Several congenital and acquired conditions, originating from the hypothalamus and pituitary, or in other organs/systems with secondary systemic dissemination, can alter GH secretion leading to transient or chronic somatotroph deficiency or excess. The evolution of radiological, histological, and molecular techniques has profoundly changed the classification as well as treatment indications and types. Management is often challenging because of the heterogeneous and insidious presentation, the multi-organ involvement, and the variable outcome, so that patients should be referred to Pituitary Centers of Excellence. This volume addresses still open issues related to the diagnosis and treatment of GH deficiency and excess, in particular challenging physiologic and pathologic circumstances, and presents the new frontiers of diagnosis – including the application of artificial intelligence – and therapy towards precision, patient-tailored approach, aimed at maximizing treatment effectiveness, tolerability and patient adherence, and consequently, the employment of socio-sanitary resources.
2024. "Subject Index", GH Excess and Deficiency from Fetus to Older Age: A Kaleidoscopic Overview, Federica Guaraldi, Diego Mazzatenta
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Acidophil stem cell tumor (ASCT), 102
Acromegaly, 232
artificial intelligence (AI), 204
atesidorsen, 209
biochemical control, 138
CAM2029, 205
cimdelisen, 209–210
clinical manifestations, 135
complications, 135–137
DEBIO 4126, 206
diagnostic delay burden, 137–138
disease control, 138–139
erectile dysfunction (ED), 228–231
fertility, 232
GH receptor inhibition, 209
HTL0030310, 208
intranasal octreotide, 206
LANPRF, 206–207
medical treatment, 203–210
mortality, 139
new devices, 204–205
ONO-5788, 208
ONO-ST-468, 208
oral octreotide, 205–206
paltusotine, 207
quality of life, 138–139
site 1-binding helix (S1H), 210
somatoprim, 208
somatostatin-dopamine chimeric compound, 210
somatostatin receptors, selective agonist of, 207–210
somatotropinomas, immune microenviroment, 204
therapeutic inertia reasons, 139–140
therapeutic inertia risks, 135–137
Adamantinomatous craniopharyngioma (ACP), 12
Adherence, 63
Adrenocorticotropic hormone (ACTH), 24
Albeit endoscopic techniques, 154
Anatomo-Clinical landscape, 102–107
Artificial intelligence (AI), 204
Aryl hydrocarbon receptor interacting protein (AIP) pathogenic variants, 88–90
Atesidorsen, 209
Biochemical control, 138
Body mass index (BMI), 62–63
Bone effects, 58–60
Bone mineral density (BMD), 23, 59
Bright spot, 4
CAM2029, 205
Cardiovascular and metabolic diseases, 145
Central nervous system (CNS), 8
Chiasmatic-hypothalamic gliomas, 14–15
Childhood onset, 21
Cimdelisen, 209–210
Continuous positive airway pressure (C-PAP), 148
Craniopharyngiomas (CPs), 12
CS ectopic micro-PAs/PitNETs, 168–169
CS invasive macro-PAs/PitNETs, 168–169
DEBIO 4126, 206
Diagnostic delay burden, 137–138
Digital phenotyping data, 218–222
Disease control, 138–139
Dyspituitarism, 99
Ectopic neurohypophysis, 7
Ectopic posterior pituitary lobe (EPP), 5
Empty sella, 9
Endoscopic endonasal approach (EEA), GH-secreting tumors
case series, 161
CS ectopic micro-PAs/PitNETs, 168–169
CS invasive macro-PAs/PitNETs, 168–169
discussion, 176–179
irregular PAs/PitNETs, 168
micro-PA/PitNETs, 163–166
patient management, 161–163
regular macro-endo-/suprasellar PAs/PitNETs, 166–168
results, 172–176
skull base invasion, 169–170
sphenoid sinus, infrasellar macro-PAs/PitNETs, 169–170
