45: Cutaneous Reactions to Drugs

Question 1

What is the range of cutaneous reaction rates according to a systematic review of the medical literature?

Answer 1

Cutaneous reaction rates vary from 0% to 8% according to a systematic review of the medical literature.

Question 2

What are the most common types of drug eruptions and their characteristics?

Answer 2

The most common types of drug eruptions are exanthematous and maculopapular eruptions, accounting for approximately 95% of skin reactions. They typically start on the trunk, spread peripherally in a symmetric fashion, and are associated with pruritus and fever.

Question 3

What populations may have an increased risk of drug reactions in hospitals?

Answer 3

Populations that may have an increased risk of drug reactions in hospitals include: 1. Patients with HIV 2. Individuals with connective tissue disorders (e.g., lupus erythematosus) 3. Patients with non-Hodgkin lymphoma 4. Individuals with hepatitis.

Question 4

What is the typical time frame for the onset of exanthematous eruptions after drug therapy initiation?

Answer 4

Exanthematous eruptions usually occur within 1 week of initiation of therapy and may appear 1 to 2 days after drug therapy has been discontinued.

Question 5

What are the clinical features of urticarial eruptions associated with drug use?

Answer 5

Urticarial eruptions are characterized by: - Pruritic red wheals of various sizes - Individual lesions generally last for less than 24 hours - New lesions may develop - Associated angioedema may last for 1 to 2 hours but can persist for 2 to 5 days.

Question 6

What are the potential long-term complications of hypersensitivity syndrome reactions?

Answer 6

Long-term complications of hypersensitivity syndrome reactions may include immune-mediated thyroid dysfunction, which can lead to hyperthyroidism or hypothyroidism. Symptoms may not present until 3 to 12 months after the first symptoms appear.

Question 7

A patient develops a morbilliform rash 2 days after discontinuing a drug. What is the most likely type of drug eruption, and what is the expected resolution time?

Answer 7

The most likely type of drug eruption is an exanthematous eruption. It typically resolves within 7-14 days, with the rash changing from bright red to brownish red, followed by desquamation.

Question 8

A patient with infectious mononucleosis is treated with ampicillin and develops a rash. What is the likelihood of this reaction, and why does it occur?

Answer 8

The likelihood of developing an exanthematous eruption increases from 3%-7% to 60%-100% in patients with infectious mononucleosis treated with aminopenicillins like ampicillin. This is due to a drug-virus interaction.

Question 9

What systemic symptoms are associated with drug-induced hypersensitivity syndrome (DIHS), and what are the long-term complications?

Answer 9

DIHS is associated with fever, malaise, and internal organ inflammation. Long-term complications include immune-mediated thyroid dysfunction, which may lead to hyperthyroidism or hypothyroidism, presenting 3-12 months after initial symptoms.

Question 10

A patient presents with pruritic red wheals lasting less than 24 hours and angioedema. What type of hypersensitivity reaction is likely, and what are the common symptoms?

Answer 10

This is likely an IgE-mediated immediate hypersensitivity reaction. Common symptoms include pruritus, urticaria, cutaneous flushing, angioedema, nausea, vomiting, diarrhea, abdominal pain, nasal congestion, rhinorrhea, laryngeal edema, bronchospasm, or hypotension.

Question 11

What are the common clinical features of exanthematous eruptions caused by drug reactions?

Answer 11

• Morbilliform or maculopapular eruptions are the most common form, accounting for approximately 95% of drug reactions. - Typically starts on the trunk and spreads peripherally in a symmetric fashion. - Pruritus is almost always present. - Usually occurs within 1 week of initiation of therapy and may appear 1 or 2 days after drug therapy has been discontinued. - Resolution typically occurs within 7-14 days, with a change in color from bright red to brownish red, possibly followed by desquamation.

Question 12

How does the risk of developing an exanthematous eruption change for patients with infectious mononucleosis when treated with aminopenicillins?

Answer 12

The risk of developing an exanthematous eruption in patients with infectious mononucleosis increases significantly when treated with aminopenicillins, rising from 3-7% to as high as 60-100%.

Question 13

What are the characteristics and potential complications of hypersensitivity syndrome reactions (HSR) associated with drug use?

Answer 13

• HSR can present with an exanthematous eruption, fever, and internal organ inflammation, which can be asymptomatic. - Common drugs involved include aromatic anticonvulsants, sulfonamide antimicrobials, and others. - Initial symptoms typically occur 1 to 6 weeks after exposure. - Long-term complications may include immune-mediated thyroid dysfunction, leading to hyperthyroidism or hypothyroidism, which may not present until 3 to 12 months after the first symptoms appear.

