1. Part II: Contact Dermatitis & Drug Eruptions
Andrew’s Chapter 6, pg 123
Bolognia Chapter 23
Michael Hohnadel, D.O.

2. Drug Reactions
Generally a low rate of adverse reactions - 1/1000 exposures.
Higher rate for commonly used meds – PCN and TMP: 30-50/1000.
Presence of HIV disease or EBV infection increases rate
One of the most common reasons pts visit dermatologist

3. Patient Evaluation Three rules:
1.) Stop all unnecessary meds
2.) Ask about nonprescription meds and meds delivered by other means: suppositories, eye drops, implants, patches, etc
3.) No matter how atypical the presentation always consider pts meds as a possible cause
Diagnose cutaneous eruption by clinical pattern(ie urticaria, exanthem, vasculitis, erythema multiforme, etc)
Ask two questions:
1.) Which med can cause this pattern of rxn?
2.) How commonly does this med cause this rxn pattern?

4. Additional testing ?
Skin testing is most useful in evaluating type I (immediate) hypersensitivity
Most frequently used in evaluating adverse rxn’s to penicillin, local anesthetics, insulin, and vaccines
Radioallergosorbent (RAST) tests have 20% false-negative rate in penicillin type I allergy and therefore RAST must be followed by skin testing
RAST test cannot replace skin testing

5. Pathogenesis In most patterns pathogenesis is UNKOWN!! Types:
Immunologic - Response by the pt to the drug or its metabolite
Nonimmunologic - may result from normal pharmacologic effects of drug (urticaria worsening from aspirin ingestion)
Likelihood may be determined by metabolism:
Anticonvulsant and sulfonamide rxn’s, the P-450 system of individuals generates toxic metabolites of the med that binds to proteins and stimulates an immunologic rxn
This defect can be found in family members (HLA subtypes)
Immune status and clinical condition may be a factor.
AIDS pts may be related to glutathione deficiency.

6. Pathogenesis

7. Exanthems Most common form of adverse cutaneous eruption
Characterized by erythema, often with papules throughout. Lesions first appear proximally - especially groin and axilla, generalizing within 1-2 days
Pruritus is usually prominent and is a distinguishing factor from a viral exanthem
Tend to occur within the first two weeks of tx.
but may occur later, even up to 10 days after tx
Most common cause: Antibiotics, especially semi-synthetic penicillin & sulfamethoxazole/trimethoprim
Ampicillin given during infectious mononucleosis and Bactrim given to AIDS pts cause exanthems in a large # of pts treated.

8. Exanthems
Secondary to Phenobarbitol

9. Treatment Simple exanthems - supportive tx Complex exanthems
Eruption may resolve even if offending med is continued
Topical steroidal medications and antihistamines may allow course of tx to be completed.
Rechallenge may or may not result in reappearance of eruption
In HIV infection and rarely, in persons with normal immune status rechallenge may result in a more severe blistering rxn
Complex exanthems
These present with fever, rash, and variably , with eosinophilia, lymphadenopathy, hepatitis, nephritis, and rarely heart, lung & brain
Hypersensitivity syndromes are seen mostly with: anticonvulsants, and long-acting sulfonamides; less commonly with allopurinol, gold, dapsone, and sorbinil.

10. Anticonvulsant Hypersensitivity Syndrome
Assoc. with: diphenylhydantoin, phenobarbital, carbamazepine, and other anticonvulsants.
1 of 5000 pts tx with these meds.
Presentation:
Initially morbilliform, but may have various morphologies including eczema, bullae, SJS like sloughing.
Syndrome begins with fever between 2 and 6 weeks after agent is started.
Eruption begins with prominent facial swelling.
Other: pharyngitis, lymphadenopathy (75%), hepatosplenomegaly.
Widespread pinpoint pustules may develop esp in dark skinned individuals.
Lab: eosinophilia, atypical lymphocytosis, elevated liver function tests (51%), and occasionally nephritis
Can lead to death from hepatitis

11. Anticonvulsant Hypersensitivity Syndrome
Pathogenesis
Inability to detoxify arene oxide metabolites of these meds
Metabolites bind to proteins and elicit an immune response leading to an adverse drug rxn
Cross rxn with different anticonvulsants are common (because meds are metabolized by same pathway)
Management
Ruling other infectious etiologies
Discontinue offending med
Supportive tx. If liver or renal involvement or if pt is ill then hospitalization, systemic steroids may be used

12. Sulfonamide Hypersensitivity Syndrome
Clinical syndrome similar to anticonvulsants.
Pts develop severe bullous rxn like Stevens-Johnson syndrome or TEN.
Pts are almost always slow acetylators who produce toxic hydroxylamine metabolites during metabolism of the sulfonamide.