statement of ethics, 179
statistical analysis, 163, 176
supradiaphragmatic extension, macro-PA/PitNET with, 170–171
surgical technique, 163–166
technical features, 179
Endoscopic endonasal surgery (EES), sellar lesions, 216–224
Erectile dysfunction (ED), 228–231
acromegaly, 228–231
growth hormone deficiency (GHD), 234
Familial isolated pituitary adenomas (FIPA), 89
Fertility
acromegaly, 232
growth hormone deficiency (GHD), 234
First-generation somatostatin analogs (fg-SSA), 183
adjuvant setting, 186
efficacy of, 187–188
indications to treatment, 186
neoadjuvant treatment, 186–187
no-surgery setting, 186–187
starting dose, 188
therapeutic monitoring, 188
therapy titration, 188
Follicular stimulating hormone (FSH), 227
Fugitive acromegaly
Anatomo-Clinical landscape, 102–107
origin of the terminology, 99–102
pathophysiological changes, 102
pituitary tumors pathogenesis, translational evidence for, 107–113
Fugitivity, 99
GH-PitNET, see Growth hormone-secreting pituitary neuroendocrine tumor
Growth hormone deficiency (GHD)
adherence, 63
body mass index (BMI), 62–63
bone effects, 58–60
empty sella, 9
erectile dysfunction (ED), 234
fertility, 234
gender effects, 62
hormone replacements, 62
isolated anterior pituitary hypoplasia, 5
magnetic resonance imaging (MRI), 3–5
metabolic effects, 60
organic, 9
pituitary dystopia, 5–9
pituitary gland aplasia, 5
pituitary gland development, 2
pituitary stalk thickening (PST), 9–12
psychological effects, 61
quality of life, 61
rationale for, 61
rGH replacement, age influence, 61–62
rGH replacement prediction models, 64
rGH therapy personalization, 64
transitional age, 29–45
traumatic brain injury (TBI), 9
tumors and treatment-related changes, 12–15
Growth hormone-releasing hormone (GHRH) secretion, 85
Growth hormone replacement treatment (GH-rT), 51–53
diagnosis, 49–51
Growth hormone-secreting pituitary neuroendocrine tumor (GH-PitNET)
biological features, 154–155
current indications for, 145–148
neoadjuvant medical treatment, 149–150
pre-operative evaluation, 148
specific challenging situations, 149
surgery specific challenges, 152–153
surgical treatment, 150–152
transsphenoidal surgery and endoscopy, 150–152
High-density lipoprotein (HDL) cholesterol, 23
Hormone replacements, 62
HTL0030310, 208
Human chorionic gonadotropin (hCG), 13
Hyperpituitarism, 99
Hypogonadism, 87
Hypopituitarism, 87, 99
HYPOPRONOS international group, 101
Hypothalamic-pituitary dysfunction, 12
Idiopathic growth hormone deficiency (IGHD), 5
Insulin growth factor 1 (IGF-1), 227
Insulin-like growth factor 1 (IGF-1), 83
Intracranial germinomas, 12
Intranasal octreotide, 206
Irregular PAs/PitNETs, 168
Isolated anterior pituitary hypoplasia, 5
Langerhans cell histiocytosis (LCH), 10–11
LANPRF, 206–207
Long-acting growth hormone, 25
Long-acting repeatable (LAR), 149
Low-density lipoprotein (LDL) cholesterol, 23
Lymphocytic hypophysitis, 11–12
Magnetic resonance imaging (MRI), 3–5
Male sexual function and fertility
acromegaly, 228–232
growth hormone deficiency (GHD), 232–234
growth hormone excess, 228–231
methods, 227
Mammosomatotroph tumors, 106
McCune-Albright syndrome (MAS), 91–92
Metabolic/bone effects, 23–24
Metabolic effects, 60
Micro-PA/PitNETs, 163–166
Mortality, 139
Multimodal therapy, 86
Multiple/combined pituitary hormone deficiency (MPHD/CPHD), 2
Multiple endocrine neoplasia type 1 (MEN1), 92
Multiple pituitary hormone deficiency groups (MPHD), 24
Neoadjuvant medical treatment, 149–150
