PharmGKB update: II. CYP3A5, cytochrome P450, family 3, subfamily A, polypeptide 5.
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Cytochrome P-450 CYP3A↗
Biomedical subjects
S Kishi
Publications and source records attributed to S Kishi.
Effect of FK506 eye drops on late and delayed-type responses in ocular allergy models.
BACKGROUND: It is well-known that FK506 strongly inhibits cytokine production by T cells in vitro. However, less evidence is available from in vivo studies of ocular allergy. OBJECTIVE: To study the anti-inflammatory effect of FK506 eye drops on late and delayed-type responses in several animal models of ocular allergy. METHODS: Rats and guinea-pigs were sensitized with egg albumin (EA) in adjuvant and later challenged by topical EA application to their eyes to examine the late response. Biopsy specimens of conjunctiva were stained with haematoxylin-eosin or stained for T cells and eosinophils. In addition, rats, rabbits and guinea-pigs were sensitized with complete Freund's adjuvant and later challenged by injecting purified protein derivatives for the delayed-type response. Bulbar conjunctival oedema and hyperaemia were graded by score in rabbits, and Evans blue (EB) extravasation was measured in rats and guinea-pigs. FK506 (0.01-1%) and steroid (0.1%) eye drops were instilled in the eyes of animals several times, before and after challenge. RESULTS: FK506 eye drops inhibited T cell and eosinophil infiltration in the late response and EB extravasation in the delayed-type response in rats. Also, they inhibited conjunctival oedema, hyperaemia and ocular mucus in the delayed-type response in rabbits. These effects were similar to those of steroid eye drops (betamethasone sodium phosphate, fluorometholone). FK506 eye drops also inhibited inflammatory cell infiltration, the loss of conjunctival epithelium and decrease of goblet cells in the late response as well as EB extravasation in the delayed-type response in guineapigs, a steroid-resistant species. CONCLUSION: FK506 eye drops inhibit late and delayed-type responses in animal models of ocular allergy.
Animals↗
Changes in hemodynamics and autonomic nervous activity in patients undergoing laparoscopic cholecystectomy: differences between the pneumoperitoneum and abdominal wall-lifting method.
BACKGROUND AND STUDY AIMS: Intraoperative changes in circulatory hemodynamics and autonomic nervous activity were evaluated in 33 patients with cholelithiasis who underwent laparoscopic cholecystectomy. PATIENTS AND METHODS: Of these patients, 18 were treated using a pneumoperitoneum (group G) and 15 using the abdominal wall-lifting method (group WL). Their ECG, blood pressure, arterial oxygen saturation, and expiratory carbon dioxide partial pressure were monitored. Autonomic nervous function was evaluated by spectral analysis of the heart rate. RESULTS: Mean blood pressure increased significantly in group G during surgery, but did not vary in group WL during any stage of surgery. The high-frequency (HF) power, an index of parasympathetic activity, decreased significantly in group G after pneumoperitoneum. However, the HF power did not decrease significantly in group WL. The LF/HF ratio, an index of sympathetic activity, increased significantly in group G after pneumoperitoneum, but did not vary in group WL. In addition, the incidence of ventricular or supraventricular arrhythmias and the severity of the arrhythmias as determined by Lown's classification were higher in group G than in group WL. These findings suggest that intraoperative changes in autonomic nervous activity, due to increased intra-abdominal pressure, were smaller in patients undergoing laparoscopic cholecystectomy using the abdominal wall-lifting method than in those undergoing laparoscopic cholecystectomy using pneumoperitoneum. The results also demonstrated that hemodynamic changes were smaller in patients undergoing the abdominal wall-lifting method than in those undergoing pneumoperitoneum. CONCLUSIONS: It was concluded that hemodynamics should be carefully monitored during pneumoperitoneum, and that the abdominal wall-lifting approach in laparoscopic cholecystectomy is a method worthy of consideration for elderly patients or those with cardiopulmonary complications.
Abdominal Muscles↗
Characterization of zebrafish caspase-3 and induction of apoptosis through ceramide generation in fish fathead minnow tailbud cells and zebrafish embryo.
