Table 4.

Illustrative pathophysiologies of putative feedback failure inferred by disorderly secretory patterns^a

	Refs.
I. Autonomous secretion
Somatotropinoma	211,218
Corticotropinoma	212,216,217,219
Prolactinoma	214,230
Parathyroid adenoma	43
Aldosteronoma	213
Cortisol-secreting adrenal adenoma	213
II. Secondary hypersecretory states
Hyperprolactinemia of stalk section	230
Hyperaldosteronism of salt depletion	43
Hyperparathyroidism in renal failure	44
Hypergonadotropism: menopause	304
Fasting-induced GH secretion	211
III. Experimental feedback depletion (signal monitored)
↓ Te (LH secretion)	109,239,340
↓ IGF-I (GH secretion)	226
IV. Puberty
LH, GH: more disorderly despite ↑ Te and ↑ IGF-I	323,324,328,329,334,367
V. Aging
LH, FSH, GH, ACTH	74,81,217,305,327,367,368
IV. Prediabetes or diabetes mellitus type II
Insulin	73
VII. Feedforward enhancement
↑ Orderliness of ACTH with low cortisol	241
↑ Orderliness of PTH with low calcium	226
VIII. Unexplained pathophysiology
PCOS ↓ orderliness of LH and Te	338
Adult GH deficiency ↓ regularity	326
Depression ↓ ACTH/cortisol orderliness	369,370,371
Visceral obesity ↓ GH orderliness	334

↓, Decreasing; ↑, increasing. 

^aDefined quantitatively by elevated ApEn.