Question 14

What distinguishes urticarial eruptions from exanthematous eruptions in drug reactions?

Answer 14

• Urticarial eruptions are characterized by pruritic red wheals of various sizes that generally last for less than 24 hours, with new lesions potentially developing. - In contrast, exanthematous eruptions are typically morbilliform or maculopapular and last longer, often resolving within 7-14 days. - Urticaria may also be associated with angioedema, which can last from 1 to 2 hours to 2 to 5 days.

Question 15

What are the characteristics and treatment options for drug-induced acneiform eruptions?

Answer 15

Characteristics: - Occurs in patients taking EGF receptor inhibitors (e.g., gefitinib, erlotinib, cetuximab) with an incidence of 81.6%. - Characterized by pruritic follicular papules and pustules without comedones, appearing within 1 to 2 weeks of treatment initiation. - Associated findings include paronychia, xerosis, and skin fissures. Treatment Options: 1. Discontinue the offending agent if possible. 2. Topical tretinoin may be useful if discontinuation is not possible. 3. Alternatives include tetracyclines and low-dose isotretinoin. 4. Target pruritus with anti-histamines and doxepin.

Question 16

What is the clinical significance of drug-induced linear immunoglobulin A disease and its common presentations?

Answer 16

Clinical Significance: - Resembles erythema multiforme, bullous pemphigoid, and dermatitis herpetiformis. - May present with erosions mimicking toxic epidermal necrolysis (TEN) and has a more severe clinical course. Common Presentations: - Mucosal and conjunctival lesions are less common. - Spontaneous remission occurs when the drug is withdrawn. - Onset time ranges from 2 days to 4 weeks. - Diagnosis requires biopsy, and the index of suspicion for drug induction is higher in cases with only IgA in the basement membrane zone. - Most frequently reported drug: Vancomycin.

Question 17

What are the key features and management strategies for drug-induced pemphigus?

Answer 17

Key Features: - Can be drug-induced or drug-triggered. - Caused by penicillamine and other thiol-containing drugs (e.g., piroxicam, captopril). - Tends to remit spontaneously in 35% to 50% of cases, presenting as pemphigus foliaceus. - Average interval to onset is about 1 year, associated with antinuclear antibodies in 25% of patients. Management Strategies: 1. Drug cessation is crucial. 2. Systemic glucocorticoids and other immunosuppressive drugs may be required. 3. Follow-up after remission to monitor serum for autoantibodies to detect early relapse.

Question 18

What are the characteristics of pseudoporphyria and its management?

Answer 18

Characteristics: - A cutaneous phototoxic disorder resembling porphyria cutanea tarda (PCT) in adults or erythropoietic protoporphyria (EPP) in children, but with normal porphyrin levels. - PCT variety is characterized by skin fragility, blister formation, and scarring in photodistribution. - EPP variety presents with cutaneous burning, erythema, vesiculation, and angular chicken pox-like scars. - Symptoms may begin within 1 day of therapy initiation or be delayed for up to 1 year. Management: - Discontinue the implicated drug if skin fragility, blistering, or scarring occurs. - Use sunscreen and protective clothing. - Consider NSAIDs, diuretics, and antibiotics for symptom management.

Question 19

A patient develops a serum sickness-like reaction after taking cefaclor. What are the key features of this reaction, and how does it differ from true serum sickness?

Answer 19

Key features include fever, urticarial rash, and arthralgias 1-3 weeks after drug initiation. Unlike true serum sickness, immune complexes, hypocomplementemia, vasculitis, and renal lesions are absent.

Question 20

What are the histopathological findings in acute generalized exanthematous pustulosis (AGEP), and what is the typical timeline for resolution?

Answer 20

Histopathological findings include spongiform subcorneal and/or intraepidermal pustules, marked edema of the papillary dermis, and perivascular infiltrates with neutrophils and some eosinophils. Generalized desquamation occurs after 2 weeks.

Question 21

A patient on epidermal growth factor receptor inhibitors develops pruritic follicular papules and pustules without comedones. What is the condition, and how is it managed?

Answer 21

The condition is drug-induced acneiform eruption. Management includes topical tretinoin, tetracyclines, or low-dose isotretinoin. Antihistamines and doxepin can target pruritus.

Question 22

A patient develops pseudoporphyria with blistering and scarring in photodistributed areas. What drugs are commonly implicated, and what preventive measures should be taken?

