ABSTRACT
We report and eight years old boy presenting with a pyogenic granuloma of the scalp, generalized alopecia, descamative plates in the neck, trunk and limbs and nail involvement. Cultures for fungus of all these lesions disclosed Microspore canis. The patient was treated with oral griseofulvin, miconazole and topical tolnaftate. Five years later and after several incomplete treatments, the patient returns with a fistulous mass of 12 x 8 cm in the dorsal area whose culture revealed Microspore canis. The mass was excised and oral ketoconazole was indicated. After three months of follow up, the patient was lost from control
Subject(s)
Humans , Male , Child , Mycetoma/microbiology , Microsporum/pathogenicity , Tolnaftate/therapeutic use , Gentamicins/therapeutic use , Cloxacillin/therapeutic use , Alopecia/microbiology , Griseofulvin/therapeutic use , Mycetoma/therapy , Miconazole/therapeutic use , Granuloma, Pyogenic/surgeryABSTRACT
Mallory bodies are hepatocyte intracytoplasmic inclusions frequently observed in liver diseases. They contain altered intermediary filaments that have immunoreactivity with epidermic antikeratin antibodies (A-QEp). They also contain Ubiquitin (Ubq) a 76 residue polypeptide that has an important role in the proteolysis of rapid exchange and abnormal cytosol proteins. To standarize an immunohistochemical method for the detection of Mallory bodies in percutaneous liver biopsies. A-QEp and A-Ubq polyclonnal antibodies were used in the study of 131 percutaneous liver biopsies obtained from patients with different liver diseases. Mallory body immunoreactivity was confirmed with immunoelectron microscopy demonstrated that Mallory bodies are partially formed by altered intermediate filaments. In conclusion, antibodies againnst ubiquitin may be very useful for the detection of Mallory bodies in liver biopsies
Subject(s)
Humans , Ubiquitin/isolation & purification , Keratins/isolation & purification , Inclusion Bodies/immunology , Immunohistochemistry/methods , Biopsy/statistics & numerical data , Hematoxylin , Liver Diseases/immunology , Microscopy, ElectronABSTRACT
La tromboastenia de Glanzmann es un trastorno hemorrágico de herencia autosómica recesiva, caracterizado por la ausencia o déficit de complejo glicoproteico IIb/IIIa de la membrana de las plaquetas, que se traduce en alteración de la agregación plaquetaria y sangramientos. Se describre el caso clínico de una niña de tres años de edad con síndrome purpúrico-equimótico y antecedente de hemorragias desde el año de vida, con recuento y morfología plaquetaria normales, tiempo de sangría prolongado, modificación en la retracción del coágulo, ausencia de agregación plaquetaria frente a ADP, colágeno, araquinodato de Na, epinefrina, ionóforo A23187 y agregación subnormal con ristocetina. Mediante técnicas de inmunofluorescencia y anticuerpos monoclonales se confirmó disminución del complejo GP IIb/IIIa de la membrana plaquetaria y reducción en el número de sitios de fijación de este complejo por plaqueta, lo que permite catalogar a la paciente como una variante de tromboastenia de Glanzmann