Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prader-Willi syndrome (PWS) is a complex genetic disorder localized to chromosome 15 and is considered the most common genetic cause of the development of life-threatening obesity. Although some morbidities associated with PWS, including respiratory disturbance/hypoventilation, diabetes, and stroke, are commonly seen in obesity, others such as osteoporosis, growth hormone deficiency, and hypogonadism, and also altered pain threshold and inability to vomit, pose unique issues. Various bariatric procedures have been used to cause gastric stasis, decrease gastric volume, and induce malabsorption, with poor results in PWS patients in comparison with normal obese individuals.
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PMID:Critical analysis of bariatric procedures in Prader-Willi syndrome. 1816 38

Low density lipoproteins (LDL) size seems to be an important predictor of cardiovascular events and progression of coronary artery disease and the predominance of small dense LDL have been accepted as an emerging cardiovascular risk factor by the National Cholesterol Education Program Adult Treatment Panel III. We recently showed increased LDL size or higher levels of small, dense LDL in different categories of patients at higher cardiovascular risk, such as those with coronary (including acute myocardial infarction) and non-coronary (including carotid disease, abdominal aortic aneurysm and peripheral arterial disease) forms of atherosclerosis or metabolic diseases (including type-II diabetes, polycystic ovary syndrome and growth hormone deficiency). Screening for the presence of small, dense LDL may potentially identify those with even higher risk and may contribute in directing specific treatments in order to prevent new cardiovascular events. This seems particularly true for statins and fibrates. Promising data are available for rosuvastatin, the latest statin molecule introduced in the market, and ezetimibe, a cholesterol absorption inhibitor. The most recent patents regarding these two hypolipidemic agents include the antiinflammatory, antithrombotic and antiplatelet activity (EP1626716B1 and CN1794987A for rosuvastatin) and the potential use for treatment of cholesterol-associated benign and malignant tumors and diabetes (US7098198 and US7071181 for ezetimibe).
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PMID:An update on the role of the quality of LDL in cardiovascular risk: the contribution of the universities of Palermo and Zurich. 1822 Nov 6

Insulin-like growth factors (IGF-I and II) are important endocrine, paracrine and autocrine mediators of physiological growth. They promote cellular proliferation, survival and differentiation. Their effects are mediated mainly through the IGF-I receptor, but IGFs also bind to the IGF-II/mannose 6-phosphate and insulin receptors. IGF activity is modulated by a family of six high-affinity IGF binding proteins (IGFBPs); in most situations, IGFBPs inhibit IGF actions but they may also enhance them. Assays are now available for IGF-I, IGF-II and individual IGFBPs. IGF-I and IGFBP-3 assays have some utility in the diagnosis and management of acromegaly and growth hormone deficiency. There is a large body of in vitro and in vivo evidence supporting a pathogenic role for alterations in the IGF system in many diseases, including diabetes, cancer, cardiovascular disease and neuromuscular disease. More recently, epidemiological studies have linked high IGF-I levels with some cancers and low IGF-I levels with ischaemic heart disease. Preliminary studies of recombinant IGF-I as a treatment for diabetes, osteoporosis and neuromuscular disease have been performed in humans. In contrast, there is considerable interest in developing IGF inhibitors for the treatment of cancer. This apparent paradox highlights the need to develop therapeutics beyond the natural ligands and inhibitors, with characteristics such as ligand and tissue specificity. This will only become possible as we increase our understanding of this complex system. Additionally, as IGF and IGFBP assays are becoming more readily available, their role in the diagnosis and monitoring of diseases should be more clearly defined in the near future.
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PMID:The insulin-like growth factor system: towards clinical applications. 1845 8