Answer 22

Commonly implicated drugs include NSAIDs, diuretics, antibiotics (e.g., tetracycline, ciprofloxacin), retinoids, and cyclosporine. Preventive measures include discontinuing the drug, using sunscreen, and wearing protective clothing.

Question 23

What is the clinical presentation of drug-induced linear IgA disease, and how is it diagnosed?

Answer 23

It presents with lesions resembling erythema multiforme, bullous pemphigoid, or dermatitis herpetiformis. Diagnosis requires biopsy and direct immunofluorescence, showing IgA deposits in the basement membrane zone.

Question 24

A patient develops drug-induced pemphigus. What are the clinical differences between thiol and non-thiol drug-induced pemphigus?

Answer 24

Thiol drug-induced pemphigus often presents as pemphigus foliaceus and remits spontaneously in 35%-50% of cases. Non-thiol pemphigus resembles idiopathic pemphigus vulgaris with mucosal involvement.

Question 25

A patient develops acute generalized exanthematous pustulosis (AGEP) after taking a beta-lactam antibiotic. What systemic features are associated with AGEP?

Answer 25

Systemic features include leukocytosis with neutrophilia, fever, elevated liver enzymes, renal insufficiency, and pleural effusions with hypoxemia.

Question 26

A patient develops erythema multiforme-like lesions after taking vancomycin. What is the likely diagnosis, and how is it confirmed?

Answer 26

The likely diagnosis is drug-induced linear IgA disease. It is confirmed by biopsy and direct immunofluorescence showing IgA deposits.

Question 27

What are the characteristics and management strategies for drug-induced acneiform eruptions associated with EGF receptor inhibitors?

Answer 27

**Characteristics:** - Occurs in the majority of patients taking EGF receptor inhibitors (e.g., gefitinib, erlotinib, cetuximab) with an incidence of 81.6%. - Characterized by pruritic follicular papules and pustules without comedones, presenting within 1 to 2 weeks of treatment initiation. - Other findings may include paronychia, xerosis, and skin fissures. **Management Strategies:** 1. Discontinue the offending agent if possible. 2. Use topical tretinoin if discontinuation is not feasible. 3. Consider alternatives such as tetracyclines and low-dose isotretinoin. 4. Target pruritus with anti-histamines and doxepin.

Question 28

How does drug-induced linear immunoglobulin A disease present and what is the significance of biopsy in its diagnosis?

Answer 28

**Presentation:** - Resembles erythema multiforme, bullous pemphigoid, and dermatitis herpetiformis. - Mucosal and conjunctival lesions are less common. - May present with erosions mimicking toxic epidermal necrolysis (TEN) and has a more severe clinical course. - Onset occurs 2 days to 4 weeks after drug exposure. **Significance of Biopsy:** - A biopsy is necessary for diagnosis to confirm the presence of linear IgA deposits. - In cases with only IgA and no IgG in the basement membrane zone, the suspicion for drug induction should be higher.

Question 29

What are the clinical features and management of drug-induced pemphigus, and how does it differ from idiopathic pemphigus vulgaris?

Answer 29

**Clinical Features:** - Drug-induced pemphigus may be triggered by penicillamine and other thiol-containing drugs (e.g., piroxicam, captopril). - Tends to remit spontaneously in 35% to 50% of cases. - Presents as pemphigus foliaceus with an average interval to onset of 1 year. - Associated with the presence of antinuclear antibodies in 25% of patients. **Management:** 1. Discontinue the offending drug. 2. Use systemic glucocorticoids and other immunosuppressive drugs as needed. 3. Follow up after remission to monitor serum for autoantibodies to detect early relapse. **Difference from Idiopathic Pemphigus Vulgaris:** - Non-thiol drug-induced pemphigus shows similar clinical, histologic, and immunologic aspects but may involve mucosal surfaces and has a 15% rate of spontaneous recovery after drug withdrawal.

Question 30

What are the characteristics of drug-induced bullous pemphigoid compared to idiopathic forms?

Answer 30

**Drug-induced bullous pemphigoid** is characterized by: - Younger patients - Positive Nikolsky sign - Lesions on normal-appearing skin, target lesions on palms and soles, involvement of lower legs, and mucosal involvement - Histopathology shows perivascular infiltration of lymphocytes, neutrophils, marked eosinophils, intraepidermal vesicles, and possible lack of tissue-bound and circulating anti-basement membrane zone IgG. In contrast, **idiopathic forms** may not present these specific features and can be more severe and chronic.

