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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diabetes epidemic continues unabated, leading to an increasing number of acute and chronic complications, including sight-threatening proliferative diabetic retinopathy. Currently, there is no accepted pharmaceutical therapy for diabetic retinopathy besides nearnormal glycemia, treatment of hypertension, and dyslipidemia. For an effective treatment of retinopathy, one would recommend a concept leading to the downregulation of endogenous angiogenic stimulators and the upregulation of endogenous angiogenic inhibitors, resulting in a restoration of the balance in angiogenic control. The naturally occurring growth hormone inhibitor, somatostatin, has been suggested as candidate for developing novel therapies. Somatostatin may exert its antiangiogenic effects, both through antagonism of the growth hormone axis and through direct antiproliferative and apoptotic effects on endothelial cells. Therefore, the use of long-acting somatostatin analogues will lead to an upregulation of antiangiogenic signaling. Use of long-acting somatostatin analogues in diabetic retinopathy would be an important extension of the initial concept that somatostatin is a regulator of growth hormone secretion only. Currently available analogues have already allowed to modulate the expression of diabetic retinopathy at various disease stages. Somatostatin analogues remain the only nondestructive therapeutic alternative to patients with proliferative diabetic retinopathy who have failed to respond to panretinal photocoagulation.
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PMID:Use of long-acting somatostatin analogue treatment in diabetic retinopathy. 1724 82

The adult growth hormone deficiency (GHD) syndrome is a well-defined clinical entity. Although the symptoms of GHD are not age specific, their relative importance differs depending on the patient's age, and the impact of GHD varies throughout adult life. Ceasing growth hormone (GH) therapy soon after final height in patients with severe GHD potentially limits somatic development by reducing accrual of bone and muscle mass. It is now recognized that the continuation of GH therapy in the transition years is required to achieve adult levels of somatic development. In middle age, the most worrying feature of GHD is the increase in cardiovascular risk, an important component of which is GHD-related dyslipidemia. One of the most profound effects of GH therapy in this age group is the durable reduction in cholesterol levels. Elderly GH-deficient patients experience the symptoms of GHD over and above the signs of normal aging. Perhaps most importantly, these patients have impaired quality of life, with fatigue as a major component. Evidence is growing for improved quality of life with GH therapy in the elderly. This review describes the diagnosis, symptoms and treatment of GHD specific to the different age groups.
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PMID:Growth hormone replacement throughout life: insights into age-related responses to treatment. 1756 Jan 53

The hormones with a strong influence on the lipid spectrum and the development of atherosclerosis include cortisol, growth hormone and oestrogens. Cortisol accelerates atherosclerosis both through dyslipidemia and through an increase in visceral fat, hypertension, increased insulin resistance and the development of reduced glucose tolerance which may result in diabetes mellitus. Even when a cortisol excess disappears, as is the case of patients cured of Cushing syndrome, arterial walls remain permanently vulnerable to the atherosclerotic process. In conditions involving a lack of growth hormone, dyslipidemia develops and increases the burden on the cardiovascular system if not treated in a timely manner by the substitution of growth hormone. Oestrogens have a double effect: they have an anti-atherogenic effect on artery walls that are not yet damaged by an atherosclerotic process, but where atherosclerosis has already developed they have a prothrombotic effect and destabilise the atheromatous plaques. If oestrogen is to be used as protection against the onset of atherogenesis, it is necessary to start in a period when the atherosclerotic process has not yet begun to damage the woman's arterial walls and it is best to use natural hormones (estradiol) and to prevent endometriosis it should be combined with crystalline progesterone applied locally--inravaginally. Oestrogens should be given in small doses, preferably parenterally. Even this will not prevent genetic oestrogen effects though.
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PMID:[How corticoids, growth hormone and oestrogens influence lipids and atherosclerosis]. 1757 71

Approximately half of patients with HIV-infection develop abnormal body fat distribution, characterized by increased abdominal, breast, and dorsocervical adiposity and decreased fat in the limbs and face in association with antiretroviral therapy. Changes in fat distribution are associated with dyslipidemia, insulin resistance, and increased cardiovascular risk in patients with HIV lipodystrophy. Growth hormone secretion is reduced and responses to standardized stimulation testing altered, suggesting relative growth hormone deficiency in this population. Growth hormone secretion is characterized by normal pulse frequency, but decreased pulse amplitude, pulse width, and trough GH levels compared to weight matched, non-HIV-infected patients. Abnormalities in GH secretion are strongly associated with body composition and metabolic abnormalities in patients with HIV lipodystrophy, particularly with increased visceral fat and elevated free fatty acids. Increased somatostatin tone and decreased ghrelin concentrations may also contribute to reduced GH levels. Administration of exogenous GH or growth hormone releasing hormone (GHRH) to normalize growth hormone concentrations is effective to reduce visceral fat and improve lipid parameters in HIV-infected patients. Treatment with supraphysiologic GH is limited by side effects and exacerbation of insulin resistance, whereas administration of physiologic doses of GH demonstrates more modest treatment effects but fewer adverse effects. Initial studies of GHRH also show significant reductions in visceral adipose tissue (VAT) with potentially fewer adverse effects. GHRH may be particularly useful to normalize GH dynamics in patients with HIV lipodystrophy by increasing endogenous GH pulse height, GH pulse width, and trough GH levels, while preserving the negative feedback of IGF-I on pituitary GH secretion.
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PMID:GH/GHRH axis in HIV lipodystrophy. 1827 Aug 41

