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Biomedical subjects

A Vidaller

Publications and source records attributed to A Vidaller.

At least 37 records · Page 2Linked to original sources
PubMed1997

Adhesion molecule expression and endothelial cell activation in cutaneous leukocytoclastic vasculitis. An immunohistologic and clinical study in 42 patients.

OBJECTIVES: To investigate the sequential expression of adhesion molecules on endothelium and inflammatory cells in cutaneous leukocytoclastic vasculitis, and the relation of these adhesive molecules with clinical and histologic variables. DESIGN: An immunohistochemical analysis (streptavidin-biotin-peroxidase technique) of 42 vasculitic lesions of up to 96 hours was performed using a panel of monoclonal antibodies specific for different adhesion molecules. Twenty normal skin samples and 3 perilesional specimens served as control samples. A clinical protocol was also performed, and patients were followed up for 1 to 5 years. SETTING: A clinicopathologic research unit of a university hospital. PATIENTS: Forty-two patients, 21 women and 21 men, aged 22 to 79 years, with cutaneous leukocytoclastic vasculitis. INTERVENTIONS: Three skin biopsy specimens of vasculitic lesions from each patient were obtained for histopathologic examination on paraffin, direct immunofluorescence, and immunohistochemical analysis on cryostatic tissue sections. MAIN OUTCOME MEASURES: The histologic characteristics and the immunohistochemical-stained specimens were evaluated by 3 independent investigators, using a semiquantitative method. RESULTS: Increased endothelial expression of very late activation antigen-1, HLA-DR, and intercellular adhesion molecule-1 was observed. The induction of E-selectin expression was more marked in recent lesions (P < .001) and correlated with the proportion of infiltrating neutrophils (P = .03). Endothelial expression of vascular cell adhesion molecule-1 was restricted to developed lesions. Most infiltrating cells were neutrophils expressing Mac-1. In 1 patient, lymphocyte function associated antigen-1 expression was also up-regulated. No significant increase in CD3, CD8, or CD71 immunoreactivity was found. An up-regulation of perivascular cells expressing HLA-DR and vascular cell adhesion molecule-1 was observed in vasculitic lesions. This cellular staining correlated with long-term evolution of the disease (P = .04). CONCLUSIONS: Adhesion molecules are sequentially upregulated in cutaneous leukocytoclastic vasculitis. The results of this study support the possible involvement of E-selectin in mediating recruitment of neutrophils expressing Mac-1.

Adult↗
PubMed1996

Tuberculous lymphadenitis presenting with cutaneous leucocytoclastic vasculitis.

Cutaneous leucocytoclastic vasculitis is an inflammatory vascular disorder due to deposition of immune complexes in dermal vessels. A direct or indirect role of infectious agents in the pathogenesis of such vasculitis has been postulated. We describe a patient with cervical lymphadenitis due to Mycobacterium tuberculosis infection who developed cutaneous vasculitis. The vasculitis resolved with standard antituberculous therapy. The association between leucocytoclastic vasculitis and tuberculous infection has only rarely been reported. Tuberculous infection may present in a number of different clinical forms depending in part on variations in the number and virulence of the bacilli, route of infection, presence or absence of an internal tuberculous focus, age and specific immunity of the host. Although the association between infection and vasculitis is well known, Mycobacterium tuberculosis as a causative agent of cutaneous leucocytoclastic vasculitis is uncommon.

Antitubercular Agents↗
PubMed1996

Changes in T-cell phenotype and adhesion molecules expression in psoriatic lesions after low-dose cyclosporin therapy.