Caspase-3 was cloned from zebrafish embryos and its properties were characterized to identify the biological implications of caspase in embryogenesis and apoptosis in zebrafish, which is a model organism in vertebrate developmental biology and genetics. The predicted amino acid sequence, totalling 282 amino acid residues, consisted of the prodomain and large and small subunits. Phylogenetic analysis showed that the cloned zebrafish caspase was a member of the caspase-3 subfamily with approx. 60% identity with caspase-3 from Xenopus, chicken and mammals. In addition, recombinant zebrafish caspase hydrolysed acetyl-Asp-Glu-Val-Asp-4-methyl-coumaryl-7-amide, and exhibited similar substrate specificity to the mammalian caspase-3 subfamily. Therefore this caspase was designated zebrafish caspase-3. Overexpression of zebrafish caspase-3 induced apoptosis and increased ceramide levels in fish fathead minnow tailbud cells and zebrafish embryos. Both ceramide generation and apoptosis induction were inhibited by treatment with a caspase inhibitor, benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone. Moreover, zebrafish caspase-3 mRNA was present in early embryos up to the 1000-cell stage as a maternal factor, and was then expressed throughout the body after the gastrula stage by zygotic expression. These findings indicate that the isolated caspase-3 plays an important role in the induction of ceramide generation as well as apoptosis in fish cells and the zebrafish embryo, and suggest that caspase-3 functions as a modulator of the pro-apoptotic signal in development.
Amino Acid Sequence↗
A specific interaction between the telomeric protein Pin2/TRF1 and the mitotic spindle.
Pin2/TRF1 was independently identified as a telomeric DNA binding protein (TRF1) [1] and as a protein (Pin2) that can bind the mitotic kinase NIMA and suppress its ability to induce mitotic catastrophe [2, 3]. Pin2/TRF1 has been shown to bind telomeric DNA as a dimer [3-7] and to negatively regulate telomere length [8-11]. Interestingly, Pin2/TRF1 levels are regulated during the cell cycle, being increased in late G2 and mitosis and degraded as cells exit from mitosis [3]. Furthermore, overexpression of Pin2/TRF1 induces mitotic entry and then apoptosis [12]. This Pin2/TRF1 activity can be significantly potentiated by the microtubule-disrupting agent nocodazole [12] but is suppressed by phosphorylation of Pin2/TRF1 by ATM; this negative regulation is important for preventing apoptosis upon DNA damage [13]. These results suggest a role for Pin2/TRF1 in mitosis. However, nothing is known about how Pin2/TRF1 is involved in mitotic progression. Here, we describe a surprising physical interaction between Pin2/TRF1 and microtubules in a cell cycle-specific manner. Both expressed and endogenous Pin2/TRF1 proteins were localized to the mitotic spindle during mitosis. Furthermore, Pin2/TRF1 directly bound microtubules via its C-terminal domain. Moreover, Pin2/TRF1 also promoted microtubule polymerization in vitro. These results demonstrate for the first time a specific interaction between Pin2/TRF1 and microtubules in a mitosis-specific manner, and they suggest a new role for Pin2/TRF1 in modulating the function of microtubules during mitosis.
Binding Sites↗
Telomeric protein Pin2/TRF1 as an important ATM target in response to double strand DNA breaks.
ATM mutations are responsible for the genetic disease ataxia-telangiectasia (A-T). ATM encodes a protein kinase that is activated by ionizing radiation-induced double strand DNA breaks. Cells derived from A-T patients show many abnormalities, including accelerated telomere loss and hypersensitivity to ionizing radiation; they enter into mitosis and apoptosis after DNA damage. Pin2 was originally identified as a protein involved in G(2)/M regulation and is almost identical to TRF1, a telomeric protein that negatively regulates telomere elongation. Pin2 and TRF1, probably encoded by the same gene, PIN2/TRF1, are regulated during the cell cycle. Furthermore, up-regulation of Pin2 or TRF1 induces mitotic entry and apoptosis, a phenotype similar to that of A-T cells after DNA damage. These results suggest that ATM may regulate the function of Pin2/TRF1, but their exact relationship remains unknown. Here we show that Pin2/TRF1 coimmunoprecipitated with ATM, and its phosphorylation was increased in an ATM-dependent manner by ionizing DNA damage. Furthermore, activated ATM directly phosphorylated Pin2/TRF1 preferentially on the conserved Ser(219)-Gln site in vitro and in vivo. The biological significance of this phosphorylation is substantiated by functional analyses of the phosphorylation site mutants. Although expression of Pin2 and its mutants has no detectable effect on telomere length in transient transfection, a Pin2 mutant refractory to ATM phosphorylation on Ser(219) potently induces mitotic entry and apoptosis and increases radiation hypersensitivity of A-T cells. In contrast, Pin2 mutants mimicking ATM phosphorylation on Ser(219) completely fail to induce apoptosis and also reduce radiation hypersensitivity of A-T cells. Interestingly, the phenotype of the phosphorylation-mimicking mutants is the same as that which resulted from inhibition of endogenous Pin2/TRF1 in A-T cells by its dominant-negative mutants. These results demonstrate for the first time that ATM interacts with and phosphorylates Pin2/TRF1 and suggest that Pin2/TRF1 may be involved in the cellular response to double strand DNA breaks.