13. Allopurinol Hypersensitivity Syndrome
Presentation: Weeks to months (average 7 wks) after allopurinol is begun, a morbilliform eruption (50%) that often evolves to an exfoliative erythroderma(20%)
Typically occurs in pts with preexisting renal failure, whose dose is not adjusted for their renal function
Bullous eruptions including TEN’s may occur(25%).
Asociated: fever, eosinophilia, sometimes hepatitis, and typically worsening renal failure
Course and Treatment:
Syndrome may be steroid responsive, but is slow to resolve and frequently lasts months after allopurinol has been stopped
25% of pts die as a consequence
Dialysis does not accelerate resolution of this syndrome

14. Allopurinol Hypersensitivity Syndrome
Exfoliative dermatitis caused by allopurinol

15. Drug-Induced Pseudolymphoma
Exposure to a medication results in cutaneous inflammatory infiltrates that resemble lymphoma such as MF. Rare reaction.
Diagnosis:
Consistent with lymphoma with atypical lympocytes.
Lymphadenopathy and circulating Sezary cells may also be present
Gene rearrangement may be positive!!
Usually, keratinocyte necrosis and dermal edema help make pseudolymphoma dx.
Resolves with discontinuation of the med.
Primary meds responsible: anticonvulsants, sulfa drugs, dapsone, and antidepressants

16. Urticaria
Meds may induce urticaria by immunologic and nonimmunologic mechanisms.
Presentation: Wheals or angioedema. My be part of a more severe anaphylactic rxn with bronchospasm, laryngospasm, or hypotension
Types:
Nonimmunologic
Aspirin and NSADS are the most common cause.
They alter prostaglandin metabolism, enhancing degranulation of mast cells.
Other agents: radiocontrast, opiates, tubocurarine, polymyxin-B.
Pretest with RAST may be helpful but will not exclude possiblity of rxn (esp with radiocontrast agents.)

17. Urticaria Immunologic
Most commonly associated with penicillin and related beta-lactam antibiotics
It is associated with IgE antibodies to penicillin or its metabolite
Skin testing is useful in evaluating pts with a history of urticaria associated with penicillin exposure.
Pt may be given a desensitization protocol.
Pts with PCN allergy have an increased rate of rxn to cephalosporins.
Third-generation cephalosporins are much less likely to induce a rxn in a pcn allergic pt than the first- or second generation ones
May not be as cross reactive as is commonly believed.

18. Urticaria
Urticaria 2nd to PCN

19. Angioedema
Known complication of the use of ACE inhibitors. Blacks 5x > Whites.
ACE inhibitors are a common cause of accuired Angioedema. (Lisinopril and enalapril > captopril).
Effect is dose dependent and may resolve with decreased dose.
ACE users with one episode of angioedema have a 10x risk of a second episode which may be more severe.
Angioedema may represent a consequence of a normal pharmacological effect of the ACE inhibitors
Blocking of kininase II by ACE inhibitors may increase tissue kinin levels, enhancing urticarial rxn’s and angioedema
Episodes may require hospitalization 45% of the time, ICU 27% of the time, and intubation 18% of the time.

20. Angioedema
Deep, poorly defined swelling

21. Angioedema

22. Photosensivity Reactions
Meds may cause phototoxic, photoallergic, lichenoid and pseudoporphyria like reactions.
Most drug-induced photosensitivity is triggered by radiation in the UVA range (spectrum and depth)
Most common drugs: NSAIDs, sulfamethoxazole/trimethoprin, thiazide diuretics and related sulfonylureas, quinine and quinidine, and certain tetracyclines.
Phototoxic vs Photoallergic:
Phototoxic reactions: (sunburn)
Related to dose of both med and UV irradiation
Does not require prior exposure or participation by the immune system
Rxn’s can appear from hrs to days after to exposure
Tetracyclines(especially demeclocyline), amiodarone, and the NSAIDs are common culprits
TX: May include dose reduction and photoprotection

