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Human insulin-like growth factor I (IGF-I) is a growth and differentiating factor produced by various adult and fetal tissues. In the kidney, it has been linked to the proliferative response of renal tubular and glomerular cells, following unilateral or partial nephrectomy, in acromegaly, in diabetes mellitus and in glomerulonephritis. To gain insight into the potential effects of IGF-I in human kidney, a quantitative analysis of IGF-I-binding sites was performed in fetal and adult tissue using 125I-IGF-I. The ligand consistently labelled renal cortex, medulla, and glomeruli while renal vessels were not uniformly marked. The highest affinity of binding sites was found in glomeruli (adult kidneys: Kd 24.7 +/- 5.1 pM; Bmax 5.2 +/- 0.5 fmol/mg tissue equivalent (TE); n = 4; fetal kidneys: Kd 17.0 +/- 2.5 pM; Bmax 4.5 +/- 0.7 fmol/mg TE; n = 4) and cortical tubules, while vessels and renal medulla (adult kidneys: kd 47 +/- 3.9 pM, Bmax 2.6 +/- 0.3 fmol/mg TE; n = 4; fetal kidneys: kd 41.6 +/- 9.2 pM, Bmax 3.5 +/- 0.4 fmol/mg TE; n = 3) had only about half the affinity of binding and a significantly reduced maximal capacity. The strong binding of 125I-IGF-I to glomeruli supports the view that IGF-I may be involved in modulating glomerular structure and function. Fetal renal growth may depend on the action of IGF-I on glomerular cells and tubular epithelia of the kidney.
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PMID:Localization and characterization of IGF-I receptors in fetal and adult human kidneys. 146 71

Growth hormone (GH) levels were measured after a 75g oral glucose load (OGTT) in normal adults, patients with impaired glucose tolerance (IGT), insulin-dependent diabetes mellitus (IDDM) and acromegaly. Nadir GH levels at 2-hour post-OGTT in normal subjects ranged from 0.4 to 8.4 mIU/L, the 95% confidence interval being 0.4-4.4 mIU/L. In IGT and IDDM subjects basal fasting GH levels were not significantly different from normal and did not alter during OGTT. The high fasting GH level measured in one each of the IGT and IDDM patients was suppressible at 1-hour after glucose intake. In contrast, acromegalic patients had elevated fasting GH levels (11.8-178 mIU/L) although in 3 patients, the levels were mildly elevated and overlapped with normal. OGTT failed or only partially suppressed GH secretion in all acromegalics. Therefore, elevated fasting GH levels are not diagnostic and OGTT is required for accurate diagnosis and assessment of treatment of acromegalic patients.
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PMID:Evaluation of suppression of growth hormone levels following a 75g oral glucose tolerance test. 149 29

Treatment with Sandostatin is established in acromegaly, thyroid-stimulating hormone (TSH)-producing pituitary, and endocrine-active gastroenteropancreatic tumors. Potential indications include ectopic hormone syndromes, medullary thyroid carcinomas, pituitary resistance to thyroid hormones, tall stature children, diabetes mellitus and diabetic complications, polycystic ovary syndrome, and Graves' ophthalmopathy. Particularly in the ectopic growth hormone-releasing hormone (GHRH) syndrome, Sandostatin is unequivocally effective and, in the ectopic corticotropin syndrome selected cases can be treated successfully with Sandostatin, leading to marked clinical improvement. In many of the above situations, only subgroups show a response to Sandostatin, which may be identified by scintigraphy with labeled Sandostatin. This pertains also to Graves' ophthalmopathy, for which Sandostatin may be particularly promising and where positive and negative Sandostatin scans have been demonstrated. However, for all these potential indications, larger, well-studied series are needed, before definitive conclusions can be drawn.
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PMID:Potential indications for octreotide in endocrinology. 151 41

