Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0033774 (
pruritus
)
14,546
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Subepidermal autoimmune bullous dermatoses are defined by clinical, histological and immunological criteria, notably the presence of anti-basement membrane antibodies detectable in vivo by direct immunofluorescence. We report three cases where anti-basement membrane antibodies were not detectable in vivo by direct immunofluorescence but were detected in high titres by indirect immunofluorescence. This situation is extremely rare in the literature. The first case concerns a 69-year old woman seen for bullous and pruriginous lesions of the lower limbs of 2 months' duration. Histological examination found dermoepidermal bullae with, in their lumen, a serous fluid spotted with numerous polymorphonuclears. A search for anti-basement membrane antibodies was positive in significant titres (1,280; 320; 480) at indirect immunofluorescence on rabbit lip whereas five successive direct immunofluorescence test in perilesional skin and on the thigh medial surface remained negative. The second case is that of a 91-year old woman suffering from generalized
pruritus
associated with erythematous lesions predominant on the extension surfaces of the forearms and thighs, without any bullous lesion. Pathological examination only showed a superficial dermal lymphocytic infiltrate. Four direct immunofluorescence tests were negative, whereas a search for anti-basement membrane antibodies on rat oesophagus was positive at 1/1,280. The third case resembles the second one. It concerns a 72-year old woman who consulted for generalized
pruritus
of several months' duration which interfered with sleep and was incompletely relieved by emollients. There was no specific skin lesion. Pathological examination revealed nothing more than a discrete perivascular mononucleate infiltrate. Direct immunofluorescence tests performed on two occasions on the skin of the abdomen and of the medial thigh surface were negative.(ABSTRACT TRUNCATED AT 250 WORDS)
Ann
Dermatol
Venereol 1992
PMID:[Does bullous pemphigoid with negative direct immunofluorescence exist? Apropos of 3 cases]. 128 98
Erythema gyratum reopens is a slowly expanding, mildly scaling dermatosis with a "wood-grain" pattern and is seen in patients with an underlying malignancy. To date only 49 cases have appeared in the literature, 41 of which (84%) were associated with a neoplasm, most commonly of the lung. Several patients also had
pruritus
, palmoplantar keratoderma, ichthyosis, vesiculobullous lesions, and/or eosinophilia. Histopathologic findings are nonspecific. The skin findings usually disappear with therapy for the underlying malignancy.
J Am Acad
Dermatol
1992 May
PMID:Erythema gyratum repens: a paraneoplastic eruption. 158 77
This article has attempted to summarize the various causes of vulvar
pruritus
and present a framework for evaluating these patients. Although not all patients have a readily classifiable disorder, symptomatic treatment and reassurance can provide considerable patient relief. There is no easy answer, yet the recognition that the process is treatable, if not curable, should provide encouragement for both patients and their physicians.
Dermatol
Clin 1992 Apr
PMID:Vulvar dermatoses and pruritus vulvae. 160 61
Sexually transmitted disorders may present on the vulva as ulcers, rashes, edema, adenopathy, or
pruritus
. Clinical and laboratory skills are needed to distinguish one from another so that the proper treatment is selected and further venereal spread is prevented.
Dermatol
Clin 1992 Apr
PMID:Sexually transmitted diseases of the vulva. 160 66
Six of nine adults who developed Red Sea coral contact dermatitis had seafood allergies. Contact with the "fire" coral was followed by a series of skin eruptions starting with an immediate pruritic urticaria-like lesion which forced the victims out of the water. Within minutes the affected area became erythematous and edematous with eventual blister formation approximately 6 hours after the initial contact. The blisters resolved, leaving violaceous papules and plaques in a streaky fashion corresponding to where the coral brushed the skin. The lesions became shiny and lichenoid in 3 weeks while
pruritus
persisted. Treatment with topical corticosteroids and oral antihistamines reduced the severity of the disease but did not stop its evolution to the lichenoid stage. Complete resolution usually occurred after 15 weeks, leaving residual hyperpigmented macules.
