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C Cursiefen

Publications and source records attributed to C Cursiefen.

At least 19 recordsLinked to original sources
PubMed2006

[The dry eye. Current concepts on classification, diagnostics, and pathogenesis].

The etiology of dysfunctional tear syndrome ("dry eye") is multifactorial and complex. Recent evidence suggests an important role of androgens in regulating tear film secretion onto the ocular surface. In addition, inflammatory processes of the ocular surface seem to be the common final pathway of all chronic forms of dry eye. Novel concepts of pathogenesis and state-of-the-art diagnostic tools are discussed. In vivo confocal microscopy allows quantification of ocular surface inflammatory cells. This is of increasing importance for evaluation of anti-inflammatory treatments in dry eye patients.

Dry Eye Syndromes↗
PubMed2006

[Current treatment for dry eye syndrome].

The therapy of dry eye disease as a chronic problem necessitates a long-term therapeutic association between patient and ophthalmologist. The aim of therapy is to relieve symptoms and improve vision as far as possible with an acceptable level of effort on the part of the patient. Therapy of dry eye follows a staged concept including tear replacement, serum eye drops, punctum plugs, novel anti-inflammatory drugs (cyclosporin A), and surgical procedures. Interdisciplinary care, especially of patients with autoimmune disease, is recommended and is best provided in a specialized dry eye outpatient clinic with quality control.

Anti-Inflammatory Agents↗
PubMed2006

[Conjunctival chemosis resistant to therapy].

We saw a 62-year-old male with a conjunctival chemosis, which was resistant to local therapy. Excisional biopsy and histological work-up of the tissue were performed. Additional immunohistochemical staining using the Lyve-1 antibody (specific for lymphatic vascular endothelium) allowed the diagnosis of a lymphangioma of the conjunctiva to be made.

Aged↗
PubMed2005

[Neurotrophic keratitis].

Neurotrophic keratitis is a degenerative disease of the cornea caused by reduced corneal innervation. Trauma, tumors, inflammatory lesions and surgical procedures can damage the first branch of the trigeminal nerve on its entire course from brainstem to and within the cornea. Loss or reduction of corneal innervation leads to a reduced aqueous phase of the tear film and due to reduced supply with neurotransmitters/trophic factors also to reduced epithelial healing capacity (impaired mitosis and migration). Combined existence of tear film deficiency and impaired epithelial healing capacity predispose to persistent epithelial defects, corneal ulcers and perforation. Early diagnosis and adequate treatment may prevent this catastrophic chain of events.

Cell Movement↗
PubMed2005

[Conservative and surgical treatment of neurotrophic keratopathy].

Neurotrophic keratopathy is one of the most challenging conditions among the disorders of wound healing of the ocular surface. In addition to bilateral assessment of corneal sensitivity, tear status and lid function must be analyzed and treated by unpreserved artificial tears and adequate lid surgery. Further conservative treatment options include hyaluronic acid and dexpanthenol as well as autologous serum. Application of recombinant growth factors (especially NGF) represents an interesting perspective. Concerning surgical interventions, temporary or permanent occlusion of the lacrimal punctum may be accompanied by lateral tarsorrhaphy which is easy to perform, potentially reversible, and in most cases successful. Depending on the type of wound healing disorder amniotic membrane transplantation may be helpful either as basal membrane transplant (graft) or as a patch, or in combination (sandwich). A tectonic keratoplasty a chaud should typically be combined with a simultaneous amniotic membrane patch and/or a lateral tarsorrhaphy to avoid persistent epithelial defects.

Adjuvants, Immunologic↗
PubMed2004

[Clinical aspects and treatment of immune reactions following penetrating normal-risk keratoplasty].

