Pruritic welts

The patient’s history and the classic morphology of raised plaques was consistent with chronic spontaneous urticaria. Erythema may be subtle or not visible in patients with skin of color.

Individual urticarial lesions last less than 24 hours with itching and burning. Angioedema also occurs, and manifests as a deeper edema with itching, burning, and pain. Symptoms typically last for 2 to 3 days and involve the eyelids, lips, and tongue.

Chronic urticaria (CU) is defined as episodes of spontaneous wheals or angioedema lasting for more than 6 weeks and is subdivided into chronic spontaneous urticaria or inducible urticaria (if there is a known cause). Triggers include infection, emotional stressors, or medications (eg, angiotensin-converting enzyme inhibitors, nonsteroidal anti-inflammatory drugs). Autoimmunity is seen in one-third of CU patients.¹

Only a limited routine-diagnostic work-up is necessary for CU and it may include a complete blood count with differential and erythrocyte sedimentation rate and C-reactive protein testing. Further diagnostic testing is based on history and may include functional autoantibodies, thyroid stimulating hormone, and thyroid autoantibodies.

The initial step in treatment involves identification and elimination of triggers. If this is not possible, first-line therapy includes second-generation antihistamines. If symptoms persist beyond 2 weeks, the dose of the antihistamine is increased up to 4-fold. Patients should be counseled that the lowest necessary dose needs to be taken habitually to prevent urticaria. If symptoms persist, omalizumab, a recombinant humanized IgG monoclonal antibody against serum IgE, cyclosporine, or montelukast, may be added. Leukotriene-receptor antagonists such as montelukast were previously second-line therapy, but they have had mixed results in randomized controlled trials. With a much lower cost than omalizumab, leukotriene-receptor antagonists are a reasonable alternative for patients who are refractory to antihistamines.¹

This patient was given high-dose nonsedating antihistamines; she experienced sedation and inadequate relief. A prior authorization was successfully obtained, and she was prescribed omalizumab.

‌

Image courtesy of Kriti Mishra, MD, Department of Dermatology, University of New Mexico School of Medicine, Albuquerque. Text courtesy of Kriti Mishra, MD, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

The patient’s history and the classic morphology of raised plaques was consistent with chronic spontaneous urticaria. Erythema may be subtle or not visible in patients with skin of color.

Individual urticarial lesions last less than 24 hours with itching and burning. Angioedema also occurs, and manifests as a deeper edema with itching, burning, and pain. Symptoms typically last for 2 to 3 days and involve the eyelids, lips, and tongue.

Chronic urticaria (CU) is defined as episodes of spontaneous wheals or angioedema lasting for more than 6 weeks and is subdivided into chronic spontaneous urticaria or inducible urticaria (if there is a known cause). Triggers include infection, emotional stressors, or medications (eg, angiotensin-converting enzyme inhibitors, nonsteroidal anti-inflammatory drugs). Autoimmunity is seen in one-third of CU patients.¹

Only a limited routine-diagnostic work-up is necessary for CU and it may include a complete blood count with differential and erythrocyte sedimentation rate and C-reactive protein testing. Further diagnostic testing is based on history and may include functional autoantibodies, thyroid stimulating hormone, and thyroid autoantibodies.

The initial step in treatment involves identification and elimination of triggers. If this is not possible, first-line therapy includes second-generation antihistamines. If symptoms persist beyond 2 weeks, the dose of the antihistamine is increased up to 4-fold. Patients should be counseled that the lowest necessary dose needs to be taken habitually to prevent urticaria. If symptoms persist, omalizumab, a recombinant humanized IgG monoclonal antibody against serum IgE, cyclosporine, or montelukast, may be added. Leukotriene-receptor antagonists such as montelukast were previously second-line therapy, but they have had mixed results in randomized controlled trials. With a much lower cost than omalizumab, leukotriene-receptor antagonists are a reasonable alternative for patients who are refractory to antihistamines.¹

This patient was given high-dose nonsedating antihistamines; she experienced sedation and inadequate relief. A prior authorization was successfully obtained, and she was prescribed omalizumab.

‌

Image courtesy of Kriti Mishra, MD, Department of Dermatology, University of New Mexico School of Medicine, Albuquerque. Text courtesy of Kriti Mishra, MD, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

The patient’s history and the classic morphology of raised plaques was consistent with chronic spontaneous urticaria. Erythema may be subtle or not visible in patients with skin of color.

Individual urticarial lesions last less than 24 hours with itching and burning. Angioedema also occurs, and manifests as a deeper edema with itching, burning, and pain. Symptoms typically last for 2 to 3 days and involve the eyelids, lips, and tongue.

Chronic urticaria (CU) is defined as episodes of spontaneous wheals or angioedema lasting for more than 6 weeks and is subdivided into chronic spontaneous urticaria or inducible urticaria (if there is a known cause). Triggers include infection, emotional stressors, or medications (eg, angiotensin-converting enzyme inhibitors, nonsteroidal anti-inflammatory drugs). Autoimmunity is seen in one-third of CU patients.¹

Only a limited routine-diagnostic work-up is necessary for CU and it may include a complete blood count with differential and erythrocyte sedimentation rate and C-reactive protein testing. Further diagnostic testing is based on history and may include functional autoantibodies, thyroid stimulating hormone, and thyroid autoantibodies.

The initial step in treatment involves identification and elimination of triggers. If this is not possible, first-line therapy includes second-generation antihistamines. If symptoms persist beyond 2 weeks, the dose of the antihistamine is increased up to 4-fold. Patients should be counseled that the lowest necessary dose needs to be taken habitually to prevent urticaria. If symptoms persist, omalizumab, a recombinant humanized IgG monoclonal antibody against serum IgE, cyclosporine, or montelukast, may be added. Leukotriene-receptor antagonists such as montelukast were previously second-line therapy, but they have had mixed results in randomized controlled trials. With a much lower cost than omalizumab, leukotriene-receptor antagonists are a reasonable alternative for patients who are refractory to antihistamines.¹

This patient was given high-dose nonsedating antihistamines; she experienced sedation and inadequate relief. A prior authorization was successfully obtained, and she was prescribed omalizumab.

‌

Image courtesy of Kriti Mishra, MD, Department of Dermatology, University of New Mexico School of Medicine, Albuquerque. Text courtesy of Kriti Mishra, MD, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.