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C Auw-Hädrich

Publications and source records attributed to C Auw-Hädrich.

11 recordsLinked to original sources
PubMed2006

[Temporal arteritis (giant cell arteritis). Clinical picture, histology, and treatment].

Giant cell arteritis (arteritis temporalis) is the most common form of systemic vasculitis in the elderly. A series of symptoms such as new-onset headache, jaw claudication, proximal myalgia, weight loss, and fever may lead to the diagnosis. However, there is also a silent or occult presentation with minor or no systemic symptoms, especially no headache. A number of laboratory values (erythrocyte sedimentation rate, CRP, fibrinogen, thrombocytes, and cardiolipin antibodies) indicate giant cell arteritis, but none of this proves the diagnosis. Temporal artery biopsy is the gold standard for diagnosis of giant cell arteritis. Due to skip lesions, a negative result does not exclude the diagnosis. The most important complication of giant cell arteritis is visual loss in one or both eyes due to AION or retinal artery occlusion. Usually, visual loss is irreversible even with therapy. Corticosteroids are the drug of choice to treat giant cell arteritis. Therapy is required for a long time, monitored by parameters of inflammation (ESR, CRP).

Adrenal Cortex Hormones↗
PubMed2006

[Arterial ocular occlusion associated with systemic venous thrombophilia--2 case reports].

BACKGROUND: Arterial ocular occlusions in apparently healthy young men are unusual. Because of inconsistent study results there is a great amount of insecurity with respect to the reasonable diagnostic approach in such a scenario. We report on the process of diagnostic steps in two young men with arterial ocular occlusion such as non-arteritic optic neuropathy (NAION) and branch retinal arterial occlusion (BRAO). CASE REPORT: Here, we report on two hitherto healthy young men who suffered from ocular arterial occlusions. Because of the apparent arterial perfusion deficit at first thrombocyte aggregation-inhibiting substances were recommended. On searching for the underlying embolic source in both men a significant arterial-venous cardiac and pulmonary shunt volume was identified. Additional screening for risk factors for venous thrombosis resulted in the identification of Factor V Leiden as well as hyperhomocysteinemia. CONCLUSION: These two cases stress the importance to exclude possible arterial-venous shunts and, if identified, the need to search for additional risk factors for venous thrombosis in patients with arterial embolic ocular disease.

Adult↗
PubMed2003

[Corneal complications after hematopoietic stem cell transplantation].

AIM: To evaluate the incidence and clinical course of corneal complications in patients with severe dry eye syndrome after hematopoietic stem cell transplantation (HSCT). PATIENTS AND METHODS: 50 consecutive patients (aged 9-65 years; average=42+/-11 years) with Sjögren-like syndrome after hematopoietic stem cell transplantation were examined. In order to assess the severity of the dry eye syndrome, the frequency of blinking and break-up time were determined and Schirmer-I, fluorescein,and rose bengal tests were carried out. Biopsy and histological examination were performed in cases with suspected conjunctival graft-versus-host reaction. RESULTS: Patients with Sjögren-like dry eye syndrome were referred within an average of 13 months after HSCT (SD+/-20 months).The follow-up was up to 83 months (mean: 10.2 months,SD+/-14.97). Of the 50 patients 15 developed severe corneal complications with significant loss of vision which resulted in enucleation of the eye in 1 patient. Of these 15 patients 4 had a viral and 2 a bacterial keratitis,7 had trophic corneal thinning and sterile ulcers. Two patients had limbal stem cell insufficiency or pseudomembranous conjunctivitis, both due to conjunctival graft-versus-host reaction. Another patient developed a toxic keratopathy, probably induced by cyclosporin A eye drops. Of 50 patients 35 presented with signs of an inactive or active conjunctival graft-versus-host reaction which could be proven histologically in 26 patients. DISCUSSION: Patients with Sjögren-like dry eye syndrome after hematopoietic stem cell transplantation are at high risk to develop corneal complications.These complications may result from an aggressive extension of the graft-versus-host reaction towards the conjunctiva and/or the lacrimal gland and seem to occur more often during the period of reduction of systemic immunosuppressive therapy.Furthermore, infectious as well as trophic or toxic corneal complications may be supported by local immunosuppressive therapy. We suggest frequent ophthalmological checks of patients receiving hematopoietic stem cell transplantation who need local immunosuppressive therapy or are in the phase of reduction of systemic immunosuppressive therapy

Adolescent↗
PubMed2003

[Atopic keratoconjunctivitis: probably a risk factor for the development of conjuntival carcinoma].