PURPOSE: Endothelial graft rejection is one of the most common causes of graft failure following penetrating keratoplasty (PK). The aim of this study was to evaluate the incidence, time course and outcome of treatment of graft rejection after normal-risk PK and to identify possible risk factors for the recurrence of immune reactions and irreversible graft failure. PATIENTS AND METHODS: The study included 500 eyes from the prospective Erlanger Normal-risk Keratoplasty Study with a mean follow-up of 42 +/- 18 (median 40) months. Indications for PK were keratoconus in 48 %, Fuchs' dystrophy in 30 %, secondary bullous keratopathy in 11 %, non-vascularized corneal scars in 7 % and stromal dystrophies in 4 %. Standardized complete ophthalmological examinations were performed on a regular basis before, during the acute graft rejection and then regularly in a defined examination raster in an cornea out-patient service. RESULTS: During follow-up 29 eyes (5.6 %) developed an episode of endothelial graft rejection (23 eyes with acute diffuse and 6 eyes with chronic focal rejection type). Episodes of endothelial graft rejection clustered between 11 and 25 months postoperatively (15 from 29, 51.7 %). Most grafts (25 of 29) regained clarity after topical and systemic steroid treatment. Only 4 patients showed an irreversible graft failure requiring a repeat PK, all of whom had secondary bullous keratopathy as the primary indication for PK. Risk factors for irreversible graft failure were pre-existing anterior synechiae in 3 patients and secondary open angle glaucoma in pseudoexfoliation syndrome in one patient. Recurrence of graft rejection was seen in 5 patients (all with keratoconus) after a time interval of 8 to 12 months. Under very low topical steroid treatment no further recurrence was observed in all 5 patients up to 2 years. CONCLUSION: Patients should be followed-up on a regular base for longer postoperative periods, since most episodes of graft rejection were observed between 1 and 2 years after PK. Development of irreversible graft failure was strongly associated with pre-existing anterior synechiae and pre-existing glaucoma. Low-dose topical steroid treatment after immunological rejection seems to prevent the recurrence of further graft rejection.

Adult↗
PubMed2003

[Angiogenesis and lymphangiogenesis in the cornea. Pathogenesis, clinical implications and treatment options].

BACKGROUND: Whereas the normal cornea is devoid of blood and lymphatic vessels,both can invade the cornea secondary to a variety of corneal diseases and after surgery. This not only reduces visual acuity, but also renders such a cornea high-risk, if subsequent corneal transplantation is performed. METHODS: A PUBMED-based literature search was carried out. RESULTS: Current knowledge on pathogenesis, clinical implications and treatment modalities for corneal neovascularization is discussed. CONCLUSIONS: Novel anti-angiogenic and antilymphangiogenic therapeutic strategies should reduce blindness associated with corneal neovascularization and subsequent graft rejection.

Angiogenesis Inhibitors↗
PubMed2003

[Classification of ocular surface disease. Part 1].

The ocular surface consists of the lid margin, conjunctiva and cornea which together with the tear system represent a functional entity. The diagnosis of ocular surface disease can be very difficult due to the similarity of various disease entities. The classification should be made on the pathological and pathophysiological characteristics of ocular surface disease. The first part of the classification comprises diseases of the lid margin, the tear system as well as diseases of the conjunctiva. Both the clinical presentation as well as the underlying pathophysiological and pathological characteristics of the most important ocular surface diseases are reviewed.

Conjunctival Diseases↗
PubMed2003

Pericyte recruitment in human corneal angiogenesis: an ultrastructural study with clinicopathological correlation.

BACKGROUND/AIM: During angiogenesis-that is, the outgrowth of new from pre-existing blood vessels, new capillaries undergo a period of "fine tuning" when vascular endothelial cells become apoptotic if sufficient supply of angiogenic factors is lacking. Morphologically, this period correlates with the absence of pericyte coverage of new vessels. Mature, pericyte covered vessels, in contrast, do not depend on elevated levels of angiogenic factors for survival. This study analyses whether, and if so when, pathological vessels in human corneal neovascularisation (CN) acquire pericyte coverage. This can be of importance for future angioregressive therapeutic strategies. METHODS: Vascularised human corneas obtained by keratoplasty were evaluated by electron microscopy for pericyte coverage of new vessels. These data were correlated with the duration of CN (mean 73 (SD 95) (range 0.5-360) months; n = 15). CN was secondary to keratitis, transplant rejection, aniridia, or trauma. RESULTS: Overall, 196 blood vessels were analysed ultrastructurally (72 (37%) capillaries, 122 (62%) venules, and two (1%) arterioles). Electron microscopically, 170 (87%) vessels were covered by pericytes and two (1%) in addition by smooth muscle cells. Pericyte recruitment increased with time, evolving between clinically noted onset of CN and keratoplasty. Already 2 weeks after onset of CN, more than 80% of new vessels were covered by pericytes. CONCLUSION: Pathological new vessels in human corneal angiogenesis are rapidly covered by pericytes. Therapeutic strategies aimed at regression of immature, not yet pericyte covered vessels by antagonising angiogenic factors should thus be most effective if applied very early in the course of corneal neovascularisation.

