Hostname: page-component-8448b6f56d-m8qmq Total loading time: 0 Render date: 2024-04-20T02:56:15.956Z Has data issue: false hasContentIssue false

The Hormone Treatment of Acromegaly

Published online by Cambridge University Press:  08 February 2018

E. L. Hutton
Affiliation:
Endocrinological Laboratory, Burden Neurological Institute, Bristol
M. Reiss
Affiliation:
Endocrinological Laboratory, Burden Neurological Institute, Bristol

Extract

The demonstration by Zondek (1936), subsequently confirmed by Cramer and Horning (1936), Gardner (1937), Collip (1936), Noble (1938), Deanesley (1938, 1939), Pybus and Miller (1938), that large doses of oestrone will impair and partly suppress the functions of the pituitary anterior lobe, especially the gonadotrophic and the growth hormone production and will produce partial degeneration of the acidophil cells, led Kirklin and Wilder (1936) to adopt this method of treatment for patients suffering from acromegaly. Their series consisted of eight patients, four men and four women, and their results may be briefly summarized as follows: There was a general improvement in three patients; headache which was originally present in six cases disappeared in four, but returned in one case, though this may have been due to a discontinuance of treatment; in three patients there was a decrease in size, in one a smaller hat was required and her dental plate became loose, in one the hands became smaller, and in one shoes became looser; the visual fields were originally altered only in three of the eight patients, and in one of these the fields returned to normal, in one there was no change, and in the third a progressive hemianopia accompanied by erosion of the sella turcica developed during treatment; hyperidrosis and intolerance of heat, originally present in two, disappeared in both; finally there was loss of libido in three cases.

Type
Part II.—Original Articles
Copyright
Copyright © Royal College of Psychiatrists, 1942 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Collip, J. B. (1936), J. Med. Franc., 25, 330.Google Scholar
Cramer, W., and Horning, E. S. (1936), Lancet, ii, 1056.Google Scholar
Deanesley, R. (1938), Nature, 141, 79; (1939), Journ. Endocrinology, 1, 36.Google Scholar
Deanesley, R. and Parkes, A. S. (1937), Proc. Roy. Soc., b, 124, 279; (1938), Lancet, i, 606.Google Scholar
Gardner, W. U. (1937), Anat. Record, 68, 339.Google Scholar
Kirklin, D. L., and Wilder, R. M. (1936), Proc. Mayo Clinic, 11, 121.Google Scholar
Noble, R. L. (1938), Lancet, i, 192; (1938), Journ. Physiol., 94, 177.Google Scholar
Pybus, F. C., and Miller, E. W. (1938), Nature, 142, 872.Google Scholar
Reiss, M., and Golla, Y. M. L. (1940), Journ. Ment. Sci., 86, 281.Google Scholar
Schrire, I., and Sharpey Schafer, E. P. (1938), Clin. Sci., 3, 369.Google Scholar
Schrire, I., and Zwarenstein, L. H. (1933), Biochem. Journ., 27, 1337; (1934), ibid., 28, 356.CrossRefGoogle Scholar
Schrire, I. (1937), Quart. J. Med., n.s, 6, 17.Google Scholar
Stephens, D. J. (1939), Journ. Endocrinology, 26, 638.Google Scholar
Zondek, B. (1936), Lancet, ii, 842.Google Scholar
Submit a response

eLetters

No eLetters have been published for this article.