Acromegaly is an uncommon disorder and may present in a variety of ways, leading to considerable delay in diagnosis. Unlike other pituitary tumors, tumors associated with acromegaly tend to be fairly large in most patients. Thus, symptoms may be commonly due to the tumor mass as well as to hormone oversecretion. Mortality is two- to threefold increased due to cardiovascular, respiratory, and neoplastic causes. An increase in diabetes mellitus and hypertension may contribute to the first of these. Early treatment may reverse the diabetes, soft tissue changes, sleep apnea, cardiovascular disease, and neuromuscular disease. The effect of early treatment on neoplasia is unclear, and patients probably should continue to be screened, especially for colon neoplasia, even after appropriate therapy for the acromegaly. Hypopituitarism may be present initially as a result of tumor mass but may also develop as a result of ablative therapy.
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PMID:Clinical manifestations of acromegaly. 152 14

The authors report a very rare case of pituitary adenoma producing both GH and ACTH. A 29-year-old female was admitted with obesity, amenorrhea, acromegaly, hirsutism, excessive pigmentation, acne, and diabetes mellitus. Computed tomography revealed an intrasellar tumor 16 mm in height, with a destroyed sellar floor. The blood concentrations of GH, ACTH and cortisol were increased (GH: 92 ng/ml, ACTH: 94 pg/ml, cortisol: 18.3 micrograms/dl). No diurnal variation in the amount of cortisol was observed. The urinary 17-OHCS was suppressed by 8 mg but not by 2 mg of dexamethasone. A subtotal adenomectomy was then performed through the transsphenoidal approach, which led to a sufficient reduction of both blood GH and ACTH (cortisol). Histologically the tumor was an acidophilic pituitary adenoma. Immunoperoxidase staining showed diffuse GH and sporadic ACTH producing cells, but failed to show any cells producing both hormones. The electron micrograms of neoplastic cells showed the ultrastructural characteristics of respective GH and ACTH cells. Another increase in both GH and cortisol, which occurred 19 months after the operation, has been controlled by bromocriptine administration. This case may be the first reported case of a pituitary adenoma producing both GH and ACTH, not accompanied by prolactin (PRL) hypersecretion, which has been fully confirmed endocrinologically and histopathologically.
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PMID:A case of pituitary adenoma producing both growth hormone (GH) and adrenocorticotropic hormone (ACTH). 166 12

Many endocrine diseases can cause fatigue. Tiredness is a frequent symptom of primary and secondary hypothyroidism, hyperthyroidism, excessive glucocorticoid or mineralocorticoid production, primary and secondary adrenal insufficiency, primary and secondary hypogonadism and hyperprolactinemia in the male, acromegaly, diabetes mellitus and diabetes insipidus. A great number of medical diseases other than those mentioned in the articles on cardiological and pneumological fatigue can also cause abnormal tiredness (infectious diseases, hematological, renal, hepatic, gastrointestinal and rheumatological disturbances, vasculitis and malignant tumors). The pathogenesis of tiredness caused by endocrine or medical illnesses, i.e. how the sensation of fatigue is produced, is not clear. The fatigue of the various endocrine or other medical diseases is not disease-specific, i.e. its characteristics do not differentiate it from the fatigue of other illnesses.
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PMID:[Endocrine and other medical causes of abnormal fatigability]. 175 71

Growth hormone (GH) counteracts in general the effects of insulin on glucose and lipid metabolism, but shares protein anabolic properties with insulin. Under physiological circumstances GH does not affect total glucose turnover directly. There is however evidence that GH acutely decreases glucose oxidation (secondary to an increase in lipid oxidation) and suppresses muscle uptake of glucose, suggesting that GH redistributes glucose fluxes into a non-oxidative pathway, which could be a build up of glycogen depots through gluconeogenesis. Since GH secretion is inhibited in the fed state these actions are mainly important in the postprandial or fasting state. Under pathological conditions of GH excess (e.g. acromegaly, poorly controlled tp. 1 diabetes or high dose GH treatment) the diabetogenic actions of GH become apparent. In these patients increased endogenous glucose production, decreased muscle glucose uptake and rising blood glucose levels are observed. In patients with intact beta-cell function these changes are counterbalanced by hyperinsulinemia--such hyperinsulinemia may in the long term induce increased cardiovascular morbidity and mortality ('Reavens syndrome X'). When stimulated with insulin these patients exhibit insulin resistance at the liver, in adipose tissue and in muscle. Few elaborate studies on the effects of GH on glucose metabolism in GH deficient patients have been conducted. These patients are hypersensitive to the actions of insulin on glucose metabolism and there is some evidence that when GH initially is given to such patients in the GH deprived state, paradox insulin-like effects of GH may be observed. Whether this may relate to increased activity of insulin-like growth factors is unsettled.
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PMID:Effects of growth hormone on glucose metabolism. 180 81

