Syphilitic Interstitial Keratitis Research Articles

Descemet Membrane Endothelial Keratoplasty for Corneal Edema and Visually Significant Descemet Membrane Scrolls Due to Syphilitic Keratitis

The presence of Descemet membrane scrolls is an uncommon finding reported in syphilitic interstitial keratitis. We herein describe a novel surgical strategy for this entity; this report demonstrates that Descemet membrane endothelial keratoplasty surgery can be performed with excellent visual outcomes in the event of corneal edema as a late sequela of syphilitic keratitis.

Endothelial Mesenchymal Transition: A Therapeutic Target in Retrocorneal Membrane

A single layer of corneal endothelial cells covers the posterior surface of the Descemet membrane. Normally, corneal endothelial cells do not proliferate, suggesting that factors inhibit their undergoing mitosis. Fibroblastic transformation of corneal endothelial cells due to syphilitic interstitial keratitis or alkali burn may result in stromal opacification. Various growth factors such as fibroblast growth factor 2 and transforming growth factor β are involved in "endothelial-mesenchymal transition (EnMT)." Endothelial wound-healing assay experiments revealed that cell migration toward artificial wound defect was mediated by p38 and c-Jun N-terminal kinase. To understand whether Smad signal might have an important role in EnMT regulation, gene transfer of Smad7 was employed to block transforming growth factor β/Smad signal in rat corneal endothelium 3 days before alkali burning. EnMT during healing interval after alkali burn was markedly suppressed by Smad7 overexpression associated with upregulation of cell proliferation. Therefore, blocking Smad signal effectively suppresses injury-induced EnMT and fibrogenic reaction by corneal endothelium without impairing repair of wound defect. Strategies that block Smad may be useful for prevention and treatment of fibrogenic disorders in the corneal endothelium.

Atypical Cogan's Syndrome with Aortitis

Cogan's syndrome is characterized by non syphilitic interstitial keratitis and Meniere's syndrome-like audiovestibular function disorder, as well as various systemic manifestations, including fever, arthralgia, vasculitis, and aortitis. We report the case of atypical Cogan's syndrome with aortitis; the patient's symptoms caused by active inflammation, including inflammatory ocular manifestations, audiovestibular symptoms, and aortitis, were improved by early administration of corticosteroids, however, her reduced visual acuity was not improved because of post-inflammatory change in her left eye.

Cystoid macular oedema in Cogans syndrome-a case report.

IntroductionCogan's Syndrome is typically characterised by a non syphilitic interstitial keratitis (IK), with or without conjunctivitis, iritis or subconjunctival bleeding and progressive sensorineural hearing loss within two years of ocular signs. Atypical ocular manifestations include episcleritis, scleritis, posterior scleritis, retinal artery occlusion, choroiditis, retinal vasculitis, and optic disc oedema. We report a case of Cogan's syndrome in with recurrent cystoid macular oedema was the main feature.Case presentationA patient was diagnosed with Cogan's syndrome nearly 2 years after first presentation. He had cystoid macular edema which failed to respond initially to steroid, methotrexate and azothiaprine however resolved after treatment with mycophenolate mofetil.ConclusionCogan's syndrome is rare and presents a challenge in terms of diagnosis and treatment. Recurrent cystoid macular oedema is a unique finding in this condition and can be difficult to control. Multidisciplinary management of this multisystem disorder is vital.

Immunohistochemistry and Electron Microscopy of Retrocorneal Scrolls in Syphilitic Interstitial Keratitis

Purpose: To describe the immunohistochemical and electron microscopic characteristics of retrocorneal scrolls in syphilitic interstitial keratitis. Methods: Five eyes of five patients with congenital syphilitic interstitial keratitis who underwent keratoplasty for corneal opacities and corneal edema were studied. The corneal buttons were processed for histologic examination with hematoxylin and eosin staining and underwent immunohistochemistry stainings for collagen types I, III, IV, V, VI, VIII, fibronectin, laminin, and decorin. The corneal buttons were also processed for transmission electron microscopy and immunoelectron microscopy. Results: Light microscopy revealed that the retrocorneal scrolls had a multilayered, amorphous, acellular matrix. All scrolls were lined with attenuated corneal endothelial cells. The Descemet membranes in all specimens had areas of irregular thickening with attenuated endothelium. Immunohistochemical assessment of the scrolls showed positive staining for collagens I, III, IV, VI, VIII, fibronectin, laminin, and decorin but not for α -SMA. Immunoelectron microscopy confirmed these findings. Transmission electron microscopy showed multilaminar disorganized structures in scrolls composed of long- and short-fiber collagens. Conclusions: We confirmed the presence of collagens I, III, IV, VI, VIII and proteoglycans in the retrocorneal scrolls lined with attenuated endothelium. Our findings may provide further insight into the pathogenesis of keratopathy in syphilitic interstitial keratitis.