Question 31

What are the common clinical features of fixed drug eruptions (FDE)?

Answer 31

**Clinical features of Fixed Drug Eruptions (FDE)** include: - Solitary round or ovoid, erythematous, bright red or dusky red macules that may evolve into edematous plaques. - Bullous type lesions may be present.

Question 32

What are the common clinical features of fixed drug eruptions (FDE)?

Answer 32

Clinical features of Fixed Drug Eruptions (FDE) include solitary round or ovoid, erythematous, bright red or dusky red macules that may evolve into edematous plaques. Bullous type lesions may be present. Commonly found on the genitalia and perianal area, but can occur anywhere on the skin surface. Women often present with lesions on hands and feet, while men present on the genitalia. Symptoms include burning, stinging, fever, malaise, and abdominal symptoms. Lesions develop from 30 minutes to 8-16 hours after medication ingestion. After the acute phase, residual grayish or slate-colored hyperpigmentation develops.

Question 33

What is the significance of challenge or provocation tests in diagnosing drug-induced skin reactions?

Answer 33

Challenge or provocation tests are significant in diagnosing drug-induced skin reactions because they help establish the diagnosis by testing the suspected drug. Patch testing at the site of a previous lesion yields a positive response in up to 43% of patients. Prick and intradermal skin tests may be positive in 24% and 67% of patients, respectively.

Question 34

What are the most frequent culprits of fixed drug eruptions?

Answer 34

The most frequent culprits of Fixed Drug Eruptions (FDE) include NSAIDs, Acetaminophen, and Antibiotics.

Question 35

What are the clinical patterns of drug-induced hyperpigmentation associated with specific drugs?

Answer 35

Clinical patterns of drug-induced hyperpigmentation associated with specific drugs include: | Causative Drug | Clinical Pattern of Pigmentation | |----------------|-------------------------------| | Antimalarials | Nail bands with transversal bands or diffuse pigmentation | | Cytotoxic drugs | Longitudinal or diffuse pigmentation, sometimes involving skin or onycholysis | | Silver | Diffuse or longitudinal pigmentation | | Phenothiazines | Diffuse or longitudinal pigmentation | | Zidovudine | Diffuse pigmentation |

Question 36

A patient develops drug-induced hyperpigmentation. What are the common causes, and how does it present?

Answer 36

Common causes include NSAIDs, antibiotics, and antimalarials. It presents as slate-gray or brownish discoloration, often in sun-exposed areas.

Question 37

A patient develops fixed drug eruptions (FDE) after taking NSAIDs. What are the hallmark features, and how is the diagnosis confirmed?

Answer 37

Hallmark features include solitary round or ovoid erythematous macules that recur in the same location upon rechallenge. Diagnosis is confirmed by a challenge test or patch testing at the site of a previous lesion.

Question 38

What are the diagnostic criteria for fixed drug eruptions (FDE), and how do they differ from SJS-TEN?

Answer 38

FDE is diagnosed by recurrent lesions at the same site upon rechallenge, often with hyperpigmentation. Unlike SJS-TEN, FDE lacks systemic involvement.

Question 39

What are the clinical features of drug-induced bullous pemphigoid, and how does it differ from the idiopathic form?

Answer 39

Drug-induced bullous pemphigoid occurs in younger patients, with lesions on normal-appearing skin and target lesions on palms and soles. It resolves after drug withdrawal, unlike the chronic idiopathic form.

Question 40

What are the distinguishing features of drug-induced bullous pemphigoid compared to idiopathic forms?

Answer 40

Drug-induced bullous pemphigoid typically presents in younger patients and shows positive Nikolsky sign, lesions on normal-appearing skin, target lesions on palms and soles, and involvement of lower legs and mucosal areas. Histopathology reveals perivascular infiltration of lymphocytes and neutrophils, marked eosinophils, and intraepidermal vesicles with necrotic keratinocytes.

Question 41

What is the clinical significance of performing a challenge or provocation test in suspected fixed drug eruptions?

Answer 41

A challenge or provocation test is clinically significant as it helps in establishing the diagnosis of fixed drug eruptions (FDE), identifying the specific drug responsible for the eruption, and understanding the patient's reaction to the drug, which can guide future medication choices. Positive responses in patch testing at previous lesion sites can occur in up to 43% of patients.

Question 42

How do the clinical presentations of fixed drug eruptions differ between genders?

Answer 42

In fixed drug eruptions, women more commonly present with lesions on the hands and feet, while men are more likely to have lesions on the genitalia. This gender difference may influence the clinical approach and management of the condition.

