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Biomedical subjects

J Perriard

Publications and source records attributed to J Perriard.

6 recordsLinked to original sources
PubMed2001

Acute genitocrural intertrigo: a sign of primary human immunodeficiency virus type 1 infection.

We describe a 49-year-old male patient who presented with an acute illness associated with a widespread maculopapular eruption and eroded lesions in the inguinal folds consistent with an acute intertrigo, for which search of mycological and bacteriological causes remained negative. Serological tests disclosed a high viral HIV-1 load and p24 antigenemia, while anti-HIV-1 antibodies were absent, a profile typical of acute HIV-1 infection. Since the maculopapular eruption regressed concomitantly with the orogenital lesions as well as the eroded inguinal lesions prior to specific therapy, our observation indicates that intertriginous lesions may constitute one of the early cutaneous markers of primary HIV-1 infection.

Acute Disease↗
PubMed2000

A new method to quantify wear using implant supported restorations.

OBJECTIVES: To design a novel technique to assess the wear of prosthodontic veneering materials. Further to determine whether accurate transfer between the oral cavity and the measuring device is achievable and assess the reproducibility of the coordinates generated by the measuring system. METHODS: The system is based on the repositioning capacity of an octagonal connector of the ITI implant system. The same type of connector was screwed onto the clinical implants that supported the experimental restorations and secured to the x-y table of the measuring device. The measuring setup also comprised a z-axis LVDT displacement gauge that allowed the entire surface of the restorations to be profiled and digitized. The system was under the control of a PC equipped with custom-made software that set the position of the stepping motors, lifted and lowered the z-axis probe, and registered and wrote the x-, y- and z-axis coordinates. Final numerical adjustments and analyses were performed using a commercial array-oriented software package. Validation procedures were performed using a specially designed calibration surface. RESULTS: On repeated profile tracings, the measurement error was less than 2 microns. When the calibration surface was removed between measurements as during clinical trials, the measurement error increased to ca. 5 microns. SIGNIFICANCE: The measurement error of the testing procedure including transfer to and from the mouth is +/- 5 microns.

Calibration↗
PubMed2000

An overlap of Cowden's disease and Bannayan-Riley-Ruvalcaba syndrome in the same family.

We describe a family with the unusual association of Cowden's disease and Bannayan-Riley-Ruvalcaba syndrome. The father has characteristic mucocutaneous features that are palmoplantar keratoses, multiple facial papules, oral papillomatoses, lipomas, and vitiligo with involvement of the thyroid and digestive tract. The son presents with pigmented macules of the penis, macrocephaly, and a lipoma that are typical for Bannaya-Riley-Ruvalcaba syndrome. Recent studies have demonstrated that these 2 diseases are allelic disorders at the PTEN locus on chromosome 10q.

Abnormalities, Multiple↗
PubMed1999

IgG autoantibodies from bullous pemphigoid (BP) patients bind antigenic sites on both the extracellular and the intracellular domains of the BP antigen 180.

Bullous pemphigoid (BP) and gestational pemphigoid (PG) are subepidermal blistering disorders associated with autoantibodies directed against two components of hemidesmosomes: the BP antigen 180 (BP180) and the BP antigen 230 (BP230). Autoantibodies against the extracellular domain (ECD) of BP180 are thought to play an initiatory role in subepidermal blister formation. To characterize the targeted antigenic sites on BP180, we have assessed the reactivity of sera from BP and PG patients against eukaryotic recombinant proteins encompassing various portions of the ECD and the intracellular domain (ICD) of BP180. Twenty-two of 22 (100%) BP sera that immunoblotted BP180 in keratinocyte extracts, bound a mutant form consisting of the entire ECD of BP180, whereas only three of these 22 sera (14%) reacted against the ECD of BP180 lacking the NC16A membrane proximal region. Thirteen out of the 22 (59%) BP sera recognized the ICD of BP180. Circulating IgG from a representative BP patient that was affinity purified against the ECD of BP180 did not bind the ICD when reblotted, indicating that there was no antigenic cross-reactivity between the ECD and the ICD of BP180. Reactivity against the ICD of BP180 was further ascertained by immunofluorescence microscopy studies showing that nine of the 22 (41%) BP sera stained COS-7 cells expressing the ICD of BP180. Using deletion mutants of the ICD of BP180, the majority of the sera was found to recognize the central region of the ICD of BP180. Specifically, an immunodominant region was localized to an 87-amino acid segment located towards the NH2-terminus of BP180. In contrast to BP sera, five of six (83%) PG sera contained IgG that recognized exclusively the NC16A region, whereas none bound to the ICD of BP180. Together, the results indicate that in BP, autoantibody reactivity to BP180 is not exclusively restricted to the NC16A region, but that additional antigenic determinants exist on the ICD of BP180. The observed heterogeneous immune response against BP180 might reflect intramolecular epitope spreading. Because the ICD ofBP180 harbors functionally important regions, it is possible that autoantibodies against the ICD of BP180 have pathogenic significance for the progression of the disease.

Adult↗