Acta medica Austriaca最新文献

Zusammenfassung: Die extraokulären Augenmuskeln sind bei der endokrinen Orbitopathie in typischer Reihenfolge betroffen. Charakteristisch daher auch die Bewegungseinschränkung eines oder beider Augen. Ist das akut entzündliche Stadium abgelaufen, und sind trotz gut eingestellter Schilddrüsenfunktion Bewegungseinschränkungen der Augen geblieben, ist die Therapie der Wahl die Augenmuskelchirurgie, die einerseits der Verbesserung der Beweglichkeit und damit der Erweiterung des Blickfeldes und andererseits der Beseitigung von Doppelbildern dient.

Endocrine Orbitopathy – Eye Muscle Surgery

Summary: Extraocular muscles show a typical involvement in Graves' disease, thus inducing a characteristic pattern of motility disorders and diplopia. Therapy of choice of fibrotic changed muscles is the operation, usually performed by recessions under local or even topical anesthesia.

Zusammenfassung: Die Immunthyreopathie vom Typ Morbus Basedow ist Folge eines systemischen Autoimmunprozesses, der bei schwerer Ausprägung neben der Schilddrüse als primärem Zielgewebe auch das in den Orbitahöhlen gelegene Binde-­, Fett- und Augenmuskelgewebe betrifft. Obwohl das primäre Antigen nach wie vor ungewiss ist, dürfte der im Orbitagewebe exprimierte TSH-Rezeptor – möglicherweise durch „molekulares Mimikry” mit bakteriellen oder viralen Epitopen – eine wesentliche Rolle spielen. Nach Toleranzverlust gegenüber dem endogenen TSH-Rezeptor kommt eine T-Zell-abhängige immunologische Entzündungsreaktion in Gang, die über Zytokine, Interleukine und Prostaglandine zu einer Akkumulation von hydrophilen Glykosaminoglykanen (v. a. Hyaluronsäure, Chondroitinsulfat) im orbitalen Binde-, Fett- und Muskelgewebe führt. Neuen Befunden zufolge spielt auch die gesteigerte Rekrutierung, Differenzierung und Ausreifung von orbitalen Präadipozyten zu Adipozyten und die damit einhergehende Expression des TSH-Rezeptors eine wichtige Rolle. Folge hiervon ist eine aus­geprägte Volumenzunahme der orbitalen Gewebe mit zunehmender räumlicher Enge in den knöchern begrenzten Orbitae. Durch den intraorbitalen Druckanstieg kommt es als natürliche Form der Druckentlastung zur Protrusio bulbi bei gleichzeitiger Lidretraktion und zu einem schwellungsbedingten Prolaps der entzündlich veränderten Binde- und Fettgewebsanteile in die Ober- und Unterlider (periorbitale Ödeme). Zusätzlich können Motilitätsstörungen der äußeren Augenmuskeln auftreten, die je nach Ausmaß der asymmetrischen Beeinträchtigung mit Doppelbildern einhergehen. Mit steigender Raumnot entwickeln sich intraorbital zunehmend mechanische Komplikationen, die durch venöse Kongestion, Gewebehypoxie und Bildung von freien Sauerstoffradikalen (Rauchen!) noch verschlimmert werden. Im Extremfall kann die massive Volumenzunahme der Orbita­gewebe zur Expositionskeratitis und Optikusneuropathie führen, die neben den kosmetischen Problemen zu den gravierenden Komplikationen der endokrinen Orbitopathie zählen.