Question 43

What are the common symptoms and timeline for the development of fixed drug eruptions after medication ingestion?

Answer 43

Common symptoms of fixed drug eruptions include burning, stinging, fever, malaise, and abdominal symptoms. Symptoms can develop from 30 minutes to 8 to 16 hours after ingestion of the medication. After the initial acute phase lasting days to weeks, residual grayish or slate-colored hyperpigmentation develops.

Question 44

What are the most frequent culprits associated with fixed drug eruptions?

Answer 44

The most frequent culprits associated with fixed drug eruptions include NSAIDs, Acetaminophen, and Antibiotics (such as penicillins and fluoroquinolones).

Question 45

What are the clinical features of drug-induced lichen planus?

Answer 45

Clinically and histologically indistinguishable from idiopathic lichen planus. Often presents as eczematous with a purple hue. Involves large areas of the trunk. Mucous membranes and nails are usually not involved. Histopathology shows focal parakeratosis, cytoid bodies, eosinophils, and plasma cells in the inflammatory infiltrate.

Question 46

What is the mean latent period for drug-induced lichen planus associated with penicillamine?

Answer 46

Mean latent period for penicillamine is approximately 2 months to 3 years.

Question 47

What triggers drug-induced pseudolymphoma and what are its characteristics?

Answer 47

Triggers include foreign agents (e.g., insect bites), infections (e.g., HIV), and idiopathic causes. Characteristics include simulating lymphoma but has benign behavior, can manifest as widespread erythematous papules, plaques, or nodules, and symptoms may resolve within 7 to 14 days after drug discontinuation.

Question 48

What are the common serologic abnormalities found in drug-induced lupus?

Answer 48

Most common serologic abnormality is (+ antinuclear antibodies with a homogenous pattern. Antihistone antibodies are positive in up to 95% but not specific. Anti-dsDNA is absent, while Anti-ssDNA is present in drug-induced lupus.

Question 49

What are the cutaneous findings associated with drug-induced dermatomyositis?

Answer 49

Classic cutaneous findings include pruritic photodistributed papulosquamous exanthema, pathognomonic heliotrope rash or Gottron papules in the majority of cases.

Question 50

What are the clinical and histological features of drug-induced lichen planus, and which drugs are commonly implicated?

Answer 50

Clinically, it presents as eczematous lesions with a purple hue, often sparing mucous membranes and nails. Histologically, it shows focal parakeratosis, cytoid bodies, and eosinophils in the inflammatory infiltrate. Common drugs include beta-blockers, ACE inhibitors, and TNF-alpha antagonists.

Question 51

A patient develops drug-induced lupus erythematosus (DILE). What serologic markers differentiate it from idiopathic lupus?

Answer 51

In DILE, anti-dsDNA antibodies are absent, while anti-ssDNA antibodies are present. Antihistone antibodies are positive in up to 95% of cases but are not specific.

Question 52

A patient on minocycline develops symmetric polyarthritis and a livedo reticularis rash. What is the likely diagnosis, and what serologic findings are expected?

Answer 52

The likely diagnosis is minocycline-induced lupus. Serologic findings may include positive antinuclear antibodies and absence of antihistone antibodies.

Question 53

What are the key features of drug-induced subacute cutaneous lupus erythematosus (SCLE), and which drugs are commonly implicated?

Answer 53

Key features include photosensitive papulosquamous or annular lesions with mild systemic involvement. Common drugs include terbinafine, thiazide diuretics, and calcium channel blockers.

Question 54

A patient develops drug-induced pseudolymphoma. What are the clinical features, and which drugs are implicated?

Answer 54

Clinical features include erythematous papules, plaques, or nodules, often with fever, lymphadenopathy, and hepatosplenomegaly. Implicated drugs include anticonvulsants, ACE inhibitors, and allopurinol.

Question 55

What are the key features of drug-induced subacute cutaneous lupus erythematosus (SCLE), and how is it managed?

Answer 55

Key features include photosensitive papulosquamous or annular lesions with mild systemic involvement. Management involves discontinuing the offending drug, with resolution in weeks.

Question 56

What are the clinical and histological characteristics of drug-induced lichen planus, and how do they compare to idiopathic lichen planus?

Answer 56

Drug-induced lichen planus is clinically and histologically indistinguishable from idiopathic lichen planus. It often presents as eczematous lesions with a purple hue and typically involves large areas of the trunk. Mucous membranes and nails are usually not affected. Histopathological findings include focal parakeratosis, cytoid bodies, eosinophils, and plasma cells in the inflammatory infiltrate.

