Three-dimensional fat-saturated T1-weighted Cartesian volumetric interpolated breath-hold examination (VIBE) for the diagnosis of aortitis in patients with suspected large vessel vasculitis: a comparative study with 18F-FDG PET applying fully integrated PET/MRI.

AIM: To evaluate the feasibility of T1-weighted (T1W) three-dimensional (3D) fat saturated Cartesian volumetric interpolated breath-hold examination (VIBE) magnetic resonance imaging (MRI) sequence for the diagnosis of aortitis in patients with suspected large vessel vasculitis (LVV) applying fully integrated 2-[18F]-fluoro-2-deoxy-d-glucose (18F-FDG) positron-emission tomography (PET)/MRI. MATERIAL AND METHODS: Fourteen patients with aortitis and 14 patients with a negative study for aortitis using 18F-FDG PET as the standard of reference for the evaluation of inflammatory aortic involvement were included retrospectively. All patients were imaged at 3 T using T1W VIBE pre- and post-contrast. Four aortic segments were evaluated for image quality (IQ), diagnostic confidence (DC), and the degree of inflammatory activity (IA) using a Likert scale. Binomial and generalised estimating equation model tests were used to assess the diagnostic performance of T1W VIBE. Cohen's k was applied to test for interobserver reproducibility with respect to IA. Spearman's rank correlation coefficient was calculated to examine correlations between IQ, DC, IA, and PET results. RESULTS: On a patient- and segment-based analysis, sensitivity, specificity, positive predictive value, negative predictive value, and accuracy were 85.7% and 59.8%, 100% and 100%, 100% and 100%, 87.5% and 68%, and 92.9% and 82.1%, respectively. IQ and DC were acceptable to good in all examinations and substantial interobserver agreement was observed for IA (Cohen's k = 0.69). IQ and DC as well as IA and 18F-FDG vessel wall uptake were significantly correlated (r=0.763 and 0.679, respectively; p<0.0001). CONCLUSION: T1W 3D fat saturated VIBE MRI allows diagnosis of aortitis and may aid in the management of patients with suspected LVV.

[Manifestations of autoimmune disorders in otorhinolaryngology : Classical symptoms and diagnostic approach]. / Manifestationen von Autoimmunerkrankungen in der HNO-Heilkunde : Klassische Symptomatik und diagnostisches Vorgehen.

Manifestations of autoimmune disorders represent a diagnostic challenge. Many autoimmune disorders show typical manifestations in the ear, nose and throat and should be taken into account in the differential diagnosis. Sjogren's syndrome, various vasculitides and sarcoidosis represent the most common autoimmune disorders in otorhinolaryngology, but IgG4-related diseases, relapsing polychondritis and autoimmune disorders of the mucosa are also observed. Autoimmune diseases can lead to sensorineural deficits. Both hypo- and hyperthyroidism can be caused by autoimmune disorders. The diagnosis is usually based on the corresponding classification criteria, whose correct application can facilitate the clarification of these diseases.

[Diffuse stromal corneal opacity and alterations of the hands]. / Diffuse stromale Hornhauttrübungen und Veränderungen der Hände.

Bilateral stromal corneal opacity is a differential diagnostic challenge for ophthalmologists. In this article 2 female patients aged 30 and 36 years old, respectively, with different degrees of expression of stromal diffuse corneal opacity will be presented. Patient 1 was of short stature (114 cm) and patient 2 was 172 cm in size. Both patients exhibited altered joint structures of the hands and feet and diffuse stromal corneal opacity. Furthermore, patient 1 had both mitral and aortal insufficiencies and patient 2 an aorta insufficiency. The stromal diffuse corneal opacity was indicative of Schleie syndrome. For patients with reduced vision a lamellary keratoplasty is to be recommended.

Fisher-Lewis kidney transplantation model as a tool for investigation of transplantation-induced cardiomyopathy.

BACKGROUND: Cardiovascular disease is a major cause of death after kidney transplantation; thus, cardiovascular protection is a major concern in transplant recipients. Data about cardiac characteristics from animal models after kidney transplantation are lacking. Therefore, we investigated cardiac structure and function in a model of chronic allograft injury. METHODS: Kidneys from Fisher 344 rats were orthotopically transplanted into Lewis rats. Eight recipient rats were treated with placebo or an angiotensin II type-1 receptor blocker (AT1RB; candesartan cilexitil, 5 mg/kg/d) for 24 weeks posttransplantation, and 8 untreated matched Lewis rats were used as healthy controls. Echocardiography was performed at 24 weeks posttransplantation to measure ejection fraction, fractional shortening, and left ventricular mass, in triplicate. Proteinuria at 24 hours was determined, and after harvesting, the heart weight-body weight ratio (HW/BW) was measured. RESULTS: At 24 weeks posttransplantation, renal transplant-recipient rats demonstrated a significantly decreased ejection fraction (mean [SD], 58.9% [3.2%] vs 70.7% [2.1%]) and fractional shortening (29.8% [2.0%] vs 38.3% [2.0%]) and increased HW/BW and left ventricular mass (7.7 [0.2] cm(3) vs 6.7 [0.2] cm(3)) compared with healthy control rats. The HW/BW and left ventricular mass were significantly ameliorated by AT1RB compared with placebo-treated transplant-recipient rats (6.8 [0.2] cm(3) vs 7.7 [0.2] cm(3)). In addition, decreased proteinuria was evident after AT1RB. CONCLUSION: The Fisher-Lewis rat kidney transplantation model resulted in cardiac hypertrophy and decreased cardiac function. AT1RB normalized cardiac hypertrophy without improving function. These findings demonstrate that the Fisher-Lewis rat renal transplantation model can be used to investigate transplantation-induced cardiomyopathy.

[Bilateral recurrent retinal thrombosis in a young man]. / Bilaterale rezidivierende retinale Thrombose bei einem jungen Mann.

A 41-year-old male patient presented with veiled vision which had appeared only a few hours previously. Funduscopy revealed a retinal edema due to venous stasis retinopathy. A previous history was unknown except for an uncorrected arterial hypertension. A retinal vein thrombosis and macula edema developed in the affected eye. An antiphospholipid antibody syndrome was diagnosed which was treated with anticoagulants.