23. Photosensivity Reactions
Photoallergic reactions
Typically eczematous, pruritic, and occur after some period of drug exposure.
They involve the immune system, and are confirmed by positive photopatch testing
In general, they are not as drug dose dependent as phototoxic reactions
Examples:
Amiodarone photosensitivity develops in 75% of tx pts, and occurs after a cumulative dose of 40g.
NSAIDs, especially piroxicam
Characteristic rxn is a vesicular eruption of dorsa of hands, sometimes associated with dyshidrosiform pattern on the lateral aspects of hands and fingers
May be related to thimersol exposure earlier in life.

24. Photo Reactions Phototoxic reaction to MTX .
Phototoxic reaction from TCN

25. Pseudoporphyria
Presentation: Photodistributed bullous rxn which clinically and histologically resembles PCT.
Not Seen: Hypertrichosis, skin fragility, dyspigmentation, and sclerodermoid changes. Porphyrin studies are normal.
Naproxen is most commonly reported cause
Resolves when the drug is discontinued.

26. Anticoagulant-Induced Skin Necrosis
Most common Patient: Obese, postmenopausal women are predisposed secondary to the fact that lesions tend to occur in areas with abundant subcutaneous fat (breast, abdomen, or buttocks)
Warfarin necrosis: 3 –5 days after therapy is begun, red, painful plaques develop that become necrotic.
The higher the initial dose, the higher the risk.
Cause: Hereditary or acquired deficiency of antithrombotic agents protein C and less commonly protein S. Temporary hypercoagulable state.
TX: Stop warfarin, admin: vit K and Protein C
Heparin necrosis: Local and widespread reactions
6-12 days after injection - tender red plaques that undergo necrosis.
Any type heparin may cause.
Heparin antibody causing platelet coagulability is often found.
May result in widespread thrombosis.

27. Warfarin Necrosis
Pt underwent knee surgery and was placed on low dose warfarin afterwards.

28. Heparin Necrosis.
Heparin induced necrosis, note ischemia.

29. Vitamin K Reactions
Presentation: 1-2 weeks after injection of vitamin-K, pruritic, deep seated, red plaques involving the dermis and subcutaneous tissue develop at the site of injection.
Commonly located on posterior arm and over hip or buttocks. Lesions on hip tend to progress around the waist and down thigh, forming a “cowboy gun belt & holster” pattern.
Most affected pts have liver disease & are being tx for elevated PTT’s

30. Allergic reaction at site of vitamin K injections

31. Injection Site Reactions
IM injection may produce a syndrome called- Embolia Cutis Medicamentosa (Nicolau syndrome)
Immediately after injection there is a local intense pain, and ischemic palor
Within mins-hrs site develops an erythematous macule that evolves into a livedoid violaceous patch with dendrites.
This becomes hemorrhagic, then ulcerates, and eventually heals with an atrophic scar
Etiology: Peri-arterial injection with thrombosis
Muscle and liver enzymes may be elevated and neurologic symptoms and sequela occur 1/3 of pts.
Uncommonly, amputation may be needed
Treatment: Conservative-dressing changes, debridement, bed rest, and pain control. Rarely surgical intervention is needed

32. Injection Site Reactions
Cutaneous reaction to IV infusion and extravasation of chemotherapeutic agent

33. Acute Generalized Exanthematous Pustulosis
Frequency: Not uncommon. 90% of time is related to medication
Eruption occurs around 5 days after med is started (50% occur within 24 hrs)
Presentation: A scarlatiniform erythema rapidly develops into > 100 non-follicular pustules less than 5 mm in diameter. Widespread desquamation occurs after a few days
Edema of face, purpura, and target lesions may appear in the background
Mucous membranes are involved in 22%
Fever is universal
Neutrophilia in 90%, and eosinophilia in 30%. Normal Liver funct.
Causes: Mercury is sole cause in 13% of cases in France, beta-lactams in 44%, and macrolides in 17%. Sulfonamides have NOT been reported to cause this rxn. 17% of pts have a history of psoriasis

