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L Puig

Publications and source records attributed to L Puig.

At least 73 records · Page 4Linked to original sources
PubMed1995

Erythema-multiforme-like eruption due to topical contactants: expression of adhesion molecules and their ligands and characterization of the infiltrate.

Erythema-multiforme-like reactions are a rare manifestation of allergic contact sensitivity, the pathomechanisms of which and their possible relationship to erythema multiforme remain unclear. We present our histopathological and immunohistochemical findings regarding the expression of several adhesion molecules and immunophenotypic markers of the infiltrate in skin biopsy specimens from 2 cases of erythema-multiforme-like reactions due to contact sensitizers and 3 cases of typical post-herpetic erythema multiforme. The histopathological pattern of erythema-multiforme-like reactions was characterized by an upper-dermal perivascular lymphoid infiltrate with exocytosis and keratinocyte necrosis; in 1 of the cases, there were foci of spongiosis and an admixture of eosinophils in the infiltrate. In comparison with biopsy specimens from cases of typical erythema multiforme, in both cases of erythema-multiforme-like reactions, the epidermal expression of ICAM-1 was more prominent, the % of CD4+ cells in the infiltrate was higher and the % of CD69+ cells was lower. There were no other significant differences in the cell phenotype of the infiltrate or in adhesion molecule expression in biopsy samples from both disorders.

Adult↗
PubMed1995

Pigmented epidermotropic ductal carcinoma of the breast in a male. Ultrastructural evidence of melanocytic colonization and melanin transfer to the tumor.

The first case of pigmented epidermotropic breast carcinoma in a male, presenting as a pigmented lesion of the areola and nipple, is described. Immunohistochemical and ultrastructural studies demonstrated that the pigmentation was found to be primarily due to colonization of tumor nests by melanocytes, with numerous melanophages interspersed in the desmoplastic stroma and only occasional compound melanosomes within the epithelial tumor cells.

Breast Neoplasms, Male↗
PubMed1995

[Blood donors seropositive for type 1 human immunodeficiency virus (HIV-1). Epidemiologic characteristics and clinical course].

PURPOSES: To evaluate retrospectively the epidemiologic profile and clinical course of the HIV-positive voluntary blood donors in the Sant Pau's Hospital Blood Bank (Barcelona-Spain) between 1986 and 1993. PATIENTS AND METHODS: A total of 119,345 blood donors were studied, and fifty seven such cases were identified. Risk behavior, causes of failure of the pre-donation procedures and clinical stage were analyzed. A follow-up of their infection was performed by the Infectious Disease Unit. RESULTS: The mean age of 57 seropositive donors was 31 +/- 8 years. Prevalence of HIV-1 infection among donors was 0.48 per 1000. Forty four (77%) were male and 13 (23%) female. Forty three (75%) were first time donors while 14 (25%) were repeat donors. The causes for the failure of the self-deferral questionnaire were: 42 subjects did not consider that they had engaged in "risk" behavior, seven donors lied in order to know if they were HIV carriers and two cases were driven to donate due to social or family pressure. The distribution of these donors according to risk behaviour was: 30 (53%) heterosexual, 11 (20%) homosexual, 11 (20%) intravenous drug users and five (7%) with no identified risk. It was noted that HIV infection progressed more rapidly to AIDS in HIV - positive homosexual donors than in heterosexual subjects (p < 0.05). CONCLUSIONS: Heterosexual donors who maintain sexual contacts with different partners without prophylactic measures for HIV infection currently represent the highest risk group for transfusion-related HIV infection. Clinical evolution of HIV infection was faster and more devastating in the homosexual group than in the heterosexual group.

Adult↗
PubMed1995

[The Gorlin syndrome. A review of 11 cases].

Gorlin syndrome is an autosomal dominant disorder with variable penetrance and expressivity. It is characterized by early onset of multiple basal cell carcinomas, mandibular keratocytes, pits of the palms and soles, cerebral ectopic calcification and several skeletal anomalies. We report a series of eleven patients (eight females and three males) with Gorlin syndrome, belonging to nine different families, which have been diagnosed in our Dermatology department during the last ten years. The ages at the moment of diagnosis ranged from 8 to 73 years. Ovarian fibromas were demonstrated in five cases and a frontal parasagittal meningioma in one case. Gorlin syndrome has been recently linked to a putative tumor suppressor gene which has been mapped to 9(q22.3-q31). Further research on the function of the protein encoded by this gene may provide additional insight on the mechanisms leading to oncogenesis in sporadic and hereditary basal cell carcinomas and other tumors.