BACKGROUND: Almost half of the patients with atopic dermatitis experience chronic inflammation of the eyelids, the conjunctiva and the cornea. Chronic inflammation is a possible cause for the development of malignancies, especially if associated with some kind of immunological defect as in atopic patients. So far, a correlation between atopic conjunctivitis and conjunctival malignancies has not yet been reported. Here, we present 7 atopic patients with conjunctival carcinoma or carcinoma in situ detected between February 2000 and August 2001. PATIENTS: All 7 patients had a long history of atopic dermatitis and chronic of inflammation of the conjunctiva and cornea. In all patients smears were examined by cytology and DNA cytometry. Furthermore, in 6 of the 7 patients a histopathological examination of conjunctival biopsies was performed. RESULTS: In 4 of the 7 patients invasive conjunctival carcinoma and in 2 carcinoma in situ were detected. Cytology and cytometry revealed conjunctival carcinoma or carcinoma in situ in the remaining patient. Histopathological examination could not be performed since the patient refused to have a conjunctival biopsy. CONCLUSIONS: These results suggest that atopic keratoconjunctivitis might be a risk factor for the development of conjunctival carcinoma.

Adult↗
PubMed2002

[Corneal dystrophies in the light of modern molecular genetic research].

Modern methods of molecular genetics have resulted in new insights into the pathogenesis of corneal dystrophies which now require a new classification. Clinical evidence, the results of histopathological and electron-microscopical examinations, especially in cases of recurrence which reflect early disease, and the immunohistochemical analysis of the deposits have already aroused the suspicion that the "old" classification dividing the dystrophies into those of the epithelium, of the so-called anterior membrane, of the stroma and of the endothelium may no longer be adequate. The detection of the BIGH 3 gene which is mainly expressed in the corneal epithelium, and its gene product keratoepithelin, have led to the insight that the so-called anterior membrane dystrophies (Reis-Bücklers, Thiel-Behnke) as well as the more common "classical" stromal dystrophies (granular dystrophies Types I and II, lattice dystrophies Types I and IIIA) are caused by different mutations of the above mentioned BIGH3 gene and are thus to be regarded as epithelial in origin. Lattice dystrophy Type II is part of the Meretoja syndrome, a systemic amyloidosis, and is caused by a mutation of the gelsoline gene on chromosome 9 (9q34). Gelsoline is also predominantly expressed in the corneal epithelium. In addition, the responsible genes, their gene-products and the mutations are known for Meesmann's epithelial dystrophy and for the so-called gelatinous drop-like dystrophy, while in other dystrophies only the location on a certain chromosome can be given, namely: 16q22 for the macular dystrophy, 1p36 for the central crystalline dystrophy of Schnyder and 20p11.2-q11.2 for the congenital hereditary endothelial and for Schlichting's posterior polymorphous dystrophies. As the production rate of new results in molecular genetics is very fast, the proposed new classification can only be of preliminary character.

Chromosome Mapping↗
PubMed1998

Retinal ganglion cell layer and visual function in a patient with optic disc drusen.

BACKGROUND: To correlate the retinal ganglion cell pattern to visual acuity and visual field data in a patient with bilateral optic disc drusen, a quantitative clinicopathological study was carried out. METHODS: Both retinae of a patient with optic drusen were whole-mounted. Retinal ganglion cell counts were made using a sampling scheme covering the whole retina and compared to the findings in 10 normal retinae. Relative ganglion cell reduction in the drusen retinae was correlated to clinical data. RESULTS: The total retinal ganglion cell count was reduced from 1244858+/-98736 in normal retinae to 305319 on the right and 527571 on the left eye with optic disc drusen. Large ganglion cells had a better chance of survival. Parafoveal ganglion cell loss was 57% for the right and 36% for the left eye, while visual acuity was 0.8 and 1.0 respectively. The mean light sensitivity loss increased from the centre (6.2 dB) to paracentral (9.9 dB), mid-peripheral (13.7 dB) and outer peripheral (15.0 dB) retina, while ganglion cell losses were smallest in outer peripheral retina (21.9%), followed by central (53.0%), mid-peripheral (70.9%) and paracentral retina (87.7%). CONCLUSION: These data validate Frisén's theory on central retinal resolution and provide the structural basis for the clinical rule that low visual acuity should not be attributed to disc drusen. Automated light sense perimetry gives an inadequate picture of retinal damage caused by optic disc drusen.

Adolescent↗
PubMed1998

[Orbital sarcoidosis--a case with an unusual course].

BACKGROUND: Most cases of orbital sarcoidosis are associated with a systemic sarcoidosis. PATIENTS AND METHODS: A 67-year-old woman suffered from an orbital mass on the right side, which led to disturbance of the ocular motility. Slight improvement was achieved by the administration of systemic steroids. RESULTS: Histologically a chronic granulomatous inflammation was revealed in the biopsy of the orbital mass. The suspected diagnosis was sarcoidosis, but three conventional chest X-rays within 10 months and the serum angiotensin-converting-enzyme were normal. Suprisingly a computertomography of the chest showed mediastinal lymphomas. CONCLUSION: Granulomatous orbital inflammation without any local cause or other systemic granulomatous disease strongly suggests a systemic sarcoidosis. In case of missing lymph node enlargement in conventional chest X-ray computertomography should be performed.

Aged↗