In a study, ten patients with chronic urticaria who had normal thyroid levels (but seven of the ten had elevated antithyroid antibodies and three controls had no antithyroid antibodies) were treated with the synthetic thyroid drug levothyroxine. March 2001 -- If you have chronic hives and rashes -- a condition known as urticaria -- that come and go, some studies have shown that one common -- but usually overlooked -- cause of such hives is infection with the Helicobacter pylori -- or H. pylori -- bacteria.
This is the same bacteria that has been found to cause some stomac ulcers. Researchers discovered that the antibiotics given to the ulcer patients to rid them of the H. Pylori also cleared up the chronic urticaria.
The researchers also believe that for some patients with chronic urticaria, there is a link to autoimmune disease, and in particular, thyroid disease, as a significant percentage of patients with urticaria also have high levels of antithyroid antibody, even though they may not have clinical thyroid disease.
While receiving the levothyroxine, the seven patients reported that their urticaria symptoms went away within 4 weeks. The three controls did not respond. In five patients, symptoms recurred after treatment was stopped; these symptoms again resolved after treatment was restarted.
Not much is known about the physiology and fate of basophils in urticaria, but it is possible that they have a direct role because "releasability" to anti-IgE has been shown to be reduced and peripheral blood basopenia appears to relate to serum histamine releasing activity in chronic disease. Preliminary findings indicate that numbers are negatively correlated with urticarial activity, supporting the hypothesis that they migrate from blood into skin during wheal formation and contribute to persistence of the wheal.
Basophils comprise about 1% of the circulating granulocytes in humans. In healthy subjects this represents about 40 basophils per l of whole blood, which equates to around 200 million in the circulation at any time. They are characterized by granules that stain with basic dyes. Despite many similarities with tissue mast cells they show developmental, phenotypic, and functional differences. Basophils and mast cells almost certainly arise from a common bone marrow stem cell. Whereas the conditions required for maturation of the basophil are unclear, the phenotype of tissue mast cells is controlled by the local cytokine environment. Mucosal mast cells containing tryptase (MCT cells) mature under the influence of interleukins 3 and 4, but connective tissue mast cells containing tryptase and chymase (MCTC) require the presence of fibroblasts. The survival of blood basophils is unknown but is probably less than mast cells. The fate of basophils that have degranulated in response to a stimulus is not certain, but recovery of the granules within 6 h appears possible There is relatively little literature on basophils in health and disease. This is partly because they are present in low numbers in peripheral blood and are difficult to quantify accurately with automated differentials. Basophils and mast cells cannot be distinguished easily in tissue with conventional stains. Most of the current literature relates to the use of basophils in the diagnosis of allergic disease and histamine releasing activity of serum in urticaria, using assays of functional activity.
The fate of the missing blood basophils in chronic urticaria remains unclear. It is possible that they are actively recruited into wheals by expression of endothelial adhesion molecules, including VCAM-1, induced by degranulation of lesional skin mast cells. This might explain the prolongation of "idiopathic" urticaria wheals well beyond the expected time course of histamine-induced wheals in healthy subjects Basophils in Chronic Urticaria by C E H Grattan
Acquired lipoprotein lipase deficiency associated with chronic urticaria. A new etiology for type I hyperlipoproteinemia AL Garcia-Otin, F Civeira, J Peinado-Onsurbe, C Gonzalvo, M Llobera, and M Pocovi Departments of Biochemistry, Molecular Biology and Medicine, University of Zaragoza, Hospital Miguel Servet, Av. Isabel La Catolica 1-3, 50009, Zaragoza, Spain.
Type I hyperlipoproteinemia (type I HLP) is a rare disorder of lipid metabolism characterized by fasting chylomicronemia and reduced postheparin plasma lipoprotein lipase (LPL) activity. Most cases of type I HLP are due to genetic defects in the LPL gene or in its activator, the apolipoprotein CII gene. Several cases of acquired type I HLP have also been described in the course of autoimmune diseases due to the presence of circulating inhibitors of LPL. Here we report a case of type I HLP due to a transient defect of LPL activity during puberty associated with chronic idiopathic urticaria (CIU). The absence of any circulating LPL inhibitor in plasma during the disease was demonstrated. The LPL genotype showed that the patient was heterozygous for the D9N variant. This mutation, previously described, can explain only minor defects in the LPL activity. The presence of HLP just after the onset of CIU, and the elevation of the LPL activity with remission of the HLP when the patient recovered from CIU, indicate that type I HLP was caused by CIU. In summary, we report a new etiology for type I HLP - a transient decrease in LPL activity associated with CIU and with absence of circulating inhibitors. This is the first description of this association, which suggests a new mechanism for type I HLP.Acquired lipoprotein lipase deficiency associated with chronic urticaria. A new etiology for type I hyperlipoproteinemia
Lyme Disease and Urticaria and possible link? Abstract no: 990500354
Urticarial vasculitis and Lyme disease source: Journal of the American Academy of Dermatology vol. 22 Number 6, Part 1, June 1990, page 1114-1116 author: Judyann Olson M.D., Nancy B. Esterly
"Erythema chronicum migrans (ECM) is the classic skin lesion of Lyme disease, a multisystem disease caused by the spirochete Borrelia burgdorferi. Other cutaneous manifestations of Lyme disease include localized and generalized urticaria, generalized macular eruptions, malar erythema in febrile patients, and septal panniculitis. We describe a child with urticarial vasculitis as the presenting feature of Lyme disease.........in endemic areas a diagnosis of Lyme disease should be considered in patients with a clinical or histologic urticarial vasculitis, because it is a potentially treatable condition." ____________________
from: Lyme Disease and Its Neurological Complications author Michael F. Finkle, MD source: Archives of Neurol--Vol. 45, Jan 1986 Lyme Disease and Urticaria
See survey below! But to see the full list of all chronic urticaria go back to the main page. http://urticariaresearch.blogspot.com/ to post or comment in areas like: your health history,Things we should know about your urticaria, diet and other information.
