, Yates RA. Sign of Leser-Trelat. Clin Dermatol 1993;11:141-8.32. Hovenden AL. Acquired hypertrichosis lanuginosa associated with malignancy. Arch Intern Med

1987;147:2013-8.33. Sindhuphak W. Vibhagool A. Acquired hypertrichosis lanuginosa. Int J Dermatol 1982;21:599-

601.34. Bolognia J. Bazexs syndrome: acrokeratosis paraneoplastica. Semin Dermatol 1995;14:84-9.35. Gross G, Pfister H, Hellenthal B, et al. Acanthosis nigricans mailgna: clinical and virological

investigations. Dermatologica 1984:168:265-72.36. Cox NH, Lawrence CM, Langtry JA, Ive FA. Dermatomyositis disease associations and an

evaluation of screening investigations for malignancy. Arch Dermatol 1990;126:61-5.

37. Nicolis GD, Helwig EB. Exfoliative dermatitis. Arch Dermatol 1973;108:788-97.38. Abrahams I, McCarthy JT, Sanders SL. 101 Cases of exfoliative dermatitis. Arch Dermatol

1963;87:96-101.39. Pal S, Haroon TS. Erythroderma: a clinicoetiologic study of 90 cases. Int J Dermatol

1998;37:104-7.


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References

Photo references: www.dermatlas.org

www.dermis.net

www.emedicine.com Habif. Clinical Dermatology, 4thed. Mosby Inc:

2004.
http://www.dermatlas.org/http://www.dermis.net/http://www.emedicine.com/http://www.emedicine.com/http://www.dermis.net/http://www.dermatlas.org/

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