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When writing on osteomalacia it is necessary to state clearly what is meant by this designation, as much confusion is met with in the liter' ' 1 t ure on this subject, especially in the Scandinavian countries.Osteomalacia is an easily recognisable disorder with characteristic signs and symptoms. It is a clinical unity, but of different etiology. The clinical and roentgenpathological features are usually alone not sufliciently characteristic to distinguish osteomalacia from certain other, similar conditions with decalcification of the bone system. The diagnosis is dependent on certain pathognomonic chemical findings in the body fluids, which make it an easy one. A s osteomalacia is adult rickets our knowledge on that disease may be utilised for our studies on its adult form, with certain modifications due to the growth factor in rickets.The cause of the primary bone changes are purely chemical and the condition arises, when the solubility product of the calcium and the inorganic phosphorus of the serum is too low for the precipitation of calciumphosphate in the osteoid tissue, laid down by the osteoblasts. This was postulated for infantile rickets by Howland and Kramer ( 1 ) already in 1922. In osteomalacia as in rickets one may find a low Ca and normal P, or a normal Ca and low P or both Ca and P are lower than normal. The brilliant work of Albright and his co-workers on the metabolism of decalcifying bonediseases has clarified many dark points and contributed largely to a clear and concise classification of these diseases.All the changes found in osteomalacia are due to a faulty calciummetabolism and to secondary changes induced by the hypocalceniia. All the known types of the disease are caused by lack of calcium, either clue to deficiency of absorption from the gut or a negative balance produced by loss of calcium through the urine. The main cause of osteomalacia due to deficient absorption is, as in rickets, Vitainin D deficiency with deficiency

Zusammenfassung. Es wird ein Fall von Sublimatvergiftung beschrieben, besonders mit Rücksicht auf die speziellen Laboratorienbefunde. Der Patient, ein junger Mann, trinkt 4 g Sublimat in konzentrierter Lösung. Unmittelbar danach bekommt er Schmerzen im Munde und Schlunde und Erbrechen, und wenige Minuten später kommt er unter Behandlung mit Magenspülung etc. 5 Stunden später findet man Albuminuric und Zylindrurie, darauf folgt eine totale Anurie von 6‐tägiger Dauer. Die Diurese kommt jetzt wieder in Gang, die Nierenfunction ist jedoch sehr mangelhaft mit herabgesetzter Clearence und Isostenurie. Mit der Nierenkrankheit verbunden ist eine bedeutende Azotaemie, die jedoch auffallend wenige klinische Symptome giebt, — eine Herabsetzung der Alkalireserve, der totalen Basen, besonders des Natriums, und verminderte Chloriden‐koncentration im Blute. Man findet Hypoproteinanaemie und Oedeme. Parotitis, Stomatitis, haemorrhagische Gastritis und ulceröse Colitis, Dermatitis und Leberdegeneration treten auf. Der Tod tritt nach 21 Tagen als Folge einer Mediastinitis ein.