What type of Urticaria have you been diagnosed with?
How Often ?
How are you feeling about your condition?
Have you been sucessful in finding treatment for your Urticaria?
What type of doctor have you seen?
What lab tests have you had?
Previous history of being diagnosed with Nephritis (kidney ) infection?
Have you been hospitalized for an infection in the past?
Muscle/Joint/Jaw/Neck Pain?
Dental problems/abcess/root canals?
NEW QUESTION Contact lens developing crystals?
Digestive issues?
Any issues after receiving childhood immunizations?
Food sensitivity/?
Had a significant vision change through the years?
MRI Brain/Angioma?
Don't forget to post "your" information!!
This site is dedicated to my husband who has battled chronic urticaria for over 29 years. For more information on your type of urticaria please click on this link http://urticariaresearch.blogspot.com/ to go back to the main page and review areas DOWN THE PAGE which include: WE NEED YOUR IMPUT TO LEARN MORE ABOUT THIS CONDITION! *Your Medical history before and after chronic urticaria *Things we should know about your urticaria *Need prayer *Does location play a part? *Do you have a question? *What are your symptoms and triggers? Together we can find a cure!
Autoimmunity and coagulation in Urticaria
ReplyDeleteScience Direct:chronic Urticaria: a disease at a crossroad between autoimmunity and coagulation
Basohilic leucopenia in different forms of Urticaria Study
ReplyDeleteBasohilic leucopenia in different forms of Urticaria Study
Reduced blood glutathion levels with Chronic Urticaria
ReplyDeleteMedical Journal result studies suggest REDUCED BLOOD GLUTATHION
LEVELS IN PATIENTS WITH CHRONIC URTICARIA
The Fibrinolytic System
ReplyDeleteThe Fibrinolytic System (Blood Urokinase Plasminogen Activator System in Chronic Urticaria)
Don't Forget The Thyroid by Dr. RW Donnell
ReplyDeleteInteresting Article: Don't forget THYROID in Chronic Urticaria by Dr. RW Donnell
Interesting Article: Don't forget THYROID in Chronic Urticaria by Dr. RW Donnell
ReplyDeleteIn a study, ten patients with chronic urticaria who had normal thyroid levels (but seven of the ten had elevated antithyroid antibodies and three controls had no antithyroid antibodies) were treated with the synthetic thyroid drug levothyroxine.
ReplyDeleteMarch 2001 -- If you have chronic hives and rashes -- a condition known as urticaria -- that come and go, some studies have shown that one common -- but usually overlooked -- cause of such hives is infection with the Helicobacter pylori -- or H. pylori -- bacteria.
This is the same bacteria that has been found to cause some stomac ulcers. Researchers discovered that the antibiotics given to the ulcer patients to rid them of the H. Pylori also cleared up the chronic urticaria.
The researchers also believe that for some patients with chronic urticaria, there is a link to autoimmune disease, and in particular, thyroid disease, as a significant percentage of patients with urticaria also have high levels of antithyroid antibody, even though they may not have clinical thyroid disease.
While receiving the levothyroxine, the seven patients reported that their urticaria symptoms went away within 4 weeks. The three controls did not respond. In five patients, symptoms recurred after treatment was stopped; these symptoms again resolved after treatment was restarted.
