Computergestützte Charakterisierung von sonographischen Plazentastrukturen

Schlu?folgerungen Aus der Me?wert-Verteilung der Grauwerte im Sonogramm lassen sich Kennwerte berechnen, die eine computergestützte sonographische Reifebeurteilung der Plazenta erm?glichen. Allerdings sind die Verteilungsparameter (Median, Varianz, Schiefe, Exze?) abh?ngig von den Ger?teparametern. Zuverl?ssiger ist die Berechnung von Kennwerten, die sich auf die strukturellen Eigenschaften des Sonogramms beziehen. Bei den hier dargestellten Untersuchungen k?nnen Kennwerte für den Kontrast bzw. für die Ansammlung gleichartiger Grauwerte um einen bestimmten Punkt die sonographische Beurteilung der Plazenta optimieren. Damit erweitern sich die M?glichkeiten für die Zustandsdiagnostik der intrauterinen Lebensbedingungen.     

Pedicled fibroma of the extrahepatic bile ducts

It is reported on the very rare occurrence of a benign tumor in common hepatic bile duct of a 33-year-old woman, associated with obstructive jaundice. Clinical diagnosis and treatment are described, histological typing like fibroblastic tumor with neurogenic parts are discussed and a short review of the literature is given.     

Hormonersatztherapie und vaskuläres Risiko

Gynäkologische Endokrinologie - Auch die neue Version der AWMF-S3-Leitlinie „Peri- und Postmenopause – Diagnostik und Interventionen“ der Deutschen Gesellschaft für...     

Prevention of deep-vein thrombosis after total hip and knee replacement. Low-molecular-weight heparin in combination with intermittent pneumatic compression

After total hip (THR) or knee replacement (TKR), there is still an appreciable risk of developing deep-vein thrombosis despite prophylaxis with low-molecular-weight heparin (LMWH). In a prospective, randomised study we examined the efficacy of LMWH in combination with intermittent pneumatic compression in patients undergoing primary unilateral THR or TKR. We administered 40 mg of enoxaparin daily to 131 patients combined with either the use of intermittent pneumatic compression or the wearing of graduated compression stockings. Compression ultrasonography showed no evidence of thrombosis after LMWH and intermittent pneumatic compression. In the group with LMWH and compression stockings the prevalence of thrombosis was 28.6% (40% after TKR, 14% after THR). This difference was significant (p < 0.0001). In the early post-operative phase after THR and TKR, combined prophylaxis with LMWH and intermittent pneumatic compression is more effective than LMWH used with graduated compression stockings.     

Vascul?re Komplikationen bei Thoracic-outlet-Syndrom: kombinierte transaxill?re Revascularisation und Rippenresektion

Am Beispiel von zwei Patienten mit Thoracic-outlet-Syndrom (TOS; Halsrippen- und costoclavicul?res Syndrom) und vascul?rer Komplikation werden anatomische Beziehungen und pathophysiologische Prinzipien als Voraussetzung für eine ad?quate chirurgische Behandlung erl?utert. Neben der kausalen Therapie des TOS mit Rippenresektion und Ausschalten der Embolisationsquelle der A. subclavia steht die Revascularisation der Peripherie in Form von Bypass, Lyse und/oder Sympathektomie. Dabei erscheint der transaxill?re Zugang die ideale Variante zu sein, da er optimal minimalinvasive Prinzipien eines geringen Traumas mit einer langstreckigen Exposition der A. subclavia Segment 3 bis zur proximalen A. axillaris vereint.     

Angiotensin-converting enzyme gene insertion/deletion polymorphism and carotid artery wall thickness in patients with peripheral arterial occlusive disease.

