RESUMEN
PURPOSE: To compare the intraocular lens calculation formulas and evaluate postoperative refractive results of patients with previous hyperopic corneal refractive surgery. DESIGN: Retrospective, comparative, observational study. SETTING: Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, USA. METHODS: Clinical charts and optical biometric data of 39 eyes from 24 consecutive patients diagnosed with previous hyperopic laser vision correction and cataract surgery were reviewed and analyzed. The Intraocular lens (IOL) power calculation using the Holladay 2 formula (Lenstar) and the American Society of Cataract and Refractive Surgery (ASCRS) Post-Refractive IOL Calculator (version 4.9, 2017) were compared to the actual manifest refractive spherical equivalent (MRSE) following cataract surgery. No pre-Lasik / PRK or post-Lasik / PRK information was used in any of the calculations. The IOL prediction error, the mean IOL prediction error, the median absolute refractive prediction error, and the percentages of eyes within ±0.50 diopter (D) and ±1.00 D of the predicted refraction were calculated. RESULTS: The Holladay 2 formula produced a mean arithmetic IOL prediction error significantly different from zero (P = 0.003). Surprisingly, the mean arithmetic IOL prediction errors generated by Shammas, Haigis-L and Barret True K No History formulas were not significantly different from zero (P = 0.14, P = 0.49, P = 0.81, respectively).There were no significant differences in the median absolute refractive prediction error or percentage of eyes within ± 0.50 D or ± 1.00 D of the predicted refraction between formulas or methods. CONCLUSION: In eyes with previous hyperopic LASIK/PRK and no prior data, there were no significant differences in the accuracy of IOL power calculation between the Holladay 2 formula and the ASCRS Post-refractive IOL calculator.
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Hiperopía/fisiopatología , Hiperopía/cirugía , Lentes Intraoculares , Refracción Ocular , Anciano , Humanos , Persona de Mediana Edad , Estudios RetrospectivosRESUMEN
We report an elderly woman who was anticoagulated and presented with a recent history of right-sided orbital contusion and a periorbital hematoma without clinical or radiological evidence of focal mass or orbital involvement. She was initially treated conservatively. Continued progression of adnexal swelling and erythema prompted further investigation, however. There was no improvement with surgical drainage alone; biopsy revealed angiosarcoma. The discovery of this vascular tumor underscores the importance of a reconsideration of the diagnosis in the face of counterintuitive findings. Additionally, we emphasize the need to consider malignancy in the differential diagnosis of prolonged periorbital swelling, regardless of a history of recent trauma.
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Neoplasias de los Párpados/diagnóstico , Hemangiosarcoma/diagnóstico , Hematoma/diagnóstico , Enfermedades Orbitales/diagnóstico , Anciano de 80 o más Años , Biomarcadores de Tumor/metabolismo , Biopsia , Diagnóstico Diferencial , Neoplasias de los Párpados/metabolismo , Neoplasias de los Párpados/cirugía , Femenino , Hemangiosarcoma/metabolismo , Hemangiosarcoma/cirugía , Hematoma/metabolismo , Hematoma/cirugía , Humanos , Imagen por Resonancia Magnética , Proteínas de Neoplasias/metabolismo , Procedimientos Quirúrgicos Oftalmológicos , Enfermedades Orbitales/metabolismo , Enfermedades Orbitales/cirugía , Neoplasias de la Parótida/diagnóstico , Neoplasias de la Parótida/cirugía , Radioterapia Adyuvante , Tomografía Computarizada por Rayos XRESUMEN
PURPOSE: To determine the tolerability of intravitreal infliximab (Remicade) in patients with refractory diabetic macular edema or choroidal neovascularization secondary to age-related macular degeneration. METHODS: This is a prospective, interventional, noncomparative, open-label, 12-week pilot study of intravitreal infliximab in four patients who failed conventional therapies. Two had diabetic macular edema and two had choroidal neovascularization secondary to age-related macular degeneration. All patients received 0.5 mg/0.05 mL intravitreal infliximab and were eligible for a second injection at 6 weeks if reinjection criteria were met. Outcome measures were best-corrected visual acuity using standard Early Treatment Diabetic Retinopathy Study refraction, central retinal thickness on optical coherence tomography, fluorescein angiography, standard electroretinography, and microperimetry. Patients were evaluated at Days 0 and 1 and Weeks 2, 6, and 12. Six months after study completion, all patients were tested for human antimouse and human antichimeric antibodies. RESULTS: At Week 12, visual acuity scores had declined in three patients. All patients had persistence of cystoid macular edema on optical coherence tomography, although two had a decrease in central retinal thickness. Three patients had an overall worsened appearance on angiography. On the final electroretinography, all patients had a decrease in maximal combined responses, from 7% to 24% from baseline, which may have been within expected variability of electroretinography data. To photopic flicker stimulus, three patients had slower latency of response, and all had decreased amplitudes. All patients declined on microperimetry. The first patient entered in the study met the criteria for a second injection because of improved standard electroretinography and microperimetry at Week 6. However, 2 weeks after the second injection, he developed panuveitis. Two other patients, after one injection only, had evidence of inflammation (vitritis or panuveitis) on examination at Week 6. Three patients developed systemic antibodies against infliximab (human antichimeric antibodies). CONCLUSION: Low-dose intravitreal infliximab was not well tolerated in this small group of patients and was both immunogenic and probably retinotoxic.
