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

Little is known on the epidemiology of Cushing's disease (CD) as relevant data on such a rare disease can only be obtained from large-scale studies. We addressed this topic analyzing the data obtained in the Italian multicenter study which comprised nearly 300 patients with CD. The number of newly diagnosed patients with CD increased markedly in the second decade of the study (from 7.4 +/- 0.71 pts/year prior to 1987 to 26.4 +/- 4.12 after 1987) probably reflecting the heightened awareness of the disease and the increased availability of diagnostic tools. Urinary free cortisol (UFC) levels were significantly higher in men than in women and were inversely correlated with the time interval between appearance of symptoms and diagnosis. Recognition of CD among patients presenting with common diseases such as obesity, diabetes and hypertension requires highly sensitive screening tests (e.g. UFC, midnight cortisol in saliva, overnight dexamethasone suppression test) which however may yield false positive results. In doubt, second line testing using dex-CRH or desmopressin may distinguish between CD and pseudo Cushing. The different prevalence of CD and ectopic ACTH secretion (ES) undermines the diagnostic accuracy of tests used for the differential diagnosis of ACTH-dependent Cushing's syndrome (i.e. CRH, high dose dexamethasone, IPSS). Tests aimed at identifying ES rather than CD are needed to overcome this bias. Transsphenoidal surgery was the preferred choice of treatment for patients with CD, resulting in remission in 70% operated patients with a 15% relapse rate over 10 years follow-up. Definition of remission after surgery and parametres predictive of relapse, however, vary according to studies and long-term follow-up is required to establish their validity. Most clinical manifestations of hypercortisolism disappeared after remission although some long-lasting effects on the cardiovascular system had been observed. Finally, according to recent reports, mortality rates for patients cured of CD appear comparable to those of the general population.
 ...
PMID:Epidemiology and follow-up of Cushing's disease. 1135 89

Chronic severe hypercortisolism is associated with life-threatening infections, diabetes and a high surgical mortality rate. Oral medical therapy can inhibit steroidogenesis and reduce the risk of these complications. However, apart from a few reports using an ethyl alcohol formulation of the iv anesthetic etomidate, there is no well-tested parenteral steroidogenesis inhibitor. We used the propylene glycol preparation of etomidate available in the United States to control hypercortisolism in a 39-yr-old man with ectopic ACTH secretion who was unable to take oral medications. Etomidate was administered over a period of 5.5 months. We titrated the dose of etomidate daily using serum cortisol levels, to avoid steroid over replacement and allow for a response to ongoing stress. A reduced dose during a period of acute renal failure achieved adequate control of hypercortisolemia. Suppression of steroidogenesis persisted for at least 14 d and perhaps as long as 6 wk after cessation of the medication. Except for transient myoclonus, the patient tolerated this preparation well. Parenteral propylene glycol containing etomidate can be used safely for a prolonged period to reduce hypercortisolemia in patients unable to take oral medications.
 ...
PMID:Use of a parenteral propylene glycol-containing etomidate preparation for the long-term management of ectopic Cushing's syndrome. 1154 33

This article highlights the advances in feline endocrinology, excluding diabetes mellitus and hyperadrenocorticism, which have recently been reviewed elsewhere. The goal will be to provide clinically relevant information regarding pathogenesis, diagnosis, and treatment options for these feline endocrine disorders.
 ...
PMID:Feline endocrinology update. 1157 Jan 26

