Biomedical subjects

V DeLeo

Publications and source records attributed to V DeLeo.

13 recordsLinked to original sources

PubMed2001

Gold allergy in North America.

OBJECTIVE: To determine the prevalence of allergic reactions to gold among patients tested by the North American Contact Dermatitis Group (NACDG) from 1996 to 1998. METHODS: This is a prospective analysis of patch test results from the 12 centers that comprise the NACDG. Gold was tested as gold sodium thiosulfate (0.5% in petrolatum [pet]), along with 49 other screening allergens, in patients presenting with possible contact dermatitis. RESULTS: Of 4,101 patients tested, 388 (9.5%) had a positive patch test result to gold. Women accounted for 62.8% of the subjects tested and 90.2% of patients positive to gold (P < .0001). The most common sites of dermatitis in gold-allergic patients were the hands (29.6%), face (19.3%), and eyelids (7.5%). Nickel and cobalt allergies, respectively, also were present in 33.5% and 18.3% of gold allergic individuals, as compared with 14.2% and 9.0% of the total population. Gold was the only positive reaction in 15.2% of the 388 patients. CONCLUSION: Gold is a more common allergen than previously reported and might cause facial and eyelid dermatitis. Hypersensitivity to gold is statistically linked to female gender and to allergic reactions to nickel and cobalt.

Allergens↗

PubMed2000

Phototesting and photopatch testing: when to do it and when not to do it.

Phototesting and photopatch testing are among the most important tests in the evaluation of photodermatoses, yet their use has been restricted to specialized centers. To assist clinicians interested in conducting these procedures and in updating their techniques, we asked 4 experts to comment on these tests in the context of diagnostic approach to the photosensitive patient. A list of photoallergens and a protocol for their use is provided.

Allergens↗

PubMed1998

Inhibition of ultraviolet B (UVB)-induced c-fos and c-jun expression in vivo by a tyrosine kinase inhibitor genistein.

We reported the inhibitory effects of genistein, an inhibitor of tyrosine protein kinase (TPK), on ultraviolet B (UVB)-induced expression of c-fos and c-jun in SENCAR mouse skin. UVB irradiation substantially increased transcript levels of c-fos and c-jun mRNA in mouse skin. Topical application of genistein 60 min before UVB radiation reduced c-fos and c-jun expression in the mouse skin in dose-dependent manner. Inhibition was more pronounced in skin exposed to the low dose (5 kJ/m2) than to the high dose (15 kJ/m2) of UVB radiation. In addition, genistein exhibited more inhibition of c-fos than that of c-jun. Post-application of genistein after UVB exposure down-regulated the expressions of c-fos and c-jun, but to a lesser extent compared with pre-application. A431 human epidermoid carcinoma cells, which excessively express epidermal growth factor receptors (EGF-R), were used to investigate the possible mechanism of genistein's action. The results showed that genistein down-regulated the UVB-mediated phosphorylation of TPK-dependent EGF-R in a dose-dependent manner. We concluded that inhibition of UVB-induced c-fos and c-jun expression in mouse skin by genistein may, at least in part, result from the inhibition of TPK activities and down-regulation of EGF-R phosphorylation. Suppression of UVB-induced proto-oncogene expression in mouse skin suggests that genistein may serve as a potential preventative agent against photodamage and photocarcinogenesis.

Animals↗

PubMed1997

Allergic and immunologic skin disorders.

The skin represents a unique immunologic organ poised to protect the host from invading organisms and environmental antigens. The skin is also an important target for a variety of allergic and autoimmune responses. Mast cells are key to the pathogenesis of urticaria, angioedema, and mastocytosis. Atopic dermatitis is the consequence of an immunoregulatory abnormality resulting in a skin-directed T helper type 2 response. Allergic contact dermatitis is an example of classic delayed type hypersensitivity. Circulating autoantibodies against the epidermis are a key mechanism by which bullous skin diseases occur.

Allergens↗

PubMed1994

Photosensitivity as the presenting illness in four patients with human immunodeficiency viral infection.