34. Acute Generalized Exanthematous Pustulosis
Treatment: Once inciting agent is discontinued, eruption usually resolves within 15 days without sequelae
Patch testing with the suspected agent may reproduce a pustular eruption on an erythematous base at 48 hrs
Histology:
Early lesions show marked papillary edema, neutrophil clusters in dermal papillae, and perivascular eosinophils
Well developed lesions show intraepidermal or subcorneal spongiform pustules
May be an associated leukocytoclastic vasculitis
Presence of eosinophils, and marked papillary edema help to distinguish this eruption from pustular psoriasis

35. Putules on Skin Acute Generalized Exanthematous Pustulosis
Histology: Pustules with neuts and edema.

36. Drug-Induced Pigmentation
Etiology: Post inflammatory hyperpigmentation or actual deposition of drug in skin.
Minocycline causes three types of pigmentation:
Blue-black discoloration in areas of prior inflammation(not related to total or daily dose exposure)
Appearance of a similar colored pigmentation on normal skin of anterior shims (is dose dependent)
Least common - Generalized, muddy brown hyperpigmentation.
Chloroquine, hydroxychloroquine, and quinacrine all may cause a blue-black pigmentation of face, extremities,ear cartilage, oral mucosa, and nails
Pretibial hyperpigmentation is most common
Amiodarone after 3-6 months causes photosensitivity in 30-57% of pts.
1-10% of pts a slate-gray hyperpigmentation develops in areas of photosensitivity
Pigmentation fades after med is discontinued

37. Minocycline
Amiodarone pigmmentation

38. Drug-Induced Pigmentation
Clofazimine may cause a pink discoloration that gradually becomes reddish blue or brown. (esp in Hansen’s disease)
Major cause of noncompliance.
Zidovudine causes a blue or brown hyperpigmentation most frequently in nails
Lunula may be blue, or whole nail plate may be dark brown
Diffuse hyperpigmentation of skin, pigmentation lateral tongue, and increased tanning are less common
Occurs in darkly pigmented pts, is dose dependent, clears after med discontinued
Chlorpromazine, thioridazine, imipramine, and clomipramine may cause a slate-gray hyperpigmentation in sun-exposed areas after long periods of ingestion
Frequently, corneal and lens opacities are present
Therefore all pts with hyperpigmentation from these meds should have ophthalmologic exam

39. Drug-Induced Pigmentation
Purple pigmentation in patient who had been on high doses of chlorpromazine
There is sparing of deep creases of the face

40. Drug-Induced Pigmentation
Heavy metals gold, silver, and bismuth produce blue to slate-gray hyperpigmentation.
Pigmentation occurs after yrs of exposure, mainly in sun-exposed areas. It is permanent.
Bismuth also pigments gingival margin.
Arsenical melanosis is characterized by black,
generalized pigmentation or by pronounced truncal hyperpigmentation that spares the face.

41. Fixed Drug Reactions Common
Present anywhere on body (50% occur on oral and genital mucosa)
Represent 2% of all genital ulcers evaluated at clinics for STD’s
Presentation:
Six or less lesions occur, typically one.
Clinically begin as a red patch that soon evolves to an iris or target lesion identical to EM.
Eventually may blister and erode.
Lesions of oral mucosa and genitalia usually present as erosions.
Postinflammatory hyperpigmentation results.

42. Fixed Drug Eruption
Causes: NSAIDs, especially pyrazolone derivatives, naproxen, mefenamic acid; sulfonamides, trimethoprim, or combinations are common.
Barbiturates, tetracyclines, phenolphthalein(in laxatives), and erythromycin
Unknown pathogenesis
Variant: Nonpigmented fixed drug eruption
It is characterized by large, tender, often symmetrical erythematous plaques that resolve completely within weeks, only to recur on re-ingestion of offending drug
Pseudoephedrine by far most common.
Baboon syndrome !!

43. Fixed Drug Eruptions Phenophthalein - A naproxen - B ,
Ciprofloxin - C ,
TMP/sulfamethoxazole - D

44. Bullous Drug Reactions
Uncommon:
per million person years for TEN
1.2 to 6.0 per million person years for Stevens-Johnson syndrome.
Definition:
SJS < 10% of body surface area involved
10-30% are overlap cases
>30 % TEN
Likely a disease spectrum.

