Nodular cutaneous amyloid tumors of the eyelids in the absence of systemic amyloidosis.

A patient was referred with recurrent bilateral, slow-growing, painless, nodular tumors of the upper eyelid margins. The tumors were excised and the base of each lesion was ablated with the CO2 laser. Histological examination of the excised tissue revealed amyloid. Despite the fact that cutaneous, amyloid lesions of the eyelid have been previously described as essentially pathognomonic for systemic amyloid disease, no evidence of systemic amyloidosis was found in this patient. We believe that this represents only the second reported case of bilateral cutaneous amyloid of the eyelids without systemic involvement. We agree with previous authors that this lesion be added to the list of painless slow-growing bilateral eyelid tumors.

Burn scar malignancies of the eyelids.

PURPOSE: To study the clinicopathologic characteristics and treatment of eyelid carcinomas developing in thermal burn scars. METHODS: A review of eight cases of eyelid burn scar malignancies: two from our own experience and six from published reports. RESULTS: Reported cases of burn scar malignancy of the eyelid are short-latency basal cell carcinomas. All carcinomas arose from small superficial burns. These potentially aggressive tumors respond well to local excision. CONCLUSION: As with other areas of the body, eyelid burn scars may undergo neoplastic degeneration. These carcinomas are predominately short latency basal cell carcinomas, rather than long-latency squamous cell carcinomas that are more common elsewhere in the body, including the head and neck region. Clinicians should be diligent in the long-term surveillance of all eyelid burns.

Cerebrospinal fluid leakage during endscopic forehead lifting.

PURPOSE: To report a case of endoscopic brow lift in which cerebrospinal fluid leakage was encountered. METHOD: A 69-year-old otherwise healthy man underwent endoscopic forehead lifting. RESULTS: An area of strong adherence was encountered in the area of the left superior paracentral scalp incision. As the adherence was released, clear fluid extruded (cerebrospinal fluid) and a burr hole was discovered. Absorbable gelatin sponge was placed over the dural defect and burr hole, and closure of the endoscopic scalp incisions was accomplished. CONCLUSION: Caution is suggested in performing this procedure when a patient has any history of a head trauma.

Nodular fasciitis of the lower eyelid in a pediatric patient.

PURPOSE: To describe a 14-year-old boy with a 1-month history of a rapidly growing, nontender, lower eyelid mass. METHODS: The specimen was studied using light microscopy. RESULTS: Although magnetic resonance imaging suggested a chronic vascular lesion, histopathologic analysis after excisional biopsy was consistent with nodular fasciitis. CONCLUSIONS: Nodular fasciitis is a relatively common soft-tissue lesion and represents a benign, reactive process. Lesions in the head and neck develop more frequently in children and adolescents than in adults, but periorbital lesions are uncommon. This is the first reported case of nodular fasciitis of the lower eyelid in a pediatric patient.

Sarcoidosis with orbital tumor outside the lacrimal gland: initial manifestation in 2 elderly white women.

Two elderly white women (aged 72 and 87 years) were first seen with painless, unilateral orbital swelling. Orbital scanning revealed masses infiltrating the soft tissue around the eye. Biopsy results showed nodular, noncaseating granulomas consistent with sarcoidosis. One patient's workup revealed systemic manifestations of sarcoidosis at the time of examination with hilar lymphadenopathy noted on gallium scan; the other refused a complete systemic workup. The orbital tumors resolved with systemic prednisone therapy. To our knowledge, our 87-year-old patient is the oldest to be seen with orbital sarcoidosis. These 2 patients demonstrate that this diagnosis must be considered with orbital tumors in the elderly and in unusual locations, such as these which occurred outside the lacrimal gland.

Reversal of iatrogenic punctal and canalicular occlusion.