Adolescent↗
PubMed1994

Interleukin-1 increases 15-hydroxyeicosatetraenoic acid production in human dermal fibroblasts.

Inhibition of the formation of pro-inflammatory eicosanoids such as leukotrienes and 12-hydroxyeicosatetraenoic acid by 15-hydroxyeicosatetraenoic acid (15-HETE) has been reported. Psoriatic dermis synthesizes reduced levels of 15-HETE and it has been postulated to play a role in the pathophysiology of this disease. Interleukin-1 stimulates the production of prostaglandin E2 in fibroblasts, but its effect on the synthesis of 15-HETE is at present unknown. The aim of this study was to investigate the modulation of 15-HETE formation by interleukin-1 in dermal fibroblasts. Cells were treated with recombinant interleukin-1 alpha or beta prior to incubation with exogenous 14C-arachidonic acid, and eicosanoids were analyzed by HPLC. Interleukin-1 significantly increased the production of 15-HETE, but also 12-hydroxy-heptadecatrienoic acid, 11-hydroxyeicosatetraenoic acid, and prostaglandins, in a concentration- and time-dependent fashion. No significant differences between the two types of interleukin-1 were found. Dexamethasone (10 nM), and the protein synthesis inhibitors actinomycin D (1 microM) and cycloheximide (3 micrograms/ml) completely abolished the effect of interleukin-1 on 15-HETE formation. Whereas indomethacin (0.5-25 microM) strongly inhibited the synthesis of 15-HETE, aspirin (100-1000 microM) was unable to significantly inhibit its formation in both untreated and interleukin-treated fibroblasts. Aspirin inhibited the 15-HETE produced by cyclooxygenase from ram seminal vesicles, although to a lesser extent than indomethacin. In cell-free extracts, the activity concerning the synthesis of 15-HETE was associated with the microsomal fraction (100,000 x g pellet). Overall, these results strongly suggest that interleukin-1 increases 15-HETE formation mainly through the expression of new cyclooxygenase.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1994

Petechial glove and sock syndrome caused by parvovirus B19.

The petechial glove and sock syndrome is a recently described febrile dermatosis characterized by acral edema, petechiae in a characteristic distribution, and enanthem, which has been associated in several cases with parvovirus B19 seroconversion. We report an additional case of petechial glove and sock syndrome that further corroborates the role of parvovirus B19 as a causative agent of this syndrome in adults.

Adult↗
PubMed1993

Acute febrile neutrophilic dermatosis (Sweet's syndrome).

BACKGROUND: Sweet's syndrome is well recognized and not infrequently diagnosed in Spain; however, the range of clinical and pathologic expression may not have been fully realized. METHODS: We reviewed 30 consecutive Spanish cases of Sweet's syndrome diagnosed in our department from 1979 to 1990, with special attention to clinical and histopathologic findings. RESULTS: Distinctive clinical features in our series included oral mucosa lesions in four patients (13%), development of pathergy phenomenon in one case, concurrent nodular lesions resembling erythema nodosum on the limbs in nine cases (30%), and lung involvement in two patients. Infectious disease and drug treatment were recorded as possible triggering factors of Sweet's syndrome in eight and seven patients respectively. Associated underlying systemic disorders were present in 15 (50%) of our patients. The most frequent associations were hematologic neoplasia in four patients, solid neoplasia in two, and chronic idiopathic inflammatory bowel disease in three patients. Dressler's syndrome and sicca syndrome were found in one patient each. Histopathologic studies of skin biopsy specimens obtained at presentation disclosed typical features of Sweet's syndrome in all cases. Epidermal involvement, with variable degrees of spongiosis, exocytosis of polymorphonuclear leukocytes and keratinocyte necrosis, was a prominent feature in 83% of biopsy specimens. CONCLUSIONS: Further characterization of the clinicopathologic spectrum of Sweet's syndrome is necessary as the recognition of the full spectrum of this syndrome will improve our diagnostic abilities and provide a solid clinical basis for prospective studies that allow dissection of the intricate patho-mechanisms involved in this fascinating disorder.

