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06.04.2014, admin  
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Growth Hormone Deficiency In Adults Gita Majdi, M.D, MRCP(UK) Endocrinology Fellow Western University November 2013. Growth Hormone Physiology: Somatotroph cells Somatotrophs are located predominantly in the lateral wings of the anterior pituitary gland Comprise between 35% and 45% of pituitary cells. Biosynthesis of Growth Hormone The human GH locus spans approximately 66 kilobases (kb) on the long arm of chromosome 17q22-24. Growth Hormone Assays Plasma GH is measured by RIA (polyclonal or monoclonal) or by IRMA (dual monoclonal). Growth Hormone Secretagogues and Ghrelin Hypothalamic somatostatin ( SRIF, Somatotropin release-inhibiting factor) and GHRH are secreted in independent waves and interact together with additional GH secretagogues to generate pulsatile GH release.
IGF 1 The IGFs (somatomedins) are a family of peptides that are, in part, GH dependent and mediate many of the anabolic and mitogenic actions of GH. GHBP Circulating growth hormone–binding proteins (GHBPs) include a 20-kd low- affinity GHBP and a 60-kd high-affinity GHBP. GH Action GH binds to the growth hormone receptor (GHR) dimer, which undergoes internal rotation, resulting in Jak2 phosphorylation (P) and subsequent signal transduction.
GH deficiency in Adults (1) GH is the most abundant hormone in the adult pituitary gland GHD in adults is recognized as a distinct entity.
GHD in Adults (2) The diagnosis of adult GHD is established by provocative testing of GH secretion Patients should receive adequate replacement for other pituitary hormonal deficits before testing.
Pathophysiology of Adult GHD Congenital Acquired causes: -50% arise from pituitary tumors -20% from extra pituitary tumors - 5% from inflammatory or infiltrative lesions - 15% of cases being idiopathic - Surgical or radiation treatment of pituitary and parasellar tumors is the most common cause of GHD, accounting for almost two thirds of cases. Presentation Of GHD in Adults Symptoms of GHD are nonspecific and include fatigue, lack of energy, social isolation, low mood, poor concentration, and reduced physical capacity. Diagnosis of GH deficiency in Adults Isolated GHD may be complete or partial Up to 67% of children initially diagnosed with idiopathic GHD had normal GH responses when subsequently retested as adults for GHD after cessation of GH treatment Therefore, children with GHD should be retested before GH treatment is continued into adulthood unless they have clearly documented panhypopituitarism or a defined genetic or developmental abnormality that causes complete and irreversible GHD.
Growth Hormone–Responsive Markers Growth hormone–responsive markers include IGF1, IGF binding protein 3 (IGFBP3), and the acid-labile subunit of the IGFBP complex. GH Therapy GH replacement improves exercise capacity and performance in cardiac output and diastolic function.
Growth Hormone Replacement Therapy Effects of recombinant human growth hormone (rhGH) replacement on lean body mass and fat mass in adults with GH deficiency. GH Therapy Computed tomographic scan through the abdomen before (top) and after treatment with human growth hormone (hGH) (bottom) in a GH-deficient patient. 1 Pediatric and Adolescent Outpatient Clinic, Quisisana Hospital, Ferrara, Italy2 Department of Pediatrics, Division of Endocrinology, Hamad General Hospital Doha, Qatar3 Department of Medical Physics, St.
The demographic, clinical, and laboratory data of the TM study population are presented in Table 1. It contains a cluster of five highly conserved genes, each consisting of five exons separated by four introns.

