Suppressor of cytokine signaling (SOCS) 2, a negative regulator of growth hormone (GH) and insulin-like growth factor 1 (IGF-1), which is associated with acromegaly and cancers, is a promising candidate molecule for treating various diseases.
A low secretory activity of these tumours might explain the normal plasma values for GH and insulin-like growth factor 1 (IGF1) and the absence of clinical signs of acromegaly.
The aim of this study was to test whether the relationship between GH and insulin-like growth factor-1 (IGF-1) concentrations is influenced by the GHR genotype in patients with acromegaly.
Acromegaly is a rare disease generally brought about by a benign tumour in the pituitary and characterized by growth hormone (GH) and insulin-like growth factor 1 (IGF-1) excess.
Although follow-up for the vast majority of these children does not yet extend beyond young adulthood, a slight increase in cancers in those with long-standing excess GH secretion (as seen in patients with acromegaly) and no overall increase in cancer with insulin treatment, have been observed.
The ratio of plasma peak GH induced by TRH administration to the basal level of plasma GH in the patients with acromegaly correlated positively with the level of TRHR-1 mRNA expression in their GH-producing adenomas (r = 0.620, P = 0.0179).
The Patient was considered as having "acromegaloidism", a term used for patients whom manifest clinical features of acromegaly but do not present a demonstrable growth hormone hypersecretion.
In conclusion, IGF1, but not GH, has pro-inflammatory effects, probably via the MAPK signalling pathway and might be involved in the pathogenesis of atherosclerosis in acromegaly.
Direct mitogenic properties of GH-IGF-1 axis on bone marrow progenitor cells may very rarely lead to erythroid hyperplasia and subsequent polycythaemia, reversible with successful therapy of acromegaly.
Improvements in understanding the structure-function relationship of the human GH molecule and of the interplay of the hormone with its receptor make it conceivable that recombinant analogues of human GH will be designed to inhibit the effects of GH excess in acromegaly.(ABSTRACT TRUNCATED AT 250 WORDS)
Increased secretion of growth hormone leads to gigantism in children and acromegaly in adults; the genetic causes of gigantism and acromegaly are poorly understood.
Acromegaly is characterized by growth hormone (GH) and insulinlike growth factor-1 (IGF-1) hypersecretion, and GH and IGF-1 play important roles in regulating body composition and glucose homeostasis.
The history of frequent and excessive administration of a progestational agent suggested that the progestational drug induced the acromegaly.During the monitoring period. soft tissue changes diminished and there was normalization of several factors: plasma growth hormone concentration, response of plasma insulin and glucose to an oral glucose load, and response of plasma glucose hormone to the injection of insulin.
The mean age of the 30 acromegaly patients (M/F:14/16) was 47.26 ± 12.52 years (range: 18-64 years) and that of the healthy volunteers (M/F: 17/13) was 44.56 ± 10.74 years (range: 19-62 years).Insulin-like growth factor-1 (IGF-1) and growth hormone (GH) levels were measured using an electrochemiluminescence method, and serum sclerostin levels using an enzyme-linked immunosorbent assay.The Mann-Whitney U test was used to compare sclerostin levels between the two groups.
Our data indicates that tissue-level properties of cortical bone are significantly altered in patients with controlled acromegaly after reversal of long-term exposure to pathologically high GH and IGF-1 levels.
Silent somatotroph pituitary neuroendocrine tumors (or silent growth hormone pituitary neuroendocrine tumors, SGH-PitNET) are neoplasias with positive immunostaining for growth hormone (GH), in patients with no signs and symptoms of acromegaly nor biochemical evidence of GH hypersecretion.
Defects in the axis' activity during childhood result in growth abnormalities, while increased secretion of GH from the pituitary results in acromegaly.
In the present study, the authors analyzed polysialylated NCAM expression in 82 pituitary tumors from humans: 49 secreting adenomas, 32 nonfunctioning adenomas, and one growth hormone and prolactin-secreting carcinoma associated with acromegaly and spinal and liver metastases.