Adult↗
PubMed1992

Epidermal cell-polymorphonuclear leukocyte cooperation in the formation of leukotriene B4 by transcellular biosynthesis.

The cellular origin of Leukotriene B4, a potent pro-inflammatory agent that is present in psoriatic lesions, has not been completely ascertained. The present study was performed in order to assess the possible contribution of epidermal cells to leukotriene B4 synthesis through 5-lipoxygenase or by means of transcellular metabolism of the epoxide intermediate leukotriene A4 from activated polymorphonuclear leukocytes. The metabolism of exogenous arachidonic acid in fresh human epidermal cell, polymorphonuclear leukocyte or mixed suspensions was determined by means of high-performance liquid chromatography. Epidermal cells transformed arachidonic acid mainly into 12-hydroxy-eicosatetraenoic acid and prostaglandin E2. Formation of prostaglandins F2 alpha and D2, 12-hydroxy-eptadecatrienoic acid, and 15- and 11-hydroxy-eicosatetraenoic acids was also detected. We did not detect any eicosanoid derived from 5-lipoxygenase pathway. Mixed suspensions of polymorphonuclear leukocytes and epidermal cells (ratio 1:4) produced 1.72 times more leukotriene B4 than leukocytes alone under the same experimental conditions. Epidermal cells incubated with 5 microM authentic leukotriene A4 for 3 min yielded 2.954 +/- 0.27 pmoles/10(6) cells of leukotriene B4, which was characterized by co-elution with authentic standard and its ultraviolet absorption spectrum. These data demonstrate the existence of a leukotriene A4 epoxide hydrolase activity in human epidermal cells. Our results suggest that epidermal cells could cooperate in leukotriene B4 biosynthesis by transcellular metabolism of leukotriene A4 in lesions of psoriasis, and possibly other inflammatory dermatoses characterized by increased leukotriene B4 levels and prominent polymorphonuclear leukocyte infiltrates.

Arachidonic Acid↗
PubMed1992

Pyoderma gangrenosum in association with erythema elevatum diutinum: report of two cases.

We report on the appearance of centrifugally spreading ulcers with undermined borders in two patients with chronic recurrent erythema elevatum diutinum controlled with dapsone. The ulcerated lesions were consistent on clinical and pathologic examination with the diagnosis of pyoderma gangrenosum. They eventually responded to treatment with oral corticosteroids. The addition of cyclosporine was required in one case. No associated disease was found in any of the patients. The possible pathophysiological mechanisms of this uncommon association are reviewed.

Adrenal Cortex Hormones↗
PubMed1991

Thrombin generation and fibrinolysis in the thrombotic thrombocytopenic purpura and the hemolytic-uremic syndrome.

Prothrombin fragment 1 + 2 (F1 + 2) and thrombin-antithrombin complexes (TAT), as well as other coagulation and fibrinolysis parameters, were studied in a series of 13 patients affected by thrombotic thrombocytopenic purpura (TTP) or hemolytic-uremic syndrome (HUS). Fragment F1 + 2 was found to be increased in all patients at diagnosis (patients' range, 1.21-19.03 nmol/l; normal limits, 0.28-1.08 nmol/l), and remained also higher than normal after treatment with plasma exchange (patients' range, 1.5-4.01 nmol/l). Even though the analysis of fibrinolysis markers did not show a definite state of hypo or hyperfibrinolysis in the systemic circulation, enhanced circulating D-dimer levels (0.53-12.6 micrograms/ml, normal levels of 0.03-0.29 micrograms/ml) indicated that a certain grade of fibrin lysis was present at previously formed thrombi. Plasma PAI-1 activities either on admission (9.2-38.2 U/ml) and after plasma exchange therapy (2.6-38.6 U/ml) showed a behavior irrespective of t-PA:Ag changes, and post-plasmapheresis values remained high only in patients with fatal neurological outcome. Nevertheless, no correlations between clinical and laboratory data could be established useful for the TTP/HUS prognosis. We conclude that increased thrombin generation occurring in damaged areas is appropriately inhibited by antithrombin III in the systemic circulation, avoiding consumption coagulopathy to develop in uncomplicated patients. In addition, fibrinolysis data suggest that elevated PAI-1 may decisively favor the development of microvascular thrombi.

Antithrombin III↗