A number of patients with adrenal incidentaloma are exposed to a slight degree of cortisol excess resulting from functional autonomy of the adrenal mass (usually a cortical adenoma). At present, there are only scant data on the unwanted effects of this endocrine condition referred to as subclinical Cushing's syndrome. The aim of the present study was to look for some features of the metabolic syndrome in patients with incidental adrenal adenoma. Forty-one patients (9 men and 32 women) bearing adrenal incidentaloma with typical computed tomography features of cortical adenoma were studied. For both patients and controls, exclusion criteria were age equal to 70 yr or greater, previous history of fasting hyperglycemia, or impaired glucose tolerance (IGT), severe hypertension, current use of medication or concomitant relevant illnesses, and body mass index (BMI) equal to 30 kg/m(2) or greater. Forty-one patients with euthyroid multinodular goiter accurately matched for sex, age, and BMI served for a 1:1 case-control analysis. The study design included an oral glucose tolerance test (75 g) and an endocrine workup aimed at the study of the hypothalamic-pituitary-adrenal axis. Age and BMI were fully comparable between patients (54.0 +/- 10.7 yr, 23.8 +/- 2.4 kg/m(2)) and controls (52.2 +/- 11.6 yr, 23.5 +/- 2.8 kg/m(2)). Fasting glucose and fasting insulin levels were not different between the two groups (4.96 +/- 0.61 mmol/liter vs. 4.88 +/- 0.58 mmol/liter; 67 +/- 34 pmol/liter vs. 59 +/- 32 pmol/liter), but the 2-h postchallenge glucose was significantly higher in patients than in controls (7.43 +/- 2.49 mmol/liter vs. 6.10 plus minus 1.44 mmol/liter, P = 0.01). Fifteen patients (36%) reached the World Health Organization criteria for IGT and two other patients (5%) reached those for diabetes, and 14% of the controls qualified for IGT (P = 0.01). No difference in the lipid pattern was seen between the two groups, but either systolic or diastolic blood pressure were higher in patients (135.4 +/- 15.5 mm Hg vs. 125.0 +/- 15.6 mm Hg, P = 0.003; 82.9 +/- 9.1 mm Hg vs. 75.3 +/- 6.6 mm Hg, P < 0.0001). We calculated the whole-body insulin sensitivity index derived from the oral glucose tolerance test that was significantly reduced in the patients (4.3 +/- 1.7 vs. 5.7 +/- 2.5, P = 0.01). In a multiple regression analysis, 2-h glucose was associated with BMI and midnight cortisol values (r(2) = 0.36, P = 0.002). The comparison of the patients with nonfunctioning adenoma (n = 29) with those with subclinical Cushing's syndrome (n = 12) yielded significant differences as to 2-h glucose and triglyceride levels, which were significantly higher in the second group (7.02 +/- 1.76 mmol/liter vs. 8.72 +/- 3.17 mmol/liter, P = 0.03; 1.06 +/- 0.4 mmol/liter vs. 1.73 +/- 0.96 mmol/liter, P = 0.002), but the insulin sensitivity index was conversely reduced (5.2 +/- 1.4 vs. 2.9 +/- 1.2, P < 0.0001). In conclusion, many patients with incidental adrenal adenoma display altered glucose tolerance, that may be explained by reduced insulin sensitivity, and increased blood pressure levels in comparison with carefully age- and BMI-matched controls. The slight hypercortisolism observed in some such patients may significantly contribute to this state of insulin resistance. Midnight serum cortisol appears as a sensitive marker of the metabolic effects of subclinical Cushing's syndrome.
 ...
PMID:Adrenal incidentaloma: a new cause of the metabolic syndrome? 1292 19

Heightened awareness of endocrine abnormalities is important in evaluation of patients presenting with musculoskeletal symptoms. Endocrine disorders such as diabetes, hyperthyroidism, hypothyroidism, hyperparathyroidism, hypoparathyroidism, hyperadrenocorticism, and acromegaly cause a unique array of rheumatic manifestations. Such conditions include Dupuytren's contracture, carpal tunnel syndrome, chondrocalcinosis, pseudogout, scleredema, and osteoporosis. Characteristic changes on radiologic evaluation and serum enzyme testing are additional clues to these atypical presentations. Consideration of a possible endocrine cause early in the evaluation may improve management in patients with such an underlying disorder.
 ...
PMID:Endocrine origins of rheumatic disease. Diagnostic clues to interrelated syndromes. 1198 36

Cushing's syndrome is the clinical expression of the overproduction of glucocorticoids and is well recognized in both human and veterinary medicine. Spontaneous diabetes mellitus is well known in Macaca spp., however the occurrence of hyperadrenocorticism and diabetes mellitus concurrently in macaques has not been reported previously. This unusual case presents a rare opportunity to examine the relationships between two important endocrine diseases in a nonhuman primate. A male, 14-year-old rhesus macaque (Macaca mulatta) was diagnosed with hyperadrenocorticism and concurrent diabetes mellitus. Initially, the monkey had mildly elevated blood glucose values upon routine semi-annual physical examination. Further diagnostic work-up demonstrated hypercortisolism. Adrenocorticotropic hormone-dependent Cushing's syndrome was subsequently diagnosed in light of results from dexamethasone testing, magnetic resonance imaging, and computed tomography scans. A therapeutic course of L-deprenyl (Anipryl(r)) was begun, and 8 weeks later, insulin therapy was initiated. The patient responded well to insulin therapy, however the dosage was rapidly increased. After 6 months, Anipryl(r) therapy was determined to be of little or no value, and ketoconazole was selected as the drug of choice to control the hypercortisolism. The monkey has shown remarkable improvement with the dual therapies of insulin and ketoconazole. Approximately 2 months after the initiation of ketoconazole therapy, the animal was returned to an experimental protocol under the conditions of twice-daily treatment and strict dietary control. The ongoing plan for clinical management includes periodic blood glucose and liver function surveillance.
 ...
PMID:Cushing's Syndrome with Concurrent Diabetes Mellitus in a Rhesus Monkey. 1208 27