Actins↗
PubMed2001

Immunohistochemical classification of primary and recurrent macular corneal dystrophy in Germany: subclassification of immunophenotype I A using a novel keratan sulfate antibody.

Macular corneal dystrophy (MCD) is an autosomal recessive disease characterized by abnormal deposition of glycosaminoglycans in corneal stroma, keratocytes, Descemet's membrane and corneal endothelium. According to the presence and distribution of sulfated keratan sulfate (KS)-epitopes in serum and cornea (using mAb 5-D-4), MCD can be classified into three immunophenotypes: type I, I A and II. The purpose of this study is to evaluate the immunophenotype of primary and recurrent MCD and to analyze the reactions of a novel KS-antibody in MCD corneas, which recognizes an epitope localized in the binding region of KS-chains to the core protein (mAb 3D12/H7). Indirect immunohistochemistry for KS (mAbs 3D12/H7 and 5-D-4) was performed on 44 corneas of 37 patients with MCD including two recurrences. Immunogold labeling was used to localize KS ultrastructurally within keratocytes. The serum concentration of KS (cKS) was determined in a serum antigen-inhibition assay. Immunohistochemically, no reaction was observed using mAb 5-D-4 in 18 corneas of 16 patients (43% of 37 patients; immunophenotype I). Positive reactions within single keratocytes but not in the stroma, were seen in 22 corneas of 17 patients (46% of 37 patients; immunophenotype I A) and positive reactions in keratocytes and extracellular stroma were found in four corneas of four patients (11% of 37 patients: immunophenotype II). For analysis of cKS a total of seven samples was available. Whereas in the samples of the five patients with immunophenotypes I and I A cKS was below the limit of detection, in the two sera from patients with immunophenotype II, cKS was normal (cKS = 1243 and 1380 nmol l(-1)). The two recurrences demonstrated immunophenotype II. Using mAb 3D12/H7, MCD immunophenotype I A can be further subclassified in type I A 1 (lacking reaction with mAb 3D12/H7 in keratocytes; 77%) and type I A 2 (positive reaction with mAb 3D12/H7 within keratocytes; 23%). MCD immunophenotype I A can not only be found in Saudi Arabia, but is as common as immunophenotype I in German patients. The only recurrences of MCD necessitating regrafting occurred in two patients with immunophenotype II possibly suggesting a higher risk for recurrence in this immunophenotype. The mAb 3D12/H7 allows a further subclassification of immunophenotype I A into type I A1 and 2. This points to a broader spectrum of MCD immunophenotypes and indirectly to a broader corneal proteoglycan pathology in MCD.

Antibodies, Monoclonal↗
PubMed2001

Blood-aqueous barrier breakdown after penetrating keratoplasty with simultaneous extracapsular cataract extraction and posterior chamber lens implantation.

BACKGROUND: The purpose of this study was to quantify breakdown of the blood-aqueous barrier (BAB) following penetrating keratoplasty (PK) with simultaneous extracapsular cataract extraction and posterior chamber lens implantation (triple procedure) and compare it with the alterations following PK only. METHODS: This study included 72 eyes after triple procedure and 227 eyes after PK only. The diagnosis for PK was Fuchs dystrophy in 39%, keratokonus in 44%, stromal corneal dystrophy in 3% and avascular corneal scars in 6% of cases. The postoperative topical steroid treatment was standardized in both groups. Aqueous flare was quantified using the laser flare-cell meter (FC-1000, Kowa) at defined postoperative intervals (10 days, 6 weeks, then every 3 months until 1 year postoperatively). Patients with conditions associated with impairment of the BAB were excluded from the study. RESULTS: In the early postoperative course, aqueous flare values (photon counts/ms) were significantly higher in patients with triple procedure (21.9 +/- 11.0) than in patients with PK only (9.8 +/- 3.2; P = 0.001). At 6 weeks postoperatively, aqueous flare returned to normal levels in patients after PK only (5.2 +/- 2.3), whereas patients with triple procedure still showed significantly increased flare values (10.8 +/- 5.6; P = 0.01). At 6 months postoperatively, aqueous flare values of patients with triple had returned to normal levels (6.8 +/- 3.8) and did not differ significantly from those after PK only (5.2 +/- 1.9; P = 0.09). CONCLUSION: Our results indicate that triple procedure causes a more extensive and longer-lasting breakdown of the blood-aqueous barrier than PK only. Quantification of aqueous flare with the laser flare-cell meter is useful in the postoperative follow-up after triple procedure. Further studies are required to investigate the clinical relevance of BAB breakdown on endothelial cell count and the incidence of subsequent immunological graft rejection.

