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)

A 59-year-old Caucasian housewife presented with a 2-year history of marked loss of tissue substance from the finger and toe pulps and the heel pads. There was no clinical evidence or history of urticaria or other inflammatory change. Investigations demonstrated a raised plasma cortisol secondary to a left adrenal adenoma. Skin biopsies showed abnormalities of dermal collagen, but no evidence of elastin destruction. This case presents an unusual variant of the cutaneous atrophy associated with Cushing's syndrome.
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PMID:Profound digital collagen atrophy: a new cutaneous presentation of adrenal-dependent Cushing's syndrome. 224 95

The porphyrias are the only group of diseases caused by endogenous phototoxic agents. While patients with erythropoietic protoporphyria and those with porphyria cutanea tarda both have skin lesions on sun-exposed areas, there are differences in their cutaneous manifestations. Based on information discussed in this chapter, the following pathophysiologic mechanisms can be proposed. In porphyria cutanea tarda, photoactivation of the complement system in the presence of uroporphyrin results in activation of dermal mast cells, which release their proteases. This results in dermal-epidermal separation, reflected clinically as skin fragility and vesicles. The interaction between activated mast cells with fibroblasts, the nature of which is still unclear, may contribute to fibrosis and sclerodermoid skin changes. The stimulatory effect of uroporphyrin on collagen biosynthesis by fibroblasts, which occurs independent of irradiation, may be responsible for the sclerodermoid lesions seen at sun-exposed as well as sun-protected areas. In erythropoietic protoporphyria, mast cell activation can occur as the result of complement activation induced by protoporphyrin and irradiation. Protoporphyrin and irradiation may also directly induce the release of preformed and generated mediators from mast cells, a process mediated at least in part by peroxidation. The release of mast cell mediators may account for the erythema, edema, and urticaria observed in patients with erythropoietic protoporphyria upon exposure to sunlight. Interaction of mast cells with fibroblasts, and the direct membrane-damaging effect of protoporphyrin and irradiation on the latter, may contribute to the waxy thickening of skin seen in chronically sun-exposed areas of these patients. There are, however, many unanswered questions. What accounts for the different biological effects of mast cell-derived mediators: dermal-epidermal separation in one, erythema and urticaria in the other? The fragmentation of dermal collagen bundles associated with cleavage beneath the lamina densa, and the hyperpigmentation and hypertrichosis observed in some patients with porphyria cutanea tarda remain unexplained. What is the mechanism of the reduplication of blood vessel basal lamina in the non-sun-exposed areas of both types of patient? Are there any roles for cytokines and epidermal cell-derived eicosanoids? While it is clear that the pathogenesis of cutaneous lesions in porphyria cutanea tarda and erythropoietic protoporphyria involves interactions among inflammatory mediators and various cells in skin, much still needs to be done to further our understanding of their pathophysiology.
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PMID:Mechanisms of phototoxicity in porphyria cutanea tarda and erythropoietic protoporphyria. 248 74

Corticosteroids, though known to act effectively against allergy and hypersensitivity, may themselves produce such reactions, ranging from urticaria to anaphylaxis. A middle-aged man with collagen vascular disease developed purpuric rash on repeated administration of steroids. This acute purpuric reaction with sequential colour changes is different than the more common senile purpura-like lesions induced by intake of steroids. It is also different than the purpuric lesions associated with collagen vascular disease per se. The present case favours an allergic aetiology.
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PMID:Prednisolone purpura. 253 97

The term necrotizing angiitis signifies a histological lesion combining an inflammatory infiltration rich in pycnotic polynuclear cells to fibrinoid deposits of the vessels wall and/or of the near by collagen. This type of lesions may affect vessels of small caliber or vessels with a muscular wall (arterioles). In the skin, with the term necrotizing angiitis, is implied a lesion affecting the small vessels of the dermis, capillaries and mostly post-capillary venules. The most frequent, by far, clinical manifestation is a palpable purpura; more seldom, it may be lesions of urticaria, livedo or necrotic lesions. these cutaneous necrotizing angiitis may represent alone the entire symptomatology; they may be associated with varied deep localizations of the same type and finally combine with or precede diseases perfectly defined in other respects, especially collagen diseases. Thus, the term necrotizing angiitis refer to a multitude of entities, syndromes which it is only possible to regroup with many clinical, immuno-pathological, etiological and biological data, each of these data alone being an insufficient reference to characterize them.
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PMID:[Cutaneous necrotizing angiitis]. 356 84

The aim of this study was to evaluate the presence of inflammatory phenomena and elastic fiber phagocytosis in mid-dermal elastolysis. The pathological and ultrastructural features of 5 Caucasian female patients (ranging from 26 to 40 years) with acquired diffuse asymptomatic areas of skin wrinkling have been reviewed. The clinical features of all cases were characteristic of this condition and only in one patient were erythematous urticaria-like, non pruriginous patches also observed. In 4 cases a history of prolonged sun bathing was present and in 3 cases there was a short history of oral contraception. The pathological study confirmed the typical absence of elastic fibers in the midreticular dermis. In two cases elastic fibers were still detectable in the periadnexal dermis. Hematoxylin and eosin sections showed a mild perivascular infiltrate in two cases, while in three patients histiocytes were scattered among collagen bundles. Multinucleated giant cells containing fragmented elastic fibers were detectable in one patient. Ultrastructural analysis revealed large mononuclear cells with phagocytic aspects toward elastic fibers in all cases.
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PMID:Mid-dermal elastolysis: a pathological and ultrastructural study of five cases. 872 51

