From post-mortem examinations performed at the Pathology Institute at Koblenz, 163 cases of wine growers affected by chronic arsenic poisoning were analyzed. While a reduction could be seen in the number of cases of liver cirrhosis, the carcinoma rate was still high and even increased when compared to earlier reports. Lung cancers were identified in 66% of all wine growers affected and are thus the leading form of the skin were observed. A particular characteristic of amount of carcinomas or precarcinogenic alterations of arsenic carcinoma. However, nearly the same amount of carcinomas or precarcinogenic alterations of the skin were observed. A particular characteristic of cases. Among the multiple tumors, up to six different carcinomas were found. As arsenic is no longer detectable by toxicologic-chemical means the deposits of arsenic have been depleted and excreted long ago and so the diagnosis of chronic poisoning today depends on morphological changes of the skin (arsenic hyperkeratosis, melanosis and M. Bowen) which have been shown to be reliable. A comparison of our analysis with much more extensive material collected by the trade association supports our experience and the determined case rates. Furthermore modern theories on the carcinogenic action of arsenic, the question of the tumor latency and the relation of specific cancers to the poison are presented. In addition medical opinions on chronic arsenic poisoning are discussed.

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Dissecting aneurysm of the aorta is often seen; similar changes in the pulmonary artery are rare. In the German literature they are unknown. 11 previously described cases have been compiled with their clinical and pathological records, and a new added. The patient, a 45 year old woman, suffered from pulmonary hypertension which resulted in medionecrosis and a large aneurysm of the trunk of the pulmonary artery. She died of haemopericardium after rupture of the artery in two stages, with a tear of 8 cm in the trunk which reached to the bifurcation of the vessel.

Fifty carcinomas that were partially to completely papillary in nature were examined. According to urethroscopic and rectal palpation findings, six of the carcinomas were located centrally, 40 tumors were in the prostate proper, and four were clinical stage T0. The epithelium of the papillary portions of the tumors was dark in some instances, light in others. Immunohistochemistry revealed that 20 of 22 tumors were positive for prostatic acid phosphatase (PAP) and prostate-specific antigen (PSA). In no case was a topical relationship to the utriculus prostaticus demonstrable. The epithelium of the utriculus in seven additional patients who were not involved in this series also stained positively for PAP and PSA. Usual carcinomas of the prostate proper can develop endometrioid structures that do not differ immunohistochemically from ordinary portions of the carcinoma. Tumors located in central portions of the prostate are, in our opinion, morphologic variants of usual prostatic carcinomas, and apparently arise in prostatic ducts. We conclude that a distinction between endometrioid carcinomas and tumors of prostatic ducts does not seem justified and that papillary prostatic carcinomas should be treated like common prostatic cancer.

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