Cyclosporin is a very effective treatment for severe psoriasis, but its exact mechanism of action in this disease is not completely understood. It has been hypothesized that the drug could act through the inhibition of the expression of certain cell adhesion molecules on the keratinocytes prior to the reduction in the number of epidermal inflammatory cells. Several studies have focused on ICAM-1 changes on keratinocytes and endothelial cells after cyclosporin treatment in psoriatic patients but their results have been somewhat contradictory. We examined changes in T-cell markers and adhesion molecules among keratinocytes, endothelial and inflammatory cells after low-dose cyclosporin treatment for severe psoriasis. We performed a histological and immunohistochemical study on psoriatic skin among 10 patients (7 males and 3 females; mean age 37 years) treated with low-dose (2.5 mg/kg/day) cyclosporin, prior to therapy, after 1 month, and after 3 months of treatment. The mean PASI (Psoriasis Area and Severity Index) before treatment was 23 +/- 4, 13 +/- 7 after the first month of therapy, and 8 +/- 2 at the end of the third month of therapy. Pretherapy samples showed a moderate to severe inflammatory infiltrate mainly due to T-lymphocytes expressing a T-cell memory (UCHL-1) and helper/inducer (CD4) phenotype. Most of these cells also expressed HLA-DR and LFA-1 and ICAM-1 antigens. After the treatment, an overall reduction in the degree of epidermal hyperplasia was seen (p = 0.01). The severity of the infiltrate was clearly reduced (p = 0.05), but no significant changes in the phenotype profile were observed. Although slightly reduced, endothelial ICAM-1 expression persisted after cyclosporin therapy. Keratinocyte ICAM-1 expression was uniformly and significantly reduced after 1 month and 3 months of therapy (p = 0.01). These results support the hypothesis that cyclosporin interferes with the expression of keratinocyte adhesion molecules in patients with psoriasis. Servitje O, Bordas X, Serón D, Vidaller A, Moreno A, Curcó N, Sais G, Peyrí J. Changes in T-cell phenotype and adhesion molecules expression in psoriatic lesions after low-dose cyclosporin therapy.

Adult↗
PubMed1995

Colchicine in the treatment of cutaneous leukocytoclastic vasculitis. Results of a prospective, randomized controlled trial.

BACKGROUND AND DESIGN: Cutaneous leukocytoclastic vasculitis is an inflammatory vascular disease with a variable course. There is no defined therapy for this entity. Contradictory data on the effect of colchicine have been reported. To determine the efficacy of colchicine in cutaneous leukocytoclastic vasculitis, 41 patients were randomly selected to receive oral colchicine, 0.5 mg twice daily, or topical emollients. Response to treatment was judged according to the reduction in the number of lesions. After 1 month, in those patients in whom a complete or no response was achieved, therapy was withdrawn; in those with a partial response, treatment was maintained for the following 2 months. At the end of 3 months, treatment was continued only in those patients in whom a relapse occurred. RESULTS: Twenty patients in each group completed 1 month of treatment. One patient taking colchicine dropped out because of diarrhea. At the end of the first month of the study, five patients in the control group and four in the colchicine group achieved a complete response. Nine patients who had a partial response (four in the colchicine group and five in the control group) continued to receive treatment for the following 2 months. Three patients in the colchicine group suffered a relapse after discontinuing therapy but experienced remission with reinstitution of therapy. At the end of the 3 month period, 12 patients in the colchicine group and 10 patients in the control group showed no significant response. Complete response was achieved in five patients in the colchicine group and in seven in the control group. At the 1-year follow-up, 10 patients in each group had no clinical evidence of cutaneous vasculitis. CONCLUSIONS: Colchicine had no significant therapeutic effect in this controlled study. However, the finding that relapse occurred on cessation of colchicine therapy in three complete responders suggests that colchicine can be effective in some patients, despite our negative results.

Administration, Cutaneous↗
PubMed1994

Sarcoid pleural effusion: a report of two cases.

Two patients with pleural effusions have been seen among 270 patients with sarcoidosis in an eighteen-year period. In both patients pleural effusions were present at the onset of sarcoidosis and associated with extensive pulmonary or extrathoracic involvement. Pleural effusions were exudative with a high lymphocyte count. One patient was successfully treated with corticosteroids and the second died from cardiac complications of the disease.

Aged↗
PubMed1994

Chronic ascites in late onset systemic lupus erythematosus with antiphospholipid antibodies.

Because doctors are reluctant to diagnose systemic lupus erythematosus (SLE) in elderly patients, the initial diagnosis in this age group is usually tardy. Furthermore, the presenting manifestations in these patients are commonly atypical. We describe a 72-year-old woman in whom chronic ascites with antiphospholipid antibodies was the initial predominant manifestation of subsequently fatal SLE. Only 13 cases of chronic lupus ascites have been reported in the English and French literature. Our patient represents the first case reported in an elderly person.

Aged↗
PubMed1992

[Renal vasculitis without hematuria in senile patients].

