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Biomedical subjects

Fulvio Parentin

Publications and source records attributed to Fulvio Parentin.

5 recordsLinked to original sources
PubMed2006

Polymicrobial keratomycosis in a three-year-old child.

PURPOSE: To describe a previously unreported case of polymicrobial mycotic keratitis caused by an association between Candida lusitaniae, C. parapsilosis, and Geotrichum candidum. METHODS: A three-year-old child with an antecedent trauma with vegetable matter and a prolonged use of corticosteroid eyedrops developed fungal keratitis. RESULTS: The isolates of the corneal scraping using Sabaraud dextrose agar grew C. lusitaniae, C. parapsilosis, and G. candidum. After topical 0.2% and systemic fluconazole treatment, the corneal lesion resolved with no recurrence. CONCLUSIONS: Corneal trauma with vegetables and the indiscriminate use of corticosteroids are important risk factors for mycotic keratitis. A combination of topical 0.2% and systemic fluconazole therapy was effective in the treatment of this mycotic association. This is the first report of fungal keratitis caused by C. lusitaniae and G. candidum.

Antifungal Agents↗
PubMed2004

Refractive evaluation in children with growth defect.

PURPOSE: Growth hormone (GH) is considered essential for postnatal somatic growth, exerting its effects on growth by hepatic production of IGF-I. IGF and other growth factors interact with the developing ocular tissues by influencing the synthesis of the extracellular matrix of the sclera and by inducing angiogenesis. The association between optic nerve hypoplasia, reduced retinal vascularization and GH deficiency (GHD) is well known. The purpose of this study is to evaluate the possible influence of congenital GHD on the refraction and on the emmetropization process. METHODS: Eighty children with congenital GHD had a thorough ophthalmologic examination, including cycloplegic refraction and axial length measurement. As a control group we enrolled 483 healthy children. RESULTS: In accordance with other epidemiological studies, the control group showed a slightly myopic mean defect; on the contrary, in GHD group we found a hyperopic defect, related to a shorter axial length, with statistically significant differences. CONCLUSIONS: Our findings emphasise the possible role of growth hormone in ocular development, and its interaction with the physiological process of emmetropization.

Adolescent↗
PubMed2003

Granulomatous anterior uveitis associated with bimatoprost: a case report.

PURPOSE: To describe a previously unreported case of anterior granulomatous uveitis in a patient using bimatoprost. METHODS: A 72-year-old woman with a long-standing history of anisometropic amblyopia and pseudoexfoliative glaucoma in the right eye started therapy with bimatoprost 0.03% once a day in the right eye. She had no previous history of ocular inflammation or ocular surgery. Her medical history was negative for systemic diseases associated with ocular inflammation. RESULTS: After one week, the patient developed severe conjunctival injection, cells and flare, and numerous 'mutton fat' keratic precipitates in the right eye. Examination of the left eye revealed no evidence of inflammation. Bimatoprost was discontinued; no topical steroid therapy was started. Systemic investigations were normal. The inflammation resolved over two weeks, solely with the discontinuation of bimatoprost. CONCLUSIONS: Bimatoprost is a synthetic prostamide, chemically related to prostamide F. Prostamides are naturally occurring substances, biosynthesized from anandamide in a pathway that includes COX2. Even though anandamide has proven suggestive potential pro-inflammatory effects, the mechanism of induction of inflammation by bimatoprost remains uncertain and speculative. In our report, the onset of acute uveitis in a patient using bimatoprost, after a long-term and well-tolerated treatment with a prostaglandin analog, suggests a distinct potential pro-inflammatory action of prostamides. This can indirectly support the concept that the target receptor of bimatoprost is different, and that the mechanism of action of prostamides is pharmacologically unique.

Aged↗
PubMedDate not supplied

Congenital growth hormone deficiency and eye refraction: a longitudinal study.

The aim of this study was to study the influence of growth hormone deficiency (GHD) on emmetropization and to evaluate the effect of growth hormone replacement therapy on eye refraction. Twenty-eight children affected by congenital GHD and undergoing substitutive therapy (group 1), and 28 healthy subjects (group 2), were prospectively studied. All patients had a thorough eye examination, including cycloplegic refraction and axial length measurement (only GHD children). After 2 years, we found in both groups a reduction of the dioptric power of the eye. A t test for paired data showed statistically significant differences in both groups (p<0.001), but the change of refraction was higher in group 2 (p<0.01). Axial length showed a statistically significant increase, according to the myopic shift (p<0.001). The change of the refraction found in GHD children could be related to the somatic growth and partially induced by growth hormone therapy. The difference between the two groups could be explained with the late beginning of the therapy in GHD children. It is possible to form the hypothesis that a correct and well-timed substitutive therapy could permit a normal emmetropization process.

Child↗