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Antiinflamatorios/efectos adversos , Anticuerpos Antiidiotipos/sangre , Anticuerpos Monoclonales/efectos adversos , Panuveítis/inducido químicamente , Retina/efectos de los fármacos , Anciano , Antiinflamatorios/inmunología , Anticuerpos Monoclonales/inmunología , Quimera/inmunología , Neovascularización Coroidal/tratamiento farmacológico , Neovascularización Coroidal/etiología , Retinopatía Diabética/complicaciones , Retinopatía Diabética/tratamiento farmacológico , Electrorretinografía , Femenino , Angiografía con Fluoresceína , Estudios de Seguimiento , Humanos , Infliximab , Inyecciones , Degeneración Macular/complicaciones , Degeneración Macular/tratamiento farmacológico , Edema Macular/tratamiento farmacológico , Edema Macular/etiología , Masculino , Persona de Mediana Edad , Panuveítis/diagnóstico , Proyectos Piloto , Estudios Prospectivos , Retina/patología , Tomografía de Coherencia Óptica , Factor de Necrosis Tumoral alfa/antagonistas & inhibidores , Factor de Necrosis Tumoral alfa/inmunología , Agudeza Visual/fisiología , Pruebas del Campo Visual , Cuerpo VítreoRESUMEN
Parity in women is associated with reduced lifetime risk of breast cancer, and hormones of pregnancy [estrogen (E), progesterone (P), human chorionic gonadotropin (hCG)] are implicated. Parity also reduces mammary cancer risk in carcinogen-exposed rats, and administering pregnancy hormones to these animals is similarly effective. Because pregnancy hormones are also able to stimulate cancer growth, we proposed to resolve this dichotomy by determining whether administered pregnancy hormones elicit the cancer-inhibiting agent alpha-fetoprotein (AFP) from the liver, which would implicate AFP as a proximal effector of hormonal anticancer activity. Accordingly, we treated groups of nitrosomethylurea-exposed rats with saline, E(3), E(2) + P, E(3) + P, hCG, or allowed them to experience pregnancy, and then monitored mammary cancer incidence and serum levels of AFP over time. Each hormone treatment reduced mammary cancer incidence and elevated serum AFP levels. To challenge human tissues, human HepG2 liver cells in culture were treated with the same hormonal agents. Each hormone regimen increased the levels of AFP in the culture medium. Medium containing AFP elicited by hCG inhibited the E(2)-stimulated proliferation of cultured human MCF7 breast cancer cells, whereas hCG alone did not inhibit their growth. Furthermore, antibodies to AFP neutralized the growth-inhibiting effect of AFP-containing HepG2 medium. We conclude that in the treatment of carcinogen-exposed rats with the hormones of pregnancy, and by inference in women who have experienced pregnancy, that AFP is a proximal agent that inhibits mammary gland cancer.