45. SJS v. TEN
Systemic symptoms, amount of epidermal involvement and confluence are key factors.

46. SJS &TEN
Causes:
Greater then 100 meds have been reported as a cause.
Most common: TMP/sulfamethoxazole(1-3/100,000) Fansidar-R, sulfadoxine with pyrimethamine (10/100,000), carbamazepine(14/100,000).
Antibiotics (especially long-acting sulfa drugs and penicillins).
Other: anticonvulsants, anti-inflammatory and allopurinol are also causes.
Mechanism: FAS – FAS ligand up-regulation and activation ?

47. Proposed TEN Mechanism and Rational for IVIG Treatment

48. Histology of TENS Late Early
A lymphocytic infiltrate at the D-E junction
Necrosis of keratinocytes that may be full thickness
Infiltrate may be marked or very scant

49. SJS &TEN Presentation:
Fever and influenza-like symptoms often precede the eruption.
Skin lesions appear on face and trunk and spread rapidly (within 4 days) to their maximum extent
Initial lesions are macular and are followed by desquamation. May also form atypical targets with purpuric centers that coalesce, form bullae, then slough.
Two or more mucosal surfaces are also eroded with oral and conjunctiva being most frequently affected.
Difficulty with swallowing, photophobia, painful urination, and extensive respiratory and alimentary tract involvement.
Workup:
Skin bx usually performed to exclude other diseases
DDX: Paraneoplastic pemphigus (excluded with DIF). Graft-versus host disease (hx) and SSSS ( superficial blister).

50. SJS Skin and conjunctival Involvement

51. SJS
TENS

52. Management Similar to an extensive burn
Fluid and electrolyte imbalances, bacteremia from loss of protective skin barrier, hypercatabolism, and sometimes ARDS
Pts who are very ill or have > 30%- 50% loss of epidermis should be transferred to burn unit
IVIG in 10 pts in doses up to 0.75 g/kg/day for 4 days led to response in 48 hrs and skin healing within 1 week
No adverse rxn’s where observed
Blocking apoptosis through blockade of the death receptor FAS(CD 95)

53. Management Immunosuppressive TX (controversial)
Benefit of immunosuppressive TX is to stop the process very quickly to reduce the ultimate amount of skin lost
Once most of skin loss has occurred, immunosuppressive TX only adds to morbidity and perhaps mortality.
Immunosuppressive therapy it should be done quickly, in adequate doses, given a short trial to see if the process can be arrested, and then tapered.
In pts who survive, the average time for epidermal re-growth is 3 weeks
Most common sequelae are ocular scarring and vision loss

54. TEN
Three weeks of healing after receiving IVIG.

55. Radiation-Induced EM
Occurs if phenytoin is given prophylactically in neurosurgical pts who are receiving whole-brain radiation therapy and systemic steroids
Presentation: Erythema and edema initially on the head in the radiation ports, as a dose of steroids is being reduced. Eruption spreads caudad and mucosal involvement may occur
Evolves over 1-2 days to lesions clinically and histologically similar to EM
Can rarely be seen with radiation therapy alone.

56. Urticarial EM Virtually always associated with antibiotic ingestion
Presentation:
Skin lesions consist of urticarial papules and plaques, some of which clear centrally forming annular lesions,but no true iris lesions
Lesions can be distinguished from true urticaia in that they are fixed for days.
Pruritis is common
Bullae are absent, and mucous membranes are uninvolved
Histologically, there is a superficial and deep dermal infiltrate containing eosinophils with dermal edema. Epidermis is not involved
Treatment: Response to systemic steroids is dramatic, with clearing in hrs

57. HIV Disease and Drug Reactions
Those with helper T-cell counts between , are at increased risk for development of adverse rxn to meds.
Morbilliform rxn’s to Bactrim occurs in 45% of AIDS pts:
Associated hepatitis or neutropenia may require discontinuation of drug
Low-dose re-challenge / desensitization may be attempted. Works 50-80% of the time.
A similar increased risk is seen in HIV pts receiving Augmentin
Severe bullous rxn’s-SJS, TEN are times more common.

58. Adverse Reactions to Chemotherapeutic Agents

59. Radiation Enhancement & Recall Reactions
Radiation dermatitis: Erythema and vesiculation at ports.
“Radiation recall” May occur if chemo agents are administered up to a week or more after radiation therapy
A similar reactivation of a sunburn after methotrexate therapy.

