Search PubMed⌕ Search

Biomedical subjects

N Bodak

Publications and source records attributed to N Bodak.

10 recordsLinked to original sources
PubMed2002

[Cutaneous hydration of the premature and new born].

The barrier function of the stratum corneum is a fundamental element in maintaining cutaneous hydration. Alteration in the stratum corneum leads to the loss of this barrier function, with increased transdermal water loss, decreased water content and installation of xerosis. Moisturizers correct cutaneous xerosis by restoring the stratum corneum. In the new born, the architectural and biochemical structure of the stratum corneum is identical to that of infants and adults. However, 60 p. cent of new born exhibit physiologic desquamation, demonstrating a transitory functional deficit in the stratum corneum, justifying emollient treatment. After this physiological desquamation period, emollients are reserved for atopic infants or those presenting keratinization disorders. In the premature, the epidermis and particularly the stratum corneum are immature; trans-epidermal water loss is elevated and the skin is dry or even fissural. The interest of applying emollients to the skin of premature new born was recently demonstrated. Emollients improved the aspect of the skin and also decreased the number of infectious episodes.

Body Water↗
PubMed2002

[Facial cellulite associated with mandibular osteomyelitis in an infant].

INTRODUCTION: The discovery of a jugular tumefaction in an infant evokes several diseases. We report the case of a 4-month-old infant whose jugular cellulite revealed mandibular osteomyelitis. CASE REPORT: A 4-month-old boy was referred for hard, hot tumefaction of the right cheek and multiple cervical adenopathies. The suggested diagnosis was cellulite of cutaneous origin. He presented 21 900/mm(3) hyperleukocytosis associated with an inflammatory biological syndrome. Standard x-ray of the facial mass was normal. Sonography of the face showed thickening of the soft subcutaneous tissues and retro and sub-mandibular adenopathies with abcedation. Antibiotherapy with amoxicillin and clavulanic acid led to rapid improvement. Three days after withdrawal of the antibiotherapy, the tumefaction recurred without fever. A facial scan eliminated cystic lymphangioma and showed osteolysis of the external plateau of the ascending branch of the mandible with periosteal appositions. Histological examination of a surgical bone biopsy showed infectious osteitis and culture revealed hemolytic beta streptococci. Six weeks of antibiotherapy (initially with amoxicillin and gentamycin, then amoxicillin in monotherapy) led to the regression of all cutaneous signs. COMMENTS: When confronted with a tumefaction in this area, malignant or benign tumoral causes such as cystic lymphangioma must be eliminated. Infectious causes (abscess, parotid inflammation and osteomyelitis) must be evoked and distinguished from infantile cortical hyperostosis (Caffey-Silverman's syndrome). Standard radiological imaging, scan or scintigraphy are useful diagnostic tools. If osteolysis is discovered, a biopsy must be taken for anatomopathological and biological examination.

Cellulitis↗
PubMed2001

[Pemphigoid gestationis: treatment by topical class I corticosteroid].

BACKGROUND: Systemic corticosteroid is the main treatment of severe forms of pemphigoid gestationis. We report a case of generalised pemphigoid gestationis successfully treated with very potent topical corticosteroid. CASE: A 37-year-old woman developed during her third pregnancy with a new partner an urticated generalised eruption associated with bullous lesions. The diagnosis of pemphigoid gestationis was confirmed by direct immunofluorescence which detected a linear C3 deposition along the basement membrane zone and the positivity of Herpes Gestationis Factor (10 units). Local treatment with potent corticosteroid (betamethasone dipropionate 0.05 p. 100) failed and the patient was successfully treated by clobetasol propionate 0.05 p. 100 cream. The infant, in good health, was not delivered prematurely. DISCUSSION: Severe form of pemphigoid gestationis are currently treated with 0.5 to 1 mg/kg/day of systemic corticosteroids, with maternal and pediatric possible side effects. As in bullous pemphigoid, this observation underlines the efficiency and good tolerance of very potent corticosteroid in severe forms of pemphigoid gestationis.

Administration, Cutaneous↗
PubMed2000

[Digital clubbing].

Explore the source record for details and available documents.

Diagnosis, Differential↗
PubMed1999

High levels of patched gene mutations in basal-cell carcinomas from patients with xeroderma pigmentosum.

Recently, hptc, a human gene homologous to the Drosophila segment polarity gene patched (ptc), has been implicated in the nevoid basal-cell carcinoma (BCC) syndrome, and somatic mutations of hptc also have been found in sporadic BCCs, the most frequent cancers found in the white population. We have analyzed the hptc gene, postulated to be a tumor suppressor gene, in 22 BCCs from patients with the hyperphotosensitive genodermatosis xeroderma pigmentosum (XP). Patients with XP are deficient in the repair of UV-induced DNA lesions and are characterized by their predisposition to cancers in sun-exposed skin. Analysis using PCR-single-strand conformation polymorphism of the hptc gene identified 19 alterations in 16 of 22 (73%) of the BCCs examined. Only two (11%) deletions of the hptc gene were found in XP BCCs compared with >30% rearrangement observed in non-XP sporadic BCCs, and 17 of 19 (89%) were base substitutions. Among the 17 base substitutions, 11 (65%) were CC --> TT tandem mutations, and 4 (23%) were C --> T substitutions, all targeted at bipyrimidine sites. Hence, a significantly higher number (15 of 19; 79%) of UV-specific alterations are seen in XP tumors, in contrast to non-XP sporadic BCCs. Interestingly, we have found that in 7 of 14 (50%) XP BCCs analyzed, both hptc and the tumor suppressor gene p53 are mutated. Not only have our data indicated the key role played by hptc in the development of BCCs, they also have substantiated the link between unrepaired UV-induced DNA lesions and skin carcinogenesis, as exemplified by the UV-specific alterations of different genes in the same tumors.

Animals↗