EXANTHEMIC DRUG ERUPTIONS

The epidermis has necrotic keratinocytes at all levels of the epidermis and a minimal dermal inflammatory infiltrate. The eosinophils suggest the drug induced etiology.   Differential Diagnosis.: Viral exanthema , TEN , EM and fixed drug eruption.

ERYTHEMA MULTIFORME there is a mild lichenoid infiltrate with dyskeratotic keratinocytes Exocytosis of lymphocytes is present  Dermal inflammatory infiltrate containing eosinophils and keratinocyte necrosis would suggest a drug mediated process

TOXIC EPIDERMAL NECROLYSIS AND STEVENS-JOHNSON SYNDROME

There is extensive dyskeratosis of the epidermis with early blister formation. A mild perivascular lymphocytic infiltrate is seen in the superficial dermis Display keratinocyte necrosis and inflammatory infiltrate

LICHENOID DRUG ERUPTION Histopathology : Histologically it is similar with LP , EM & TEN

FIXED DRUG ERUPTION Similar to EM and TEN Characteristic lichenoid lymphocytic infiltrate and abundant pigment incontinence with scattered melanophages. In addition, basal vacuolar alteration and dyskeratotic cells occur in the epidermis.

FIGURE 11-6. Fixed drug eruption FIGURE 11-6.Fixed drug eruption. This section shows the characteristic lichenoid lymphocytic infiltrate and abundant pigment incontinence with scattered melanophages. In addition, basal vacuolar alteration and dyskeratotic cells occur in the epidermis.

ACUTE GENERALIZED EXANTHEMATOUS PUSTULOSIS have subcorneal or intraepidermal pustules, papillary dermal edema, lymphohistiocyticj perivascular infiltrate with some eosinophils and neutrophils Differential diagnosis: pustularpsoriasis subcornealpustulardermatos

FIGURE 11-8. Acute generalized exanthematouspustulosis FIGURE 11-8. Acute generalized exanthematouspustulosis. Diffuse spongiosis and a mild upper dermal perivascular inflammatory infiltrate are seen in this case caused by amoxicillin.

vacuolar degeneration of basilar keratinocytes with cleft formation. TOXIC ACRAL ERYTHEMA (Hand-foot syndrome, palmar-plantar erythrodysethesia syndrome,) vacuolar degeneration of basilar keratinocytes with cleft formation. Mild epidermal dysmaturation may be seen.   Keratinocyte necrosis is also present in the lower third of the epidermis. In the dermis, there is a mild perivascular infiltrate of lymphocytes with few eosinophils.

DRUG-INDUCED SCLERODERMA-LIKE CONDITIONS   fibrosis of the dermis and subcutis, adnexal structure entrapment, mild vascular dilation with minimal to no inflammatory infiltrate.

NEPHROGENIC SYSTEMIC FIBROSIs mild to moderate increased fibrous cellularity in the mid to deep reticular dermis. Increased collagen and dermal mucin are also characteristically seen. The cellularity and collagen deposition may extend along the subcutaneous septa and fascia.

Nephrogenic systemic fibrosis Nephrogenic systemic fibrosis. The deep dermis shows increased cellularity composed of activated fibroblasts with stellate morphology and occasional multinucleation. Increased collagen and dermal mucin are also present.

BULLAE AND SWEAT GLAND NECROSIS IN DRUG-INDUCED COMA The epidermis shows varying degrees of necrosis. In areas of complete necrosis of the epidermis, the bullae arise subepidermally

Drug-induced coma bulla Drug-induced coma bulla. There is extensive necrosis of the epidermis with subepidermal blister formation. Inflammation in the blister cavity is secondary to adjacent ulceration. The dermis shows only a mild inflammatory infiltrate.  

DRUG-INDUCED BULLOUS DISORDERS   a picture identical to that seen in pemphigus vulgaris and/or pemphigus foliaceus. The autoantibody response to desmoglein 1 and desmoglein3 is similar in both

DRUG-INDUCED LUPUS ERYTHEMATOSUS

DRUG-INDUCED LUPUS ERYTHEMATOSUS same as in lupus erythematosus Pathogenesis:genetic predisposition, in particular, HLA-DR4, has a role in drug-induced lupus. ANA is positive

Photoallergic Drug Eruption Similar to allergic contact dermatitis and includes spongiosis, mild acanthosis, and a superficial perivascular lymphocytic infiltrate with eosinophilis

Photoallergic dermatitis Photoallergic dermatitis. There is spongiosis with microvesicle formation, exocytosis of lymphocytes, and a perivascular lymphocytic infiltrate admixed with scattered eosinophils.

