Urticaria is a group of disorders that share a distinct skin reaction pattern, namely the occurrence of itchy wheals anywhere on the skin (Yosipovitch et al., 2002).
Urticaria is characterized by raised, pink/erythematous skin lesions that range from a few millimeters in size to several centimeters and may coalesce. An important characteristic of urticaria is that they are evanescent, meaning that old lesions vanish as new ones appear during a span of 24 hours. Typically, urticarial lesions leave no scarring and are generally worsened by scratching. Any area of the body may be involved. However, the most commonly affected regions are the perioral and periorbital regions, tongue, genitalia and extremities (Kaplan, 2002).
Chronic urticaria (CU) …show more content…
pylori may be different in chronic urticaria. Several pathogen-host interactions have been described in the pathogenesis of H. pylori infection. In chronic urticaria it was demonstrated that H. pylori-infected patients showed a higher prevalence of immunoglobulin G (IgG) and in part also immunoglobulin A (IgA) antibodies to the H. pylori-associated lipoprotein lpp20 than H. pylori-infected patients without chronic urticaria (Wedi et al., 2004).
Several mechanisms have been implicated in the pathogenesis of such chronic diseasis. One proposed mechanism is that an increase in gastric vascular permeability during infection results in greater exposure of the host to alimentary allergens (Buhner et al., 2004).
In support of this suggestion that duodenal ulcer patients have a higher incidence of allergic manifestations than controls. Immunoglobulin E (IgE)-containing cells in gastric and duodenal mucosa seem to be the culprits
(Shiotani et al., 2001), although there is limited evidence for H. pylori-specific IgE . Thus, the possibility that patients with urticaria develop specific IgE against H. pylori is an attractive pathogenic explanation that unfortunately has not been confirmed yet (Liutu et al., …show more content…
pylori infection in CU is a subject of intensive debate. This immunomodulation is not only dependent on the virulence of H. pylori but also on host and environmental factors. An alternative possibility is that immunological stimulation by chronic infection may produce, through mediator release, a nonspecific increase in sensitivity of the cutaneous vasculature to agents that enhance vascular permeability.
Furthermore, IgG and IgA antibodies to 19-kDa H. pyloriassociated lipoprotein were found to play a role in the pathogenesis of CU (Mini et al., 2005).
There is a pronounced complement consumption due to H. pylori specific antibodies, which contributes further to the pathogenesis of CU (Greaves, 2002). Some studies have demonstrated, IgG autoantibodies against IgE and/or Fc εRi α in the sera of one-third of patients with CU, and it was postulated that infection with H. pylori may induce production of pathogenetic antibodies possibly by molecular mimicry (Appelmelk et al., 1996).
A growing body of evidence suggests that 30-50% of CU results from an autoimmune process involving functional histamine releasing anti-Fc ε RI α autoantibodies or less commonly, anti-IgE-autoantibodies (Sabroe et al.,
Urticaria is characterized by raised, pink/erythematous skin lesions that range from a few millimeters in size to several centimeters and may coalesce. An important characteristic of urticaria is that they are evanescent, meaning that old lesions vanish as new ones appear during a span of 24 hours. Typically, urticarial lesions leave no scarring and are generally worsened by scratching. Any area of the body may be involved. However, the most commonly affected regions are the perioral and periorbital regions, tongue, genitalia and extremities (Kaplan, 2002).
Chronic urticaria (CU) …show more content…
pylori may be different in chronic urticaria. Several pathogen-host interactions have been described in the pathogenesis of H. pylori infection. In chronic urticaria it was demonstrated that H. pylori-infected patients showed a higher prevalence of immunoglobulin G (IgG) and in part also immunoglobulin A (IgA) antibodies to the H. pylori-associated lipoprotein lpp20 than H. pylori-infected patients without chronic urticaria (Wedi et al., 2004).
Several mechanisms have been implicated in the pathogenesis of such chronic diseasis. One proposed mechanism is that an increase in gastric vascular permeability during infection results in greater exposure of the host to alimentary allergens (Buhner et al., 2004).
In support of this suggestion that duodenal ulcer patients have a higher incidence of allergic manifestations than controls. Immunoglobulin E (IgE)-containing cells in gastric and duodenal mucosa seem to be the culprits
(Shiotani et al., 2001), although there is limited evidence for H. pylori-specific IgE . Thus, the possibility that patients with urticaria develop specific IgE against H. pylori is an attractive pathogenic explanation that unfortunately has not been confirmed yet (Liutu et al., …show more content…
pylori infection in CU is a subject of intensive debate. This immunomodulation is not only dependent on the virulence of H. pylori but also on host and environmental factors. An alternative possibility is that immunological stimulation by chronic infection may produce, through mediator release, a nonspecific increase in sensitivity of the cutaneous vasculature to agents that enhance vascular permeability.
Furthermore, IgG and IgA antibodies to 19-kDa H. pyloriassociated lipoprotein were found to play a role in the pathogenesis of CU (Mini et al., 2005).
There is a pronounced complement consumption due to H. pylori specific antibodies, which contributes further to the pathogenesis of CU (Greaves, 2002). Some studies have demonstrated, IgG autoantibodies against IgE and/or Fc εRi α in the sera of one-third of patients with CU, and it was postulated that infection with H. pylori may induce production of pathogenetic antibodies possibly by molecular mimicry (Appelmelk et al., 1996).
A growing body of evidence suggests that 30-50% of CU results from an autoimmune process involving functional histamine releasing anti-Fc ε RI α autoantibodies or less commonly, anti-IgE-autoantibodies (Sabroe et al.,