Skin Findings In Sick Patients

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Contact or photocontact allergy is most likely due to...

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Oxybenzone
Isopropyl debenzoylmethane

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Risk of Actinic Keratoses in sunscreen vs. nonsunscreen appliers

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no sunscreen = increase by 1 AK per subject
sunscreen = decreased by 0.6 AK per subject

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Does solar protection protect you from skin cancer?

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Nonmelanoma skin cancer is prevented...
Melanoma may not be prevented by solar protection b/c it is multifactorial

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The mean protection values (MPF) for hat covered sites was as follows:

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Forehead 6
Nose 3
Cheek 2

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Purpura

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non-blanchable erythema caused by extravasation of erythrocytes into the dermis

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Non-inflammatory purpura

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nonpalpable
causes: quantitative platelet defects (e.g. chemotherapy, idiopathic thrombocytopenic purpura, etc.), qualitative platelet defects (e.g. aspirin therapy), or reduced connective tissue support (e.g. solar purpura, corticosteroid therapy, Ehlers Danlos syndrome)

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Inflammatory Pupura

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Vasculitis

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Systemic Lupus Erythematosus
Definition (ARA criteria)

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Four or more criteria required:
1. Malar rash
2. Discoid lupus
3. Photosensitivity
4. Oral ulcers
5. Arthritis
6. Proteinuria > 0.5 g/day, or cellular casts
7. Seizures or psychosis
8. Pleuritis or pericarditis
9. Hemolytic anemia or leukopenia or lymphopenia or thrombocytopenia
10. Antibody to DNA or Sm antigen or the presence of LE cells or a biologically false positive VDRL
11. Positive FANA

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Systemic Lupus Erythematosus
Etiology

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Immune complex role in pathogenesis of many systemic and cutaneous (i.e. vasculitis) manifestations is well studied. UV light - DNA produced in epidermis - Possible cytotoxic T-cell effect on the epidermis. Genetic factors including complement deficient families. Drug induced LE especially hydralazine and procainamide, INH, dilantin, penicillamine. Sun exposure is a provoker.

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Systemic Lupus Erythematosus
Incidence

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27.5/million for white females, 75.4/million for black females. F:M=8:1 (peak at third decade).
Higher male percentage in children and elderly.

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Systemic Lupus Erythematosus
Clinical Features - Skin

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Skin - Butterfly erythema - heals without scarring, more persistent than sunburn. Common presenting manifestation of SLE.
Poikiloderma - hyper and hypopigmentation, telangiectasia, and epidermal atrophy
Maculopapular rash - may be purpuric, but can be identical to “drug rash”

Discoid lesions

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Systemic Lupus Erythematosus
Clinical Features - Hair

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Alopecia - diffuse, bifrontal or scarring; Periungual telangiectasia; vasculitis lesions - palpable purpura, ulcers, gangrene; palmar erythema, livedo reticularis, rare bullous lesions, Raynaud’s phenomenon, urticaria, oral ulceration and nasal septal ulcerations, erythema multiforme, panniculitis lupus profundus

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Systemic Lupus Erythematosus
Treatment

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Assess all systems involved. Systemic corticosteroids. Azathioprine (Imuran) or cyclophosphamide (Cytoxan) may have steroid sparing effects. Antimalarials (see DLE above) benefit skin and joints, but do not help vasculitis. Non steroidal anti-inflammatory agents.

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Systemic Lupus Erythematosus
Prognosis

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five year survival approaching 95% in some trials. Five year survival in early days of corticosteroids was only 70%.

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Progressive Systemic Sclerosis

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Scleroderma

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Scleroderma
Etiology

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Unknown
1) Primary vascular disorder
2) abnormality of connective tissue formation
3) autoimmune disease

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Scleroderma
Incidence

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F:M= 3:1, 2.7 new patients per 1 million population. Onset often 30-50 years of age

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Scleroderma
Clinical Features

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Skin involvement almost always present. High incidence of Raynaud’s phenomenon. Characteristic facies with shiny bound skin on forehead, pinched nose, mouth with constricting radial furrows. Telangiectatic mats. Sclerodactyly of hands. Calcinosis of fingers, elbows. Periungual telangiectasia, “Salt and Pepper” hypo and hyperpigmentation

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Scleroderma
Laboratory CREST Patients

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anticentromere antibody

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CREST

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calcinosis, Raynaud’s, esophageal dysmotility, sclerodactyly and telangiectasia - less fulminant course often than rapidly progressive, truncal patten.

clinical feature of Scleroderma

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Scleroderma
Esophagus

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dysmotility leads to reflux and stricture; also intestinal involvement

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Scleroderma
Lung

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restrictive disease and impaired diffusion capacity

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Scleroderma
Cardiac

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pericarditis, arrhythmias

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Scleroderma
Renal

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malignant hypertension

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Scleroderma
Therapy

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No specific treatment. Emollients to skin. Physical therapy to prevent disuss atrophy. Minipress 1 mg b.i.d. orally (or Nifedipine or Captopril) for Raynaud’s. Penicillamine under investigation.