BACKGROUND: It has been suggested that the deletion polymorphism of the angiotensin converting enzyme (ACE) gene is linked to a high risk of cardiovascular disease. The relationship between the insertion/deletion (I/D) polymorphism of the ACE gene and the carotid intima-media thickness in patients with peripheral arterial occlusive disease is unknown. We tested the hypothesis that the early progression of atherosclerosis in the extracranial carotid arteries in patients with peripheral arterial disease is associated with a genetic predisposition. METHODS: This prospective trial included 98 patients who only had manifestations of arteriosclerotic disease in peripheral arterial vascular regions of the lower extremities (stable stage II PAOD). Maximal common carotid intima-media thickness (mIMT) was measured using high resolution B-mode ultrasonography. Determinations of ACE gene polymorphism were made using a polymerase chain reaction technique. Multivariate regression analysis was performed to assess the influence of ACE genotypes, ACE activity and vascular risk factors on intima-media thickness. RESULTS: There was no significant association between intima-media thickness and ACE gene polymorphism. History of symptomatic peripheral arterial disease without local or systemic progression exists in subjects with the II-genotype significantly longer than in subjects with the DD genotype (p=0.01). With the presence of an II-genotype, there was also a tendency towards a thinner intima-media thickness. We found significant correlations between intima-media thickness and age (p<0.0001), fasting serum insulin (p=0.001), and lipoprotein (a) (p=0.008). CONCLUSIONS: In the present study involving patients with stage II peripheral arterial occlusive disease, ACE gene polymorphism could not be identified as a determining marker for the development of intima-media thickening in the common carotid artery. However, it can be assumed that there is a reduced risk for the systemic progression of atherosclerosis in patients with the II genotype.     

Common Carotid Intima-media Thickness in Peripheral Arterial Disease

The common carotid intima-media thickness (IMT) is regarded as a reliable predictor of cardiovascular morbidity. Patients with peripheral arterial disease (PAD) have an increased risk of cardiovascular morbidity and mortality, and PAD is associated with increases in IMT. The aim of this study was to establish whether IMT would be a suitable parameter for predicting cardiovascular risk in individual patients with PAD and the factors involved in determining IMT in these patients. This prospective study included 314 subjects: 112 patients with isolated PAD, 85 patients with PAD and additional coronary and/or cerebrovascular atherosclerosis, and 117 subjects without atherosclerotic disease. Maximum IMT (mIMT) was measured using high-resolution B-mode ultrasonography. Patients with isolated PAD were examined for influencing factors on mIMT. The mIMT in patients with isolated PAD (1.01±0.2 mm) was not significantly different from that of patients with PAD and additional systemic atherosclerosis (1.01±0.17 mm). Controls showed a significantly lower mIMT (0.71±0.15 mm). In multivariate stepwise regression analysis, the chief influencing factors on mIMT in patients with isolated PAD included age as well as fasting insulin and plasminogen activator inhibitor-1 (PAI-1). We found significant correlations between mIMT and the presence of microalbuminuria in nondiabetics with PAD. The highly increased mIMT values of patients with isolated PAD reflect the elevated cardiovascular risk which is already present in the early clinical stages of PAD. The links between fasting insulin, PAI-1, microalbuminuria, and older age with mIMT in isolated PAD are at the same time important predictors of the development of systemic atherosclerosis in PAD.     

Premature Collagen Fibril Formation,Fibroblast-Mast Cell Interactions and Mast Cell-Mediated Phagocytosis of Collagen in Keloids

Keloids are benign hyper-proliferative growths of fibrous tissue where increased fibroblast activity results in abnormal collagen deposition. Excessive inflammation is a characteristic feature of keloids, but little is known about the underlying ultrastructural features of keloids related to collagen processing, fibril and fiber formation, the interaction between fibroblasts and associated collagen fibers and mast cells. In this study, the ultrastructure of the dermis of keloid patients was evaluated using light and transmission electron microscopy techniques. Abnormal intracellular premature collagen fibril formation was observed. Phagocytosis of collagen fibrils by mast cells was a common ultrastructural feature of keloid tissue as was a close or direct association between fibroblasts and mast cells. Based on these findings and recent advances in knowledge related to collagen synthesis, fibril formation and processing, we hypothesize that keloid formation is primarily due to abnormal collagen synthesis where the consequent accumulation of collagen fibers causes increased mast cell recruitment and collagen phagocytosis. Subsequent release of mast cell-derived mediators then promotes further collagen synthesis. The observation of early formation in keloid tissue of premature insoluble collagen fibrils supports previous studies that enzymes such as procollagen C-proteinase are important early therapeutic targets.