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P Bigliardi

Publications and source records attributed to P Bigliardi.

10 recordsLinked to original sources
PubMed2005

How best to fight that nasty itch - from new insights into the neuroimmunological, neuroendocrine, and neurophysiological bases of pruritus to novel therapeutic approaches.

While the enormous clinical and psychosocial importance of pruritus in many areas of medicine and the detrimental effects of chronic 'itch' on the quality of life of an affected individual are widely appreciated, the complexity of this sensation is still often grossly underestimated. The current Controversies feature highlights this complexity by portraying pruritus as a truly interdisciplinary problem at the crossroads of neurophysiology, neuroimmunology, neuropharmacology, protease research, internal medicine, and dermatology, which is combated most successfully if one keeps the multilayered nature of 'itch' in mind and adopts a holistic treatment approach - beyond the customary, frequently frustrane monotherapy with histamine receptor antagonists. In view of the often unsatisfactory, unidimensional, and altogether rather crude standard instruments for pruritus management that we still tend to use in clinical practice today, an interdisciplinary team of pruritus experts here critically examines recent progress in pruritus research that future itch management must take into consideration. Focusing on new insights into the neuroimmunological, neuroendocrine, and neurophysiological bases of pruritus, and discussing available neuropharmacological tools, specific research avenues are highlighted, whose pursuit promises to lead to novel, and hopefully more effective, forms of pruritus management.

Dermatology↗
PubMed2000

Delayed generalized allergic reactions to corticosteroids.

A 37-year-old patient presented with a severe allergic local reaction upon inhalation of budesonide for asthma. Skin tests were positive for budesonide and amcinonide (group B) and elicited a strong local reaction and a disseminated macular exanthema. Corticosteroids from other groups were well tolerated. A 38-year-old male patient had first an allergic contact dermatitis to topically applied prednisolone acetate and then a disseminated eczematous exanthema upon oral intake of prednisone. A delayed-type sensitization to corticosteroids from group A such as hydrocortisone, prednisone and tixocortol pivalate was identified. A detailed diagnosis in patients with allergic reactions to corticosteroids is crucial with regard to their use in emergency therapy.

Adrenal Cortex Hormones↗
PubMed1999

Association of a syndrome resembling Wegener's granulomatosis with low surface expression of HLA class-I molecules.

BACKGROUND: Granulomatous syndromes, such as Wegener's granulomatosis, are defined according to complex criteria, but the underlying cause is rarely identified. We present evidence for a new aetiology for chronic granulomatous lesions associated with a recessive genetic defect, which is linked to the human leucocyte antigen (HLA) locus. METHODS: Five adults with necrotising granulomatous lesions in the upper respiratory tract and skin, associated with recurrent bacterial respiratory infections and skin vasculitis, were identified. A diagnosis of Wegener's granulomatosis was considered in all of them, but abandoned because of an incompatible disease course and resistance to immunosuppressive treatments. Peripheral-blood samples were taken and analysed by immunohistochemistry and fluorescent-activated-cell-sorter analysis. Since all five patients were homozygous for the HLA locus, we looked for genetic defects located within the HLA-locus with PCR and restriction fragment length polymorphism. FINDINGS: A severe decrease in cell-surface expression of HLA class-I molecule was seen in all patients. Defective expression of the transporter associated with antigen presentation (TAP) genes was responsible for the HLA class-I down-regulation, and in two patients we identified a mutation in the TAP2 gene responsible for the defective expression of the TAP complex. We showed the presence of autoreactive natural killer (NK) cells and gammadelta T lymphocytes in the peripheral blood cells of two patients. Correction of the genetic defect in vitro restored normal expression of HLA class-I molecules and prevented self-reactivity in the patients' cells. Histology of granulomatous lesions showed the presence of a large proportion of activated NK cells. INTERPRETATION: Our findings define the cause and pathogenesis of a new syndrome that affects patients with a defective surface expression of HLA class-I molecules. The syndrome resembles Wegener's granulomatosis both clinically and histologically. Patients have chronic necrotising granulomatous lesions in the upper respiratory tract and skin, recurrent infections of the respiratory tract, and skin vasculitis. A predominant NK population within the granulomatous lesions suggests that the pathophysiology of the skin lesions may relate to the inability of HLA class-I molecules to turn off NK cell responses. Accurate genetic analysis of a defined syndrome can provide a better understanding of the cause and pathogenesis of a disease.

ATP-Binding Cassette Transporters↗
PubMed1985

Double-blind comparison of astemizole, terfenadine and placebo in hay fever with special regard to onset of action.

In this double-blind study forty-seven patients with hay fever were treated for 8 days with either terfenadine 60 mg twice a day, astemizole 10 mg once a day or placebo. On the second day of treatment terfenadine was statistically significantly superior to astemizole and placebo according to the ratings of symptomatology, efficacy and individual symptoms. The median onset of symptom alleviation was 3 hours for terfenadine and 2 days for astemizole. On the eighth day both astemizole and terfenadine were statistically significantly more efficacious than placebo, but no significant differences were found between the two drugs. Both drugs were well tolerated.

Adult↗