Amino Acid Sequence↗
Telomeric protein Pin2/TRF1 induces mitotic entry and apoptosis in cells with short telomeres and is down-regulated in human breast tumors.
Telomeres are essential for cell survival and have been implicated in the mitotic control. The telomeric protein Pin2/TRF1 controls telomere elongation and its expression is tightly regulated during cell cycle. We previously reported that overexpression of Pin2/TRF1 affects mitotic progression. However, the role of Pin2/TRF1 at the interface between cell division and cell survival remains to be determined. Here we show that overexpression of Pin2 induced apoptosis in cells containing short telomeres, but not in cells with long telomeres. Furthermore, before entering apoptosis, Pin2-expressing cells first accumulated in mitosis and strongly stained with the mitosis-specific MPM2 antibody. Moreover, Pin2-induced apoptosis is potentiated by arresting cells in mitosis, but suppressed by accumulating cells in G1. In addition, overexpression of Pin2 also resulted in activation of caspase-3, and its proapoptotic activity was significantly reduced by inhibition of caspase-3. These results indicate that up-regulation of Pin2/TRF1 can specifically induce entry into mitosis and apoptosis, likely via a mechanism related to activation of caspase-3. Significantly, we also found that, out of 51 human breast cancer tissues and 10 normal controls examined, protein levels of Pin2/TRF1 in tumors were significantly lower than in normal tissues, as detected by immunoblotting analysis and immunocytochemistry. Since down-regulation of Pin2/TRF1 allows cells to maintain long telomeres, these results suggest that down-regulation of Pin2/TRF1 may be important for cancer cells to extend their proliferative potential.
Adaptor Proteins, Signal Transducing↗
Tomographic findings of foveal hard exudates in diabetic macular edema.
PURPOSE: To report the intraretinal location of foveal hard exudates after vitrectomy to treat diabetic macular edema and to evaluate the visual outcome. METHODS: In a prospective study, the tomographic features of 11 eyes (8 patients) with diabetic macular edema were evaluated with optical coherence tomography after vitrectomy. The intraretinal location of hard exudates at the fovea (anatomic foveola) and the relationship with visual acuity were investigated. RESULTS: With optical coherence tomography, hard exudates were observed as highly reflective spots in the cross-sectional images. In six of 11 eyes (54.5%), the hard exudates were in the inner portion of the neurosensory retina; the final best-corrected visual acuity averaged 20/70 in the six eyes. In the remaining five eyes (45.5%), hard exudates were deposited not only in the neurosensory retina but also in the subretinal space. In optical coherence tomographic images, subretinal hard exudates were observed as highly reflective plaques, which were slightly elevated over the retinal pigment epithelium. The five eyes developed a serous retinal detachment at the fovea before or after vitrectomy. Subretinal hard exudates bridged the detached neurosensory retina and the retinal pigment epithelium in two eyes. The average final visual acuity level in the five eyes was 20/300. The visual outcome was significantly worse in five eyes with subretinal hard exudates than in six eyes with an intraretinal one (P <.05, Wilcoxon rank sum tests). CONCLUSIONS: If serous retinal detachment develops before or after vitrectomy for diabetic macular edema, hard exudates tend to accumulate not only in the neurosensory retina but also in the subretinal space. The visual prognosis is worse in cases of subretinal exudation.
Aged↗
Histological study of PIVKA-II expression in hepatocellular carcinoma and adenomatous hyperplasia.
