Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperactivity of the sympathetic nervous system produces many of the skin changes of hyperthyroidism, while the hypometabolic state and the accumulation of mucopolysaccharides in the dermis are responsible for hypothyroid cutaneous manifestations. Acropachy, atopic eczema, localized myxedema and nail changes are associated with thyrotoxicosis. Vitiligo may be seen in all three thyroid diseases of autoimmune origin. Hyperpigmentation, pruritus and urticaria are associated with hyperthyroidism.
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PMID:Cutaneous signs of thyroid disease. 376 64

Hormones of the thyroid gland (thyroxine, tri-iodothyronine) control the metabolism of cells and tissue of the body, while parathormone and calcitonine are balancing the intra- and extracellular levels of calcium and phosphorus by governing some metabolic functions of bones, kidney and small intestine. Growth, maturation and metabolic homeostasis of the organism depend, among other intrinsic factors, on a normal production and secretory rate of both thyroidal and parathyroidal hormones. Clinical conditions of hyperthyroidism induce 1. increased metabolic turnover of the body with transcutaneous heat loss, 2. disordered growth of hairs and nails, 3. hyperpigmentation of skin, 4. pruritus with or without urticaria. Pretibial (usually symmetrical) myxedema may be associated with conditions of either hyper- or hypothyroidism (e.g., Hashimoto's thyroiditis); if combined with bilateral exophthalmus and acropachyderma of fingers and toes, it is called Diamond syndrome, or E.M.O. syndrome. In hypothyroidism, the skin feels chilly and dry, looks pale, and may present follicular keratoses with or without secondary eczema. The hair appears dull and sparse due to disordered anagen phase. Skin wounds heal with delay. Diffuse myxedema originates in the papillary and periadnexal connective tissue and eventually extends to the dermis as a whole. Clinical conditions of hyperparathyroidism rarely cause secondary calcification of the skin; they may induce severe pruritus, particularly in secondary hyperparathyroidism due to renal failure. Impetigo herpetiformis or generalized pustular psoriasis, resp., may be set off by excessive surgical removal of the goiter. Congenital maldevelopment of both thymus and parathyroid gland leads to cellular immune deficiency with secondary chronic muco-cutaneous candidosis.
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PMID:[The thyroid gland, the parathyroid gland and the skin]. 648 58

The cutaneous mucinoses are a heterogeneous group of diseases in which mucin accumulates in the skin or within the hair follicle. We divide the cutaneous mucinoses into two groups: the distinctive cutaneous mucinoses in which the mucin deposit is a distinctive histopathologic feature that manifests as a clinically specific lesion, and the diseases associated with histopathologic mucin deposition as an additional finding. This article deals with the clinical and histopathologic features and the treatment of the distinctive cutaneous mucinoses and updates their classification. They may be divided, according to the microscopic location of mucin, into dermal and follicular mucinoses. The former group includes; lichen myxedematosus, acral persistent papular mucinosis, reticular erythematous mucinosis, scleredema, dysthyroidotic mucinoses (i.e. localized myxedema, generalized myxedema, papular mucinoses associated with thyroid diseases), papular and nodular mucinosis associated with lupus erythematosus, self-healing juvenile cutaneous mucinosis, cutaneous mucinosis of the infancy, cutaneous toxic mucinoses (papular mucinosis of the toxic oil syndrome and of eosinophiliamyalgia syndrome), neuropathia mucinosa cutanea, cutaneous focal mucinosis, mucous cyst (digital and of the oral mucosa), while the latter group includes Pinkus' follicular mucinosis and urticaria-like follicular mucinosis.
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PMID:[Cutaneous mucinosis]. 833 31

There has been a rapid expansion in the use of IGIV for an ever-growing number of conditions. It is a product with an excellent safety record without the side effects of steroids or other immunosuppressive agents. There have been numerous recent advances in our understanding of the mechanisms of action of IGIV in many of the conditions for which it is being used, but there is still much to be learned. IGIV has had a major impact in neurology, haematology, immunology, rheumatology and dermatology. The limitations for IGIV are cost of the preparation itself and the logistical problems associated with its administration. Here we describe the published evidence for the use of high-dose IGIV in the dermatological conditions atopic dermatitis, urticaria, scleromyxedema, pyoderma gangrenosum, psoriasis and pretibial myxedema. These conditions have an emerging evidence base for hdIGIV which is relatively small consisting mainly of case reports and small case series. The outcomes in a number of these conditions appear encouraging, but as the reports are likely to reflect a bias for positive results, one must be cautious about drawing firm conclusions.
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PMID:Use of IGIV in the treatment of atopic dermatitis, urticaria, scleromyxedema, pyoderma gangrenosum, psoriasis, and pretibial myxedema. 1650 20

Angioedema is a self-limiting edema of the subcutaneous or submucosal tissues due to localised increase of microvascular permeability whose mediator may be histamine or bradykinin. Patients present to emergency department when angioedema involves oral cavity and larynx (life-threatening conditions) or gut (mimicking an acute abdomen). After initial evaluation of consciousness and vital signs to manage breathing and to support circulation if necessary, a simple approach can be applied for a correct diagnosis and treatment. Forms of edema such as anasarca, myxedema, superior vena cava syndrome and acute dermatitis should be ruled out. Then, effort should be done to differentiate histaminergic from non-histaminergic angioedema. Concomitant urticaria and pruritus suggest a histaminergic origin. Exposure to allergens and drugs (mainly ACE inhibitors and non steroidal anti-inflammatory drugs) should be investigated as well as a family history of similar symptoms. Allergic histaminergic angioedema has a rapid course (minutes) whereas non histaminergic angioedema is slower (hours). Since frequently the intervention needs to be immediate, the initial diagnosis is only clinical. However, laboratory tests can be subsequently confirmatory. Allergic angioedema is sensitive to standard therapies such as epinephrine, glucocorticoids and antihistamines whereas non histaminergic angioedema is often resistant to these drugs. Therapeutic options for angioedema due C1-inhibitor deficiencies are C1-inhibitor concentrates, icatibant and ecallantide. If these drugs are not available, fresh frozen plasma can be considered. All these medications have been used also in ACE inhibitor-induced angioedema with variable results thus they are not currently recommended whereas experts agree on the discontinuation of the causative drug.
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PMID:Angioedema and emergency medicine: From pathophysiology to diagnosis and treatment. 3022 Apr 53