Botulinum toxin type a for dysthyroid upper eyelid retraction.

PURPOSE: To evaluate the safety and efficacy of botulinum toxin type A for treatment of eyelid retraction resulting from thyroid eye disease (TED) during the inflammatory phase of the condition. METHODS: In this prospective, nonrandomized case series, 18 patients with inflammatory eyelid retraction caused by active TED received botulinum toxin type A injection (10, 5, or 2.5 U) for treatment of upper eyelid retraction. Botulinum toxin type A (Allergan, Irvine, CA, U.S.A.) was injected transconjunctivally just above the superior tarsal border in the elevator complex of the upper eyelid. RESULTS: Seventeen of 18 patients (94%) demonstrated a reduced marginal reflex distance (MRD1) after botulinum toxin injection. The average change in MRD1 of the treated eyelid after injection was -2.35 mm (range, 0 to -8.0 mm). Of the 27 eyelids injected, 33% had a 0- to 1-mm drop in eyelid height, 30% had a 1.5- to 2-mm decrease, 22% had a 2.5- to 3-mm decrease, and 15% had a greater than 3-mm decrease in eyelid height. None of the treated eyelids were noted to increase in height. One patient showed no alteration inafter treatment. One patient had clinically MRD1 significant ptosis and one patient reported worsening of preexisting diplopia after injection. Three patients undergoing unilateral injection had relative contralateral eyelid elevation. All untoward effects resolved spontaneously without sequelae. CONCLUSIONS: : Botulinum toxin type A may be used in the inflammatory stage of thyroid eye disease to improve upper eyelid retraction. Individual response to treatment is variable, but this modality should be considered as a temporizing measure until stability for surgery is reached.

Nasolacrimal obstruction secondary to I(131) therapy.

PURPOSE: To report the finding of nasolacrimal drainage system obstruction associated with I(131) therapy for thyroid carcinoma from an updated and expanded cohort. METHODS: Patients with a history of epithelial derived thyroid carcinoma who had tearing were offered referral for evaluation by an oculoplastic surgeon. Patients underwent nasolacrimal probing and irrigation procedures with localization of their nasolacrimal obstruction. Therapy for the site of obstruction was instituted. RESULTS: Clinically significant tearing was identified in 26 patients, all of whom had previously undergone I(131) therapy (n = 563). Nineteen patients were evaluated and confirmed to have nasolacrimal drainage system obstruction; 7 have yet to be formally evaluated. Areas of obstruction included nasolacrimal duct, common canaliculus, and, rarely, distal upper and lower canaliculi. Patients were treated with a variety of modalities including silicone intubation, balloon dacryoplasty, dacryocystorhinostomy, and conjunctival dacryocystorhinostomy. CONCLUSIONS: The use of I(131) for thyroid carcinoma is associated with a 3.4% incidence of documented nasolacrimal drainage obstruction and an overall 4.6% incidence of documented or suspected obstruction. The true incidence may be higher, since - I(131) treated individuals were neither systematically evaluated nor questioned about tearing. It has yet to be established if the obstructions result from local toxicity caused by the passive flow of radioactive iodine containing tears through these tissues or the active uptake and concentration of I(131) in lacrimal drainage system tissues through the sodium/iodide supporter.

Advances in cosmetic oculoplastic surgery.

According to the American Society for Aesthetic Plastic Surgery, in the year 2000 over 5.7 million cosmetic surgical and nonsurgical procedures were performed in the United States. This was a 25% increase above the total number performed in 1999. The most popular of these procedures was botulinum toxin injection, followed by chemical peels and microdermabrasion. As the field of plastic and reconstructive surgery changes, so does the scope of the oculoplastic surgeon. This review article summarizes those developments in aesthetic surgery that are recent additions to the practice of aesthetic oculoplastic surgery. It highlights the most recent literature discussing brow and midface lifts, skin lasers, microdermabrasion, upper and lower blepharoplasty, chemical peels, botulinum toxin, and fat sculpturing.

Calmodulin regulation of gallbladder ion transport becomes dysfunctional during gallstone formation in prairie dogs.