Question 57

What is the typical latent period for drug-induced lupus, and how does it differ from idiopathic lupus?

Answer 57

The typical latent period for drug-induced lupus varies depending on the drug: Hydralazine: 3 weeks to 2 years; Minocycline: typically occurs after 2 years of therapy; Other drugs may have varying onset times. In contrast, idiopathic lupus does not have a drug-related onset period and can develop spontaneously without a specific trigger.

Question 58

What are the common triggers and clinical manifestations of drug-induced pseudolymphoma?

Answer 58

Common triggers for drug-induced pseudolymphoma include anticonvulsants (e.g., carbamazepine, phenytoin), ACE inhibitors, allopurinol, cyclosporine, and fluoxetine and other antidepressants. Clinical manifestations typically include erythematous papules, plaques, or nodules, fever, marked lymphadenopathy, and hepatosplenomegaly. Symptoms may resolve within 7 to 14 days after drug discontinuation.

Question 59

How does the clinical presentation of drug-induced dermatomyositis differ from idiopathic dermatomyositis?

Answer 59

Drug-induced dermatomyositis is characterized by papulosquamous or annular cutaneous lesions, often photosensitive, and absent or mild systemic involvement. Clinical morphology and histopathology are indistinguishable from idiopathic dermatomyositis, which may present with more severe systemic symptoms and a broader range of cutaneous findings.

Question 60

What are the common medications implicated in purpuric eruptions?

Answer 60

Common medications include Hydroxyurea, Penicillamine, Granulocyte colony-stimulating factor, Allopurinol, Cefaclor, Minocycline, Phenytoin, Isotretinoin, and Anti-TNF agents (e.g., etanercept, infliximab, adalimumab, rituximab, levamisole).

Question 61

What is the clinical hallmark of purpuric eruptions?

Answer 61

The clinical hallmark of purpuric eruptions is palpable purpura, which is typically found on the lower extremities.

Question 62

What is the typical onset time for purpuric eruptions after initiation of therapy?

Answer 62

Purpuric eruptions typically occur 7 to 21 days after the initiation of therapy.

Question 63

What are the characteristics of anticoagulant-induced skin necrosis?

Answer 63

Characteristics include begins 3 to 5 days after initiation of treatment, early red, painful plaques develop in adipose-rich sites (e.g., breasts, buttocks, hips), plaques may blister, ulcerate, or develop into necrotic areas, and incidence is 1 in 10,000, higher in women, especially those who are obese and in their 6th and 7th decades of life.

Question 64

What is the treatment for anticoagulant-induced skin necrosis?

Answer 64

Treatment includes discontinuation of warfarin, administration of vitamin K, infusion of heparin at therapeutic dosages, fresh-frozen plasma and purified protein C concentrates, and supportive measures for the skin.

Question 65

What is neutrophilic eccrine hidradenitis and how is it diagnosed?

Answer 65

Neutrophilic eccrine hidradenitis is a benign condition described in patients with leukemia receiving chemotherapy. It can also occur in the absence of drug triggers. Diagnosis is based on histopathology, showing neutrophilic infiltrate of the eccrine unit and necrosis of the eccrine coils and glands with dermal edema.

Question 66

What are potential causative agents for most cutaneous eruptions?

Answer 66

Potential causative agents for most cutaneous eruptions include new drugs started within the preceding 3 months, especially those within 6 weeks, and drugs used intermittently. Exceptions include drug-induced lupus, drug-induced pemphigus, and drug-induced cutaneous pseudolymphoma.

Question 67

What are the clinical and histological features of neutrophilic eccrine hidradenitis, and how is it managed?

Answer 67

Clinically, it presents as dark erythematous plaques that mimic cellulitis. Histologically, it shows neutrophilic infiltrates in eccrine units. Management includes antineutrophilic agents like colchicine or dapsone.

Question 68

A patient develops palpable purpura on the lower extremities 10 days after starting hydralazine. What is the likely diagnosis, and what systemic involvement should be considered?

Answer 68

The likely diagnosis is drug-induced small-vessel vasculitis. Systemic involvement may include the liver, kidneys, gut, and CNS, which can be life-threatening.

Question 69

A patient on warfarin develops painful red plaques on adipose-rich sites. What is the condition, and what is the pathogenesis?

Answer 69

The condition is anticoagulant-induced skin necrosis.

Question 70

What is the likely diagnosis for a patient with palpable purpura on the lower extremities after starting hydralazine?