Phototoxic Drug Eruption like a sunburn reaction, shows vacuolated keratinocytes, and apoptotic keratinocytes

Dermal edema and enlargement of endothelial cells

PHOTODISTRIBUTED HYPERPIGMENTATION  There is variable amount of melanin in the basal layer of the epidermis. Accumulation of pigment-laden macrophages in dermis . Fontana-Masson silver stain is positive

Chlorpromazine pigmentation Chlorpromazine pigmentation. Perivascular pigmentladen macrophages are seen in this case of chlorpromazine pigmentation.

DRUG-INDUCED PSEUDOLYMPHOMA SYNDROME similar to MF(also known as psudo MF). In cutaneous nodules, large masses of atypical lymphocytes are present in the dermis.

Cutaneous pseudolymphoma Cutaneous pseudolymphoma. There is a dense inflammatory infiltrate with exocytosis of atypical-appearing lymphocytes and absence of spongiosis in this Dilantin-induced pseudolymphoma.

CUTANEOUS REACTIONS TO ANTINEOPLASTIC CHEMOTHERAPEUTIC DRUGS

CUTANEOUS REACTIONS TO ANTINEOPLASTIC CHEMOTHERAPEUTIC DRUGS Epidermal dysmaturation, may develop in epidermis after chemotherapeutic administration. Accompanied by upper dermal melanophage Neutrophili ceccrine hidradenitis consists of variable infiltration of the eccrine coil by neutrophils and lymphocytes with necrosis of secretory epithelium.

Severe epidermal dysmaturation due to antineoplasticchemotherapy Severe epidermal dysmaturation due to antineoplasticchemotherapy. Loss of polarity and disorganization of keratinocytesare specimen

CUTANEOUS ERUPTIONS RESULTING FROM ADMINISTRATION OF HUMANRE COMBINANT PROTEINS The upper dermis contains a perivascular and interstitial infiltrate of neutrophils, eosinophils, and lymphocytes. The epidermis may display intercellular edema with exocytosis of inflammatory cells. Vasculitis is absent.

A diffuse perivascular and interstitial inflammatory cell infiltrate is present with associated vascular dilation and spongiosis.

MINOCYCLINE PIGMENTATION increased melanization of the basal cell layer and melanin within macrophages in the upper dermis.

Minocycline hyperpigmentation Minocycline hyperpigmentation. Pigment is presentin dermal melanophages and dendritic cells

CLOFAZIMINE-INDUCED PIGMENTATION The upper dermis contains numerous foamy macrophages that possess cytoplasm with brown granular pigment.

Penicillamine-Induced Atrophy of the Skin The anetoderma shows diminution or absence of elastic tissue and the areas of easy bruising of the skin.

HALOGEN ERUPTIONS

Bromoderma. There is downward proliferation of the epidermis with a large intraepidermal abscess. A dense inflammatory infiltrate is present in the dermis.

HALOGEN ERUPTIONS bromoderma and iododerma shows a dense infiltrate of neutrophils, which, in areas of dermal necrosis, show nuclear dust. There may be intradermal abscesses. Eosinophils are present in most cases and may be numerous

ARGYRIA In the dermis, there are extracellular fine,small, round, uniformly sized brown-black silver granules. They are present in the greatest numbers in the basement membrane zone surrounding the sweat glands and dermal papillae In addition to silver, there is an increase in the amount of epidermal melanin

Argyria. Silver granules are present in the basement membrane surrounding the sweat glands

CHRYSIASIS Gold granules are found predominantly within cells, particularly within endothelial cells and macrophages. However, extracellular granules may also be observe

MERCURY PIGMENTATION Irregular, brown-black granules are found in the upper dermis, both extracellularly and within macrophages. Traumatic implantation of mercury results in variably sized, often large amorphous deposits of mercury in the dermis and subcutis Chronic changes include dermal fibrosis and granulomatous inflammation.