Systemic vasculitis is a disease whose prognosis has improved considerably with steroid and immunosuppressive treatment, which points up the importance of early diagnosis. In elderly, diagnosis is made more difficult because the frequent onset in the form of a febrile syndrome with non-specific disturbances in general condition. In these patients it is not uncommon that a kidney involvement is what leads to diagnosis of the disease. Hematuria is almost a constant in vasculitis nephropathy. In their absence, acute renal failure in elderly is usually attributed to hemodynamic causes and the frequent presence of iatrogenic tubular factors. This is a report on the case of three elderly patients who presented a febrile syndrome with asthenia, anorexia and weight loss. The three cases progressed to acute renal failure with no disorders in urinary sediment. In two cases was a history of administration of gentamycin, indomethacin and iodated contrast. The clinical diagnosis was toxic and ischemic tubulopathy and, when dialysis became necessary, a renal biopsy was done which showed granulomatous vasculitis, intersticial nephritis and in two cases, necrotizing glomerulitis and crescent formation. Treatment with steroids and cyclophosphamide was started which improved general condition and renal function in one case. Early renal biopsy is advisable in senile patients with non specific systemic symptoms and progressive acute renal failure of unclear origin, even when hematuria is lacking. In this setting, the appearance of underdiagnosed renal vasculitis is possible, and consequent immunosuppressive treatment is a factor for consideration.

Acute Kidney Injury↗
PubMed1992

Salivary testosterone levels in women with systemic lupus erythematosus.

OBJECTIVE: To measure salivary testosterone in women with systemic lupus erythematosus (SLE). METHODS: We investigated concentrations of salivary testosterone in 13 women with active SLE and 47 women with inactive SLE, and in 72 healthy female controls. RESULTS: We found a significant decrease in salivary testosterone concentrations in glucocorticoid-treated SLE patients (mean +/- SD 0.06 +/- 0.04 nmoles/liter) but no differences in concentrations in untreated patients (0.09 +/- 0.03 nmoles/liter), compared with the healthy controls (0.11 +/- 0.04 nmoles/liter). CONCLUSION: Glucocorticoid treatment appears to cause a decrease in the salivary testosterone level. Measurement of salivary testosterone is a simple way of monitoring androgen metabolism in patients with SLE.

Adult↗
PubMed1992

Hyperprolactinemia inhibits natural killer (NK) cell function in vivo and its bromocriptine treatment not only corrects it but makes it more efficient.

We studied NK cell function in eight patients with pathological hyperprolactinemia by measuring 51Cr release by K562 cells exposed to their mononuclear cells and found it decreased compared to normal controls (P less than 0.01). Bromocriptine (BrC) treatment corrected NK function but also made it more efficient at 12:1 than at 25:1 or 50:1 effector:target ratios (ANOVA; P = 0.01). The study of NK cell function in agarose revealed that its decrease in hyperprolactinemia is due to their low active binding to target cells, active killing, and recycling capacity. BrC tended to correct them but also increased recycling capacity to levels higher than those of controls (P less than 0.05). Sequential studies in three hyperprolactinemic patients before and after BrC showed correction of NK function within 1 week but its increased efficiency at the 12:1 effector:target ratio required 8 weeks. We conclude that hyperprolactinemia decreases NK cell function. BrC corrects this by decreasing prolactin levels but also makes NK function more efficient by increasing the capacity of NK cells to recycle after killing.

Adult↗
PubMed1990

Vasculitis as a paraneoplastic syndrome. Report of 11 cases and review of the literature.

In a study of 222 patients with vasculitis, we identified 11 who had an associated neoplasia. Seven had hematological neoplasia and 4 had solid malignant tumors. In 4 patients vasculitis gave the first evidence of the neoplasia or of its recurrence. Nine of our patients had cutaneous vasculitis. The other 2 had vasculitis involving the intestine and resulted in acute abdomens. These 2 patients needed prednisone treatment for the vasculitis. Neoplasia should be considered in patients with vasculitis without an apparent cause.

Aged↗
PubMed1988

Peripheral neuropathy associated with angioimmunoblastic lymphadenopathy.

A 49-year-old man developed mononeuritis multiplex associated with angioimmunoblastic lymphadenopathy. The biopsy of the sural nerve revealed focal reduction of myelinated fibres and axonal degeneration, as well as perivascular inflammatory infiltrates composed of lymphocytes and plasma cells, exhibiting policlonal immunoglobulin expression, proliferation of blood vessels, thickening of the vessel wall and endothelial hyperplasia. These latter changes are similar to those commonly encountered in the lymph nodes, as well as in other organs, in patients suffering from angioimmunoblastic lymphadenopathy.

Adult↗