Aqueous Humor↗
PubMed2001

Persisting retinal ganglion cell axons in blind atrophic human eyes.

PURPOSE: To evaluate enucleated blind atrophic human eyes for the persistence of retinal ganglion cell axons. This might be of relevance for contact to an electronic prosthesis in the future. METHODS: A total of 2460 surgically enucleated eyes were studied in our ophthalmic pathology laboratory between 1981 and 1996. All eyes histopathologically classified as displaying ocular atrophy with shrinkage (axial length < or = 21 mm) and with an available optic nerve cross section without crush artifacts were selected. Only eyes of patients older than 18 years and without light perception prior to enucleation were analyzed (n = 57). Optic nerve fibers were counted under light microscopy in semithin optic nerve sections. RESULTS: Axons amounting to more than 5% of the mean axon count in normal eyes (> 57,950 axons) were detected in 24 (42%) of 57 optic nerves, and an axon count more than 10% of the mean normal count (> 115,900 axons) was found in 15 (26%) of 57 optic nerves. The retina was at least partially detached and disoriented in all 57 eyes. The inner nuclear layer was detectable in 46 (81%) of eyes, whereas the outer nuclear layer was present in 13 (23%) of 57 eyes; photoreceptors were detectable by light microscopy in only 3 eyes (5%). Intraocular calcification due to osseous metaplasia of the retinal pigment epithelium was present in 62% of the globes. CONCLUSION: Blind atrophic human eyes reveal persisting retinal ganglion cell axons. Whether direct electrical stimulation of these axons or their retinal ganglion cells has the potential to create visual information remains to be studied.

Adolescent↗
PubMed2001

Impact of short-term versus long-term topical steroids on corneal neovascularization after non-high-risk keratoplasty.

PURPOSE: To analyze incidence and extent of corneal neovascularization (CN) after non-high-risk keratoplasty and to find out whether duration of postoperative topical steroid therapy (6 vs 12 months) affects CN, corneal endothelial cell count, pachymetry, aqueous flare values, and best-corrected visual acuity at 1 year after keratoplasty. METHODS: Patients of the prospective Erlangen non-high-risk keratoplasty study with available high-quality corneal photographs taken preoperatively and 1 year later were analyzed (n=136). Corneal photographs were evaluated by two independent observers in a standardized semiquantitative fashion. Slides were projected with 100x magnification and corneal vessels classified into five grades with regard to the limbus, sutures and host-graft junction in each of 12 corneal sectors. Incidence and extent of CN after keratoplasty and relation to short-term (0-6 months) versus long-term (0-12 months) postoperative topical steroid therapy were analyzed. The effect of duration of topical steroid therapy on corneal endothelial cell count, pachymetry, aqueous flare values, and best corrected visual acuity was also analyzed. Of the 136 patients, 69 (51%) were randomly assigned to short-term and 67 to long-term topical prednisolone acetate 1%. RESULTS: Fifty-eight percent of patients (n=79) developed a CN within 1 year after keratoplasty in at least one corneal sector (mean 3.1 +/- 2.2, range 1-10). At 1 year after keratoplasty, only in 12% of these patients did at least one vessel reach the host-graft junction or grow into the donor cornea, whereas in 51% vessels were seen beyond the outer suture ends of the double running suture without reaching the host-graft junction. In 37%, capillaries were located between limbus and outer suture ends. New vessels usually pointed directly or indirectly to the outer suture ends and usually were located around the 12 o'clock and 6 o'clock positions. There was no significant difference regarding incidence and extent of CN 1 year after keratoplasty between the long-term and the short-term group. Duration of topical steroid therapy had no significant effect on corneal endothelial cell count and thickness, aqueous flare values and best-corrected visual acuity at 6 and 12 months postoperatively (only at 12 months, corneas in the long-term treatment group were slightly thicker; P=0.03). Interobserver correlation of vessel assessment was 0.77 (Kendall's tau B). CONCLUSIONS: CN is a common phenomenon after non-high-risk keratoplasty. New vessels rarely reach the host-graft junction, most commonly develop from the 6 o'clock and 12 o'clock positions and are usually located between epithelium and Bowman's layer (i.e., at the level of the superficial suture). The direction of vessel growth from the limbus towards the outer suture ends suggests release of angiogenic factors in this area. Prolongation of topical steroid therapy after non-high-risk keratoplasty beyond 6 months in this study did not significantly influence incidence and extent of CN, corneal endothelial cell count, aqueous flare values and best-corrected visual acuity observed 1 year after keratoplasty.