Although serum concentration of protein induced vitamin K absence or antagonist II (PIVKA-II) has been widely used for diagnosing hepatocellular carcinoma (HCC), little information is available concerning tissue PIVKA-II as an immunohistochemical marker for liver histology. In this study, we examined the expression of PIVKA-II in precancerous nodules (adenomatous hyperplasia) and various differentiation grades of HCC by immunohistochemical study using the monoclonal anti-PIVKA-II antibody (MU-3). We examined the relationship between tissue PIVKA-II staining and serum PIVKA-II level, tumor histology and tumor size. PIVKA-II was mainly detected in the cytoplasm of the HCC cells. The positive rates of PIVKA-II were as follows: adenomatous hyperplasia (AH), 0% (0/9); well-differentiated HCC, 65% (15/23); moderately differentiated HCC, 85% (22/26); poorly differentiated HCC, 54% (7/13). The expression of tissue PIVKA-II staining in moderately differentiated HCC was significantly higher than in well- or poorly differentiated HCC, whereas the serum PIVKA-II level in poorly differentiated HCC was higher than well- or moderately differentiated HCC. There was no relationship between the expression of PIVKA-II in cancer tissues and serum levels of PIVKA-II. Immunohistochemical studies revealed that PIVKA-II was expressed even in small-sized or well-differentiated HCC cells, but expression was not detected in AH. It was concluded that PIVKA-II is a useful immunohistochemical marker, even in small-sized or well-differentiated HCC.
Adenoma↗
Monitoring of intracellular 1-beta-D-arabinofuranosylcytosine 5'-triphosphate in 1-beta-D-arabinofuranosylcytosine therapy at low and conventional doses.
1-beta-D-Arabinofuranosylcytosine (ara-C) is used empirically at a low, conventional, or high dose. Ara-C therapy may be optimal if it is directed by the clinical pharmacokinetics of the intracellular active metabolite of ara-C, 1-beta-D-arabinofuranosylcytosine 5'-triphosphate (ara-CTP). However, ara-CTP has seldom been monitored during low- and conventional-dose ara-C therapies because detection methods were insufficiently sensitive. Here, with the use of our newly established method (Cancer Res., 56, 1800 -- 1804 (1996)), ara-CTP was monitored in leukemic cells from acute myelogenous leukemia patients receiving low- or conventional-dose ara-C [subcutaneous ara-C administration (10 mg / m(2) ) (3 patients), continuous ara-C infusion (20 or 70 mg / m(2) / 24 h) (7 patients), 2-h ara-C infusion (70 mg / m(2) ) (4 patients), and 2-h infusion of N(4)-behenoyl-1-beta-D-arabinofuranosylcytosine, a deaminase-resistant ara-C derivative (70 mg / m(2) ) (6 patients)]. Ara-CTP could be determined at levels under 1 microM. There was a close correlation between the elimination half-life values of the plasma ara-C and the intracellular ara-CTP. The presence of ara-C in the plasma was important to maintain ara-CTP. The continuous ara-C and the 2-h N(4)-behenoyl-1-beta-D-arabinofuranosylcytosine infusions maintained ara-CTP and the plasma ara-C longer than the subcutaneous ara-C or the 2-h ara-C infusion. They also afforded relatively higher ara-CTP concentrations, and consequently produced ara-CTP more efficiently than the 2-h ara-C infusion. Different administration methods produced different quantities of ara-CTP even at the same dose.
Adult↗
Close correlation of 1-beta-D-arabinofuranosylcytosine 5'-triphosphate, an intracellular active metabolite, to the therapeutic efficacy of N(4)-behenoyl-1-beta-D-arabinofuranosylcytosine therapy for acute myelogenous leukemia.
N(4)-Behenoyl-1-beta-D-arabinofuranosylcytosine (BHAC), a prodrug of 1-beta-D-arabinofuranosylcytosine, is used effectively for the treatment of leukemia in Japan. BHAC therapy may be more effective if it is delivered in conjunction with monitoring of 1-beta-D-arabinofuranosylcytosine 5'-triphosphate (ara-CTP), the intracellular active metabolite of ara-C derived from BHAC. However, previous monitoring methods for ara-CTP were insufficiently sensitive. Here, using our new sensitive method, we evaluated the ara-CTP pharmacokinetics in relation to the therapeutic response in 11 acute myelogenous leukemia patients who received a 2-h infusion of BHAC (70 mg / m(2)) in combination remission induction therapy. ara-CTP could be monitored at levels under 1 mM. BHAC maintained effective levels of plasma ara-C and intracellular ara-CTP for a longer time, even compared with historical values of high-dose ara-C. The area under the concentration-time curve of ara-CTP was significantly greater in the patients with complete remission than in the patients without response. This greater amount of ara-CTP was attributed to the higher ara-CTP concentrations achieved in the responding patients. There was no apparent difference of plasma ara-C pharmacokinetics between the two groups. Thus, for the first time, the ara-CTP pharmacokinetics was evaluated in relation to the therapeutic effect of BHAC, and the importance of ara-CTP was proven. Administration of optimal BHAC therapy may require monitoring of the ara-CTP pharmacokinetics in each individual patient.