The role of hormonal and metabolic alterations in HIV-associated lipodystrophy syndrome is not yet clear. In patients with HIV-1 undergoing antiretroviral treatment, lipodystrophy is associated with peripheral fat wasting and central adiposity, dyslipidemia, insulin resistance, and increased intramuscular fat accumulation. In HIV lipodystrophy, changes in fat distribution are heterogeneous and can include reduced subcutaneous fat as well as increased visceral fat. In the literature, there is evidence showing that overnight growth hormone (GH) secretion and pulse amplitude decrease in patients with HIV lipodystrophy, with rates of response to standardized GH stimulation being abnormal in at least 20% of these patients. Excess accumulation of visceral fat, central obesity, and increased intra-abdominal adiposity are also typical features of patients with GH deficiency. Recombinant human GH (rhGH) is a potential treatment to diminish excess visceral fat. Our group recently demonstrated that GH therapy in HIV-infected patients with syndromes of fat accumulation produced a significant decrease in body fat and a gain in lean tissue. In this article, we discuss the origin of lipodystrophy in HIV patients, and the use of rhGH treatment (benefits and adverse effects) in HIV-related lipodystrophy.
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PMID:Recombinant human growth hormone: rationale for use in the treatment of HIV-associated lipodystrophy. 1834 7

The cluster of cardiovascular risk factors-abdominal obesity, dyslipidaemia, insulin resistance and hypertension-has been recognized as the core of the metabolic syndrome. Adults with severe growth hormone (GH) deficiency have, to a large extent, features of the metabolic syndrome, and there is a strong inverse association between visceral fat accumulation and blunted GH secretion in adults. Hyposomatotropism in abdominal obesity has therefore been suggested to be of importance for its metabolic consequences. However, the underlying pathophysiological mechanisms are poorly understood. Prevalence of the metabolic syndrome is steadily increasing worldwide. Overnutrition and sedentary habits are the stigmata of modern society that predispose genetically susceptible individuals to develop central obesity and other features of the metabolic syndrome including glucose intolerance, hypertension and dyslipidemia. Although there are still no unified definitions of the syndrome, it is clear that this condition is associated with an increased risk for development of cardiovascular disease (CVD) and diabetes mellitus (DM). In this review, we discuss current evidence regarding alterations in the GH-IGF- 1 axis in abdominal obesity and its possible impact on other features of the metabolic syndrome.
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PMID:The GH/IGF-1 Axis in Obesity: Physiological and Pathological Aspects. 1837 Jul 71

Patients with adult growth hormone deficiency apparently can develop a clinical picture with pronounced obesity, dyslipidemia, decreased bone density, and increased fracture rate as well as psychosocial limitations irrespective of the loss and replacement of further hypophyseal axes. The extent of these changes is strongly dependent on interindividual variations. Retrospective analyses have indicated a possibility of elevated morbidity and mortality among this patient cohort which can be due to the proatherogenic alterations (central obesity, dyslipidemia). Treatment with recombinant growth hormone in controlled trials resulted in evident improvement in quality of life, better body composition and lipid profile as well as an increase in bone density. Whether these improvements will also pay off in terms of reduction of endpoints (decline in fracture rates, decrease of cardiovascular morbidity and mortality) has not yet been confirmed by controlled studies. When administered at low doses, titrated according to the IGF-1 level, growth hormone replacement appears to be a safe and well-tolerated therapeutic regimen.
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PMID:[Growth hormone therapy in adults. Attempt to assess a decade of use]. 1841 67