60. Chemo-induced acral erythema
Common syndrome induced most frequently by 5-florouracil, doxorubicin, cystosine arabinoside (up to 40% of pts). Dose dependent.
May appear with bolus short-term infusions or low-dose, long-term infusions. May present days to months after treatments are started
Presentation:
Initially, dysesthesia or tingling of the palms and soles
This is followed by painful, symmetric erythema and edema most pronounced over the distal pads of the digits
May be accompanied by a morbilliform eruption
Erythema becomes dusky develops areas of pallor, blisters, desquamates, then reepithelializes
Etiology:
Likely a direct toxic effect of chemotherapeutic agents on the skin
Large number of sweat glands on the palms and soles that may concentrate the chemotherapeutic agent explaining the localization of the toxicity

61. Chemo-induced acral erythema
Histology: Nonspecific.
Treatment:
Pts usually recover without complications
Most cases require only local supportive care
Cold compresses and elevation are helpful; cooling of hands during tx may reduce severity of rxn
Modification of dose decreases the pain of fluorouracil induced syndrome

62. Neutrophilic Eccrine Hidradenitis
Occurs in neutropenic pts with malignancies, usually AML -most commonly associated with chemo, especially cytoarabine
Presentation: After 7-10 days of tx, the patient becomes febrile and erythematous papules, plaques or nodules appear, localized to trunk, extremities, axillae, or pubic area. May be generalized.
Histology: a neutrophilic infiltrate involving glandular and ductal portions of the eccrine gland
Treatment:
Bx performed to exclude infection, sweets syndrome.
Skin lesions resolve in 10 days, but in severe cases may be tx with corticosteroids

63. Neutrophilic Eccrine Hidradenitis

64. Chemotherapy-Induced Hyperpigmentation
Adriamycin causes marked hyperpigmentation of nails, skin and tongue
Most commonly seen in black pts
Cyclophosphamide causes transverse banding of nails or diffuse nail hyperpigmentation
Bleomycin and 5FU causes similar transverse bands
Busulfan and 5FU induce diffuse hyperpigmentation that may be photoaccentuated
Bleomycin induces characteristic flagellate erythematous urticarial wheals associated with pruritis within hrs - days of infusion
Fluorouracil causes a serpentine hyperpigmentation overlying veins of infusion.

65. A. - Ulceration due to extravasation of doxorubicin.
B - Horizontal melanonychia due to 5-fluorouracil.
C - Erythema of the ears due to the cytarabine (cytosine arabinoside), sometimes referred to as ‘Ara-C ears’; the petechiae are due to thrombocytopenia.
D - Erythrodysesthesia due to cytarabine with erythema of the plantar surface.
E - Necrosis of psoriatic plaques due to an ‘overdose’ of methotrexate.
F - Raynaud's phenomenon and digital necrosis due to systemic bleomycin.

66. Acrodynia
Caused by mercury poisoning, usually in infancy and has pathognomonic skin changes.
Presentation: Painful swelling of hands and feet. Hands & feet are dusky red, pink, cold & clammy Sometimes with pruritis. Erythema is usually blotchy but may be diffuse. Hemorrrhagic puncta are sometimes evident
Other signs:
On trunk, a blotchy macular or papular erythema is usually present
Stomatitis and loss of teeth may occur
Fever, irritability, photophobia, increased perspiration
Always moderate upper respiratory inflammation and sore throat
Albuminuria and hematuria are usually present
Diagnosis is made by finding mercury in the urine

67. Acrodynia
Stomatitis
Sweeling of feet.

68. Acrodynia Etiology: Treatment: Broken thermometers Teething powders
Poisoned fish
Broken phosphorescent bulbs
Treatment:
Chelating agents - Dimercaprol

69. Bromoderma Presentation:
Most common is acneform erruption with inflammatory pustules in hairy parts of body and butterfly area of face(must be differentiated from rosacea). Vesicular lesions and bullae are common.
Nodular lesions with a violaceous color are mistaken for malignant lymphoma of skin
It may occur after a small dose or after protracted use of bromides. Bromides are excreted in milk.
Treatment:
Cessation of bromide ingestion with rapid resolution.
In acute intoxication 2 to 4 g of sodium chloride by mouth, taken daily, rapidly replaces the bromide in body fluids.
In severe cases of intoxication in which the pt is badly confused, ethacrynic acid rapidly decreases the bromide level, with clearing of lesions