PURPOSE: Significant epiphora occasionally develops after therapeutic punctal occlusion. When this complication occurs from combined scarring of the upper and lower proximal canaliculi, correction usually requires a conjunctivodacryocystorhinostomy. METHODS: The authors describe a new microsurgical technique for reversing iatrogenic occlusion of both the upper and lower canaliculi. The relatively straightforward reconstruction uses the remaining canalicular system to create new tear outflow sites. RESULTS: This procedure has been used successfully to repair eight of nine consecutive cases of iatrogenic canalicular occlusion, with an average follow-up of 2 years. CONCLUSION: Iatrogenic canalicular occlusion can be reversed microsurgically without a conjunctivodacryocystorhinostomy.

Changes in Müller cell plasma membrane specializations during subretinal scar formation in the rabbit.

The aim of this study was to identify changes in Müller cell plasma membrane specializations during experimentally induced subretinal gliosis in rabbits. When rabbits are dosed with sodium iodate, large expanses of retinal pigment epithelium and photoreceptors are destroyed. They are replaced by a subretinal scar consisting mainly of the ascending processes of Müller cells. These processes transform from the slender, highly polarized structures seen in normal animals into irregular processes that form a glia limitans along the basement membrane of the pigment epithelium, left bare following its degeneration. As the scar processes extend through the subretinal space and contract this basement membrane, they undergo dramatic changes in shape that are especially apparent in three-dimensional computer reconstructions of serial thick sections examined by high-voltage electron microscopy. Other changes involve the intercellular junctions and apical microvilli normally associated with the external limiting membrane. These structures become scattered over the surfaces of the ascending processes and are eventually lost. Loss of microvilli is associated with disappearance of immunostaining for a specific glycoconjugate normally associated with the microvillar plasma membrane. The observations document profound changes in Müller cell structural and functional polarity during subretinal scar formation.

A region in the steroid binding domain determines formation of the non-DNA-binding, 9 S glucocorticoid receptor complex.

This work was initiated to determine if a specific region of the glucocorticoid receptor determines the formation of the inactive (i.e. non-DNA-binding) 9 S form of the receptor recovered in cytosol preparations. It is known that the murine glucocorticoid receptor of the nti phenotype, which consists of only the carboxyl-terminal 40-kDa peptide containing the DNA-binding and steroid-binding domains separated by a short linker region, is recovered in hypotonic lysates as a 9 S heteromeric complex (Gehring, U., and Arndt, H. (1985) FEBS Lett. 179, 138-142). To further localize the domain required for formation of the 9 S complex, we have determined the sedimentation coefficients of receptors produced in COS-7 cells transfected with several mutants of the human glucocorticoid receptor gene. Deletion of the DNA-binding domain results in a 9 S complex that is somewhat less stable than the wild type receptor during sucrose gradient centrifugation. Deletion of the linker region yields a molybdate-stabilized 9 S complex, but deletion of the entire steroid-binding domain or internal deletion of the amino-terminal two-thirds of this domain yields receptors that are constitutive transcriptional activators and are present in cytosol only in the 4 S form. Taken together, these observations demonstrate that the steroid-binding domain contains the features required for formation of the 9 S heteromeric complex, and they are consistent with the proposal that the steroid-binding domain normally represses receptor function.

The kinetics of glucocorticoid binding to the soluble specific binding protein of mouse fibroblasts.

The kinetics of binding of glucocorticoids to the soluble, specific binding protein of mouse fibroblasts has been examined. The rate at which both potent and weak glucocorticoids achieve binding equilibrium is very slow. Second order rate constants of association range from 3 times 10-5 M- minus 1 min- minus 1 for cortisol to 6.7 times 10-5 M- minus 1 min- minus 1 for triamcinolone acetonide. Studies of the rates of binding at high steroid concentrations suggest that the slow rate of binding may be explained by a two-step mechanism. Active glucocorticoids, regardless of their potency, bind initially in a rapid manner to form a weak complex with the binding protein. The dissociation constant for the weak binding reaction is 0.87 times 10- minus 7 M for triamcinolone acetonide and 2.4 times 10- minus 7 M for cortisol. The weak binding complex becomes converted slowly to a tight complex. The first order rate constants for this conversion and the rate constants of dissociation from the tight complex have been determined for cortisol, dexamethasone and triamcinolone acetonide. The binding affinity of steroids of different biological potency is correlated with their rate of dissociation from this second tight binding state.