The secondary occurrence of type 2 diabetes with various hormonal diseases (e.g. pituitary, adrenal and/or thyroid diseases) is a recurrent observation. Indeed, impaired glucose tolerance (IGT) and overt diabetes mellitus are frequently associated with acromegaly and hypercortisolism (Cushing syndrome). The increased cardiovascular morbidity and mortality associated with acromegaly and Cushing syndrome may partly be a consequence of increased insulin resistance that normally accompanies hormone excess. Acromegalic patients are insulin resistant, both in the liver and in the periphery, displaying hyperinsulinemia and increased glucose turnover in the basal post-absorptive states. The prevalence of diabetes mellitus and that of IGT in acromegaly is reported to range 16-56%, whereas the degree of glucose tolerance seems correlated with circulating growth hormone (GH) levels, age, and disease duration. Moreover, a family history of diabetes and concomitant presence of arterial hypertension have been found to predispose to diabetes as well. GH has physiological effects on glucose metabolism, stimulating gluconeogenesis and lipolysis, which results in increased blood glucose and free fatty acid levels. Conversely, insulin-like growth factor 1 (IGF-I) enhances insulin sensitivity primarily on skeletal muscles. However, in acromegaly, increased IGF-I levels are unable to counteract the insulin-resistance status determined by GH excess. Therapy with somatostatin analogues (SSAs) induce control of GH and IGF-I excess in the majority of patients, but their inhibitory effect on pancreatic insulin secretion might complicate the overall effect of this treatment on glucose tolerance. Hypercortisolism produces visceral obesity, insulin resistance, and dyslipidemia that together with hypertension, hypercoagulability, and ventricular morphologic and functional abnormalities increase cardiovascular risk, and persist up to 5 years after resolution of hypercortisolism. Hypercortisolism leads to hyperglycaemia and reduced glucose tolerance, determines insulin resistance, stimulates hepatic gluconeogenesis and glicogenolisis. In Cushing syndrome the prevalence of diabetes varies between 20 and 50%, but probably this prevalence is underestimated, as not always an oral glucose tolerance test is performed in the presence of an apparently normal fasting glycaemia. Again, disease duration, rather than hormone levels, seems to be the major determinant in the occurrence of systemic complications in Cushing syndrome. Due to the impact they have on mortality and morbidity in both acromegaly and Cushing syndrome, these complications should be treated aggressively. In patients with neuroendocrine tumours (NETs) the occurrence of altered glucose tolerance may be due to a decreased insulin secretion, like it happens in patients who underwent pancreatic surgery and in those with pheochromocytoma, or to an altered counterbalance between hormones, such as in patients with glucagonoma and somatostatinoma. Moreover, SSAs represent a valid therapeutic choice in the symptomatic treatment of NETs, and also in this case the medical therapy of the primary disease, may have a significant impact on the prevalence of glucose metabolism imbalance. In thyroid disorders, an abnormal glucose tolerance may be principally encountered in hyperthyroidism. The pathogenesis is complex and scant data on prevalence and severity are found in the literature. Adequate treatment for glucose imbalance is mandatory in these peculiar patients in line with the American Diabetes Association and the European Association for the Study of Diabetes consensus statement. In particular, since traditional insulins have two features that may complicate therapy (absorption profiles, delayed onset of action and peak activity), the new insulin analogues could be of particular interest in the management of the secondary diabetes associated with endocrinopathies, considering the frailty of these patients. Indeed, it has been demonstrated that insulin glargine, given once daily, reduces the risk of hypoglycaemia compared with other formulations, and can facilitate a more aggressive insulin treatment in this class of patients.
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PMID:Secondary diabetes associated with principal endocrinopathies: the impact of new treatment modalities. 1932 13

Intrauterine growth restriction (IUGR) can lead to infants being born small for gestational age (SGA). SGA is associated with increased neonatal morbidity and mortality as well as short stature, cardiovascular disease, insulin resistance, diabetes mellitus type 2, dyslipidemia and end-stage renal disease in adulthood. In addition, SGA children have decreased levels of intelligence and cognition, although the effects are mostly subtle. The overall outcome of each child is the result of a complex interaction between intrauterine and extrauterine factors. Animal and human studies show structural alterations in the brains of individuals with IUGR/SGA. The presence of growth hormone (GH) receptors in the brain implies that the brain is also a target for GH. Exogenous GH theoretically has the ability to act on the brain. This is exemplified by the effects of GH on cognition in GH-deficient adults. In SGA children, data on the effect of exogenous GH on intelligence and cognition are scant and contradictory.
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PMID:Brain development, intelligence and cognitive outcome in children born small for gestational age. 2019 May 35

Growth without growth hormone (GH) has occasionally been described in patients who have had tumors removed in the hypothalamic-pituitary area. Most of these patients have metabolic abnormalities such as obesity, dyslipidemia and fatty liver. This report describes the metabolic beneficial effects of GH replacement in pediatric patients with growth without GH. Two children in whom the growth without GH phenomenon occurred after therapy for brain tumors participated in this study. Case 1 is a 15-yr-old Japanese girl, diagnosed as having Langerhans cell histiocytosis with multiple intracranial lesions at the age of two. She showed a slight body fat increase, dyslipidemia and fatty liver. Case 2 is a 10-yr-old Indonesian boy, diagnosed with craniopharyngioma at the age of three. He was obese and had low bone mineral density (BMD). In both cases, GH replacement therapy was started at 0.042 mg/kg/week for 12 months. Body composition, BMD, and visceral abdominal area were measured every 3 months. Serum fasting blood glucose, insulin, ALT, lipid profile, leptin, and adiponectin levels were also measured every 3 months. Case 1 showed improvement of transaminase (ALT from 64 to 16 IU/L) and triglyceride (from 239 to 129 mg/dL) over 12 months, but did not show a decrease in visceral fat area or of body fat percentage. Case 2 showed a decrease in body fat percentage and visceral fat area, accompanied by elevated serum adiponectin and decreased leptin levels. In conclusion, twelve months GH replacement therapy improves metabolic abnormalities in pediatric patients with growth without GH.
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PMID:Metabolic effects of growth hormone replacement in two pediatric patients with growth without growth hormone. 2066 Sep 85


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