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Traunstein, Germany

Hilberath J.M.,Klinikum Traunstein | Schmidt H.,Ludwig Maximilians University of Munich | Wolf G.K.,Klinikum Traunstein | Wolf G.K.,Harvard University
European Journal of Pediatrics | Year: 2014

Steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), also termed Hashimoto’s encephalopathy (HE), is a rare immune-mediated disorder and is also affecting children and adolescents. It is characterized by altered mental status, seizures, and cognitive dysfunction. Therapeutic options include steroid treatment and prognosis range from complete recovery, a relapsing course to long-term cognitive sequelae. We describe a previously healthy 13-year-old girl presenting to the emergency room with coma and refractory status epilepticus. Generalized tonic-clonic seizures persisted after pre-hospital infusion of antiepileptic medication. She was found to have highly elevated levels of thyroid-stimulating hormone and anti-thyroid peroxidase antibodies not only in blood but also in cerebrospinal fluid while showing negative results for traumatic, infectious, metabolic, toxic, neoplastic, or other known specific autoimmune diseases. Cranial neuroimaging revealed no abnormality. A diagnosis of SREAT was established, and the patient improved rapidly on corticosteroids and levothyroxine therapy. However, 3 months after the discontinuation of steroid treatment, the girl relapsed. The current literature regarding SREAT is reviewed and summarized. Conclusion: In children with SREAT, early diagnosis and treatment with corticosteroids is crucial and can lead to rapid clinical improvement. Clinicians should be aware of this uncommon but treatable condition, especially in female adolescents with unexplained seizures or an encephalopathic state. © 2014, Springer-Verlag Berlin Heidelberg. Source

Schindlbeck C.,Klinikum Traunstein | Dziura D.,Klinikum Traunstein | Mylonas I.,Ludwig Maximilians University of Munich
Archives of Gynecology and Obstetrics | Year: 2014

Introduction: Pelvic inflammatory disease (PID) is frequent in adolescents and younger women. Diagnosis is usually based on the clinical findings, and the threshold for empiric antibiotic therapy should be low. However, at least in cases of resistance toward therapy or deterioration of symptoms, laparoscopic evaluation can be helpful. Methods: We searched the hospital charts for in-house patients who were treated for PID or tubo-ovarian abscess between 2007 and 2010. In cases with both vaginal and intraabdominal bacterial cultures, results of those were compared. Results 73 patients with suspected PID or tubo-ovarian abscess were included. Median patients' age was 40 years (18-88), 18 of 73 (24.7%) patients had an IUD at the time of consultation. 58 patients underwent laparoscopy or laparotomy. In 41 patients (70.7%) tubo-ovarian abscess could be confirmed, four patients had differential gynecologic diagnoses, and two patients appendicitis. In vaginal swabs, most frequent bacteria were Streptococcus sp. (28.5%), Escherichia coli (22.2%), Enterococcus faecalis (15.9%), and Staphylococcus sp. (9.5%). In eight patients (11%) Chlamydia trachomatis could be found, there was no case of Neisseria gonorrhea. In 33 patients both vaginal and abdominal cultures were available. In nine cases (27.3%), identical bacteria could be found, however, 11 cases (33.3%) showed different results. Conclusion: In severe cases of PID, laparoscopic evaluation and taking an intra-abdominal bacterial culture are helpful for the confirmation of diagnosis, accurate microbiologic testing and specific therapy. © Springer-Verlag 2014. Source

Sander D.,Benedictus Krankenhaus | Sander D.,TU Munich | Poppert H.,TU Munich | Sander K.,TU Munich | And 2 more authors.
European Journal of Neurology | Year: 2012

Background: Despite important advances in therapeutic approaches in stroke, the options of acute treatment are still limited. Primary prevention represents another potentially highly efficient strategy. For effective prevention the early detection of subjects at risk is of utmost importance. Coinciding with a change in current understanding of atherosclerosis as an inflammatory, cross-organ disease, new parameters to assess the individual risk are emerging. Methods: Systematic review of the potential of selected parameters for prediction of cerebrovascular events beyond detection of traditional risk factors that might expand the repertoire of primary prevention programs in stroke. Results: An absolute carotid intima-media thickness difference of 0.1mm increases the future risk of stroke by 13-18%. An ankle-brachial index <0.9 was associated with a relative risk of 2.33 (95% CI 2.02-2.68) for stroke. In patients with acute stroke and ABI values < 0.9 the risk for a new vascular event is significantly increased (HR 2.1; 95% CI 1.6-2.8). Measurements of several molecular biomarkers may be used to predict future vascular events independently of traditional risk factors. Conclusions: Based on the data presented, there is clear evidence that measurement of the ankle-brachial index identifies subjects of increased stroke risk in primary and secondary care settings as well as of stroke recurrence in acute stroke. © 2011 The Author(s). European Journal of Neurology © 2011 EFNS. Source

