Biomedical subjects

F R Hu

Publications and source records attributed to F R Hu.

41 records · Page 3Linked to original sources

PubMedDate not supplied

Clinicopathologic study of satellite lesions in nontuberculous mycobacterial keratitis.

Multifocal stromal infiltrates or "satellite lesions" have been considered a characteristic feature of fungal keratitis. We examined two patients with nontuberculous mycobacterial keratitis who clinically presented with satellite lesions. The keratitis consisted of multifocal stromal infiltrates with indistinct white and fluffy margins. Both patients received topical fortified amikacin therapy with poor response. Lamellar keratectomy or penetrating keratoplasty was performed, respectively, in the two patients because of progressive stromal thinning and enlarging satellite lesions. Histopathologically, the main lesions consisted of dense infiltration of inflammatory cells with numerous acid-fast bacilli, while the satellite lesions were composed chiefly of inflammatory cells with fewer mycobacteria. Besides fungal keratitis, nontuberculous mycobacterial keratitis should also be considered when satellite lesions are present.

Adult↗

PubMedDate not supplied

Effects of contact lenses on corneal endothelium - a morphological and functional study.

PURPOSE: To study the corneal endothelial morphological changes and endothelial barrier function in contact lens wearers. METHODS: Specular microscopy and anterior segment fluorophotometry were performed on 116 controls (group 1) and 76 daily wear soft contact lens wearers. Group 2 patients (n = 34) had been wearing contact lenses for less than 5 years and group 3 (n = 42) for more than 5 years. The relationship of corneal thickness, endothelial cell density, hexagonal cell percentage, coefficient of variation in cell area, corneal autofluorescence and corneal endothelial permeability to the contact lens wear duration was studied. RESULTS: The average corneal thickness of contact lens wearers did not differ significantly from controls (0.533 +/- 0.031, 0.538 +/- 0.044, 0.532 +/- 0.031 mm for groups 1, 2 and 3, respectively; p = 0.89). However, there was a significant tendency toward corneal thinning with a longer history of contact lens wear (r = -0.31, p = 0.002 in groups 2 and 3). The percentage of hexagonal cells decreased with both increasing hours of contact lens wear per day (r = -0.36, p < 0.001) and the duration of contact lens wear in years (r = -0.33, p < 0.001), but there was no significant change in endothelial cell density in contact lens wearers. The coefficient of variation in cell size correlated more closely with increased hours of contact lens wear per day (r = 0.35, p = 0.002) than with the duration of contact lens wear in years (r = 0.12; p = 0.31). In the functional study, corneal autofluorescence increased in contact lens wearers (5.13 +/- 0.71 ng/ml in group 1, 6.45 +/- 2.03 ng/ml in group 2 and 7.21 +/- 1.51 ng/ml in group 3, respectively, p < 0.001) and the mean endothelial permeability decreased in contact lens wearers (3.89 +/- 0.95 x10(-4)/cm in group 1, 2.71 +/- 0.73 x 10(-4)/cm in group 2 and 2.95 +/- 0.91 x 10(-4)/cm in group 3, respectively, p = 0.003). CONCLUSIONS: Daily wear soft contact lenses caused morphological changes in the corneal endothelium. With an increasing span of contact lens wear, there was a significantly increased variation in cell size, a decreased hexagonal cell percentage, an evident intercellular dark area and rosette formation. The corneal autofluorescence increased and the overall endothelial permeability decreased as a consequence of contact lens wear. Contact lens wear also caused corneal thinning, and the cornea became thinner with increasing duration of contact lens wear.

Adult↗

PubMedDate not supplied

Corneal autofluorescence and epithelial barrier function in diabetic patients.

Corneal autofluorescence and corneal epithelial barrier function of 146 diabetic patients and 121 controls were examined using anterior segment fluorophotometry. Corneal autofluorescence in diabetic patients was significantly higher when compared with that of controls (14.6 +/- 3.7 vs. 10.9 +/- 2.7 ng/ml, p < 0.001), and was increased in patients with more severe diabetic retinopathy (r = 0.23, p = 0.005), higher postprandial blood glucose level (r = 0.25, p = 0.009), and higher glycosylated hemoglobin (r = 0.21, p = 0.047). No correlation existed between corneal autofluorescence and the duration of diabetes mellitus. The corneal fluorescein concentration 45 min after topical application of 20 microliters of 2% sodium fluorescein was also significantly higher in diabetics than in controls (1,373.2 +/- 1,081.5 vs. 363.0 +/- 308.3 ng/ml, p < 0.001). No correlation existed with postprandial blood sugar (r = -0.19, p = 0.056) nor with glycosylated hemoglobin (r = -0.13, p = 0.20). The corneas in diabetics became more hypesthetic with longer duration of diabetes mellitus (r = -0.19, p = 0.02), although the mean corneal sensitivity threshold was not statistically higher in the diabetic group (p = 0.57). There was no correlation of the epithelial barrier function with the duration of diabetes (r = -0.07, p = 0.38), the severity of diabetic retinopathy (r = 0.07, p = 0.38), and the corneal sensitivity threshold (r = -0.06, p = 0.43).

Aged↗

PubMedDate not supplied

Immunohistochemical study of subepithelial haze after phototherapeutic keratectomy.

PURPOSE: Subepithelial haze is a frequent complication and is often the cause of regression after photorefractive keratectomy (PRK). The lack of understanding of this undesirable complication following PRK is in part due to the limited availability of suitable tissues for pathological studies. METHODS: We examined the expression of various extracellular components in the cornea of a 46-year-old man who underwent phototherapeutic keratectomy (PTK) to remove a central corneal scar secondary to trauma. The patient subsequently underwent penetrating keratoplasty. A scar-free region containing an area of slight subepithelial haze adjacent to normal cornea was used for immunohistochemical staining with antibodies directed against cytoskeletal proteins, ie, vimentin, desmin and smooth muscle actin, and the extracellular components, laminin, heparan sulfate, keratan sulfate, and collagen types III, IV, V, and VII. RESULTS: Immunohistochemistry revealed that basal epithelial cells expressed components of basement membrane. The stromal fibroblasts within the haze tissue were labeled by anti-smooth muscle actin antibodies, a characteristic of myofibroblasts, which synthesized and secreted extracellular matrix components that contributed to the formation of the disorganized collagenous matrix and may account for subepithelial haze. CONCLUSIONS: The expression patterns for the cytoskeletal proteins and extracellular components indicated that the formation of subepithelial haze is a process of tissue remodeling, involving both corneal basal epithelial cells and keratocytes during wound repair.

Cornea↗

PubMedDate not supplied

Corneal opacity and congenital glaucoma associated with massive heparan sulfaturia: report of one case.

A four month-old male infant was noted to have had severe corneal opacity since birth. Buphthalmos, increased intraocular pressure and corneal opacity with neovascularization were noted during physical examination. There was neither dysmorphic face nor hirsutism and the liver and spleen were impalpable. In addition, hypotonia, poor head control, and absence of Moro and grasping reflexes were also noted. There was no evidence of congenital infection by TORCH study. Tests of both urine and plasma amino acids were within normal limits. However, excessive urinary excretion of heparan sulfate was detected by thin-layer chromatography. Corneal transplantation was performed at 6 months old. Histopathological examination of the corneal button showed homogeneous thickening of Bowmen's membrane and intracytoplasmic pinkish substances in corneal stroma. The Alcian blue stain was positive, which was consistent with mucopolysaccharidosis of cornea. The manifestation of this case may be a clinical variant of Sanfilippo's syndrome (Mucopolysaccharidosis type III).

Corneal Opacity↗