1940
DOI: 10.1001/archpedi.1940.02000040142013
|View full text |Cite
|
Sign up to set email alerts
|

Adrenocortical Obesity in Children

Abstract: The adrenogenital syndrome in children has been described and reviewed repeatedly (Bullock and Sequeria;1 Glynn;2 Reilly, Lisser and Hinman3). Most observers have been especially interested in the sexual precocity or pseudoprecocity caused by hypertrophy, adenoma or cancer of the adrenal cortex. Useful hypotheses have been advanced to explain the syndrome (Krabbe,4 Grollman5), and progress has been made in its early diagnosis and treatment; but with few exceptions (Weber;6 Guthrie and Emery 7) little attention… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1

Citation Types

0
1
0

Year Published

1941
1941
1972
1972

Publication Types

Select...
6

Relationship

0
6

Authors

Journals

citations
Cited by 14 publications
(1 citation statement)
references
References 19 publications
0
1
0
Order By: Relevance
“…This may be due to the better diagnostic techniques now available to detect the condition in children, who may be relatively asymptomatic (Schletter et al, 1967). In children, as in adults, bilateral adrenocortical hyperplasia occurs in one of three forms (Neville and Symington, 1967): simple hyperplasia, nodular hyperplasia or hyperplasia associated with " non-endocrine " tumours that secrete ACTH or an " ACTH-like " peptide (table 111) previously considered to be bilateral adrenocortical adenomas or adenomas with attached hyperplastic glands (Lightwood, 1932;Marks, Thomas and Warkany, 1940;Powell, Newman and Hooker, 1955). Hyperplasia with so-called " nonendocrine " tumours was detected in three boys (table 111); a thymoma, neuroblastoma and islet-cell carcinoma were the sources of ACTH.…”
Section: 0mentioning
confidence: 99%
“…This may be due to the better diagnostic techniques now available to detect the condition in children, who may be relatively asymptomatic (Schletter et al, 1967). In children, as in adults, bilateral adrenocortical hyperplasia occurs in one of three forms (Neville and Symington, 1967): simple hyperplasia, nodular hyperplasia or hyperplasia associated with " non-endocrine " tumours that secrete ACTH or an " ACTH-like " peptide (table 111) previously considered to be bilateral adrenocortical adenomas or adenomas with attached hyperplastic glands (Lightwood, 1932;Marks, Thomas and Warkany, 1940;Powell, Newman and Hooker, 1955). Hyperplasia with so-called " nonendocrine " tumours was detected in three boys (table 111); a thymoma, neuroblastoma and islet-cell carcinoma were the sources of ACTH.…”
Section: 0mentioning
confidence: 99%