Answer 70

The likely diagnosis is drug-induced small-vessel vasculitis. Systemic involvement may include the liver, kidneys, gut, and CNS, which can be life-threatening.

Question 71

What condition develops in a patient on warfarin who has painful red plaques on adipose-rich sites?

Answer 71

The condition is anticoagulant-induced skin necrosis. It results from a transient hypercoagulable state due to suppression of protein C at a greater rate than natural procoagulant factors.

Question 72

What is the diagnosis for a patient who develops heliotrope rash and Gottron papules after starting hydroxyurea?

Answer 72

The diagnosis is drug-induced dermatomyositis. Systemic involvement may include proximal muscle weakness and pulmonary involvement.

Question 73

What is the pathogenesis of drug-induced vasculitis?

Answer 73

Drug-induced vasculitis involves immune complex deposition and tissue eosinophilia, with less progression to glomerulonephritis and better outcomes compared to autoimmune vasculitis.

Question 74

What is the treatment for anticoagulant-induced skin necrosis?

Answer 74

Treatment includes discontinuing warfarin, administering vitamin K, heparin infusion, fresh-frozen plasma, and supportive skin care.

Question 75

What are the clinical features of purpuric eruptions associated with drug-induced vasculitis?

Answer 75

**Clinical Features:** - Represents approximately 10% of acute cutaneous vasculitides. - Clinical hallmark: **palpable purpura** found on lower extremities. - Other features may include hemorrhagic bullae, ulcers, and nodules. - Can affect internal organs (liver, kidney, gut, CNS).

Question 76

What are the management strategies for purpuric eruptions associated with drug-induced vasculitis?

Answer 76

**Management Strategies:** 1. **Drug withdrawal** is often sufficient. 2. **Systemic glucocorticoids** may provide benefit in severe cases. 3. Monitor for potential progression to glomerulonephritis.

Question 77

What is the pathogenesis and treatment approach for anticoagulant-induced skin necrosis?

Answer 77

**Pathogenesis:** - Occurs 3 to 5 days after initiation of treatment with coumarin congeners. - Results from a **transient hypercoagulable state** due to suppression of natural anticoagulant protein C. **Treatment Approach:** 1. **Discontinuation of warfarin.** 2. **Administration of vitamin K.** 3. **Infusion of heparin** at therapeutic dosages. 4. **Supportive measures** for skin management. 5. In severe cases, **plastic surgery** may be required.

Question 78

How does neutrophilic eccrine hidradenitis present?

Answer 78

**Presentation:** - Benign condition often seen in patients with leukemia undergoing chemotherapy. - Characterized by dark erythematous to violaceous edematous plaques, which can be asymptomatic or tender. - Can mimic cellulitis and lesions may occur on the face or extremities.

Question 79

What are the treatment options for neutrophilic eccrine hidradenitis?

Answer 79

**Treatment Options:** 1. **Antineutrophilic agents** such as colchicine. 2. **Dapsone** may be used as prophylaxis.

Question 80

What are the key factors in the etiology of drug-induced cutaneous eruptions?

Answer 80

**Key Factors:** - New drugs started within the **preceding 3 months** are potential causative agents. - **Exceptions** include drug-induced lupus, pemphigus, and cutaneous pseudolymphoma. - Most eruptions result from an **immune-mediated reaction** to a medication, involving IgE or IgG.

Question 81

What role do constitutional factors play in drug-induced lupus?

Answer 81

Constitutional factors, such as pharmacogenetic variation in drug-metabolizing enzymes and human leukocyte antigen (HLA) associations, can alter the risk of developing drug-induced lupus.

Question 82

How do toxic metabolites of aromatic anticonvulsants contribute to hypersensitivity reactions?

Answer 82

Toxic metabolites of aromatic anticonvulsants can act as haptens, initiating immune responses, stimulating apoptosis, or causing cell necrosis.

Question 83

What is the significance of HLA class I and II in drug hypersensitivity reactions?

Answer 83

HLA class I presents intracellular antigens to CD8+ T cells, while HLA class II presents extracellular antigens to CD4+ T-helper cells. Specific HLA alleles are associated with severe drug reactions.

Question 84

What clinical features may indicate a drug-associated eruption?

Answer 84

Clinical features may include systemic symptoms, erythroderma, blistering, skin tenderness, purpura, or pustulation.

Question 85

What diagnostic approaches are recommended for suspected drug hypersensitivity reactions?

Answer 85

Diagnostic approaches include analyzing features of the reaction, timing of exposure and onset, course of reaction with drug withdrawal, and similar response to cross-reacting medications.