Gallbladder absorption is increased prior to gallstone formation in prairie dogs and may promote cholesterol crystallization. Recent studies indicate that Ca2+-calmodulin (CaM) tonically inhibits gallbladder electrolyte absorption in prairie dogs fed a nonlithogenic diet. We hypothesized that dietary cholesterol alters CaM-dependent regulation of gallbladder ion transport, a possible link between increased gallbladder absorption and gallstone formation. Gallbladders from prairie dogs fed control (N = 24) or 1.2% cholesterol-enriched chow (N = 32) were mounted in Ussing chambers. Electrophysiology and ion flux were measured while exposing the epithelia sequentially to trifluoperazine (TFP), a CaM antagonist, followed by the calcium ionophore A23187. Animals fed the high cholesterol diet developed crystals and gallstones in a time-dependent fashion. Mucosal addition of 50 microM TFP decreased short-circuit current (Isc), transepithelial potential, and tissue conductance in control, crystal, and gallstone animals, but the magnitude of its effect was significantly decreased in animals fed cholesterol. TFP stimulated mucosa-to-serosa Na+ flux by 6.9 +/- 0.9 microeq/cm2/hr in control animals but only 3.1 +/- 0.8 microeq/cm2/hr in gallstone animals. Similarly, TFP increased mucosa-to-serosa Cl- flux by 11.9 +/- 1.4 microeq/cm2/hr in controls but only 4.9 +/- 1.4 microeq/cm2/hr in cholesterol-fed animals. TFP effects were not reversed by A23187, which caused differential effects on Isc and ion transport in cholesterol-fed animals. In conclusion, CaM-mediated inhibition of gallbladder Na+ and Cl- transport is diminished in prairie dogs fed cholesterol. We conclude that gallbladder ion transport is partially released from basal inhibition during gallstone formation and propose that dysfunctional CaM regulation may be a stimulus to increased gallbladder absorption.

Endogenous prostaglandins modulate chloride secretion by prairie dog gallbladder.

In addition to concentrating bile, the gallbladder secretes chloride (Cl-) and mucus into its lumen. We recently observed that gallbladder Cl- secretion is increased in prairie dogs during the formation of cholesterol crystals, a period of altered mucosal prostaglandin synthesis. Pathologic Cl- secretion is characteristic of other epithelial disorders such as cystic fibrosis and hypercalciuric nephrolithiasis and may be important in gallstone pathogenesis. We hypothesized that concentrations of endogenous prostaglandin E2 (PGE2) found during experimental gallstone formation may mediate increased Cl- secretion by prairie dog gallbladder. Prairie dog gallbladders were harvested by cholecystectomy and mounted in Ussing chambers. Unidirectional transepithelial Cl-, Na+, and H20 fluxes were measured before and after inhibition of endogenous prostaglandin synthesis with 10 micromol/L indomethacin. Gallbladders were then exposed to increasing concentrations of PGE2 to a maximal dose of 1 micromol/L, as found in animals with gallstones. Standard electrophysiologic parameters were recorded simultaneously. Indomethacin increased mucosal resistance and stimulated gallbladder Na+ and Cl- absorption. These effects were rapidly reversed by PGE2. PGE2 promoted Cl- secretion and decreased mucosal Na+ absorption at concentrations found in the gallbladder bile of animals with gallstones. Endogenous prostaglandin metabolism modulates gallbladder Cl- secretion and may promote changes in Cl- transport associated with cholelithiasis.

Octreotide stimulates Ca++ secretion by the gallbladder: a risk factor for gallstones.

BACKGROUND: Gallstone formation during octreotide therapy has been linked to elevated levels of gallbladder bile Ca++, a well-known prolithogenic factor. Although the subcutaneous administration of octreotide raises gallbladder bile Ca++ in prairie dogs, the mechanism for this effect is unknown. Octreotide has been shown to increase gallbladder Na+ and water absorption in Ussing chamber studies. Given the known effects of octreotide on gallbladder ion transport, we hypothesized that octreotide may also promote gallstone formation by stimulating gallbladder Ca++ secretion, thereby raising the lumenal concentration of biliary Ca++. METHODS: After cholecystectomy, prairie dog gallbladders were mounted in Ussing chambers, and standard electrophysiologic parameters were recorded. Unidirectional fluxes of Ca++ and Na+ were measured before and after serosal exposure to 50 nmol/L octreotide. RESULTS: Under basal conditions normal prairie dog gallbladder absorbed mucosal Ca++. Serosal octreotide converted the gallbladder from a state of basal Ca++ absorption to one of net Ca++ secretion by stimulating serosa to mucosa Ca++ flux. As anticipated, octreotide increased net Na+ absorption by stimulating mucosa to serosa Na+ flux and decreased tissue conductance and short-circuit current significantly compared with baseline values. CONCLUSION: Fifty nanomoles per liter octreotide stimulated Ca++ secretion by gallbladder epithelium, a possible mechanism for increased biliary Ca++ in prairie dogs receiving subcutaneous injections. Ca++ secretion linked to octreotide therapy may induce gallstones by raising biliary levels of Ca++, a known prolithogenic factor.