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Neoplasias de la Mama/etiología , Gonadotropina Coriónica/metabolismo , Estradiol/metabolismo , Embarazo/fisiología , Progesterona/metabolismo , alfa-Fetoproteínas/metabolismo , Animales , Neoplasias de la Mama/epidemiología , Gonadotropina Coriónica/farmacología , Estradiol/farmacología , Femenino , Humanos , Neoplasias Mamarias Experimentales/epidemiología , Neoplasias Mamarias Experimentales/etiología , Paridad/fisiología , Progesterona/farmacología , Ratas , Ratas Sprague-Dawley , Factores de RiesgoRESUMEN
Parity profoundly reduces breast cancer (BC) risk later in life. It has been reasoned that hormones (either estradiol E2 or estriol E3), progesterone (P) or human chorionic gonadotropin (hCG) in the serum of pregnant women might lead to that reduction in risk. These agents have been shown to reduce BC incidence in nonpregnant rats. We investigated the hypothesis that exogenously added E2, E3, P, or hCG are not the proximal effectors of risk reduction, but that they elicit alpha-fetoprotein (alphaFP) from the nonpregnant liver, and that cFP is the proximal agent by which reduction of BC risk is obtained. Methylnitrosourea (MNU)-exposed animals were treated with saline, E3, E2 + P, E3 + P, hCG, or were allowed to experience pregnancy, and AFP levels were measured in the serum and subsequent tumor incidence was recorded. Human HepG2 liver cells in culture were treated with E3, E2 + P, P, or hCG and elicited AFP was measured in the media. The HepG2 culture media containing elicited AFP was assessed for its ability to inhibit proliferation of T47D cells when applied to these human BC cells in culture, and to inhibit the estrogen-induced phosphorylation of the estrogen receptor in T47D cells. For each condition in the prevention studies, hormone treatment reduced the incidence of BC to an extent similar to that reported by the original studies. In each condition, alphaFP levels in serum were elevated over that in control animals. In culture, treatment of human liver cells with E3, E2 + P, or hCG, but not P alone, led to increased levels of AFP in the media. Media containing hCG-elicited AFP inhibited the estrogen-stimulated proliferation of T47D cells in culture, and inhibited phosphorylation of the estrogen receptor, whereas, estrogens and hCG did not inhibit the growth of these tumor cells in culture. In conclusion, since the hormones of pregnancy elicit alphaFP from the liver, and alphaFP but not the hormones of pregnancy has direct antitumor properties, it is concluded that alphaFP is the proximal agent through which reduction in BC incidence is realized from the experience of pregnancy.
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Neoplasias de la Mama/prevención & control , Proliferación Celular/efectos de los fármacos , Estrógenos/uso terapéutico , alfa-Fetoproteínas/metabolismo , Animales , Neoplasias de la Mama/inducido químicamente , Neoplasias de la Mama/metabolismo , Carcinógenos , Carcinoma Hepatocelular/tratamiento farmacológico , Carcinoma Hepatocelular/metabolismo , Carcinoma Hepatocelular/patología , Gonadotropina Coriónica/uso terapéutico , Estradiol/uso terapéutico , Estriol/uso terapéutico , Femenino , Humanos , Neoplasias Hepáticas/tratamiento farmacológico , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/patología , Metilnitrosourea , Embarazo , Progesterona/uso terapéutico , Ratas , Sustancias para el Control de la Reproducción/uso terapéutico , Factores de Riesgo , Células Tumorales CultivadasRESUMEN
PURPOSE: alpha-Fetoprotein (AFP) is a protein of pregnancy associated with a decrease in lifetime risk of breast cancer in parous women. A synthetic, cyclic nonapeptide has been developed that mimics the antioncogenic active site of AFP. To test the hypothesis that the AFP-derived peptide (AFPep) can prevent breast cancer, the N-methyl-N-nitrosourea-induced breast cancer model was used in rats. EXPERIMENTAL DESIGN: AFPep was given daily by injection beginning 10 days after N-methyl-N-nitrosourea treatment and continued for 23 days (a time designed to mimic pregnancy) or for other times to assess efficacy as a function of drug duration. Tumor incidence, multiplicity, and latency were noted as end points. At necropsy, pathology analysis of tumors and major organs were obtained. RESULTS: AFPep prevented cancer in a dose-dependent fashion. Significantly longer mean tumor-free days (P < 0.02), lower tumor incidence (P = 0.004), and lower tumor multiplicity were observed for AFPep-treated groups. No evidence of host toxicity as measured by body weight, cage activity, fur texture, and organ weights (liver, uterus, heart, kidney, and spleen) were found in animals treated with AFPep. Mechanistic studies using transplantable human breast cancer xenografts showed that the peptide interfered with estrogen-dependent breast cancer growth inhibited the phosphorylation of the estrogen receptor and activated phosphorylation of p53. CONCLUSIONS: AFPep is a well-tolerated, mechanistically novel, chemopreventive agent in models of breast cancer and warrants further development for the prevention and treatment of this disease in humans.