Acute Disease↗
[Murine typhus infected in Oku-etsu area, Fukui Prefecture].
A 15-year-old girl, high school student, became febrile (38-39 degrees C) with chills, sore throat and cough on April 20, 1994. Until the onset, she was healthy and she had been camping with her classmates in a wooded mountainous area in Oku-etsu, Fukui Prefecture. She consulted a local clinic on April 21 and bacampicillin was initially administered and then changed to cefaclor on April 23. However, high body temperature continued and a maclopapular rash appeared on her face on April 24 and gradually spread to her anterior chest and back. Blood examination showed a WBC count of 2,200/microliter, and she was admitted to our hospital on April 25. On admission, peripheral blood data showed leukocytopenia (WBC 2,300/microliter) with 5% atypical lymphocytes. Titers of anti-Rickettsia typhi serum antibodies (IgM, -G) were elevated (1:80, 1:640) and she was diagnosed as having murine typhus. On the second hospital day, 200 mg of minocycline (MINO) was administered per os and her body temperature fell to within the normal limits on the third hospital day. On the 7th hospital day, the skin rash disappeared and she was discharged. Altogether, 320 high school students went camping with this patient. Among them, approximately 30 students had similar symptoms and signs as this case and had been diagnosed suspected viral infection. Twelve students of the 30 were admitted to other hospitals. It was considered that this case was part of an outbreak of murine typhus in the Oku-etsu area, Fukui Prefecture, but no further investigation was performed. Murine typhus is usually a benign disease that is controllable by the administration of MINO. In rare cases, infection can worsen to multiorganic failure, severe complications have been reported in 1-4% of cases, and death has been reported in less than 3%. Recently, it has also been reported that MINO not only has an antibiotic effect, but also play acts as a cytokine modulator in patients with rickettsial infection. Thus, in febrile patients in whom uncommon Rickettsia infection is suspected, serological test for murine typhus should be examined and the immediate administration of MINO is important.
Adolescent↗
Three-dimensional observations of developing macular holes.
PURPOSE: To describe the morphologic features of idiopathic macular holes and vitreous traction during macular hole evolution. METHODS: We prospectively examined 89 eyes of 82 patients with idiopathic macular holes (stage 1, 15 eyes; stage 2, 16 eyes; stage 3, 50 eyes; stage 4, eight eyes) using optical coherence tomography. In addition to optical coherence tomography, scanning laser ophthalmoscopy was performed in all 15 eyes with stage 1 hole, six of 16 eyes with stage 2, and 19 of 50 eyes with stage 3. RESULTS: In stage 1 eyes, optical coherence tomography revealed retinal split or cystic changes at the fovea in 11 of 15 eyes (73%) and foveal retinal detachment in four eyes (27%). Two eyes with foveal cysts progressed to stage 2, and one developed a stage 3 hole. In one eye with retinal detachment, the detached retina thinned and developed dehiscence. Optical coherence tomography showed a vitreous cortex that was detached in the perifoveal area but attached on the fovea in 11 of the 15 stage 1 eyes. In stage 2 macular holes, retinal tissue extending from the perifoveal retina formed a flap. Scanning laser ophthalmoscopy demonstrated intraretinal radiating striae, which corresponded to a foveal cyst or perifoveal cystic changes. CONCLUSIONS: Macular holes start as retinal splits or foveal cysts in most cases. The anterior wall of the cyst serves as a flap in stage 2 and an operculum in stage 3 holes. Radiating striae correspond to retinal splits or cysts and presumably represent an elevation of Henle fiber. In a few macular holes, foveal detachment is the initial change. The detached retina thins and eventually develops a hole. In both courses, anterior traction of the slightly detached vitreous cortex appears to be a major contributing factor to macular hole formation.
