Chirurgie der Hyperthyreose

Pathophysiologie, Diagnostik, Operationsindikation und Vorbehandlung, chirurgisches Krankengut, Operationsverfahren und Nachbehandlung mit funktionellen Spätergebnissen wurden gezeigt. Der ätiologisch bedingte Unterschied in Therapie und Prognose der Hyperthyreose vom Typ des M. Basedow gegenüber den anderen Hyperthyreoseformen war dargestellt. Von 1891 schilddrüsenoperierten Patienten in den letzten 10 Jahren waren fast (n = 625) hyperthyreot; 22,7% der Hyperthyreosen waren vom Typ des M. Basedow, 26,5 % multinoduläre Strumen, der Rest autonome AdenomePathophysiology, diagnosis, indication for operation and pretreatment, data of operated patients, surgical treatment, and postoperative care with late results are demonstrated. The differences between Graves' disease and other kinds of hyperthyroidism are pointed out. About (n = 625) of all patients operated upon for goiter (n= 1891) within the last ten years had hyperthyroidism. Exophthalmia was present in 22.7 %, toxic multinodular goiter in 26.5 %; the rest of the patients had autonomous adenoma. The importance of radioimmunoassays to determine preoperative treatment and postoperative hormone levels for long-term results is stressed

Dringliche Eingriffe in der endokrinen Chirurgie

Während Notfalloperationen aus mechanischer Indikation immer wieder vorkommen (z. B. Chiasma-Syndrom, Atemwegsobstruktion), sind die kritischen Überfunktionen der endokrinen Drüsen in der Regel durch konservativ-medikamentöse Therapie ausreichend zu beherrschen. Ausnahmen: z. B. thyreotoxische Krise (bei nur kurz anhaltender Besserung durch Plasmapherese bei einer jodinduzierten Hyperthyreose) oder akutes Cushing-Syndrom (nicht beherrschbare hypokaliämische Alkalose). Solche Einzelfälle hängen von der optimalen Kooperation von Anaesthesie, Chirurgie und internistischer Intensivmedizin ab. Gesetze der Diagnose und der konservativen Vorbereitung für die operative Behandlung von endokrinen Überfunktionszuständen nur ultima ratio übertreten!Urgent surgery for emergency situations in endocrine diseases is needed for mechanical problems (e.g., chiasma syndrome or tracheal obstruction) and very rarely for endocrine hyperfunction, which can usually be treated by nonsurgical means. Exceptions are patients suffering from thyroid storm (impending early relapse after plasmapheresis due to excess iodine) or from acute Cushing's syndrome (intractable potassium loss and alkalosis whom we have successfully transferred to surgery. The rules for diagnosis and medical preparation for surgery of endocrine hyperfunctional states should only be disregarded ultima ratio

Diagnostik und Therapie des Hyperparathyreodismus

Seiten 693+694 Werbung

Photodissociation and chemistry of N 2 in the circumstellar envelope of carbon-rich AGB stars

Context. The envelopes of asymptotic giant branch (AGB) stars are irradiated externally by ultraviolet photons; hence, the chemistry is sensitive to the photodissociation of N2 and CO, which are major reservoirs of nitrogen and carbon, respectively. The photodissociation of N2 has recently been quantified by laboratory and theoretical studies. Improvements have also been made for CO photodissociation. Aims. For the first time, we use accurate N2 and CO photodissociation rates and shielding functions in a model of the circumstellar envelope of the carbon-rich AGB star, IRC +10216. Methods. We use a state-of-the-art chemical model of an AGB envelope, the latest CO and N2 photodissociation data, and a new method for implementing molecular shielding functions in full spherical geometry with isotropic incident radiation. We compare computed column densities and radial distributions of molecules with observations. Results. The transition of N2→ N (also, CO → C → C+) is shifted towards the outer envelope relative to previous models. This leads to different column densities and radial distributions of N-bearing species, especially those species whose formation/destruction processes largely depend on the availability of atomic or molecular nitrogen, for example, CnN (n = 1, 3, 5), CnN− (n = 1, 3, 5), HCnN (n = 1, 3, 5, 7, 9), H2CN and CH2CN. Conclusions. The chemistry of many species is directly or indirectly affected by the photodissociation of N2 and CO, especially in the outer shell of AGB stars where photodissociation is important. Thus, it is important to include N2 and CO shielding in astrochemical models of AGB envelopes and other irradiated environments. In general, while differences remain between our model of IRC +10216 and the observed molecular column densities, better agreement is found between the calculated and observed radii of peak abundance

TGF-β Inducible Early Gene 1 Regulates Osteoclast Differentiation and Survival by Mediating the NFATc1, AKT, and MEK/ERK Signaling Pathways

TGF-β Inducible Early Gene-1 (TIEG1) is a Krüppel-like transcription factor (KLF10) that was originally cloned from human osteoblasts as an early response gene to TGF-β treatment. As reported previously, TIEG1−/− mice have decreased cortical bone thickness and vertebral bone volume and have increased spacing between the trabeculae in the femoral head relative to wildtype controls. Here, we have investigated the role of TIEG1 in osteoclasts to further determine their potential role in mediating this phenotype. We have found that TIEG1−/− osteoclast precursors differentiated more slowly compared to wildtype precursors in vitro and high RANKL doses are able to overcome this defect. We also discovered that TIEG1−/− precursors exhibit defective RANKL-induced phosphorylation and accumulation of NFATc1 and the NFATc1 target gene DC-STAMP. Higher RANKL concentrations reversed defective NFATc1 signaling and restored differentiation. After differentiation, wildtype osteoclasts underwent apoptosis more quickly than TIEG1−/− osteoclasts. We observed increased AKT and MEK/ERK signaling pathway activation in TIEG1−/− osteoclasts, consistent with the roles of these kinases in promoting osteoclast survival. Adenoviral delivery of TIEG1 (AdTIEG1) to TIEG1−/− cells reversed the RANKL-induced NFATc1 signaling defect in TIEG1−/− precursors and eliminated the differentiation and apoptosis defects. Suppression of TIEG1 with siRNA in wildtype cells reduced differentiation and NFATc1 activation. Together, these data provide evidence that TIEG1 controls osteoclast differentiation by reducing NFATc1 pathway activation and reduces osteoclast survival by suppressing AKT and MEK/ERK signaling