Administration, Topical↗
PubMed2001

Orbital lymphangioma with positive immunohistochemistry of lymphatic endothelial markers (vascular endothelial growth factor receptor 3 and podoplanin).

BACKGROUND: Existence of true orbital lymphangiomas has been questioned in recent years. Therefore an orbital lymphangioma was analyzed with two new specific markers of lymphatic endothelium. METHODS: Case-report with clinicopathological, immunohistochemical, and ultrastructural findings. A 25-year-old man presented with recurrent lower lid "hematomas" and a pea-sized tumor palpable in the left lower lid. Magnetic resonance imaging showed an inferonasally located orbital tumor which extended to the posterior pole of the eye. The highly vascularized tumor was excised by medial orbitotomy. RESULTS: Histopathologically, the mass consisted of large, erythrocyte-filled cavernous vessels without evidence of smooth muscle cells or pericytes surrounding them. Numerous lymph follicles and small arterioles were scattered between them. Immunohistochemically, endothelial cells lining the lumina of the cavernous vessels were partly positive for podoplanin and vascular endothelial growth factor receptor 3 (flt-4), two markers of lymphatic endothelium. These markers did not react with endothelial cells lining the arterioles. Ultrastructurally, cavernous vessels displayed features characteristic of lymphatic vessels, and the smaller vessels demonstrated signs of arterioles. CONCLUSION: Ultrastructural analysis and immunohistochemistry using two new markers of lymphatic endothelium suggest a lymphatic nature of large vessels in an orbital lymphangioma. A greater series of vascular orbital tumors must be studied with these new lymph endothelial markers to confirm the existence of true orbital lymphangiomas and to analyze different profiles of lymph endothelial marker expression.

Adult↗
PubMed2001

Primary intraosseous cavernous hemangioma of the orbit.

PURPOSE: Primary orbital intraosseous hemangioma is a rare, benign neoplasm presenting most frequently in patients in their fourth or fifth decade of life. We describe an elderly patient affected by this tumor. METHODS: Case report. RESULTS: A 75-year-old man presented with a slowly growing, bony mass in the left orbital rim inferolaterally. He had a history of nephrectomy because of a renal carcinoma. Computed tomography showed a bony lesion with internal radiating trabeculations. A biopsy was performed. Histopathologically, the tumor was an intraosseous cavernous hemangioma. CONCLUSION: Primary intraosseous cavernous hemangioma of the orbit may infrequently affect elderly patients. One indication for surgical removal of these tumors in the absence of visual disturbances is to rule out metastatic disease in patients with a history of malignancy.

Aged↗
PubMed2001

Silicone oil-associated optic nerve degeneration.

PURPOSE: To report the frequency and extent of silicone oil migration into the optic nerve during silicone oil endotamponade. METHODS: Histopathologic analysis of 74 eyes enucleated after silicone oil endotamponade. RESULTS: In 14 of 74 enucleated eyes (24%), optically empty vacuoles regarded as silicone oil vacuoles were observed in the retrolaminar optic nerve. In three eyes, silicone oil in the optic nerve was surrounded by a granulomatous inflammatory reaction. In serial cross sections, the vacuoles extended up to the line of surgical transsection (up to 9 mm) of the optic nerve and constituted up to 40% of the total cross-sectional area. CONCLUSIONS: After silicone oil endotamponade, silicone oil may replace a considerable amount of tissue of the retrolaminar optic nerve. A granulomatous inflammatory reaction surrounding silicone oil may add to optic nerve damage.

Eye Enucleation↗