Chronic plaque psoriasis.

A 69-year-old man presented with a flare of chronic plaque psoriasis worsening over the last 18 months. There was no relevant past medical history (except for mild emphysema), known allergy, or recent treatment. Narrow-band UVB phototherapy was proposed. Treatment was discontinued after five sessions due to the worsening of lesions and the occurrence of a burning sensation, and he sought advice at the emergency department. Clinical examination showed erythema of >90% of the body surface area with diffuse desquamation (Figure 1) and mild edema of the extremities. 

 

On admission, he had normal vital parameters and blood pressure of 110/60 mm Hg. Biological exams at entrance were normal, except for a mildly increased CRP (21 mg/dL, normal <10 mg/dL). Chest X-ray was normal at admission (Figure 2a). A skin biopsy was performed. The erythroderma was presumed to be secondary to phototherapy and was treated with local clobetasol propionate 0.05% and oral ciclosporin at 2.5 mg/kg/day (150 mg/day) with initial improvement. 

 

On day 4 of admission, the patient developed hypoxemia. He was apyrexial and had no cough. Clinical examination revealed bilateral crackles at both lung bases and worsening lower limb edema. There was no hepatojugular regurgitation or jugular vein distension. Blood gas analysis showed pH 7.47, severe hypoxemia (pO2 at 44 mm Hg), hypocapnia secondary to hyperventilation (pCO2 at 27 mm Hg), and a lactate level at 2.3 mmol/L (normal <2 mmol/L). Chest X-ray revealed new bilateral lung infiltrates (Figure 2b). 

 

He was transferred to the ICU, where noninvasive ventilation with continuous positive airway pressure was performed. Biological investigations revealed leukocytosis (WBC 13,000/mm3, normal 4,000–8,000), increased CRP at 80 mg/dL (normal <10 mg/dL), normal renal function, elevated D-dimer (2,988 ng/dL, normal <500 ng/dL), and elevated VEGF (707 pg/mL, normal <500 pg/mL). Bronchoalveolar lavage (BAL) and aspiration were performed. Cellular analysis showed an increased neutrophil count (59%), contrasting with a normal lymphocyte count (2%). The direct examination and culture of BAL fluid were negative. Pharynx cultures were negative for bacteria or viruses. Thoracic computed tomography (Figure 4a) showed bilateral ground-glass infiltrates with alveolar condensation. Cardiac ultrasound was normal with no sign of cardiac dysfunction, cardiomegaly, overload, or elevation of filling pressure. 

 

Treatment with a high dose of systemic corticosteroids (2 mg/kg of methylprednisolone) was initiated 24 h after the symptoms had begun. Ciclosporin was also stopped. Clinical improvement was observed with oxygen shutdown on day 7 after ICU admission. Favourable evolution was observed with progressive oxygen shut down and progressive tapering of corticosteroids (at discharge from the hospital, the dose of methylprednisolone was 8 mg/day). Two months later, the patient's lung lesions had returned to baseline.