Neuronal differentiation 4 (NEUROD4), 103
Noonan syndrome, 21
Obstructive sleep apnea (OSAS), 145
ONO-5788, 208
ONO-ST-468, 208
Oral octreotide, 205–206
Paltusotine, 207
Papillary craniopharyngioma, 12
PA/PitNETs, see Pituitary adenomas/pituitary neuroendocrine tumors
Parathyroid hormone (PTH), 58
Penile doppler ultrasound (PDU), 229
Physical status, 149
Pituitary acrogigantism
AIP pathogenic variants, 88–90
clinical features, 85–87
genetics and genomics of, 87–92
history, 83–85
insulin-like growth factor 1 (IGF-1), 83
management, 85–87
McCune-Albright syndrome (MAS), 91–92
multiple endocrine neoplasia type 1 (MEN1), 92
X-linked acrogigantism, 90–91
Pituitary adenomas/pituitary neuroendocrine tumors (PA/PitNETs)
classification and peculiar clinico-histological features, 124–127
classification of, 123–124
early identification of, 127–128
future perspectives, 128
GH-secreting/somatotroph cells in physiology, 121–122
histological subtypes, 121
nomenclature changes, rationale and clinical significance of, 122–123
Pituitary dystopia, 5–9
Pituitary gland aplasia, 5
Pituitary gland development, 2
Pituitary stalk thickening (PST), 9–10, 9–12
Prader-Willi syndrome, 21
Psychological effects, 61
Pubertal hyperplasia, 4
Puberty, 4
Quality of life, 61, 138–139
Rathke’s pouch, 2
Recombinant growth hormone (rhGH) therapy
childhood onset, 21
efficacy, 22–23
long-acting growth hormone, 25
metabolic and bone effects, 23–24
monitoring GH therapy, 24
personalization, 64
replacement, 57, 61–62, 64
safety of, 24–25
therapy indications, 20–21
treatment of, 21–22
Regular macro-endo-/suprasellar PAs/PitNETs, 166–168
Replacement therapy, adults
challenges, 76–79
characteristics of, 71–72
clinical picture of, 69
guidelines on, 73
insulin-like growth factor-I (IGF-I), 70
monitoring, 74–75
side effects, 75–76
Safety and Appropriateness of Growth Hormone Treatments in Europe (SAGhE) Consortium., 24
Second-generation somatostatin analogs (sg-SSA), 184–185
efficacy of, 189–190
indications to, 189
starting dose, 190
therapeutic monitoring, 190
therapy titration, 190
Sellar lesions, endoscopic endonasal surgery (EES), 216–224
Site 1-binding helix (S1H), 210
Skull base invasion, 169–170
Somatoprim, 208
Somatostatin analogs (SSA)
acromegalic headache, 196
combined therapy, 193
contraindications, 193
first-generation somatostatin analogs (fg-SSA), 183
gastrointestinal effects, 193–194
history of, 182–183
lanreotide, 184
limitations, 193–195
metabolic effects, 194–195
octreotide, 183–184
pitfalls, 193–195
pregnancy, 195–196
response predictors, 190–193
second-generation somatostatin analogs (sg-SSA), 184–185
side effects, 195
Somatostatin-dopamine chimeric compound, 210
Somatostatin receptors, selective agonist of, 207–210
Somatostatin receptor subtype 2 (SST2), 89
Somatotropinoma, 86
Sparsely granulated somatotroph tumors (SGSTs), 99
Sphenoid sinus, infrasellar macro-PAs/PitNETs, 169–170
Subcutaneous injections, 73
Supradiaphragmatic extension, macro-PA/PitNET with, 170–171
Suprasellar germinomas, 12–14
Testosterone (T), 227
Thyroxine (T4), 75
Topologically associated domain (TAD), 90
Transitional age
causes of, 31–32
diagnosis, 33
follow-up, 41–42
nutrition, 44–45
rhGH, treatment with, 39–41
safety, 42–44
stimulation tests, 34–38
Transsphenoidal (TS) corridor, 150
Transsphenoidal surgery/endoscopy, 150–152
Traumatic brain injury (TBI), 9
Tri-iodothyronin (T3), 75
Tumors/treatment-related changes, 12–15
Turner syndrome, 21
X-linked acrogigantism, 90–91