Interactions of Fibroblasts, Adipocytes and Immunocompetent Cells in the Pathogenesis of Graves’ Ophthalmopathy

Summary: Graves’ ophthalmopathy is thought to result from a complex interplay of genetic and environmental factors. Various genes including those coding for HLA may determine a patient’s susceptibility to the disease and its severity, but in addition numerous and often unknown environmental factors may determine its course. The orbital immune process is thought to be initiated, on the background of a permissive immunogenetic milieu, by circulating T cells directed against certain antigens on thyroid follicular cells that also recognize antigenic epitopes which are shared by tissues contained in the orbital space. Analysis of variable region genes of T cell antigen receptors in orbital T cells of patients with active Graves’ ophthalmopathy has revealed limited variability of Tc

Methods: Twenty patients suffering from malignancy received furosemide, twenty patients were examined by FDG-PET without diuretics. Urine volume and radioactivity were measured before and after acquisition. Bladder activity was evaluated qualitatively and quantitatively.

Results: Radioactivity in the bladder was lower and the image quality higher in the furosemide group. SUV values showed a median of 3.0 in the furosemide and 6.0 in the control group. With furosemide, a larger excreted volume was seen compared to the control group. The furosemide group showed a significantly higher ratio of excreted/ injected radioactivity early after injection. However, the totally excreted radioactivity was not significantly different (p = 0.93).

Conclusion: Diuretics cause a higher urine volume with a diluted FDG concentration leading to an improved image quality. Furosemide accelerates early renal FDG elimination, reducing radiation exposure.

Lipoprotein (a) [Lp(a)] may produce thrombogenic effects by modulating the fibrinolytic system. Elevated levels of Lp(a) have also been associated with an increased risk for atherosclerosis. Because atherosclerosis is more prevalent among patients with end-stage renal disease, the role of Lp(a) among patients on hemodialysis is analyzed. Twenty patients were studied. Lp(a) was measured before and after a hemodialysis session and before the following session. Between the first and second measures there was no statistical difference but when first and third measures were compared, a statistical difference (increase) was found. In conclusion, changes in Lp(a) levels were found and perhaps these changes are related to the episodic inflammation affecting patients on hemodialysis. The significance of these changes and the role in accelerating atherosclerosis in patients with end-stage renal disease are unknown.

Coronary calcification is a strong predictor of significant coronary stenosis in symptomatic patients. While discrete calcification within coronary arteries is only detected by sensitive methods such as computed tomography, severe calcification can already be seen on the plain chest radiograph. In this article, we describe a patient with a high grade left main stem coronary artery stenosis who presented with a severe focal calcification on the plain chest radiograph in projection of the offspring of the left coronary artery.

Background: Cardiovascular risk factors are a significant burden in end-stage renal disease patients under hemodialysis. Cardiovascular-related diseases are the leading cause of death among these patients and responsible for almost half of all deaths in dialysis patients. The influence of parathormone (PTH) on myocardial function as a toxin of uremia is attracting more attention and evaluation because of growing evidence that the effects of PTH on cardiac function may be the most serious consequence of secondary hyperparathyroidism in renal failure. In this study we aimed to consider the role of the excess PTH in the development of left ventricular hypertrophy (LVH) and its effects on LV ejection fraction in patients with end-stage renal disease under regular hemodialysis.

Methods: This cross-sectional study was done on patients with end-stage renal disease (ESRD) undergoing maintenance hemodialysis treatment. Calcium, phosphorus, alkaline phosphatase and intact PTH (iPTH) were measured. Hypertensive patients were stratified into stages one to three. Echocardiography for left ventricular (LV) hypertrophy and ejection fraction (percent) were done and LV stratified into normal, mild, moderate and severe hypertrophy.

Results: The total number of patients was 73 (F = 28, M = 45), consisting of 58 non-diabetic hemodialysis patients (F = 22, M = 36) and 15 diabetic hemodialysis patients (F = 6, M = 9). The age of patients was 46.5 +/- 16 years. The length of time patients had been on hemodialysis was 21.5 +/- 23.5 months. The LV ejection fraction (EF%) was 51 +/- 8 percent. Mean +/- SD of iPTH of total patients was 309 +/- 349 pg/ml. Mean +/- SD of iPTH of diabetic group and non-diabetic group was 234 +/- 265 pg/ml and 329 +/- 368 pg/ml respectively. The value of serum alkaline phosphatase of total patients was also 413 +/- 348 IU/L. Serum alkaline phosphatase (ALP) of diabetic group and non-diabetic group was 295 +/- 179 IU/L and 443 +/- 375 IU/L respectively. Serum albumin of total patients was 4 +/- 0.75 g/dl. Serum albumin of diabetic group and non-diabetic group was 3.6 +/- 0.7 g/dl and 4.2 +/- 0.7 g/dl respectively. Significant inverse correlation of serum ALP with percent of LV ejection fraction and marginal significant correlation of serum ALP with LVH were seen and marginal significant correlation of serum iPTH with LVH was also found. Significant inverse correlation between serum iPTH with percent of LV ejection fraction in non-diabetic HD patients was observed.