Often, the source of a musculoskeletal problem can be traced to an endocrine disorder. For example, carpal tunnel syndrome is not uncommon in patients who are pregnant or have diabetes, hypothyroidism, or acromegaly. Joint problems and arthritis are other common findings in diabetes, pregnancy, and hyperparathyroidism. Muscle weakness or stiffness is seen in both hypothyroidism and hyperthyroidism, and muscle wasting is a characteristic of adrenocorticoid insufficiency. Bone disorders are common with glucocorticoid excess, acromegaly, and hyperparathyroidism. Some presentations are a classic picture of a specific endocrine condition and are readily recognized if the index of suspicion is appropriately high.
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PMID:Musculoskeletal disorders. When are they caused by hormone imbalance? 194 4

Radionuclides provide sensitive reporter molecules for labeling pharmaceuticals. Hormone measurements using radioimmunoassays are commonplace today, increasing our understanding of the pathophysiology of endocrine disease. In turn, hormones tagged with radionuclides are opening studies on new fields of receptor defects both at the receptor site and beyond. Common disorders such as diabetes mellitus, hyperthyroidism and acromegaly have been the first to benefit. Tracer methods to study secretory and clearance rates and the size of metabolic pools are mainly based on the use of radionuclides. DNA probes are useful in unravelling endocrine defects at the genome level. Originally using radioiodine but now an increasing number of newly synthesised radiopharmaceuticals, the individual organs are being visualised more specifically. Among these agents are labelled monoclonal antibodies hunting for neoplasias and analogs of adrenal medullary hormones such as metaiodobenzylguanidine (MIBG). From these studies the therapy of endocrine disorders will ultimately benefit.
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PMID:Use of radionuclides in clinical endocrinology. 197 63

The manifestations of endocrine derangements in the musculoskeletal system in infancy and childhood are disturbances in growth and maturation and in adulthood are disturbances in maintenance and metabolism. Hypercortisolism during skeletal immaturity suppresses growth. In the adult, hypercortisolism leads to osteoporosis, osteonecrosis, and muscle wasting. Deficiency of growth hormone during skeletal development results in short stature. An excess of growth hormone in a skeletally immature individual results in gigantism, an excess in a skeletally mature individual results in acromegaly. Patients with gigantism have extreme height with normal body proportions. Musculoskeletal manifestations of acromegaly include soft-tissue thickening, vertebral body enlargement, characteristic hand and foot changes, and enthesal bony proliferation. Hyperthyroidism causes catabolism of protein and loss of connective tissue, which manifest as muscle wasting. Deficient levels of thyroid hormone cause defects in growth and development. Severe growth retardation from congenital hypothyroidism is rare because neonatal screening recognizes the disorder and leads to early treatment. The skeletal manifestation of hypergonadism in children is precocious growth and early skeletal maturation. Although the initial precocious growth spurt results in a tall child, early closure of the growth plates results in a short adult. Hypogonadism in the prepubertal child results in delayed adolescence and delayed skeletal maturation. Diabetes mellitus in childhood results in decreased growth, a phenomenon presumed to be secondary to nutritional abnormalities. Generalized osteoporosis and short stature are common. In the adult, generalized osteoporosis may accompany insulin-dependent diabetes mellitus if obesity is absent. Calcification of interdigital arteries of the foot is common in diabetics and uncommon in other conditions. Additional skeletal manifestations relate to complications of diabetes such as peripheral neuropathy and diabetic foot disease.
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PMID:Radiologic manifestations in the musculoskeletal system of miscellaneous endocrine disorders. 198 24


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