BACKGROUND: A multitude of skin lesions have been reported in individuals with human immunodeficiency virus (HIV) infection. Some of them, eg, severe seborrheic dermatitis and herpes zoster infections, may predate the onset of the diagnostic criteria for the acquired immunodeficiency syndrome and may actually raise the suspicion of HIV infection in healthy-appearing individuals. We have recently evaluated four individuals who presented with a severe idiopathic photosensitivity of eczematous morphologic features who eventuated in a diagnosis of HIV seropositivity. Four individuals who presented with an eczematous eruption of sun-exposed skin were referred to the Environmental Dermatology Unit of Columbia-Presbyterian Medical Center (New York, NY) for evaluation of possible photosensitive disease. They were examined and underwent photobiological testing (minimal erythema dose testing and photopatch testing) to confirm and classify their suspected photosensitivity. OBSERVATIONS: All four patients fulfilled the criteria for chronic actinic dermatitis, a rare idiopathic photosensitivity characterized by debilitating, unremitting dermatitis with eczematous or lymphomalike histologic features and reproduction of lesions by small quantities of mid-wave UV-B radiation (290 to 320 nm). All four individuals were HIV seropositive and CD4 counts were markedly suppressed in all four. The photosensitivity predated the finding of seropositivity and the diagnosis of acquired immunodeficiency syndrome in all four patients. CONCLUSION: The presentation of healthy-appearing individuals with photodistributed dermatitis of unknown cause should alert the physician to the possibility of HIV infection.

Adult↗

PubMed1990

Long-wave ultraviolet light induces phospholipase activation in cultured human epidermal keratinocytes.

Long wave ultraviolet radiation (UVA) has been shown to play an important role in the overall response of skin to solar radiation, including sunburn, tanning, premature aging, and non-melanoma skin cancer. UVA induction of inflammation in human skin is thought to be mediated by membrane lipid derived products. In order to investigate the mechanism of this response we examined the effect of UVA on phospholipid metabolism of human epidermal keratinocytes in culture. Keratinocytes were grown in serum free low calcium medium. The cells were prelabeled with [3H] arachidonic acid or [3H] choline and irradiated with UVA (Honle 2002-Hg vapor lamp). Identification and quantitation of specific membrane phospholipid-derived components was achieved using high-performance liquid chromatography, paper chromatography, and radioimmunoassay. UVA resulted in a linear dose dependent release of [3H] arachidonic acid into medium between 1 and 20 joule/cm2. This response was inhibited in an oxygen-reduced environment. The radiolabel released was predominantly free arachidonate and cyclooxygenase metabolites. Cyclooxygenase metabolites prostaglandin E2 and prostacyclin derivative, 6-keto-prostaglandin F1a, were stimulated following UVA irradiation, but the lipoxygenase metabolite, leukotriene B was not detected. Maximal release was measured immediately after irradiation and changed little over 24 h post-irradiation. UVA stimulated an increase of [3H] choline metabolites glycerophosphorylcholine and phosphorylcholine in media extracts suggesting UVA activation of phospholipase C and phospholipase A2 or diacylglyceride lipase.

Arachidonic Acid↗

PubMed1989

Ultraviolet-B (290-320 nm)-irradiation inhibits epidermal growth-factor binding to mammalian cells.

Mitogens, such as polypeptide growth factors and phorbol ester tumor promoters, act by binding to specific receptors and inducing a pleiotropic response in cultured mammalian cells, which results in the induction of cellular proliferation. An early effect of such agents is the inhibition of binding of epidermal growth factor (EGF) to its receptor. Ultraviolet radiation has also been shown to induce a proliferative response in vivo and in vitro and to act as a tumor promoter in animal skin. We, therefore, examined the effect of ultraviolet radiation (UVB - 290-320 nm) on EGF binding to cells in culture. We found that UVB (100-300 J/m2) induced a rapid, dose-dependent inhibition of EGF binding in a mouse fibroblast cell line, which resulted from a decrease in both number and affinity of binding sites. Phosphorylation of the EGF receptor by protein kinase C (PKC) is not likely to be the mechanism for inhibition, since UVB treatment did not result in PKC activation or modulation of phorbol diester binding.

Animals↗

PubMed1989

Photoallergy to benzophenone.

Incorrect diagnosis of photoallergy to sunscreen products represents a unique clinical dilemma. Increasing sunscreen usage for suspected idiopathic photosensitivity or a change to a sunscreen containing the same photoallergen only worsens the problem. While photoallergy to p-aminobenzoic acid and its esters is well known by dermatologists and the lay public, benzophenone photoallergy is not well appreciated. We report herein the cases of four individuals with photoallergy to oxybenzone in sunscreens. It is likely that such reactions will become more commonplace since oxybenzone is by far the most frequently used agent in modern, high sun protection factor sunscreens (greater than 8 sun protection factor) being marketed today.

