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Amiodarone, ein häufig verwendetes iodhaltiges Antiarrhythmikum, kann häufig zu Hypothyreose oder Hyperthyreose führen. Während die Hypothyreose, die mehr Frauen betrifft und in iodsuffizienten Gegenden auftritt, einfach zu behandeln ist, kann für den Kliniker die Hyperthyreose eine therapeutische Challenge sein. Neben Absetzen der Therapie kann die amiodarone-induzierte Hyperthyreose Typ 1, die einer iodinduzierten Hyperthyreose entspricht, primär mit einem Thyreostatikum behandelt werden. Bei der amiodarone-induzierten Hyperthyreose Typ 2, die durch einen direkt toxischen Effekt des Amiodarones auf die Schilddrüse verursacht wird und einer Thyreoditis ähnlich ist, wird eine Therapie mit Steroiden primär eingesetzt. Jedoch ist die Unterscheidung zwischen beiden Formen häufig nicht möglich und der Kliniker wird oft mit einer Ungewissheit konfrontiert.

Chronic mountain sickness (CMS) is an important public health problem and is characterized by exaggerated hypoxemia, erythrocytosis, and pulmonary hypertension. While pulmonary hypertension is a leading cause of morbidity and mortality in patients with CMS, it is relatively mild and its underlying mechanisms are not known. We speculated that during mild exercise associated with daily activities, pulmonary hypertension in CMS is much more pronounced.

Invasive studies suggest that healthy children living at high altitude display pulmonary hypertension, but the data to support this assumption are sparse. Nitric oxide (NO) synthesized by the respiratory epithelium regulates pulmonary artery pressure, and its synthesis was reported to be increased in Aymara high-altitude dwellers. We hypothesized that pulmonary artery pressure will be lower in Aymara children than in children of European ancestry at high altitude, and that this will be related to increased respiratory NO. We therefore compared pulmonary artery pressure and exhaled NO (a marker of respiratory epithelial NO synthesis) between large groups of healthy children of Aymara (n = 200; mean ± SD age, 9.5 ± 3.6 years) and European ancestry (n = 77) living at high altitude (3,600 to 4,000 m). We also studied a group of European children (n = 29) living at low altitude. The systolic right ventricular to right atrial pressure gradient in the Aymara children was normal, even though significantly higher than the gradient measured in European children at low altitude (22.5 ± 6.1 mm Hg vs 17.7 ± 3.1 mm Hg, p < 0.001). In children of European ancestry studied at high altitude, the pressure gradient was 33% higher than in the Aymara children (30.0 ± 5.3 mm Hg vs 22.5 ± 6.1 mm Hg, p < 0.0001). In contrast to what was expected, exhaled NO tended to be lower in Aymara children than in European children living at the same altitude (12.4 ± 8.8 parts per billion [ppb] vs 16.1 ± 11.1 ppb, p = 0.06) and was not related to pulmonary artery pressure in either group. Aymara children are protected from hypoxic pulmonary hypertension at high altitude. This protection does not appear to be related to increased respiratory NO synthesis.