Recent studies indicate that neuroendocrine dysfunction is a more frequent sequel of aneurysmal subarachnoid hemorrhage (SAH), than has so far been recognized. However, from the available data it remains unclear whether certain subgroups of SAH patients carry a higher risk to sustain endocrine sequelae due to the hemorrhage than others and should be specifically followed up in terms of hormone assessment. To investigate whether a basal hormone screening is a practical method in clinical routine to single out patients in whom endocrine function testing is warranted, we established a screening protocol, based on the findings from a cohort of 40 SAH patients (study group) who had all been investigated by basal hormone para meters as well as standardized endocrinological function testing, within the framework of a previously published clinical study. We then applied this protocol to 45 newly investigated SAH-patients (screening group). According to the thus established protocol, 20 of the 45 screened patients (44.4 %) were recommended further investigations, 12 of whom agreed to undergo dynamic endocrine function testing. Altogether, the percentage of test-confirmed neuroendocrine dysfunction was only 13.3 % (6/ 45) in the screening group as compared to 55 % in the study group. Low IGF-I (2 SD below normal) did not serve to predict growth hormone deficiency, whereas low 9 am serum cortisol was of limited value to single out ACTH-deficiency in SAH-patients. In summary we conclude that basal hormone screening is not sufficient to identify SAH patients with impaired hypothalamo-pituitary function, at least not in the context of clinical routine practice.
Exp Clin Endocrinol Diabetes 2008 May
PMID:Diagnosing neuroendocrine dysfunction in patients after aneurysmal subarachnoid hemorrhage in clinical practice - does basal hormone screening make sense? 1858 91

GH therapy was approved in 2006 for treatment of adult growth hormone deficiency (GHD) in Japan. Until then, GH was used only to treat short stature in children with GHD and the treatment was stopped when the final height was reached. In the present study, we investigated metabolic co-morbidities experienced by adults with childhood-onset (CO) GHD after the cessation of GH. Forty-two patients with COGHD (M/F 22/20, age at follow up when the retrospective analysis was carried out: 18-52 yr) treated with GH in childhood were studied. We reviewed the medical records of these patients to determine the metabolic co-morbidities that developed after cessation of GH. The median age was 19 yrs (range: 14-38) at cessation of GH, and the following co-morbidities were observed: hypertriglyceridemia in 15 (41%) patients, non-alcoholic fatty liver disease (NAFLD) in 11 (29%) patients, hypercholesterolemia in 10 (26%) patients, diabetes mellitus (DM) in 4 (10%) patients, and hypertension in 1 (2.4%) patient. The median BMI when these complications became overt was 23.5 kg/m(2) for those with hypertriglyceridemia, 26.0 kg/m(2) for those with NAFLD, 20.9 kg/m(2) for those with hypercholesterolemia, and 27.2 kg/m(2 ) for those with DM. More than two co-morbidities were experienced by 32% of men and 30% of women. In conclusion, adults with COGHD after the cessation of GH have multiple metabolic co-morbidities. Lifelong GH replacement might be important for improving the overall metabolic profiles in these patients.
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PMID:Metabolic co-morbidities revealed in patients with childhood-onset adult GH deficiency after cessation of GH replacement therapy for short stature. 1861 81

In this article cases of two sisters with premature atherosclerosis have been described. The first one aged 31 with diagnosis of growth hormone deficiency (GHD) and diabetes mellitus presented with calf intermittent claudication as a result of tibial arteries occlusions. The second one aged 34 with impaired fasting glycemia and without any sign of GHD presented with sudden calf pain as a result of tibial posterior arterial acute occlusion. These cases support the hypothesis that in GH deficiency patients is a higher incidence of diabetes mellitus and early atherosclerosis and they are more vulnerable to vascular thrombotic events (Tab. 1, Ref. 5).
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PMID:Premature atherosclerosis in patients with growth hormone deficiency and diabetes mellitus. 1870 Apr 42

This perspective is the first part of an annual series of papers discussing drugs dropped from clinical development in the previous year. Specifically, this paper focuses on the 14 renal, endocrine and metabolic drugs discontinued in 2007. The candidates covered in this summary were being developed for treatment of diabetes, obesity, reproductive and urogenital health issues, and growth hormone deficiency. Information for this perspective was derived from a search of the Pharmaprojects database for drugs discontinued after reaching Phase I - III clinical trials.
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PMID:Discontinued drug in 2007: renal, endocrine and metabolic drugs. 1892 1

