886 WALTEK TIMME 



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1. Uniglandular syndrome with secondary or subsidiary pluri; 

 glandular manifestations; e.g., myxedema, Addison's disease. 



2. Transitional groups. Frohlich's dystrophy. 



3. Pluriglandular insufficiency syndromes (Claude and Gougerot). 



4. Pluriglandular hyperfunctioning syndromes ; e. g., hyper thyroid- 

 ism with hyperadrenalism. 



5. Pluriglandular compensatory syndromes; e. g., thymus-adrenal- 

 pituitary type (Timme). 



6. Pluriglandular antagonistic syndromes ; e. g., combinations of 

 myxedema and exophthalmic goiter. 



7. Syndromes frustes. 



For the present, it perhaps is wise to confine the discussion to the 

 two more or less well defined large classes pluriglandular insufficiency 

 and pluriglandular compensation. A consideration and study of these 

 will give the reader the salient features of pluriglandular disturbances in 

 general. The remaining classes above given will be discussed under the 

 separate chapters devoted to the particular glands involved and it would 

 be supererogatory to include them here. The syndromes frustes need no 

 particular attention. In general, however, it may be said that the 

 pluriglandular syndromes are as yet but very poorly understood. Knowl- 

 edge in this department is as yet at its very beginning. Longer experi- 

 ence and more exact analyses will be required to illuminate this domain. 

 Ideas presented here are current at present but may undergo great 

 changes later as endocrinology advances. 



Chief Types of Pluriglandular Insufficiency 

 1. Insuffisance Pluriglaudulaire of Claude and Gougerot 



Description. Perhaps the most widely recognized of the pluriglandu- 

 lar syndromes is that known and termed by Claude and Gougerot (a.) (6) 

 as pluriglandular insufficiency. Under this heading these writers de- 

 scribe a condition in which more or less simultaneously various glands of 

 internal secretion gradually undergo atrophy and the manifestations of 

 their deficiency become part of a clinical picture. This clinical picture is 

 subject to the greatest variations depending upon such factors as the in- 

 tensity of the process on the several glands, the degree of compensatory 

 possibilities and the natural resistance of the patient. So that in combina- 

 tion with gonadal disturbances we may get Addison's suprarenal disease, 

 or myxedema or a combination of acromegaly with exophthalmic goiter; 

 in short, practically any combination of a deficiency character. 



Etiology. By far the greatest factor in the etiology is the hereditary 

 one, predisposing the individual to the development of the syndrome as a 