4-Aminobenzoic Acid↗

PubMed1988

Ultraviolet radiation alters choline phospholipid metabolism in human keratinocytes.

Ultraviolet radiation B (UVB-290-320 nm) induces inflammation and hyperproliferation in human epidermis. This response is associated with the recovery from irradiated skin of inflammatory mediators derived from membrane phospholipids. We have previously reported that UVB stimulates the production of such mediators by human keratinocytes (HK) in culture. In these studies we examined the effect of UVB on the metabolism of choline containing phospholipids in HK prelabeled with [3H] choline. UVB (400-1600J/m2) stimulated a dose dependent release of [3H] choline from HK within minutes of irradiation. Examination of media extracts by paper chromatography revealed that the released [3H] choline was predominately in the form of glycerophosphorylcholine. Examination of label remaining in membranes of cells after irradiation by acid precipitation and HPLC revealed that the origin of the released [3H] choline was the membrane phosphatidylcholine/lysophosphatidylcholine. These data support a concept of UVB stimulation of both a phospholipase A (1 or 2) and a lysophospholipase. These UVB induced alterations of HK membrane phospholipid metabolism likely have profound effects on UVB-induced inflammation and control of cell growth in human skin.

Cells, Cultured↗

PubMed1987

Immunological detection and visualization of 8-methoxypsoralen-DNA photoadducts.

Monoclonal antibodies specific for DNA damaged by 8-methoxypsoralen (8-MOP) plus ultraviolet A (UVA) light were used to study adduct formation in human keratinocytes and mouse and rat skin in vivo. This antibody does not cross-react with nonmodified DNA or free 8-MOP. Sensitive competitive enzyme-linked immunosorbent assays with color or fluorescence endpoints were used to quantitate adducts on DNA isolated from treated keratinocytes or skin samples. Localization of 8-MOP-DNA adducts was studied by indirect immunofluorescence with fluorescein-conjugated anti-mouse-IgG antibodies. When cultured keratinocytes were treated with 8-MOP and UVA, immunofluorescence was localized in the nucleus. There was no fluorescence in untreated control cells or treated cells incubated with nonspecific serum. Comparison of intensity of immunofluorescence staining with quantitation of adduct levels by enzyme-linked immunosorbent assay indicated that the limit of sensitivity of the immunofluorescence technique is 9.0 fmol adduct/micrograms DNA or 2.9 adducts/10(6) nucleotides.

Animals↗

PubMed1987

Allergic contact dermatitis from bacitracin.

Bacitracin is a commonly used topical antibiotic. Although occasional reports of adverse reactions to bacitracin have appeared in the medical literature, it is considered to be a nonsensitizing agent by most dermatologists. A description of two patients who demonstrated allergic contact dermatitis from bacitracin is presented, with a review of the pertinent literature.

Adult↗

PubMed1983

Prolactin lowering effect of amphetamine in normoprolactinemic subjects and in physiological and pathological hyperprolactinemia.

The effect on plasma prolactin (PRL) of d-amphetamine (Amph) was studied in normo- and hyperprolactinemic subjects. In normoprolactinemic women Amph failed to lower plasma PRL levels when infused intravenously over 1 h at the dose of 7.5 mg, but induced at the dose of 15.0 mg a modest inhibition of plasma PRL (maximum PRL inhibition 20 +/- 4.5% at 45 min). Likewise, in puerperal women Amph at the dose of 7.5 mg did not decrease significantly plasma PRL levels but it was active in this respect (maximum inhibition 37 +/- 10% at 120 min) at the dose of 15.0 mg. In subjects with presumptive evidence of a PRL-secreting adenoma, Amph at either the 7.5 mg or the 15.0 mg dose failed to alter baseline PRL levels. These results indicate that Amph is a poor PRL suppressor in either normo- or hyperprolactinemic subjects. It is proposed that this may be due to the drug's ability to effect release of dopamine mainly from a non-granular pool of the amine.

Adenoma↗

PubMed1978

Hydroa vacciniforme.

Two patients with hydroa vacciniforme, a rare photodermatosis of unknown etiology, demonstrated distinctive scarring and vesiculobullous skin lesions on light-exposed body areas. Results of blood and urine porphyrin studies were normal, and no systemic abnormalities were noted. A small bullous lesion was produced in normal skin in case 1 with 15 times the minimal erythema dose of ultraviolet energy. The conditions of both patients improved while they were taking beta carotene orally.

Carotenoids↗