Int J
Dermatol
1991 Apr
PMID:Red sea coral contact dermatitis. 167 31
Atopic dermatitis is a genetically determined inflammatory condition in which the primary defect is expressed in one or more hematopoietic cells that infiltrate the skin. It is a multifactorial disease with inflammation triggered by a variety of factors. Among these, atopic dermatitis has been experimentally induced and reproduced by emotional-stress interviews and food challenges only. The inflammatory events of atopic dermatitis appear to initiated by mast cells, but eosinophils, monocytes, and T lymphocytes (predominantly CD4) also are present in lesions. The secondary effects of inflammation are a dry, brittle stratum corneum and
pruritus
, causing excoriation and a lichenified epidermal layer resulting from chronic rubbing. Therapeutic approaches to atopic dermatitis may be directed at several points in the evolution of the disease. Agents including emollients are needed to preserve and restore the stratum corneum barrier, and effective antipruritics are required to reduce the self-inflicted damage to the involved skin. Various other agents may be needed to antagonize mediators or cytokines and to inhibit cytokine expression and release from lesional, immune-effector cells. Likewise, new phosphodiesterase inhibitors, calcium-active agents, and antiallergic drugs may be used to reduce the quantity and pathologic functioning of inflammatory infiltrating cells in the skin.
J Am Acad
Dermatol
1991 Jun
PMID:Atopic dermatitis: new therapeutic considerations. 167 14
A double blind study against placebo was carried out in order to assess the inhibition induced by oxatomide gel in specific and aspecific cutaneous responses (prick test). Twenty allergic patients (8 M, 12 F) aged between 15 and 59 years (average 31) were treated for 7 days with oxatomide gel 5% or with placebo (2 applications a day). The results show a significant reduction of
itching
and of wheal size (considering either major diameter and area) only in the oxatomide group (p less than 0.01 between times and p less than 0.001 between treatments), whereas among controls
itching
remained unchanged and wheal size increased. During the follow-up a gradual return of wheal size to initial values in the patients treated was observed.
G Ital
Dermatol
Venereol 1990 Aug
PMID:[Evaluation of the inhibition of allergen-specific and nonspecific skin responses by topical oxatomide]. 168 30
A multicenter, randomized, investigator-blind controlled trial was conducted to compare the safety and efficacy of a single, whole-body application of 5% permethrin cream with that of 1% lindane lotion for the treatment of scabies in 467 patients. At 14 +/- 3 days after treatment, the mean active lesion count decreased from pretreatment levels of 85 (range, 4 to 600) in both treatment groups to 14 (range, 0 to 133) in the permethrin group and to 15 lesions (range, 0 to 500) in the lindane group. At 28 +/- 7 days after treatment, complete resolution had occurred in 181 (91%) of 199 patients treated with permethrin and in 176 (86%) of 205 patients given lindane.
Pruritus
due to scabies persisted at 28 +/- 7 days in 14% of the permethrin group and in 25% of the lindane group. The most frequent adverse effects were new or increased
pruritus
and mild, transient burning or stinging; the latter was slightly more frequent following permethrin treatment and appeared to be related to severity of infestation. Because of a lower potential for neurologic toxicity, permethrin may be preferable to lindane for the treatment of scabies particularly in children.
Arch
Dermatol
1990 Feb
PMID:Comparative study of 5% permethrin cream and 1% lindane lotion for the treatment of scabies. 169 22
Pediculosis can be caused by two distinctly different organisms, the head louse and the pubic louse. Although differing anatomically, they produce equivalent disorders, with
itching
, bites, and nits on the hairs. The head louse causes disease of the scalp, while the pubic louse lives in short hair in the pubic regions, the body, the axillae, the eyebrows, and the eyelashes. Both can be treated with gamma isomer of hexachlorobenzene, but various mixtures of pyrethrins seem more effective. The body louse, which exactly resembles the head louse, is the only one that can transmit disease. Treatment of body louse infestation is mainly cleanliness: washing the patient and changing his clothing.
Dermatol
Clin 1990 Apr
PMID:Pediculosis. 169 87
The onset of mastocytosis occurs between birth and 2 years of age in approximately 55% of all cases; an additional 10% develop the disease before the age of 15 years. Mastocytosis in these age groups differs in many respects from mastocytosis that has its onset in adulthood. The typical presentation of pediatric-onset mastocytosis consists of cutaneous manifestations: either a solitary mastocytoma, urticaria pigmentosa, or, less commonly, diffuse cutaneous mastocytosis. Particularly in infants, bullous eruptions may occur. Mastocytosis in infants and children may involve internal organs, including the bone marrow and the gastrointestinal tract, although such manifestations appear to be less common in children than in adults. Plasma histamine levels may be elevated in pediatric-onset mastocytosis. Treatment usually involves the use of H1 and H2 antihistamines to control
itching
and to control the hypersecretion of gastric acid that may occur. The prognosis for children with mast cell disease is variable; approximately half of the children with urticaria pigmentosa may experience resolution of lesions and symptoms by adolescence.
J Invest
Dermatol
1991 Mar
PMID:Pediatric mastocytosis. 170 49
<< Previous
1
2
3
4
5
6
7
8
9
10
Next >>