Aged↗
Tomographic features of early macular hole closure after vitreous surgery.
PURPOSE: To report the optical coherence tomographic features of macular hole closure in the first months after vitreous surgery. METHODS: We studied prospectively the tomographic features of 28 eyes (28 patients) with idiopathic macular holes before and after vitreous surgery by optical coherence tomography. We compared the best-corrected visual acuity levels with the postoperative tomographic features. RESULTS: The 25 eyes with successfully sealed macular holes had one of two tomographic features within 1 month postoperatively: simple closure (normal foveal configuration) in 14 eyes (56%) or a bridge formation at the fovea that mimicked a foveal retinal detachment in 11 eyes (44%). It took an average of 2.0 months (range, 0.8 to 3.5 months) for the bridge tissue to attach to the retinal pigment epithelium. Best-corrected visual acuity quickly improved in the former group; visual improvement began 1 month after attachment of the bridge tissue in the latter group. A closed hole reopened 4 months postoperatively in one eye with a bridge formation. CONCLUSIONS: Idiopathic macular holes have one of two patterns early after surgical closure, simple closure or a bridge formation. Visual improvement starts after the fovea assumes a normal configuration. The bridge formation appears to reflect an early phase and fragile condition in the anatomic closure of macular holes.
Aged↗
Tomographic features of a lamellar macular hole formation and a lamellar hole that progressed to a full-thickness macular hole.
PURPOSE: To report optical coherence tomography of a lamellar macular hole and a lamellar macular hole that progressed to a full-thickness macular hole. METHODS: Case Reports. RESULTS: Case 1. In the right eye of a 66-year old man, a lenticular-shaped split was present in the inner neurosensory retina corresponding to the fovea. Three months later, an operculum formed anterior to the fovea where the retina was attenuated. Case 2. In the left eye of a 58-year old woman, a foveal cyst was seen in the inner neurosensory retina and the inner wall of the cyst was elevated, where a slightly detached posterior vitreous cortex was attached. One month later, the inner wall was operculated, leaving a thin foveal bottom. Four months later, the hole progressed to a full-thickness macular hole. CONCLUSION: Lamellar macular hole appears to form when the inner wall of a split or cyst in the neurosensory retina at the fovea is avulsed by vitreous traction.
Aged↗
Optical coherence tomographic features of idiopathic submacular choroidal neovascularization.
PURPOSE: To clarify the morphologic features of idiopathic submacular choroidal neovascularization using optical coherence tomography. METHODS: Using optical coherence tomography, we prospectively examined 17 consecutive eyes (17 patients; eight men, nine women; mean age +/- SD, 36.0 +/- 9.3 years) with idiopathic submacular choroidal neovascularization. During the follow-up period (mean +/- SD, 7.5 +/- 3.8 months), we repeated optical coherence tomography in 15 eyes; optical coherence tomography was performed only at the initial examination in two eyes that underwent submacular surgery. RESULTS: Choroidal neovascularization was observed in the subsensory retinal space anterior to the retinal pigment epithelium as a highly or moderately reflective mass, which protruded from the retinal pigment epithelium in 13 of 17 eyes (protruding type). In four eyes, choroidal neovascularization was a highly reflective fusiform mass at the level of the retinal pigment epithelium and choriocapillaris (fusiform type). During the follow-up period, choroidal neovascularization regressed and the protruding mass became a highly reflective fusiform mass in 10 of 11 eyes with the protruding type that underwent repeated examination. In three of the 10 eyes, during 5 to 10 months from initial examination, the choroidal neovascularization was exacerbated and it again protruded into the subsensory retinal space anterior to the retinal pigment epithelium. Four eyes with the fusiform type remained the same throughout the follow-up period. The overlying retina was thickened and had low reflectivity in all 17 eyes at the initial examination. Optical coherence tomography identified subretinal fluid in only 11 of the 13 eyes with protruding type choroidal neovascularization. CONCLUSIONS: Optical coherence tomography confirmed subsensory retinal location of idiopathic submacular choroidal neovascularization anterior to the retinal pigment epithelium. Protruding choroidal neovascularization transforms to fusiform tissue at the level of the retinal pigment epithelium during the process of regression. Sensory retinal edema was always associated with choroidal neovascularization.
Adult↗
Evaluation of central serous chorioretinopathy with optical coherence tomography.