Pscherer S.,Klinikum Traunstein | Freude T.,Trauma Center Tubingen | Forst T.,Ikfe Mainz University Mainz | Nussler A.K.,Trauma Center Tubingen | And 2 more authors.
Diabetology and Metabolic Syndrome | Year: 2013

Background: The single-center, open-label, four-arm, exploratory study investigates the relation of different anti-diabetics to serum levels of active TGF-β, a known pro-fibrotic stimulus, before and after a defined test meal. Findings. We investigated sera of patients with type 2 diabetes mellitus (T2DM) treated with metformin and sulfonylurea, insulin glargine or a DPP-4 inhibitor (DPP4i). Patients' sera were analyzed before and 5 h after a defined test meal at intervals of 30 min.The sulfonylurea/metformin group exhibited the highest basal levels of active TGF-β (31.50 ± 3.58 ng/ml). The glargine/metformin group had active TGF-β levels (24.98 ± 1.90 ng/ml) that were comparable to those of the healthy participants (22.12 ± 2.34 ng/ml). The lowest basal levels of active TGF-β were detected in the DPP-4i/metformin group (12.28 ± 0.84 ng/ml). Following the intake of a standardized meal, active TGF-β levels decreased (approx. 30%) in healthy subjects as well as in the sulfonylurea/metformin group and in the glargine/metformin group. After 5 h, the active TGF-β levels were normalized to basal levels. Active TGF-β levels in the DPP-4i/metformin group did not change significantly after the test meal. Overall plasma levels of insulin and proinsulin were comparable between healthy participants, and T2DM patients in the glargin/metformin group and in the DPP4i/metformin group. However, no correlation between active TGF-β levels, glucose, insulin or pro-insulin levels was detected. Conclusions: T2DM patients often exhibit elevated levels of pro-fibrotic active TGF-β. Our results suggest that glargine/metformin and DPP4i/metformin treatment may more effectively reduce active TGF-β serum levels than the sulfonylurea/metformin treatment. © 2013 Pscherer et al.; licensee BioMed Central Ltd. Source

Freude T.,University of Tubingen | Braun K.F.,TU Munich | Haug A.,TU Munich | Pscherer S.,Klinikum Traunstein | And 4 more authors.
Journal of Molecular Medicine | Year: 2012

Affecting more than 230,000,000 patients, diabetes mellitus is one of the most frequent metabolic disorders in developed countries. Among other complications, diabetic patients have an increased fracture risk and show delayed fracture healing. During the disease progression, these patients' blood glucose and insulin levels vary significantly. Thus, the aim of this study was to analyze the effects of glucose and insulin on primary human osteoblasts. Although, in the presence of insulin and glucose, proliferation of osteoblasts was increased (1.2- to 1.7-fold), their alkaline phosphatase activity and, consequently, production of mineralized matrix were significantly reduced down to 55 % as compared to control cells (p < 0.001). Interestingly, the observed effects were mainly due to stimulation with insulin. Increase in glucose did not alter osteoblasts' function significantly but further enhanced the effects of insulin. Expression of active and total transforming growth factor beta (TGF-β) was increased by glucose and insulin. Stimulation with both glucose and insulin induced gene expression changes (e.g., osteocalcin, Runx2, Satb2, or Stat1) comparable to treatment with recombinant TGF-β1, further indicating osteoblasts' dysfunction. Inhibition of TGF-β signaling completely abolished the negative effects of glucose and insulin. In summary, glucose and insulin treatment causes osteoblast dysfunction, which is accompanied by an increased TGF-β expression. Blocking TGF-β signaling abrogates the functional loss observed in glucose- and insulin-treated osteoblasts, thus identifying TGF-β as a key regulator. Therefore, increased TGF-β expression during diabetes may be a feasible pathogenic mechanism underlying poor bone formation in uncontrolled diabetes mellitus. © 2012 Springer-Verlag. Source

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