Examinando por Autor "Vanaclocha, Francisco"

Mostrando 1 - 2 de 2

Febrile ulceronecrotic Mucha-Habermann disease
(MOSBY-ELSEVIER, 1993) López Estebaranz, Jose Luis; Vanaclocha, Francisco; Gil, Ricardo; García, Beatriz; Iglesias, Luis
Febrile ulceronecrotic Mucha-Habermann disease in an 18-year-old man is reported. This disease is a severe form of pityriasis lichenoides et varioliformis acuta (PLEVA) and is characterized by the sudden onset of diffuse coalescent ulcerations associated with high fever and systemic symptoms. In the present case the disease was preceded by typical PLEVA. Histologically, a leukocytoclastic vasculitis was seen in addition to the usual features of PLEVA. Findings of laboratory studies revealed an elevated erythrocyte sedimentation rate, a high white blood cell count, and a mild increase in liver enzymes. No systemic involvement was detected. Findings of T cell receptor gene analysis in skin and peripheral blood showed no abnormality. The patient was treated with PUVA and methotrexate with a good response. We review the eight previously reported cases of febrile ulceronecrotic Mucha-Habermann disease.
Genetic analysis of the GRM1 gene in human melanoma susceptibility
(SPRINGERNATURE, 2007) Ortiz, Pablo; Vanaclocha, Francisco; López-Bran, Eduardo; Esquivias, Jose Ignacio; López Estebaranz, Jose Luis; Martín González, Manuel; Arrue, Itziar; García Romero, Diana; Ochoa, Carolina; González Pérez, Antonio; Ruiz, Agustín; Real, Luis Miguel
Data obtained from a mouse model indicated that the ectopic expression of the Grm1 gene is sufficient for transforming melanocytes and causing malignant melanoma in vivo. In addition, it has also been documented that the GRM1 gene is aberrantly expressed in human melanomas. Here we have performed a genetic association study to elucidate whether the GRM1 gene contributes to human melanoma susceptibility. To carry out this study, we initially genotyped 250 melanoma patients and 329 nonselected and nonrelated controls with three single nucleotide polymorphisms, rs854145, rs362962 and rs6923492, located in the intron 1, intron 4 and exon 10 of the GRM1 gene, respectively. To perform sample genotyping, we used pyrosequencing techniques. Regarding rs854145 and rs6923492, there were no differences in genotypic distribution or allelic frequency between patients and controls. However, we observed (i) a higher frequency of patients carrying the C allele of rs362962 than in controls (OR ¼ 1.40, CI ¼ [1.01–1.95], P ¼ 0.045), and (ii) that difference became greater in a subgroup of patients with a low level of sun exposure and tumours located on the trunk and extremities (OR ¼ 2.10, CI ¼ [1.26–3.51], P ¼ 0.0039). To confirm these observations, the sample size of both patient and control groups was increased. In total, 464 patients and 561 controls were genotyped for the rs362962 polymorphism. Only the second observation was confirmed (OR ¼ 1.69, CI ¼ [1.16–2.47], P ¼ 0.0064). Our results suggest that the GRM1 gene may contribute to melanoma susceptibility in that specific group of patients.