Papular urticaria

Management Strategy

The exact cause of papular urticaria is often unidentified; hence, it is a diagnosis of exclusion. Initial evaluation should include complete blood count with differential, serum IgE, scratch test for dermographism, environmental evaluation, and even skin biopsy if considering systemic treatment.

Given the lack of evidence-based treatments for papular urticaria, we have suggested a therapeutic ladder that addresses (1) a presumed arthropod assault; (2) the pathophysiology of the allergic and inflammatory response; and (3) the severity of the inflammation at presentation.

The most effective treatment for papular urticaria is the identification and removal of the offending arthropod . This may require intense investigation by both physician and patient. Empiric therapy for scabies should be given because benefits outweigh the risks. This can be achieved with application of permethrin cream 5% or malathion lotion 0.5% once and reapplication 3–7 days later. In the case of suspected bed bugs and fleas, fumigation of the home is required using professional services. Fumigation of the home should also be considered in recurrent cases of papular urticaria. Clothes and bedding should be laundered before and after treatment; specifically, they should be placed in a dryer at 60°C for 10 min to dehydrate and kill scabies and bed bugs. In persistent cases, application of diethyl-m-toluamide (DEET) before bed may help. If there are pets in the home, aggressive flea control and veterinary evaluation may be necessary. If the exposure is thought to be from the outdoors, prevention can be achieved through protective clothing and insect repellents .

While the cause of papular urticaria is being investigated and treated, symptomatic therapy should be implemented immediately for patient comfort. The goal of symptomatic therapy is to reduce and prevent inflammation. The degree of aggressiveness in therapy depends on the degree of inflammation at presentation. For milder cases, topical steroids should be prescribed, with choice of class depending on the severity of lesions. For individual refractory or severe lesion, intralesional triamcinolone is often helpful. If these are ineffective or if the inflammatory response is severe on initial presentation, proceed to systemic immunosuppression – for example, a 10-day oral prednisone taper starting at 1 mg/kg or 1 mg/kg of intramuscular triamcinolone. Systemic corticosteroids will often permanently blunt the inflammatory reaction, provided the antigenic stimulus has been removed. If papular urticaria becomes chronic in the context of two failed courses of systemic steroids and negative pest control investigations, a biopsy and consideration of a broadened differential diagnosis could precede other systemic immunosuppressants, such as phototherapy, ciclosporin, methotrexate, or biologic agents (i.e., dupilumab and omalizumab) .

Pruritus control is often achieved with antihistamines. In milder cases, non-sedating antihistamines such as loratadine, desloratadine, fexofenadine, cetirizine, or levocetirizine can help alleviate symptoms. Doses above those given on the product labeling may be necessary. With more severe itching, diphenhydramine and hydroxyzine are favored. In chronic or recurrent cases, T-cell–mediated lesions, in contrast to the histamine-mediated lesions of early papular urticaria, may render antihistamines ineffective. In that case, topical agents, such as camphor/menthol, calamine lotion, crotamiton, lidocaine, and pramoxine can help.

Careful attention should be paid to any signs of infection secondary to scratching, and appropriate topical or oral antibiotics should be used.

Infrequently, cases of papular urticaria persist without the offending arthropod ultimately being identified. Although rare, hospitalizing the patient for a period of 3–7 days, while simultaneously treating for scabies on admission, results in resolution as reexposure to arthropod antigenic stimuli ceases in the hospital environment. In refractory cases, eruptions will continue until the patient is naturally hyposensitized over time. Hyposensitization can take years to develop, and the concept can be especially confusing to those who have no pets in the home or for those where only one family member is affected.

Bed bugs ( Cimex lectularius ) tend to live in wallpaper, mattress seams, couches, and headboards but can also be found in luggage, vehicles, and clothing. Importantly, they can live away from a host for up to 1 year after just one blood meal and can be spread via used furniture as well as travelers (clothing, baggage). They feed at night every 4–12 min and typically cause a painless bite of which the host is unaware. In vitro, bed bugs have been found to transmit hepatitis B, but there is no evidence for human transmission. Bed bugs are detected by human inspection, bed bug–sniffing dogs, and carbon dioxide–emitting monitoring systems.