Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatomedins are polypeptide hormones (MW: 7500 Daltons) whose plasma concentrations are largely governed by growth hormone secretion. Somatomedins stimulate cartilage growth and mitosis and growth of several extraskeletal cell types. Somatomedins also display insulin-like activity in adipose tissue. Presently four different human somatomedins are known. Somatomedin C (SmC) and insulin like growth factor I (IGF I) turned out to be identical peptides. TO a large extent they are regulated by growth hormone. Thus they mediate growth hormone action at the tissue level. Insulin-like growth factor II (IGF II) is only minimally dependent on growth hormone secretion. Its definite biological role for growth remains to be established. The somatomedins are bound to larger carrier proteins in the circulation. Somatomedins are synthesized in mesenchymal cells of multiple organs, especially in the liver and kidneys. Somatomedins are of clinical relevance for the diagnosis of growth disturbances due to pituitary disorders. In pituitary dwarfism radioimmunological SmC/IGF plasma levels are decreased whereas in acromegaly they are increased. In a small percentage of patients both with pituitary dwarfism and acromegaly normal SmC/IGF I concentrations are encountered. These facts demonstrate that SmC/IGF I determinations cannot replace common diagnostic procedures in the analysis of growth disorders. The reliability of low SmC/IGF I concentrations is limited in conditions like low-calorie malnutrition, malabsorption, various storage diseases, hypothyroidism, chronic liver and kidney diseases, because in these disorders low SmC/IGF I plasma concentrations occur despite high growth hormone levels.
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PMID:[Somatomedins and their significance in pediatrics]. 390 54

It has been shown by others that offspring of mothers who had been exposed to dioxins and polychlorinated biphenyls (PCBs) during pregnancy have elevated plasma levels of thyroid-stimulating hormone (TSH) for at least 3 months after birth and reduced plasma levels of free and total thyroxine during the second week after birth. As elevated levels of dioxins and PCB s can thus alter thyroid hormone status, the relation between the levels of some polychlorinated organic compounds in the blood lipids and growth and thyroid hormone status was studied in 12 hospitalized schoolchildren from the Aral Sea region known to have high exposure to such compounds. Their level of PCBs was two to four times higher than in healthy Stockholm children. Their height was found to be lower than in healthy Swedish children of the same age mean (SDS -0.52) and the body mass index (BMI) was inversely correlated to the total concentrations of PCBs and dichlorodiphenyltrichloroethane (DDT) and its metabolite dichlorophenyldichloroethylene (DDE) in the blood lipids. As the levels of insulin-like growth factor- were reduced to the same extent as the BMI it seems likely that PCBs and DDT cause malnutrition as a result of malabsorption. None of the children had any impairment of thyroid function, as revealed by the plasma levels of TSH and thyroxine. Although the concentrations of beta-hexachlorocyclohexane (beta-HCH) and DDE were extremely high in some of the children there was no relation between thyroid hormone status and the blood lipid levels of PCBs, hexachlorocyclohexane and DDT. However, the concentration of dioxins was not analysed.
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PMID:Chlorinated contaminants, growth and thyroid function in schoolchildren from the Aral Sea region in Kazakhstan. 976 96

Osteoporosis is increasingly recognised in men. Low bone mass, risk factors for falling and factors causing fractures in women are likely to cause fractures in men. Bone mass is largely genetically determined, but environmental factors also contribute. Greater muscle strength and physical activity are associated with higher bone mass, while radial bone loss is greater in cigarette smokers or those with a moderate alcohol intake. Sex hormones have important effects on bone physiology. In men, there is no abrupt cessation of testicular function or 'andropause' comparable with the menopause in women; however, both total and free testosterone levels decline with age. A common secondary cause of osteoporosis in men is hypogonadism. There is increasing evidence that estrogens are important in skeletal maintenance in men as well as women. Peripheral aromatisation of androgens to estrogens occurs and osteoblast-like cells can aromatise androgens into estrogens. Human models exist for the effects of estrogens on the male skeleton. In men aged > 65 years, there is a positive association between bone mineral density (BMD) and greater serum estradiol levels at all skeletal sites and a negative association between BMD and testosterone at some sites. It is crucial to exclude pathological causes of osteoporosis, because 30 to 60% of men with vertebral fractures have another illness contributing to bone disease. Glucocorticoid excess (predominantly exogenous) is common. Gastrointestinal disease predisposes patients to bone disease as a result of intestinal malabsorption of calcium and colecalciferol (vitamin D). Hypercalciuria and nephrolithiasis, anticonvulsant drug use, thyrotoxicosis, immobilisation, liver and renal disease, multiple myeloma and systemic mastocytosis have all been associated with osteoporosis in men. It is possible that low-dose estrogen therapy or specific estrogen receptor-modulating drugs might increase BMD in men as well as in women. In the future, parathyroid hormone peptides may be an effective treatment for osteoporosis, particularly in patients in whom other treatments, such as bisphosphonates, have failed. Men with idiopathic osteoporosis have low circulating insulin-like growth factor-1 (IGF-1; somatomedin-1) concentrations, and IGF-1 administration to these men increases bone formation markers more than resorption markers. Studies of changes in BMD with IGF-1 treatment in osteoporotic men and women are underway. Osteoporosis in men will become an increasing worldwide public health problem over the next 20 years, so it is vital that safe and effective therapies for this disabling condition become available. Effective public health measures also need to be established and targeted to men at risk of developing the disease.
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PMID:Osteoporosis in men. New insights into aetiology, pathogenesis, prevention and management. 988 98