Question 86

What is the relationship between valproic acid and lamotrigine regarding cutaneous adverse reactions?

Answer 86

Valproic acid increases the risk of severe cutaneous adverse reactions to lamotrigine.

Question 87

What genetic factors increase the risk of severe drug reactions?

Answer 87

HLA-B*1502 is associated with carbamazepine-induced SJS-TEN, HLA-B*5801 with allopurinol-induced SJS-TEN, and HLA-B*5701 with abacavir hypersensitivity.

Question 88

What is the role of toxic metabolites in SJS-TEN after taking sulfonamide antibiotics?

Answer 88

Toxic metabolites may act as haptens, initiating immune responses, apoptosis, or direct cell necrosis.

Question 89

What diagnostic steps should be taken for a cutaneous drug eruption with systemic symptoms?

Answer 89

Diagnostic steps include a clinical review of systems, full blood count, liver and renal function tests, urine analysis, and biopsy if systemic symptoms or uncertain diagnosis are present.

Question 90

What is the role of lymphocyte transformation assays in diagnosing drug allergies?

Answer 90

Lymphocyte transformation assays can identify drug allergies by detecting lymphocyte activation in response to specific drugs.

Question 91

What role do genetic factors play in drug-induced lupus?

Answer 91

Genetic factors influence the risk of developing drug-induced lupus, with the acetylator phenotype altering this risk.

Question 92

How do toxic metabolites from aromatic anticonvulsants contribute to hypersensitivity reactions?

Answer 92

Toxic metabolites can act as haptens, initiating immune responses that stimulate apoptosis or cause cell necrosis.

Question 93

What is the significance of HLA-B*1502 and HLA-B*5801 in drug hypersensitivity reactions?

Answer 93

HLA-B*1502 is associated with carbamazepine-induced SJS-TEN, while HLA-B*5801 is linked to allopurinol-induced SJS-TEN.

Question 94

What clinical features should prompt a review for potential drug-induced hypersensitivity reactions?

Answer 94

Minor cutaneous eruptions should trigger a clinical review of systems, as severity does not always correlate with skin manifestations.

Question 95

What are the implications of drug-drug interactions in hypersensitivity reactions?

Answer 95

Drug-drug interactions can exacerbate hypersensitivity reactions, as seen with valproic acid increasing the risk of severe cutaneous adverse reactions to lamotrigine.

Question 96

What is the significance of the SCORTEN score in SJS-TEN?

Answer 96

The SCORTEN score is used to assess the severity and predict mortality in patients with SJS-TEN.

Question 97

What are the management strategies for SJS-TEN?

Answer 97

Management strategies include discontinuance of the suspected drug(s), supportive measures, and possibly corticosteroids or intravenous immunoglobulin.

Question 98

What are the potential outcomes and complications associated with SJS-TEN?

Answer 98

Potential outcomes include recurrence rates, scarring affecting multiple systems, and immune-mediated thyroid disorders.

Question 99

What are the recommendations for preventing cutaneous drug reactions?

Answer 99

Recommendations include recognizing that reactions are largely idiosyncratic, wearing a bracelet for severe reactions, and reporting reactions to manufacturers.

Question 100

What is the SCORTEN score, and how is it used in SJS-TEN management?

Answer 100

The SCORTEN score assesses severity and predicts mortality in SJS-TEN, including criteria like age >40 and laboratory indices.

Question 101

What are the long-term complications affecting multiple systems in SJS-TEN?

Answer 101

Long-term complications include hyperpigmentation, alopecia, dry eyes, and chronic bronchitis.

Question 102

What are the management principles for SJS-TEN?

Answer 102

Management includes discontinuing the suspected drug, supportive care, and avoiding drug rechallenge.

Question 103

What are the key criteria used in the SCORTEN score?

Answer 103

The SCORTEN score includes age older than 40, laboratory indices, tachycardia, malignancy, and body surface area >10%.

Question 104

What is the recommended management approach for patients diagnosed with SJS-TEN?

Answer 104

The management approach includes discontinuance of the suspected drug(s) and supportive measures.

Question 105

What are the potential long-term sequelae of SJS-TEN?

Answer 105

Long-term sequelae can affect skin, eyes, genitalia, and lungs, leading to significant morbidity.

Question 106

What are the considerations for drug desensitization in patients with IgE-mediated reactions?

Answer 106

Drug desensitization is indicated for IgE-mediated reactions caused by penicillin and monoclonal antibodies.