Conclusions: Adverse effects of secondary hyperparathyroidism on LV function and structure in this study shows the role of excess PTH in the development of left ventricular hypertrophy as well as low LV ejection fraction. In patients with end-stage renal disease under hemodialysis, more attention needs to be given to the control of secondary hyperparathyroidism to reduce the risk of cardiovascular

The Pentalogy of Cantrell (PC) is a rare association of defects involving the lower sternum, abdominal wall, diaphragm, pericardium and heart. We report two rare cases of the PC (variant form), showing fatal progression. Case 1 only survived two hours because of severe cardio-respiratory failure. Physical examination showed midline abdominal and thoracic defects, ectopic heart, pericardial defect, diaphragmatic defect, bilateral undescended testis, scoliosis, and adherence between left upper limb and trunk. In addition, the autopsy revealed diaphragmatic agenesia, intraabdominal testis, bilateral lung hypoplasia and lymphocytic meningitis. Case 2 only survived 15 minutes. In addition to the physical findings, including lower sternal defect, ectopic heart, epigastric omphalocele and scoliosis, the autopsy showed left diaphragmatic agenesia, pericardial agenesia, bilateral lung hypoplasia, deformed rib cage, anterior thoracic myeloschisis, adreno-hepatic fusion, left renal agenesia, meckel diverticulum and multiple accessory spleens. When comparing with other cases of PC, the concurrence of bilateral intraabdominal testis and lymphocytic meningitis in case 1, and adreno-hepatic fusion, anterior myeloschisis, meckel diverticulum, multiple accessory spleens, and renal agenesia in case 2 have not been described previously.

Breast cancer is the malignant neoplasm most commonly associated with hypercalcemia. In breast cancer the majority of the hypercalcemia cases result from osteolytic metastatic bone disease of the primary tumor. In a few patients hypercalcemia results from other conditions like primary hyperparathyroidism. Here, we present two female patients who were treated for breast cancer. Hypercalcemia in these two patients was diagnosed as being due to primary hyperparathyroidism. One of them was submitted to surgery and the calcium level dropped to the normal level thereafter. The other one refused surgery and was treated with biphosphonate and calcitonin. We suggest that when hypercalcemia occurs in breast cancer, primary hyperparathyroidism should be considered as possible cause.

Our knowledge about risk factors of atherosclerosis and their associations has considerably changed and improved. The importance of type 2 diabetes and hypertension was detected earlier, hyperlipidemia and dyslipidemia (disturbance of lipoprotein composition) have been recently implemented. We have learnt that the android obesity form and especially visceral fat serve as central trigger-factor of the resulting "metabolic syndrome" and other related disturbances like acute phase proteins, inflammation markers and procoagulatory state. Altogether atherothrombotic events are increased and result in clinically relevant macrovascular disease (myocardial infarction, cerebrovascular und peripheral arterial disease), blood glucose itself causing additionally microvascular disease. The newest comprehensive guidelines of European Associations try to use most of the known factors for treatment guidelines but will fail due to the fact that they cannot be easily used in clinical practice. In additon, visceral fat, that central factor, and body fat mass have not been integrated. We suggest that the risk should be evaluated in the context of body mass index (BMI) and especially of waist circumference which could be THE central intervention factor in the treatment of our patients.