A case of contact urticaria associated with a serous rhinitis, dyspnea, wheezing, and a dry cough appearing after the application of a hair conditioner on the scalp is reported. Prick test results with the conditioner diluted at 1/16 and 1/8 were strongly positive (+3), as well as a prick test (+3) with one component of the conditioner called "hydrolyzed proteins," which contained hydrolyzed bovine collagen and stearyl trimethylammonium chloride.
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PMID:Contact urticaria with systemic symptoms caused by bovine collagen in a hair conditioner. 879 44

Wells' syndrome, or eosinophilic cellulitis, is characterized by recurrent cutaneous swellings which resemble acute bacterial cellulitis, and by distinctive histopathological changes. Skin lesions show dermal eosinophilic infiltration and the characteristic 'flame figures', which are composed of eosinophil major protein deposited on collagen bundles. The idiopathic hypereosinophilic syndrome is a multisystem disease with a high mortality rate. It is characterized by peripheral blood eosinophilia and eosinophilic infiltration of many organs, including the skin. The most common skin lesions are pruritic maculopapules and nodules over the trunk and limbs, with urticaria and angio-oedema. In contrast to Wells' syndrome, the pathology of these skin lesions is non-specific with variable eosinophil infiltration. We report overlapping clinical and histopathological findings characteristic of both syndromes in one patient. Our data favour the hypothesis that both syndromes represent an abnormal eosinophilic, response to a variety of underlying diseases or causative agents and thus are different expressions of one disease entity linked to the immunobiology of eosinophils.
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PMID:Wells' syndrome associated with idiopathic hypereosinophilic syndrome. 947 Sep 19

Protein hydrolysates (PHs) are added to hair-care products (to "repair" broken hair), soaps, bath gels, creams, etc. From one to 22 PHs used in hair-care products (collagen, keratin, elastin, milk, wheat, almond, and silk) were tested in three patient groups: A) 11 hairdressers with hand dermatitis B) 2160 consecutive adults with suspected allergic respiratory disease subjected to routine skin prick tests C) 28 adults with atopic dermatitis. In group A, all the 22 PHs were tested with scratch and patch tests. In groups B and C, one to three PHs were tested with prick tests. Positive scratch/prick test reactions were seen in 12 patients from three PHs altogether. All were women with atopic dermatitis, and all reacted to at least hydroxypropyl trimonium hydrolyzed collagen (Crotein Q). In three patients, prick and open tests with a hair conditioner containing Crotein Q were performed with positive results. One patient reported contact urticaria on her hands, and two reported acute urticaria on their head, face, and upper body from a hair conditioner containing Crotein Q. In seven of the eight studied sera, specific IgE to Crotein Q was detected. In conclusion, PHs of hair cosmetics can cause contact urticaria, especially in patients with atopic dermatitis.
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PMID:Contact urticaria from protein hydrolysates in hair conditioners. 986 Feb 41

This review of recent articles on ocular toxicology concentrates on undesirable effects on the eye induced by systemically used xenobiotics. These include color vision deficiencies or visual field deterioration related to antiepileptic drugs, elevated intraocular pressure associated with inhaled corticosteroids, retinal detachments associated with systemic corticosteroids, rifabutin-induced uveitis, cocaine-related retinal hemorrhagic lesions in utero, deferoxamine-related decreases in vision, ocular allergy to bovine-derived collagen, and a large case study of hydroxychloroquine retinotoxicity. Other publications reviewed include a controlled study showing that glucose levels do not seem to alter color vision, a report that intravenous methotrexate can reach clinically meaningful levels in the aqueous humor, and a study showing the effect of systemic pentoxifylline on ocular blood flow and diabetes. With respect to systemic effects of topical ocular medications, there was a case report of apparent systemic exposure to pilocarpine from an Ocusert (Alza Corp., Palo Alto, CA), generalized urticaria after a single application of 1% cyclopentolate, and asthma induced with topical ketorolac. Readers are reminded that no drug achieves ultimate efficacy or ultimate safety. Thus, the decision to employ a given therapy involves a physician's evaluation of its therapeutic index, that is, the ratio between efficacy and toxicity.
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PMID:Ocular toxicology. 1017 10

A 16-year-old Vietnamese man presented to the Dermatology Clinic with a 10-year history of bizarre brown patches, which initially started as red asymptomatic "bumps" on the trunk, upper and lower extremities, and face. His past medical history was significant for hypothyroidism and idiopathic urticaria. He was on Eltroxin for hypothyroidism. The family history was noncontributory. Physical examination revealed two types of lesion: erythematous, well-circumscribed papules in a linear configuration along with linear hyperpigmented atrophic patches following Blaschko's lines were noted on the lower extremities (Fig. 1), right upper extremity, right flank (Fig. 2), and right jawline. Initial biopsies taken from the papular lesions on the right thigh and right elbow revealed the following changes. The first biopsy showed a slightly thinned epidermis with prominent dilated blood vessels in the superficial dermis. There also appeared to be a slight increase in the amount of collagen in the deep dermis. The findings were reported as in keeping with "epithelial atrophy." The second biopsy from the lesion on the right elbow revealed an acanthotic epidermis. The granular layer was absent in several areas and there was marked overlying parakeratosis. In the dermis, there was a heavy perivascular lymphocytic infiltrate. The appearances were consistent with a psoriasiform dermatitis (Fig. 3). A biopsy taken from the left thigh approximately 18 months later showed slight irregular acanthosis with dermal edema, dilated blood vessels, and a patchy lymphocytic infiltrate. The appearances were compatible with mild inflammation.
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PMID:Atrophoderma of moulin with preceding inflammation. 1112 48


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