Syndrome de Cogan révélé par une diarrhée glairo-sanglante

Cogan's syndrome is defined by the combination of non syphilitic interstitial keratitis and inner ear dysfunction, similar to Meniere's disease. Cogan's syndrome was revealed by haemorrhagic glaireous diarrhoea in a 21 year-old woman whose medical history included Hirschsprung's disease. Cerebral MRI revealed viral-like bilateral neuritis of the eighth cranial nerve, never described in the literature before. The auditory and visual disorders regressed after treatment with corticosteroids. The early diagnosis of Cogan's syndrome permits the cure of the visual and auditory and notably inner ear symptoms with corticosteroid therapy.

Syndrome de Cogan ou sarcoïdose ?

Introduction – The Cogan’s syndrome is characterized by the association of vestibulo-auditory dysfunction, non syphilitic interstitial keratitis or another significant inflammatory eye lesion. Some authors consider this disease as a vasculitis, because it is frequently associated with systemic manifestations. Based on Cogan’s diagnostic criteria, Cogan’s syndrome may be part of other systemic diseases, as polyarteritis nodosa or Wegener’s granulomatosis. Exegesis – We report the case of a patient who presented with a Cogan’s syndrome and developped further sarcoidosis. Conclusion – If Cogan's syndrome is characterized as systemic disease because of its association with aortitis or other vasculitis, on the other hand, clinical presentation may be part of many other systemic diseases.

Angle-Closure Glaucoma as a Presumed Presenting Sign in Patients with Syphilis

Background: Angle-closure glaucoma is a well-known sequel to syphilitic interstitial keratitis. This study describes angle-closure glaucoma in the absence of corneal opacity as a presumed presenting sign of syphilis. Cases: Two patients presented with angle-closure glaucoma with high peripheral anterior synechiae to the level over Schwalbe's line extending the whole circumference of the angle. Neither corneal opacity nor aqueous inflammation was present. Diffuse or localized retinochoroidal degeneration with pigmentation was found in 1 eye of 1 patient and in both eyes of the other patient. Observations: Fluorescein angiography revealed dotty retinal pigment epithelial damage even in normal appearing areas of the fundus. The patients showed a positive test for Treponema pallidum hemagglutination and also a low titer of serological tests for syphilis. No systemic activity, such as skin rashes, had been noted. Conclusions: Syphilis should be considered in patients presenting high peripheral anterior synechiae involving the whole circumference of the angle even in the absence of preceding interstitial keratitis.

Rupture of Descemet's membrane secondary to presumed forceps trauma

Ruptures in Descemet's membrane can occur secondary to forceps injury at birth, prolonged labor, blunt trauma, keratoconus, and congenital glaucoma as well as other less frequent causes. The rupture initially causes acute comeal hydrops which resolves within weeks to leave permanent linear thickening of Descemet's membrane. It is important to differentiate Descemet's rupture from other entities like syphilitic interstitial keratitis, posterior polymorphous dystrophy and congenital hereditary endothelial dystrophy which may have a similar clinical presentation. Although treatment is rarely required, proper diagnosis is important to prevent unnecessary referrals and provide appropriate counseling. This case report examines a 66-year-old female with Descemet's rupture secondary to presumed forceps trauma at birth. Discussion of clinical presentation, differential diagnosis and clinical management are presented.

Syndrome de Cogan et claudication intermittente. A propos d'un cas

We describe the case of a 35-year-old woman who first presented with a typical Cogan's syndrome (non syphilitic interstitial keratitis associated with audiovestibular dysfunction) and who subsequently developed intermittent claudication secundary to a non-atheromatous involvement of iliac arteries.

Scrolls of Descemet's Membrane in Healed Syphilitic Interstitial Keratitis

A 45-year-old woman with healed syphilitic interstitial keratitis presented with decreased vision, foreign-body sensation of the right eye, and bilateral conjunctival injection. Examination disclosed a network of tissue on the posterior corneal surface, with extension into the anterior chamber. Bullous keratopathy developed after intracapsular cataract extraction, and a keratoplasty was performed. Pathologic examination of the corneal button disclosed corneal edema, posterior stromal vascularization, much thickening of Descemet's membrane, and concentrically laminated scrolls of Descemet's membrane-like tissue that extended from the posterior corneal surface into the anterior chamber. Endothelium was attenuated considerably throughout and in one area was replaced by a single layer of iris melanocytes.

Zum Cogan-Syndrom

Cogan's Syndrom is the clinical entity of non syphilitic interstitial keratitis with vestibuloauditory symptoms. Although the disease is not rate the pathohistological findings in temporal bones are only reported twice. Our communication deals with observations made on a temporal bone out of O. Mayer's collection. The most striking findings are: the endolymphatic hydrops, the degeneration of the organ of Corti, the pathology of the ductus reuniens, the fibrosis within the cisterna perilymphatica, the destruction of the maculae and the most uncommon ossification within the scala vestibuli of the basal turn. The vessels seem to show signs of angitis.

