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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of our work was to study non-insulin-mediated glucose uptake (NIMGU), in the postabsorptive state, in several pathologies characterized by peripheral insulin resistance, namely, obesity (n = 10), NIDDM (n = 7), acromegaly (n = 7) and Cushing's disease (n = 6). These groups were compared with a group of 16 healthy subjects. To estimate peripheral insulin sensitivity (SI) and glucose effectiveness (SG), we used the minimal model of glucose metabolism. Although all of these pathologies showed severe insulin resistance (control: 6.44 +/- 2.63, obesity: 2.84 +/- 1.57, NIDDM: 1.71 +/- 0.77, acromegaly: 1.88 +/- 1.23, Cushing's disease: 1.87 +/- 0.66 x 10(-4) min-1 (microU/ml)-1, P < 0.01), fasting insulin-mediated glucose uptake (IMGU) did not differ significantly among the five groups, because reactive hyperinsulinaemia was present in all of these states. The contribution of NIMGU to whole-body glucose uptake did not differ significantly among the five groups (control: 77 +/- 8%; obesity: 77 +/- 9%; acromegaly: 82 +/- 8%; Cushing's disease: 83 +/- 8%; NIDDM: 84 +/- 7%). In conclusion, our data show that, in the postabsorptive period, non-insulin mediated glucose uptake is a major determinant of glucose disposal and is similar in the different pathologies studied; on the other hand, although absolute rates of basal insulin-mediated glucose uptake are reduced in insulin-resistant states, they did not achieve statistical value compared with control subjects because of compensatory hyperinsulinaemia.
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PMID:Non-insulin-mediated glucose uptake in several insulin-resistant states in the postabsortive period. 959 80

The pertinent literature on the prevalence, clinical manifestations and pathogenic mechanisms of sleep apnoea (SA) in endocrine diseases, namely acromegaly, Cushing syndrome, hypothyroidism and diabetes mellitus was reviewed. An increased prevalence is well documented in patients with active and treated acromegaly. While most authors report peripheral obstruction, due to hypertrophy of tongue and pharyngeal tissues, to be the cause of SA in acromegaly, some findings argue for a role of hormone-induced changes of central respiratory control. SA is also more common in hypothyroidism, especially when myxedema is present. The associated edema and myopathy appear to be of pathogenic importance. Thyroxin substitution is frequently effective for the treatment of SA but nCPAP can be necessary initially and in some patients even after remission of clinical signs of hypothyroidism. In Cushing disease and syndrome, parapharyngeal fat accumulation can cause SA, but no epidemiological information is available. In non insulin dependent diabetes (NIDDM), obesity is the common risk factor for both, nocturnal hypoxia and insulin resistance. In IDDM, the development of autonomic neuropathy may predispose to SA. Where treatment of the underlying endocrine disease is unable cure the associated SA, nCPAP is usually the treatment of first choice. More prospective studies are clearly needed to establish prevalences and resolve the controversies regarding pathogenesis.
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PMID:Sleep apnoea in endocrine diseases. 961 23

The purpose of this study was to compare the results of bilateral laparoscopic adrenalectomy (BLA) to bilateral open adrenalectomy (BOA) in the treatment of Cushing's disease. Twenty-four patients (23 Cushing's disease, 1 congenital adrenal hyperplasia) were divided into 3 groups. Group 1 patients (n = 15) underwent BCA using the lateral transabdominal approach, Group while 2 patients (n = 9) underwent laparoscopic adrenalectomy on one side and conventional open adrenalectomy on the contralateral side. Groups 1 and 2 were compared retrospectively to 15 patients (Group 3) who underwent BOA as part of larger series of 61 patients. There was no difference in the degree of hypercortisolism in the 3 groups. At the beginning of the experience, the duration of surgery was longer in Groups 1 and 2 compared to the open surgery group, but this difference subsequently decreased during the study. There was no difference in intraoperative blood loss or transfusion rate. Group 1 patients experienced fewer wound and intraabdominal complications and less postoperative pain, shorter hospitalization, and quicker recovery than groups 2 and 3 patients. Technically obesity and tissue fragility are easily overcome by the laparoscopic approach. BCA also achieves success rate of hypercortisolism correction. In conclusion, BLA is the surgical procedure of choice for the treatment of Cushing's disease when surgical therapy is indicated.
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PMID:[Bilateral video-endoscopic adrenalectomy in Cushing's disease. Experience in 24 patients]. 975 69

The clinical course and diagnosis of a patient with Cushing's disease complicated by pregnancy is described, and the anaesthetic management of trans-sphenoidal selective adenomectomy performed during the second trimester outlined. Problems included obesity, diabetes, hypertension and a suboptimal airway. Fibreoptic awake intubation and intravenous anaesthesia were used. Insulin requirements decreased substantially after surgery. Early administration of hydrocortisone after surgery avoided the risk of an addisonian crisis but delayed biochemical confirmation of a metabolic cure.
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PMID:Cushing's disease treated by trans-sphenoidal selective adenomectomy in mid-pregnancy. 977 23

The development of lipodystrophy as evidenced by central obesity, "moon facies," and a "buffalo hump" is a classical feature of Cushing's disease. Recently an association of "lipodystrophy" with the use of protease inhibitors has been reported. We describe a patient with lipodystrophy secondary to protease inhibitor therapy for HIV infection.
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PMID:Protease inhibitor-induced lipodystrophy. 1018 89

