Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with hypopituitarism develop a phenotype similar to metabolic syndrome with central obesity and diabetes. Similarly, patients with hypothalamic damage may develop central obesity, insulin resistance, and hyperphagia. We sought to examine the clinical associations between hypopituitarism, hypothalamic dysfunction, and nonalcoholic fatty liver disease (NAFLD). A case series of patients seen at our institution with diagnoses of hypopituitarism, hypothalamic obesity, or craniopharyngioma and NAFLD was undertaken. Clinical, laboratory, and liver biopsy features were reviewed. Twenty-one patients were identified. NAFLD was diagnosed 6.4 +/- 7.5 years (median 3 years) after the diagnosis of hypothalamic/pituitary dysfunction. Mean gain in body mass index (BMI) between diagnoses of hypothalamic/pituitary disease and NAFLD was 11.3 +/- 8.9 kg/m(2) at an average yearly rate of 2.2 +/- 2.2 kg/m(2). The majority of patients developed elevated glucose levels and dyslipidemia by time of diagnosis of NAFLD. Of the 10 patients biopsied, six were cirrhotic, two had nonalcoholic steatohepatitis (NASH) with fibrosis, and two had simple steatosis. Long-term follow-up of 66 +/- 33 months (range 12-120) was available for 18 patients. Two required liver transplantation. Six patients died, two from liver related causes. In conclusion, patients with hypothalamic and/or pituitary disease are at risk of excessive weight gain, impaired glucose tolerance, and dyslipidemia with subsequent development of NAFLD. This group has a high prevalence of cirrhosis placing them at risk for liver-related death. The novel evidence that hypothalamic/pituitary dysfunction may be accompanied by progressive NAFLD has important implications for the work-up and management of patients with hypothalamic/pituitary disease.
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PMID:Nonalcoholic fatty liver disease among patients with hypothalamic and pituitary dysfunction. 1505 93

Design Data on lipids, body composition, and blood pressure (BP) from all published KIMS papers are summarized and compared with a literature review. Results KIMS data confirm and extend previous research showing that adults with GH deficiency (GHD) have an adverse cardiovascular risk profile. GHD patients have high levels of dyslipidemia, elevated body mass index, unfavorable waist-to-hip ratio and body composition, and a high risk of hypertension. These abnormalities are likely to explain the increased cardiovascular mortality observed in patients with hypopituitarism. When given GH replacement therapy, an improvement is seen in KIMS as well as earlier studies for lipid profile, body composition, and BP. The added value of the different KIMS papers over previous research is that KIMS involves a much larger number of patients, that lipid concentrations and IGF1 are measured in a single central laboratory, and that the effects of GH replacement therapy can be followed longer than the duration of earlier trials. By the large number of patients, KIMS gives insight into the effects of GH in different patients' subgroups such as elderly patients, patients with idiopathic GHD, patients with craniopharyngioma, patients after irradiation, and so on. In addition, KIMS has made it possible to calculate more exactly the influence of baseline parameters on these cardiovascular risk parameters and their response to GH. Conclusions Taken together, data from KIMS confirm earlier knowledge about the important benefits of GH replacement therapy, but also on the use of GH in specific subgroups such as isolated GHD, patients above 65 years, and patients after irradiation. No subgroup yet has been identified as not responding well to GH.
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PMID:Cardiovascular risk factors in hypopituitary GH-deficient adults. 1968 57

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

Growth hormone (GH) is an essential element for normal growth. However, reports of normal growth without GH have been made in patients who have undergone brain surgery for craniopharyngioma. Normal growth without GH can be explained by hyperinsulinemia, hyperprolactinemia, elevated leptin levels, and GH variants; however, its exact mechanism has not been elucidated yet. We diagnosed a female patient aged 13 with combined pituitary hormone deficiency (CPHD) caused by pituitary stalk interruption syndrome (PSIS). The patient has experienced recurrent hypoglycemic seizures since birth, but reached the height of 160 cm at the age of 13, showing normal growth. She grew another 8 cm for 3 years after the diagnosis, and she reached her final adult height of 168 cm which was greater than the midparental height, at the age of 16. The patient's blood GH and insulin-like growth factor-I levels were consistently subnormal, although her insulin levels were normal. Her physical examination conducted at the age of 15 showed truncal obesity, dyslipidemia, and osteoporosis, which are metabolic features of GH deficiency (GHD). Herein, we report a case in which a PSIS-induced CPHD patient attained her final height above mid parental height despite a severe GHD.
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PMID:Growth without growth hormone in combined pituitary hormone deficiency caused by pituitary stalk interruption syndrome. 2844 60