Evaluation of the Efficacy of Narrow Band Ultraviolet B in the Treatment of Chronic Urticaria
Ayat Ali Mahmoud Bersy;
Abstract
Chronic urticaria is defined as the presence of urticarial wheals (hives), that persists for longer than six weeks. It occurs with or without angioedema. It occurs at a prevalence of 0.1% in up to 3% of the population. It is more common in adults and more in middle aged females. Urticaria is not a life-threatening disease; however, CU has been shown to have a negative impact on the quality of life of affected patients. Chronic idiopathic urticaria are hives with unknown cause.
There are various types of CU including: idiopathic urticaria (50%), autoimmune urticaria (30-40%), physical urticaria, dermatographism, cholinergic urticaria, cold urticaria, delayed pressure urticaria, solar urticaria, urticarial vasculitis and papular urticaria.
There are multiple causes of urticaria that include drugs, food and food additives, physical triggers, underlying infections, autoimmune disease, underlying malignancy and thyroid diseases.
Chronic urticaria is a heterogeneous disorder with varying underlying pathophysiologic abnormalities. The timing of the cellular infiltrate is unknown, largely because it is difficult to establish the duration of one single hive. The infiltrating cells, T-cells, monocytes, neutrophils, and eosinophils release additional mediators, cytokines, and chemokines, amplifying the initial urticarial response that results from the activation of the cutaneous mast cells.
Mast cell is the principal effector cell of urticaria. They express high affinity IgE receptors (FcєRIs) that enable their involvement in IgE-dependent allergic reactions. When IgE forms a complex with FcєRI on mast cell to which an allergen binds, degranulation occurs.
Histamine is the key mediator and other preformed cytokines are also released. Histamine, TNF-, and IL-8 upregulate the expression of adhesion molecules on endothelial cells and encourage the migration of circulating inflammatory cells from the blood into the urticarial lesion.
The pathogenesis of CIU has long remained a mystery and the cause is rarely identified. Thus it is called idiopathic. Many studies suggested different etiopathogenesis for CU including autoimmunity disorders as FcεRI and IgE auto-antibodies and thyroid auto-antibodies; coagulation; diet; infections as hepatitis, parasitic infestations and helicobacter pylori; and malignancy.
The diagnosis is based primarily on the clinical history and further investigations may not be required. A variety of skin tests may be required such as: skin prick test, intradermal skin test, patch skin test, autologous serum skin test (ASST) and skin biopsy. Other important laboratory tests may be of value in distinguishing the etiology of chronic urticaria such as: complete blood count with differential, ESR, thyroid function and auto-antibodies, hepatitis B and C titer, parasitology and urine analysis.
Chronic urticaria is a frequent problem where response to treatment is often disappointing. Treatment of patients with chronic urticaria involves reduction of symptoms with the least invasive therapy and carefully balancing risk and benefit. First-line therapy includes patient education and general measures including avoidance of aggravating factors followed by a trial of histamine H1 receptor antihistamines if symptoms persist. If urticarial symptoms are not controlled by antihistamines alone, second line therapies should be considered, Several classes of drugs may be useful in second-line therapy, including antidepressants, corticosteroids, leukotriene receptor antagnosits and thyroxine. Phototherapy and photochemotherapy have been also considered as a second line of therapy in CU. Third-line therapy for patients who do not respond to first and second line treatments typically involves the use of immunomodulatory agents, which include cyclosporine, tacrolimus, methotrexate, mycophenolate, antimalarial agents and intravenous immunoglobulins.
The treatment of skin diseases with ultraviolet radiation represents an important therapeutic modality in clinical dermatology, and the number of skin diseases that improve under the phototherapeutic modalities is still growing.
There are various types of CU including: idiopathic urticaria (50%), autoimmune urticaria (30-40%), physical urticaria, dermatographism, cholinergic urticaria, cold urticaria, delayed pressure urticaria, solar urticaria, urticarial vasculitis and papular urticaria.
There are multiple causes of urticaria that include drugs, food and food additives, physical triggers, underlying infections, autoimmune disease, underlying malignancy and thyroid diseases.
Chronic urticaria is a heterogeneous disorder with varying underlying pathophysiologic abnormalities. The timing of the cellular infiltrate is unknown, largely because it is difficult to establish the duration of one single hive. The infiltrating cells, T-cells, monocytes, neutrophils, and eosinophils release additional mediators, cytokines, and chemokines, amplifying the initial urticarial response that results from the activation of the cutaneous mast cells.
Mast cell is the principal effector cell of urticaria. They express high affinity IgE receptors (FcєRIs) that enable their involvement in IgE-dependent allergic reactions. When IgE forms a complex with FcєRI on mast cell to which an allergen binds, degranulation occurs.
Histamine is the key mediator and other preformed cytokines are also released. Histamine, TNF-, and IL-8 upregulate the expression of adhesion molecules on endothelial cells and encourage the migration of circulating inflammatory cells from the blood into the urticarial lesion.
The pathogenesis of CIU has long remained a mystery and the cause is rarely identified. Thus it is called idiopathic. Many studies suggested different etiopathogenesis for CU including autoimmunity disorders as FcεRI and IgE auto-antibodies and thyroid auto-antibodies; coagulation; diet; infections as hepatitis, parasitic infestations and helicobacter pylori; and malignancy.
The diagnosis is based primarily on the clinical history and further investigations may not be required. A variety of skin tests may be required such as: skin prick test, intradermal skin test, patch skin test, autologous serum skin test (ASST) and skin biopsy. Other important laboratory tests may be of value in distinguishing the etiology of chronic urticaria such as: complete blood count with differential, ESR, thyroid function and auto-antibodies, hepatitis B and C titer, parasitology and urine analysis.
Chronic urticaria is a frequent problem where response to treatment is often disappointing. Treatment of patients with chronic urticaria involves reduction of symptoms with the least invasive therapy and carefully balancing risk and benefit. First-line therapy includes patient education and general measures including avoidance of aggravating factors followed by a trial of histamine H1 receptor antihistamines if symptoms persist. If urticarial symptoms are not controlled by antihistamines alone, second line therapies should be considered, Several classes of drugs may be useful in second-line therapy, including antidepressants, corticosteroids, leukotriene receptor antagnosits and thyroxine. Phototherapy and photochemotherapy have been also considered as a second line of therapy in CU. Third-line therapy for patients who do not respond to first and second line treatments typically involves the use of immunomodulatory agents, which include cyclosporine, tacrolimus, methotrexate, mycophenolate, antimalarial agents and intravenous immunoglobulins.
The treatment of skin diseases with ultraviolet radiation represents an important therapeutic modality in clinical dermatology, and the number of skin diseases that improve under the phototherapeutic modalities is still growing.
Other data
| Title | Evaluation of the Efficacy of Narrow Band Ultraviolet B in the Treatment of Chronic Urticaria | Other Titles | تقييم كفاءة استخدام الآشعة فوق البنفسجية ب ضيقة النطاق في علاج الشرية المزمنة | Authors | Ayat Ali Mahmoud Bersy | Issue Date | 2012 |
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