Chronic Hives, Rashes Associated with Bacteria, Autoimmunity: Antibiotics or Thyroid Drugs May Be an Effective Treatment for Urticaria
UpToDate, electronic clinical resource tool for physicians and patients that provides information on Adult Primary Care and Internal Medicine
ReplyDeleteBACK TO CHRONIC URTICARIA RESEARCH MAIN PAGE
ReplyDeleteNot much is known about the physiology and fate of basophils in urticaria, but it is possible that they have a direct role because "releasability" to anti-IgE has been shown to be reduced and peripheral blood basopenia appears to relate to serum histamine releasing activity in chronic disease. Preliminary findings indicate that numbers are negatively correlated with urticarial activity, supporting the hypothesis that they migrate from blood into skin during wheal formation and contribute to persistence of the wheal.
ReplyDeleteBasophils comprise about 1% of the circulating granulocytes in humans. In healthy subjects this represents about 40 basophils per l of whole blood, which equates to around 200 million in the circulation at any time. They are characterized by granules that stain with basic dyes. Despite many similarities with tissue mast cells they show developmental, phenotypic, and functional differences. Basophils and mast cells almost certainly arise from a common bone marrow stem cell. Whereas the conditions required for maturation of the basophil are unclear, the phenotype of tissue mast cells is controlled by the local cytokine environment. Mucosal mast cells containing tryptase (MCT cells) mature under the influence of interleukins 3 and 4, but connective tissue mast cells containing tryptase and chymase (MCTC) require the presence of fibroblasts. The survival of blood basophils is unknown but is probably less than mast cells. The fate of basophils that have degranulated in response to a stimulus is not certain, but recovery of the granules within 6 h appears possible
There is relatively little literature on basophils in health and disease. This is partly because they are present in low numbers in peripheral blood and are difficult to quantify accurately with automated differentials. Basophils and mast cells cannot be distinguished easily in tissue with conventional stains. Most of the current literature relates to the use of basophils in the diagnosis of allergic disease and histamine releasing activity of serum in urticaria, using assays of functional activity.
The fate of the missing blood basophils in chronic urticaria remains unclear. It is possible that they are actively recruited into wheals by expression of endothelial adhesion molecules, including VCAM-1, induced by degranulation of lesional skin mast cells. This might explain the prolongation of "idiopathic" urticaria wheals well beyond the expected time course of histamine-induced wheals in healthy subjects Basophils in Chronic Urticaria by C E H Grattan
Acquired lipoprotein lipase deficiency associated with chronic urticaria. A new etiology for type I hyperlipoproteinemia
ReplyDeleteAL Garcia-Otin, F Civeira, J Peinado-Onsurbe, C Gonzalvo, M Llobera, and M Pocovi
Departments of Biochemistry, Molecular Biology and Medicine, University of Zaragoza, Hospital Miguel Servet, Av. Isabel La Catolica 1-3, 50009, Zaragoza, Spain.
Type I hyperlipoproteinemia (type I HLP) is a rare disorder of lipid metabolism characterized by fasting chylomicronemia and reduced postheparin plasma lipoprotein lipase (LPL) activity. Most cases of type I HLP are due to genetic defects in the LPL gene or in its activator, the apolipoprotein CII gene. Several cases of acquired type I HLP have also been described in the course of autoimmune diseases due to the presence of circulating inhibitors of LPL. Here we report a case of type I HLP due to a transient defect of LPL activity during puberty associated with chronic idiopathic urticaria (CIU). The absence of any circulating LPL inhibitor in plasma during the disease was demonstrated. The LPL genotype showed that the patient was heterozygous for the D9N variant. This mutation, previously described, can explain only minor defects in the LPL activity. The presence of HLP just after the onset of CIU, and the elevation of the LPL activity with remission of the HLP when the patient recovered from CIU, indicate that type I HLP was caused by CIU. In summary, we report a new etiology for type I HLP - a transient decrease in LPL activity associated with CIU and with absence of circulating inhibitors. This is the first description of this association, which suggests a new mechanism for type I HLP.Acquired lipoprotein lipase deficiency associated with chronic urticaria. A new etiology for type I hyperlipoproteinemia
Lyme Disease and Urticaria and possible link?
ReplyDeleteAbstract no: 990500354
Urticarial vasculitis and Lyme disease
source: Journal of the American Academy of Dermatology vol. 22 Number 6,
Part
1, June 1990, page 1114-1116
author: Judyann Olson M.D., Nancy B. Esterly
"Erythema chronicum migrans (ECM) is the classic skin lesion of Lyme
disease, a multisystem disease caused by the spirochete Borrelia burgdorferi.
Other cutaneous manifestations of Lyme disease include localized and
generalized urticaria, generalized macular eruptions, malar erythema in
febrile
patients, and septal panniculitis. We describe a child with urticarial
vasculitis as the presenting feature of Lyme disease.........in endemic areas
a
diagnosis of Lyme disease should be considered in patients with a clinical or
histologic urticarial vasculitis, because it is a potentially treatable
condition."
____________________
from: Lyme Disease and Its Neurological Complications
author Michael F. Finkle, MD
source: Archives of Neurol--Vol. 45, Jan 1986
Lyme Disease and Urticaria