PURPOSE: To evaluate central serous chorioretinopathy with optical coherence tomography during the acute phase and after resolution of the acute phase. METHODS: In a prospective study, 23 consecutive eyes of 23 patients (19 men, four women; mean age +/- SD, 46.0+/-8.1 years; range, 29 to 60 years) with central serous chorioretinopathy were examined with optical coherence tomography during the acute phase and after resolution of the retinal detachment. After the initial examination, the patients were reexamined for 3 to 6 months (mean, 4.7+/-1.1 months). Cross-sectional retinal images through the center of the fovea were obtained from all eyes by optical coherence tomography. The retinal thickness at the center of the fovea was measured. The difference between the retinal thickness during the acute phase and after resolution of the retinal detachment was statistically analyzed using the Wilcoxon test. We also examined a grayish-white lesion that corresponded to the leakage point in fluorescein angiography in four eyes. RESULTS: In the acute phase, neurosensory retina was thickened within the area of serous retinal detachment in all 23 eyes. The detached retina was thicker than the reattached retina after resolution of the retinal detachment in all eyes. The retinal thickness at the center of the fovea during the acute phase (range, 157 to 236 microm; mean +/- SD, 196.9+/-22.6 microm) was significantly thickened compared with that after resolution (range, 105 to 152 microm; mean +/- SD, 124.8+/-10.7 microm; P<.0001, Wilcoxon test). In the acute phase, areas of low reflectivity localized within the detached retina were observed in 18 of the 23 eyes. In the area of the grayish-white lesion, optical coherence tomography showed a moderately reflective mass bridging the detached neurosensory retina and retinal pigment epithelium in the four eyes; the outer layer of the detached retina was more highly reflective in these eyes. The retinal pigment epithelium was focally detached beneath the subretinal reflective mass in three of the four eyes. CONCLUSIONS: In all eyes studied, neurosensory retina was thickened within the area of serous retinal detachment in the acute phase of central serous chorioretinopathy. The grayish-white lesion seems to be a fibrinous exudate that accumulates in the subretinal space and infiltrates into the outer retina.
Acute Disease↗
Optical coherence tomography of the neurosensory retina in rhegmatogenous retinal detachment.
PURPOSE: To clarify the pathologic changes of the detached neurosensory retina in rhegmatogenous retinal detachment. METHODS: Retinal images were prospectively examined by optical coherence tomography in 25 eyes of 25 consecutive patients with rhegmatogenous retinal detachment. We excluded the patients whose retinal detachment did not involve the central fovea or patients with poor fixation during optical coherence tomography (OCT) examination. Optical coherence tomography was scanned through the center of the fovea. The patients ranged in age from 15 to 77 years (mean, 45 years; SD, 20 years). The period from onset of subjective symptoms of retinal detachment to OCT ranged from 2 to 60 days (mean, 16 days; SD, 18 days). Optical coherence tomography findings, best-corrected visual acuity, and the height of the retinal detachment at the central fovea were statistically analyzed using ANCOVA (analysis of covariance) and the Mann-Whitney U test. RESULTS: In 25 eyes of 25 patients, OCT of the detached neurosensory retina at and adjacent to the center of the fovea demonstrated normal retinal structure (10 eyes, 40%), intraretinal separation (7 eyes, 28%), and an undulated separated outer retina (8 eyes, 32%). Three statistically significant factors affected best-corrected visual acuity: intraretinal separation (P = .001), intraretinal separation with undulated outer retina (P = .001), and height of retinal detachment at the central fovea (P<.001). Best-corrected visual acuity was significantly worse in the 15 eyes with intraretinal separation with or without an undulated outer retina than in the 10 eyes with retinal thickening but no intraretinal separation (P = .036). The eight eyes with undulated separated outer retina showed significantly higher retinal detachment at the central fovea than the seven eyes with intraretinal separation but no undulated outer retina (P = .009) and the 10 eyes without intraretinal separation (P = .016). The duration from onset of subjective symptoms to OCT was not related to the occurrence of intraretinal separation of the detached retina. CONCLUSIONS: Intraretinal separation of the detached retina occurred frequently and shortly after retinal detachment in rhegmatogenous retinal detachment and was one of the factors associated with poor vision in rhegmatogenous retinal detachment. Best-corrected visual acuity significantly decreased in the highly detached retina.
Adolescent↗