Increased cytokine release and increased activity of osteoclasts (reduced osteoclast apoptosis) due to a fall in estrogen is of causal significance in postmenopausal bone loss as well as malfunction of the vitamin D activation and concomitant calcium (Ca) malabsorption. Alfacalcidol prevents rapid postmenopausal bone loss by elimination of Ca malabsorption and by blocking resorbing cytokines. Established osteoporosis in older patients of both sexes is characterized by decoupled bone remodeling induced by sex hormone deficits and by a so-called somatopause (insulin-like growth factor [IGF]-deficit), but also by lack of vitamin D and, very importantly, by reduced synthesis of D-hormone (Calcitriol) in kidneys and bone as well as by a lack of receptors or receptor affinity for D-hormone in the target organs. As a consequence of these facts, a rise in parathormone (PTH) frequently occurs. The lack of D-hormone and IGF-1 evidently causes a reduction in muscle strength as well and reinforces the risk of falling and, thus, the risk of a fracture. Alfacalcidol, a prodrug of D-hormone, is a specific antiosteoporotic therapy. In alfacalcidol therapy, D-hormone is provided to the body in circumvention of its own regulation, by means of which much higher hormone concentrations can be achieved in the target tissues than by administration of plain vitamin D. Chances have been significantly improved of reducing and frequently preventing the real osteoporosis complication for older male and female patients, i. e., bone fractures, by alfacalcidol. A clear distinction should be made between supplementation with low-dosed plain vitamin D and calcium as base supply in elderly housebound subjects or as adjuvant to antiosteoporotic drugs and the specific antiosteoporotic therapy with alfacalcidol in patients with osteoporosis. The expanded understanding of the pathogenesis of corticosteroid-induced osteoporosis with its disturbed Ca homeostasis and the pharmacological effects of alfacalcidol, counteracting such iatrogenic bone loss, explain the particularly good clinical efficacy in this most frequent form of secondary osteoporosis. Normalizing de-coupled bone remodeling due to cytokine modulation and the potential influence on deteriorated bone quality in patients with rheumatoid arthritis and Crohn's disease predestine this form of therapy for prevention and treatment of osteoporosis as a result of chronic inflammatory diseases as well as of transplantation osteoporosis cases in particular.
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PMID:Rationale for treatment of involutional osteoporosis in women and for prevention and treatment of corticosteroid-induced osteoporosis with alfacalcidol. 1048 85

Delayed onset of puberty and a reduced pubertal growth spurt are often reported in patients suffering from chronic diseases. The basis of abnormal puberty in these patients is multifactorial. Nutritional deficiency may contribute to growth disorders and delayed puberty. Insufficient food supply and/or eating disorders and/or malabsorption of nutrients can be observed in these patients. Moreover, increased energy supplies are often needed in patients with chronic lung disease, infection or inflammation. More specific factors due to the disease itself may be involved in growth and puberty disorders. Abnormalities of the growth hormone (GH)-insulin-like growth factor (IGF)1 axis and gonadotrophin secretion have been described in patients with chronic renal failure, cystic fibrosis and Crohn's disease. More recently, it has been shown that cytokines produced during chronic diseases such as juvenile idiopathic arthritis may affect the GH-IGF1 axis. Finally, concomitant medication, namely corticosteroids, which are often given to these patients, may contribute to delayed puberty and poor pubertal growth.
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PMID:Puberty in chronically diseased patients. 1206 28

Multiple growth hormones (GHs) and factors are relevant to inflammatory bowel disease (IBD) due to their trophic effects on epithelial cells to promote mucosal integrity, renewal, and repair, on mesenchymal cells to promote wound healing, and on intestinal immune cells to modulate inflammation. The anabolic effects of GHs and factors outside the intestine are relevant to minimizing nutritional insufficiency, catabolic state, and the inability to maintain body weight due to inflammation-induced malabsorption. GHs and factors can, however, have a dual role, whereby trophic effects can be beneficial but, if excessive, can promote complications including the increased risk of intestinal tumors/adenocarcinoma and fibrosis. This review focuses on GH and insulin-like growth factor (IGF-I), for which evidence suggests such a dual role may exist. The actions of GH and IGF-I on the healthy intestine are compared with effects during intestinal inflammation or associated complications. Interactions between these growth factors and others relevant to IBD are considered. The role of the newly discovered suppressors of cytokine signaling proteins, which may dictate the balance between beneficial and excessive actions of GH and IGF-I, is also addressed.
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PMID:Growth factors in inflammatory bowel disease: the actions and interactions of growth hormone and insulin-like growth factor-I. 1562 5

It is well known that insulin resistance affects osteodystrophy, and there is an important relationship between insulin resistance and hepato-biliary disease. It is also well known that hepato-biliary and pancreatic disease is associated with osteodystrophy. In the present review, we describe the mechanism of diabetes and osteodystrophy due to hepato-biliary and pancreatic disease. Hepatic osteodystrophy is associated with malabsorption, abnormalities of vitamin D metabolism, inflammatory cytokines, receptor activator of NF-kappaB ligand, and insulin-like growth factor-1. In particular, tumor necrosis factor-alpha and malabsorption are important factors for viral and alcoholic hepatitis, respectively. Malabsorption due to steatorrhea is important for cholestatic disease and chronic pancreatitis. A greater focus on non-alcoholic steatohepatitis (NASH) and further investigations to clarify the relationship between osteodystrophy and NASH are needed.
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PMID:[Hepato-biliary and pancreatic disease and osteodystrophy]. 1972 Nov 98