Extensor Scaly Plaques Following Recent Medication Use

Question

A 36-year-old woman develops clearly defined, red, flaky plaques over the extensor aspect of her forearms. The lesions are interfering with her ability to handle her infant.

She had a cesarean delivery 5 weeks ago and has been using simple analgesics since then. She is not lactating.

Two weeks back, she was prescribed the following:

  • A beta-blocker for episodic anxiety
  • An antihistamine for sleep
  • A short course of oral steroids for facial nerve palsy

Which of the following is the most likely trigger for her current skin condition?

a. Antihistamine medication
b. Simple analgesic use
c. Oral corticosteroid therapy
d. Hormonal increase during pregnancy
e. Beta-blocker therapy


Answer
e. Beta-blocker therapy


Explanation

This clinical picture is classic for plaque psoriasis, characterized by:

  • Well-demarcated erythematous plaques
  • Silvery scales
  • Predilection for extensor surfaces (elbows, knees)

Among the options, beta-blockers (especially lipophilic ones like Propranolol) are well-known triggers that can:

  • Induce new-onset psoriasis
  • Exacerbate pre-existing disease

Why beta-blockers?

  • They interfere with cyclic AMP signaling in keratinocytes
  • This promotes keratinocyte proliferation and inflammation
  • Lipophilic agents (e.g., propranolol) cross cell membranes more easily → stronger effect

Why not others?

  • Antihistamines (e.g., Promethazine) → no association
  • Paracetamol → not linked to psoriasis flares
  • Oral steroids (e.g., Prednisolone) → may actually improve psoriasis (but withdrawal can worsen it)
  • Pregnancy hormones → psoriasis usually improves during pregnancy due to immunomodulation; flares occur postpartum, not during progesterone rise

Cheat Sheet: Psoriasis Triggers

Drugs that worsen psoriasis:

  • Beta-blockers (propranolol)
  • Lithium
  • Antimalarials (chloroquine, hydroxychloroquine)
  • NSAIDs
  • ACE inhibitors
  • Interferons

Other triggers:

  • Trauma (Koebner phenomenon)
  • Alcohol
  • Stress
  • Infection (esp. streptococcal → guttate psoriasis)
  • Withdrawal of systemic steroids

Flashcards

Q1. Which drug class is most commonly associated with psoriasis exacerbation?
A: Beta-blockers
Explanation: Particularly lipophilic ones like propranolol

Q2. What is the typical site of plaque psoriasis?
A: Extensor surfaces (elbows, knees)
Explanation: Classic distribution pattern

Q3. How does pregnancy affect psoriasis?
A: Usually improves
Explanation: Progesterone suppresses immune overactivity

Q4. What happens after steroid withdrawal in psoriasis?
A: Severe rebound flare
Explanation: Sudden immune rebound


MCQs

1. A patient develops new-onset psoriasis after starting medication. Which drug is most likely responsible?
a. Cetirizine
b. Propranolol
c. Paracetamol
d. Amoxicillin

Answer: b
Explanation: Beta-blockers are classic triggers; others are not associated


2. Which of the following is false regarding psoriasis?
a. It commonly affects extensor surfaces
b. Beta-blockers may exacerbate it
c. Pregnancy worsens it in most patients
d. Withdrawal of steroids can trigger flare

Answer: c
Explanation: Pregnancy usually improves psoriasis


3. Which mechanism best explains beta-blocker-induced psoriasis?
a. Increased histamine release
b. Reduced keratinocyte proliferation
c. Altered cAMP signaling in skin cells
d. Direct bacterial infection

Answer: c
Explanation: Beta-blockers reduce cAMP → increased proliferation


4. A patient on long-term steroids develops severe psoriasis after stopping them. This is due to:
a. Drug toxicity
b. Rebound immune activation
c. Allergy
d. Infection

Answer: b
Explanation: Steroid withdrawal leads to immune rebound


5. Which drug is least likely to worsen psoriasis?
a. Lithium
b. Propranolol
c. Paracetamol
d. Chloroquine

Answer: c
Explanation: Paracetamol has no known association


Summary for Quick Exam Revision

Plaque psoriasis presents with well-demarcated, erythematous, scaly plaques, typically on extensor surfaces such as elbows and knees. It is an immune-mediated condition driven by keratinocyte hyperproliferation. Several triggers can exacerbate psoriasis, with drugs being particularly important in exam settings. Among these, beta-blockers—especially lipophilic ones like propranolol—are high-yield causes. Other drug triggers include lithium, antimalarials, NSAIDs, and ACE inhibitors. Pregnancy generally improves psoriasis due to immunomodulatory effects of progesterone, while postpartum flares are common. Systemic corticosteroids may transiently improve psoriasis but their withdrawal can precipitate severe rebound flares. Recognizing drug-induced exacerbation is crucial, especially when new medications precede symptom onset.

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