Late Glaucoma After Interstitial Keratitis

In a systematic study of 45 patients who had syphilitic interstitial keratitis early in life and, many years later, were discovered to have glaucoma, there was evidence of two different but equally common mechanisms. In one group of patients, a deep-chamber type of glaucoma was superimposed on old inflammatory changes, was characteristically refractory to medical treatment, but did well with filtering surgery. The other group of patients had reversible angle-closure glaucoma associated with anatomically small anterior segments, and typically responded well to iridectomy. The late, refractory, deep-chamber type of glaucoma may involve endothelialization and formation of glass membrane in the angle, as seen in one excised eye. Occurrence of the shallow-chamber, reversible angle-closure type of glaucoma after interstitial keratitis may be coincidental, since no other evidence supports the idea that small anterior segments might be particularly prevalent among patients who have had congenital syphilis or interstitial keratitis.

Ultrastructural Pathology of Syphilitic Interstitial Keratitis

Gradual loss of corneal transparency and resultant reduction of visual acuity may be a late manifestation of congenital syphilis. These changes may occur years after the acute attack of syphilitic interstitial keratitis which leaves “ghost vessels” in the deep layers of the stroma as permanent proof of the previous attack. In this study, six corneal buttons obtained at the time of transplantation surgery in five adult patients with congenital syphilis were examined by light and electron microscopy.

Late Glaucoma Associated with Inactive Syphilitic Interstitial Keratitis

Late Glaucoma Associated with Inactive Syphilitic Interstitial Keratitis

Glaucoma Following Syphilitic Interstitial Keratitis

Glaucoma in patients with old inactive syphilitic interstitial keratitis is an entity which presents some unique problems in clinical diagnosis and management. While it is true that penicillin therapy for syphilis has markedly decreased the incidence of acute interstitial keratitis from congenital syphilis, nevertheless the late sequelae continue to present problems. Among the most important of these is the development of glaucoma. The onset of this glaucoma may be insidious with a slow destruction of vision, or it may be acute with an inflamed, painful eye. Sugar1describes this glaucoma as resulting from healed anterior uveitis which has left open angles but probably an obstruction of the trabecular framework by connective tissue. An analysis of the clinical symptomatology in 23 patients and the histological examination of one eye permits an amplification of his description. Literature The scanty literature on the glaucoma which may follow interstitial keratitis can be quickly

Results of local cortisone therapy in syphilitic interstitial keratitis.

Results of local cortisone therapy in syphilitic interstitial keratitis.

Topical cortisone in syphilitic interstitial keratitis; review of twenty-three cases (29 eyes).

(1) Ignorance of its Value.-This has led to scepticism of good results that have been reported. (2) Contradictory Verdicts on its Value in the Literature.-Two years ago Woods (presumably representing American opinion) wrote that " syphilologists and ophthalmologists doubt whether cortisone therapy in interstitial keratitis is a justifiable procedure " (Woods, 1 952a). Also in America Purnell and Leopold (1952) included syphilitic interstitial keratitis in the list of ocular conditions " not improved " by cortisone. Klauder and Meyer (1954) wrote that in the light of their experience they had stopped using cortisone in this condition. At a discussion on a paper on this subject read in November, 1952, at a meeting of the Medical Society for the Study of Venereal Diseases, caution was expressed about its value (Ashworth, 1953). Minton (1952) did not include syphilitic interstitial keratitis in a list of conditions " responding favourably " to cortisone. On the other hand, many apparently excellent results have been reported, for example by Crane and McPherson (1951), Salomaa and Swanljung (1952), Ashworth (1953), Drews, Barton, and Mikkelsen (1953), Oksala (1953), and North (1954). These contradictory and frequently pessimistic reports on cortisone in interstitial keratitis are probably due to several factors:

Topical cortisone in the treatment of syphilitic interstitial keratitis; preliminary report of 20 cases (26 eyes).

Topical cortisone in the treatment of syphilitic interstitial keratitis; preliminary report of 20 cases (26 eyes).

Corticotropin, cortisone, thyroid testosterone in syphilitic interstitial keratitis.

THIS STUDY reports the results of the treatment of 36 patients (56 affected eyes) with acute syphilitic interstitial keratitis who received one or a combination of the following drugs, corticotropin, cortisone, extract thyroid, and testosterone. Other treatment, except for the use of mydriatics, was withheld during administration of these agents in order more easily to evaluate their effect; but sooner or later, out of consideration for the welfare of the patient, we resorted to more efficacious therapy, namely, fever and antisyphilitic medicaments. Our previous experience with these older methods served as a control in judging the effectiveness of the newer ones. Results of treatment were evaluated by the effect on the keratitis: the speed of clearing of the cornea, the time necessary for the eye to become quiet, the rate of improvement in visual acuity, and the best final vision. The real challenge in treatment is the elimination of resultant