Johanson-Blizzard syndrome (JBS) is a rare autosomal recessive condition associated with exocrine pancreatic insufficiency, and is characterized by hypoplastic nasal alae, mental retardation, sensorineural hearing loss, short stature, scalp defects, dental abnormalities and abnormal hair patterns. Growth hormone deficiency, hypopituitarism, and impaired glucagon secretion response to insulin-induced hypoglycemia have been reported. Congenital heart defects have also been described in this condition. Mental retardation is typically moderate to severe in patients with JBS; however, normal intelligence can occur. In the pancreas, there is a selective defect of acinar tissue, whereas the islets of Langerhans and ducts are preserved. Diabetes has been reported in older children, suggesting the progressive nature of pancreatic disease. The molecular basis of JBS has recently been mapped to chromosome 15q15-q21 with identified mutations in the UBR1 gene. We report the case of a 7-year-old female with pancreatic insufficiency and mild phenotypic features, in whom the diagnosis of JBS was established using recently described molecular testing for the UBR1 gene.
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PMID:Johanson-Blizzard syndrome with mild phenotypic features confirmed by UBR1 gene testing. 1905 15

Impairment of glucose metabolism (in particular insulin resistance and type 2 diabetes mellitus) has been reported in patients who have undergone hematopoietic SCT (HSCT) during childhood, especially those treated with TBI. This pilot study was conducted to determine prevalence of and possible underlying mechanisms for impaired glucose homeostasis in young adults treated with HSCT and TBI and who were not previously known to have diabetes mellitus. A total of 10 subjects (6 males, 4 females) were evaluated. Mean ages were 13.0+/-1.0 years at the time of TBI and 24.0+/-1.1 years at the time of this study. Five subjects had laboratory evidence of insulin resistance using the homeostasis model assessment and the quantitative insulin sensitivity check index indices. Two of these subjects had impaired fasting glucose and four had decreased plasma insulin-like growth factor 1 levels. All 10 subjects had evidence of abdominal obesity. Insulin resistance is frequently observed in adult survivors of HSCT treated with TBI in childhood. Underlying mechanisms may include radiation-induced growth hormone deficiency and changes in body composition.
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PMID:Disorders of glucose homeostasis in young adults treated with total body irradiation during childhood: a pilot study. 1930 39

Higher plasma triglyceride levels and decreased HDL-cholesterol concentrations are usually accompanied by the presence of small, dense LDL in the so-called lipid triad or 'atherogenic lipoprotein phenotype'. This phenotype is highly atherogenic and its prevalence may suggest an even higher overall burden of atherosclerotic disease as compared with that associated with hypercholesterolemia. As stated by the National Cholesterol Education Program Adult Treatment Panel III, there is evidence suggesting each component of this lipid triad is individually atherogenic. However, the relative contribution of each component cannot be easily determined. Therefore, it has been suggested to consider the atherogenic lipoprotein phenotype as a whole as a risk factor. This is supported by data from epidemiological studies considering high-risk populations, which showed that the contribution to cardiovascular risk of each individual component cannot be dissected from the sum of all factors. We recently investigated the prevalence of the atherogenic lipoprotein phenotype in different categories of patients at higher cardiovascular risk: with coronary and noncoronary forms of atherosclerosis or metabolic diseases, including Type 2 diabetes, polycystic ovary syndrome and growth hormone deficiency. Subjects with higher triglyceride levels, decreased HDL-cholesterol concentrations and increased levels of small, dense LDL (i.e., subjects with the atherogenic lipoprotein phenotype) are common in coronary and noncoronary forms of atherosclerosis. In the future, it may be possible to measure the presence of small, dense LDL to identify subgroups at higher cardiovascular risk.
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PMID:Update on the role of the atherogenic lipoprotein phenotype in cardiovascular prevention. 1980 10


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