70. Bromoderma

71. Bromoderma
Bromide eruption on shin with bullae and granulomas

72. Iododerma
Presentation - acneiform eruption with numerous acutely inflamed follicular pustules, surrounded by a ring of hyperemia. Swelling, redness, and scaling of eyelids occurs.
Bullous lesions are also common and may become ulcerated and crusted
Pruitus and urticaria may be only manifestations of mild iodism
Acne vulgaris and rosacea are worsened by iodine
Treatment is same as bromoderma

73. Iododerma
Edematous erythematous papules on the buttocks with central crusts
Only brief duration distinguishes it clinically from basal cell carcinoma.

74. Topical Corticosteroids
Appearance of these side effects depends on three factors:
Strength of steroid
Area to which it is applied
The individual’s predisposition to certain side effects
Common Side effects:
Atrophy, striae, telangiectasia, skin fragility, and purpura are the most frequent changes seen. Hypo pigmentation in dark skinned individuals.
Telangiectasias in fair-skinned individuals using fluorinated corticosteroids on the face may or may not persist.

75. Topical Corticosteroids
Repeated application of corticosteroids to the face, scrotum or vulva may lead to marked atrophy of these tissues ( First marriage….Now This ! )
Tissue becomes “addicted” to the topical steroid, so that withdrawing it results in severe itching or burning.
Difficult to manage
Treatment: Reduce strength of steroid, add topicals like doxepin, pramoxine, or menthol and camphor.
Also TIMS may help during taper.
Telangiectasiases usually disappear in a few months after corticosteroid applications are stopped. Lasers of hyfercation may be needed.

76. Topical Corticosteroids
Atopic children with more than 50% body surface area involvement may have short stature. Some believe this is related to chronic steroid use.
If used over a large area, sufficient topical steroids may be absorbed to suppress the hypothalamic pituitary axis in any patient.
May affect growth of children with atopic dermatitis and has led to Addisonian steroid dependency and also Cushing’s syndrome.
Bone mineral density is reduced in adults whose chronic atopic dermatitis is severe enough to require steroids stronger than hydrocortisone.

77. Topical Corticosteroids
Other Reactions:
Topical corticosteroids may induce allergic contact dermatitis (esp in stasis dermatitis with long term use.)
Consider this complication in any pt with an eczematous dermatitis who becomes worse or is refractory to topical steroid tx.
Systemic corticosteroid administration may be tolerated, but in some pts there is a cross reaction manifested by whole-body allergic dermatitis
Steroid Acne, perioral dermatitis

78. Side effects…
Atrophy and purpura caused by prolonged applications of corticosteroid preparations

79. Steroid Acne due to mid potency application to the face.

80. Injected Corticosteroids
Intralesional injection may produce subcutaneous atrophy at site of injection and may migrate along lymphatics causing not only local side effects but linear atrophic hypopigmented hairless streaks
These may take years to resolve
To avoid these complications-inject directly into the lesion, not into the fat, and use only minimal concentration and volume
Intramuscular steroid injections should always be given in the buttocks with a long needle (at least 1.5 inches in adults)
Injection into deltoid muscle sometimes causes subcutaneous atrophy
Pt can be assured that this will fill in but it may take several yrs

81. SE of Injected Corticosteriods
Lipoatrophy of the buttock resulting from a corticosteroid injection

82. Systemic Corticosteroids Side Effects

83. Systemic Corticosteroids Side Effects
Acneiform Erruption
Osteonecrosis of head of femur

84. How to combat side effects…
Bone loss can occur early in course of tx and is important to manage preemptively:
Supplement with calcium & vitamin D ( g calcium and U of cholecalciferol daily)
Stop smoking
Decrease alcohol consumption
Obtain bone mineral density at baseline (via DEXA scan) & throughout tx period if long term steroid use is anticipated (yearly?)
Hypogonadism which contributes to osteoporosis can be treated in men and women with testosterone and estrogen respectively
Calcitonin and bisphosphonates may be added to management as needed

85. THE END