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Scleroderma
Prognosis

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Death can occur usually from cardiac or renal disease

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Sarcoidosis

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A multisystem granulomatous disease with prominent cutaneous features including lesion characterized by dermal granulomas. The dermatologist can confirm the diagnosis by skin biopsy.

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Rheumatoid Nodules

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These dermal nodules often occur over pressure sites and correlate with more severe, erosive rheumatoid arthritis

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Necrobiosis Lipoidica Dibeticorum

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These yellowish plaques classically occur on the lower extremities in diabetics. They may ulcerate. Recognition and histologic confirmation of this diagnosis by the dermatologist may occur in patients with previously unsuspected diabetes mellitus.

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Xanthomas

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Xanthelasmas, tuberous and tendinous xanthomas are associated with deposition of cholesterol in the dermis. They may be a marker for Type II or other cholesterol related hyperlipemias and increased risk for cardiovascular disease. Eruptive xanthomas occur due to triglyceride deposition. They occur in types I, IV and V hyperlipidermisas especially in diabetic patients.

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Pretibial myxedema

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These plaques which usually occur on the skin are associated with hyperthyroidism. The dermatologist can confirm their clinical suspicion histologically. This condition may be induced by long acting thyroid stimulator (LATS).

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Porphyria Cutanea Tarda

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This disease is characterized by hypertrichosis on the face and by bullae in a photodistribution. It occurs due to uroporphyrinogen decarboxylase deficiency. Alcohol induced liver disease the most common precipitant. The ringed molecules (uro and copro porphyrinogen) which cause the photosensitivity are detectable in the urine.

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Pyoderma Gangrenosum

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This condition is characterized by rapidly progressive cutaneous ulcers with typical undermined borders. Vasculitis, granulomatous infection and squamous carcinoma must be excluded histologically and by culture before this diagnosis can be made. Inflammatory bowel disease, chronic active hepatitis, leukemia and erosive arthritis have been associated with pyoderma grangrenosum.

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Dermatomyositis

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Patients with this collagen vascular disease have a myositis with proximal extensor muscle weakness and a characteristic cutaneous eruption. The heliotrope sign (periorbital violaceous poikiloderma - see lupus) and Gottron’s sign (poikilodermatous papules or plaques over the extensors) are typical. Up to 25-30% of adults with dermatomyositis have an associated malignancy

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Acanthosis Nigricans

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This distinctive velvety, hyperpigmented thickening occurs classically in the axillae and flexures. It may be a marker for occult malignancy or for insulin resistance.
Insulin - like growth factors may account for the epidermal proliferation in the second setting and tumor associated similar factors in the first setting.

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Neurofibromatosus

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This is a not uncommon dominantly inherited genodermatosus. Cafe-au-lait macules and cutaneous neurofibromas are diagnostic. The dermatologist can confirm the diagnosis histologically.

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Tuberous Sclerosis

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This autosomal dominant disorder is also characterized by numerous cutaneous markers. These include angiofibromas which present as the classic adenoma sebaceum, and periungual fibromas. The chagrin patch is actually a connective tissue hamartoma which occurs on the back. The ash leaf macules are areas of hypopigmentation which may be the first sign of the disease detectable by the dermatologist.

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Process of Cutaneous Small Vessel Vasculitis

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1. Endothelial cell retraction my occur by effects of vasoactive amines (eg. histamines).
2. CIC may lodge in vessel walls after the above.
3. Complement is activated after the above step.
4. Complement component C5a is a potent chemotactic agent for neutrophils.
5. Neutrophils not only phagocytize CIC, but they release potent hydrolytic enzymes that damage blood vessel walls.
6. Role for adhesion molecules – active participation of blood vessel endothelial cells.

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What do you do when you see a small vessel vasculitis?

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-confirm clinical diagnosis histopathologically (b/c the pathologist report is good for general practitioners)
-assess extent of disease (b/c drugs have risk/benefit ratio)
-attempt to establish etiology (treat cause instead of symptoms)

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Where can immune complexes deposit?

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(at good filters)
synovium
CNS and PNS
GI Tract
Kidney
Pleura
Pericardium
Retina
Adrenal Gland

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sclera

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thickening

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What is the dermis filled with in scleroderma?

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Collagen (which is produced by fibroblasts)

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Raynaud phenomenon

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A circulatory disorder in which the hands, and less commonly the feet, are persistently cold and blue

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Percentage of People with SLE that present with Discoid lesions

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20%