A retrospective analysis of Cushing's syndrome from the retrieved records of 24 out of a total of 27 referred cases over a period of 10 years (January 1985-January 1995) showed confirmation in 16 cases. Fourteen (88%) were females, 9 (56%) were in their third decade. Duration of symptoms before admission was one year or less in eleven (69%) patients. Among symptoms weakness, fatigue and weight gain and among signs moon face, truncal obesity and buffalo hump were found in all patients. Amenorrhea occurred in all the women of childbearing age. Basal urinary 17-hydroxycorticoid (17-OHCS) values were elevated in 9/12 patients and low dose dexamethasone suppression test favoured Cushing's syndrome in 8/9 patients. Definitive treatment consisted of bilateral adrenalectomy in 7 and transfrontal pituitary adenomectomy in 3. Two patients declined surgery; 4 patients were lost to follow up before definitive treatment. Two patients who had bilateral adrenalectomy and two who had transfrontal adenomectomy died subsequently while three remained in good health on corticosteroid replacement therapy. Three of the 7 patients who had bilateral adrenalectomy developed Nelson's syndrome. It is concluded that Cushing's disease is the most frequent cause of Cushing's syndrome in our series. The patients presented with the well-known clinical manifestations of hypercortisolism. However, our laboratory facilities require considerable improvement to serve as a reliable adjunct to clinical evaluation. Since Cushing's syndrome, whatever the cause, is eventually fatal if left untreated, surgical intervention is mandatory after confirmation of the cause with appropriate laboratory tests.
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PMID:Cushing's syndrome: a ten year experience at Tikur Anbassa Hospital. 1021 44

Cushing's disease (CD) in adolescence and childhood is a rare pathology and has some different clinical and therapeutic characteristics than in adults. We report 3 cases treated surgically, with the diagnosis of CD. Their common complaints were short stature and obesity. Endocrinological investigations and radiological evaluation pointed out the diagnosis of CD for all children. They were operated on by the transsphenoidal route, and adenoma resection was performed. Histopathologic and immunohistochemical examination of the tissue specimens confirmed the diagnosis of CD. Long-term follow-up demonstrated weight loss and increase in height.
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PMID:Clinical and therapeutic properties of Cushing's disease in childhood. 1054 17

Obesity results from a greater consumption of energy than is used by the body. As this energy is stored, fat cells enlarge, producing the characteristic pathology of obesity. The pathologic enlargement of fat cells, in turn, produces altered levels of many peptide and nutrient signals that are responsible for the disease we call "obesity." The genetic makeup of human beings, which reflects a long history of relative scarcity of foodstuffs, has run into an age of surfeit, and many people cannot readily adapt. Thus, the increased intake of food does not signal satiety, and there is a gradual increase in energy stores as intake of energy outpaces need as we grow older. Against this background of struggle between nature and nurture, it is possible to identify an increasing number of defects or etiologies that produce obesity. For most patients, however, it is not possible to connect obesity to a specific cause. Leptin deficiency and defects in the leptin receptor both produce human obesity. Defects in the pro-opiomelanocortin receptor system, the peroxisome proliferator-activated receptor-gamma, the agouti-related peptide, and a few other rare genetic syndromes are also associated with human obesity. Of the genetic causes, Prader-Willi syndrome is the most common. Hypothalamic injury following craniopharyngioma is the most common neuroendocrine cause. Endocrine disorders such as Cushing's disease, polycystic ovary disease, and growth-hormone deficiency can lead to increased body fat. In the modern world, exposure to a high-fat diet predisposes many people to obesity, and this problem is compounded by the low levels of activity now required for daily living. Treatment strategies must be developed against this background.
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PMID:Etiology and pathogenesis of obesity. 1069 81

Myelolipoma is a tumor-like growth composed of mature fat tissue and bone marrow elements. It occurs in the adrenal gland or as an isolated soft tissue mass. It may be associated with endocrine disorders such as hermaphroditism, Cushing's disease, Addison's disease and obesity of unknown cause. These lesions rarely measure more than 5 cm in diameter, although giant tumors have been reported in the literature. The fifth largest surgically resected adrenal myelolipoma in the literature is reported and its clinical associations and, macroscopic and microscopic features are discussed.
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PMID:Giant adrenal myelolipoma: case report and review of the literature. 1088 28

The most common endogenous cause of Cushing's syndrome is Cushing's disease. Frequent clinical findings include weight gain, truncal obesity, striae, hypertension, glucose intolerance and infections. Cranial nerve II may be affected by enlarging pituitary adenomas in Cushing's disease; cranial nerves III, IV and VI may also be affected. The evaluation of patients with suspected Cushing's disease and syndrome requires an understanding of the proper use and limitations of the tests commonly included in the diagnostic work-up. The best screening test for Cushing's syndrome is a 24-hour urine collection with analysis for urinary free cortisol excretion. Low-dose and high-dose dexamethasone suppression tests, corticotropin assays, a corticotropin-releasing hormone stimulation test and inferior petrosal sinus catheterization may be required for a definitive diagnosis. Magnetic resonance imaging is useful in localizing the lesion. Surgical removal of the lesion by a transphenoidal approach is usually successful, but long-term follow-up is required. Some patients require lifetime glucocorticoid replacement therapy.
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PMID:Cushing's disease: clinical manifestations and diagnostic evaluation. 1099 35


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