The cluster contains five genes, three PL and two GH genes that evolved from a common ancestral precursor by recombination events involving moderately repeated sequences.
The GHBPs function to dampen acute oscillations in serum GH levels associated with pulsatile pituitary GH secretion, and plasma GH half-life is prolonged by decreased renal GH clearance of bound GH.
Measured GH concentrations are antibody dependent, and different antibodies bind to a heterogeneous spectrum of GH isoforms. Ghrelin is a 28-amino-acid peptide that binds the GHS receptor to induce hypothalamic GHRH and pituitary GH. Ligand binding to a preformed GHR dimer results in internal rotation and subsequent phosphorylation cascades. GHD has negative effects on body composition, cardiovascular risk, quality of life, and physical functioning. Provocative tests include the insulin tolerance test (ITT), arginine, glucagon, clonidine, growth hormone–releasing peptide (GHRP), (GURP), and GHRH, alone or in combination with arginine or pyridostigmine. The signs are also nonspecific and include general and central adiposity, reduced lean tissue, and bone mineral density along with unfavorable biochemical changes such as hyperlipidemia and glucose intolerance. Serum IGF1 concentrations are useful for diagnosis only when age-adjusted normal ranges are used. Quadriceps or hip muscle strength improves significantly after 6 months of treatment, but muscle strength normalized after 2 years, without further significant change at 5 years. GH replacement induces profound effects on protein, fat, and energy metabolism, resulting in increased lean body mass and decreased fat mass without a significant change in body weight (Reproduced with permission from Salomon F, Cuneo RC, Hesp R, et al. Anna Hospital, Ferrara, Italy4 Department of Hematology, Alamal Hospital, Hamad Medical Center, Doha, Qatar5 Department of Paediatrics, Pugliese-Ciaccio Hospital, Catanzaro, Italy6 Department of Haematology, Thalassaemia and Prenatal Diagnosis Regional Center, Pugliese-Ciaccio Hospital, Catanzaro, Italy7 Department of Primary Health Care (PHC), Doha, Qatar8 Department of Pediatrics, Ain Shams University, Cairo, Egypt 9 St. Encode the various forms of human growth hormone (hGH) and human chorionic somatomammotropin.
Monomeric 22-kd GH1, the most abundant circulating form, is the only GH standard of sufficient purity and quantity, and it is used as the basis for GH measurement; however, it accounts for only about 25% of circulating immunoreactivity.
The GHBPs function to dampen acute oscillations in serum GH levels Plasma GH half-life is prolonged by decreased renal GH clearance of bound GH.
1- growth hormone (GH) stimulates production of insulin-like growth factor 1 (IGF-1); circulating IGF-1 (endocrine IGF-1) then acts at the growth plate. GH targets include insulin-like growth factor 1 (IGF1), c- fos, cell proliferation genes, glucose metabolism, and cytoskeletal proteins. Life expectancy is reduced in hypopituitary patients with GHD, largely as a consequence of cardiovascular and cerebrovascular events, especially in female subjects.
Some patients have established evidence of macrovascular disease, such as increased carotid intimal thickness. A large survey in 304 patients showed improved quality of life and also significant reduction in the numbers of sick leave and doctor visits during 12 months of GH therapy.

The effects of treatment with recombinant human growth hormone on body composition and metabolism in adults with growth hormone deficiency.
Polyclonal antibodies, used in earlier RIAs, recognized several molecular forms of GH; newer immunometric assays employ highly specific monoclonal antibodies. 2- GH regulates hepatic production of IGF- binding protein 3 (IGFBP-3) and the acid- labile subunit (ALS) of the IGFBP complex; IGF-1 binds to IGFBP-3 and with ALS, forming the 150-kd ternary complex. Neither estrogen nor thyroid deficiency accounts for this increased risk and reduced survival. As provocative tests vary in their ability to evoke GH release, a single value cannot be applied as a diagnostic threshold across different tests. GHD may also be associated with heart abnormalities including reduced left ventricular mass.
Reduce IGF1 levels are associated with malnutrition, liver disease, poorly controlled diabetes mellitus, and hypothyroidism. A latency period up to 3 months is required before patients recognize benefits of hGH replacement, and these benefits are most obvious in those patients with the most profound symptoms and signs of GHD. New GH assays based on measurement of GH bioactivity have been developed, including the eluted stain assay (ESTA) and the immunofunctional assay (IFA). Proteases then cleave this complex into fragments that release IGFBP-3 and IGF-1 in the intravascular space and at the growth plate. ITT is a more potent stimulator of GH release than arginine, clonidine, or l- dopa, and combinations such as arginine plus GHRH, or GHRP plus GHRH are more potent than ITT alone.
A subnormal IGF1 level in an adult patient with coexisting pituitary hormone deficits is strongly suggestive of GHD. 3- GH induces differentiation and local IGF-1 production, and IGF-1 acts via autocrine and paracrine mechanisms to stimulate cell division. The separation of IGF1 values between GH-deficient and normal subjects is greatest in the young. IGF1 measurements become less reliable as a biochemical marker of GHD in patients older than 50 years.
Measurement of IGFBP3 or the acid-labile subunit does not offer any advantage over that of IGF1. In patients with organic hypothalamic-pituitary disease, the prevalence of GHD is strongly linked to the number of pituitary hormone deficits, ranging from approximately 25% to 40% in those with no other deficit to 95% to 100% when more than three pituitary hormone deficiencies are present.
Patients with three or more pituitary hormone deficiencies and an IGF1 level lower than the reference range have a greater than 97% chance of being GH deficient and therefore do not require GH stimulation testing.

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