The diagnosis of Cushing's syndrome rests on the demonstration of clinical features and biochemical abnormalities that reflect hypercortisolism. If a patient presents with typical clinical features such as weight gain with truncal obesity and supraclavicular fat deposition, wide purple striae, and proximal muscle weakness, the diagnosis is clear-cut and is nearly always substantiated by a 24-hour urine free cortisol excretion value more than four times the normal level. However, many patients present with signs and symptoms that are common in the general population, such as hypertension, generalized weight gain, reproductive abnormalities, and depression. Many of these patients have normal cortisol excretion and do not have Cushing's syndrome. Others have mild hypercortisolism caused by psychiatric disorders, obligate exercise, morbid obesity, sleep apnea, or uncontrolled diabetes mellitus. These patients may be confused with those with the true Cushing's syndrome, and thus are considered to have a "pseudo-Cushing" state. Additional observation over time, and testing with midnight cortisol measurements, the 2-day-2-mg dexamethasone suppression test, or the dexamethasone suppression-CRH stimulation test may be useful to identify true Cushing's syndrome in these patients.
 ...
PMID:Diagnostic tests for Cushing's syndrome. 1238 46

During pregnancy, major changes of the corticotroph axis activity are observed. The placenta synthetizes Corticotropin-Releasing Hormone (CRH) and pro-opio-melanocortin (POMC), and the plasma levels of both peptides are highly increased during pregnancy. The cortisol plasma levels are two-fold elevated compared to the levels observed in non pregnant women. This increase in cortisol level is mainly due to the doubling of the Cortisol Binding Globulin (CBG). Untreated Cushing's syndrome during pregnancy is associated with a high maternal as well as fetal morbidity (hypertension, preeclampsia, diabetes mellitus, premature birth.). Adrenocortical tumors are the major cause of Cushing's syndrome diagnosed in pregnancy. The treatment of hypercortisolism during pregnancy required a multidisciplinary approach by highly specialized teams. Adrenal insufficiency is rarely diagnosed during pregnancy. Untreated adrenal failure is associated with a high maternal and fetal morbidity and mortality. On the other hand, steroid replacement therapy appropriately monitored during pregnancy is associated with a very favorable outcome in pregnant women with adrenal insufficiency. During labor steroid replacement therapy should be adapted as for any surgical procedure.
 ...
PMID:[Cushing's syndrome and adrenal insufficiency in pregnancy]. 1244 88

A 45-year-old woman with adrenocorticotropin (ACTH)-independent hypercortisolism, diabetes mellitus, and hypertension had undergone left adrenalectomy for ACTH-independent Cushing's syndrome 20 years prior to this presentation. There was cushingoid appearance 1 year after surgery. However, Cushing's syndrome recurred; ACTH-independent Cushing's syndrome was diagnosed and abdominal computerized tomography showed a right adrenal tumor, which was removed. Histology revealed primary pigmented nodular adrenocortical disease (PPNAD). The patient had also undergone hysterectomy for uterine masses diagnosed as uterine myxoma. Right breast and neck skin masses were also found, both of which were removed and diagnosed as mammary myxoid fibroadenoma and cutaneous myxoma. She had a homozygotic twin sister who also had Cushing's syndrome and had undergone bilateral adrenalectomy 13 years previously with a pathologic diagnosis of PPNAD. The twin sister also had skin, breast, and uterine masses, all of which were resected. The pathologic results were the same as this patient's. According to the clinical presentations, histologic findings, and positive family history, familial PPNAD (Carney complex) was diagnosed.
 ...
PMID:Carney complex, a familial Cushing's syndrome due to primary pigmented nodular adrenocortical disease: a case report. 1267 39

The pathogenesis of nephrolithiasis in Cushing's syndrome is still not completely clarified. The current study aimed at investigating prevalence of nephrolithiasis and role of different lithogenic factors in Cushing's disease (CD). Forty-six CD patients (24 with active and 22 with cured disease) and 46 sex- and age-matched controls entered the study. Body mass index, blood pressure, fasting glucose and insulin, serum and urinary creatinine, urea, uric acid, electrolytes, and cystine, urinary volume, pH, oxalate, and citrate levels, and renal ultrasonography (US) were performed in all patients and controls. Nephrolithiasis was found in 50% of active patients, 27.3% of cured patients, and 6.5% of controls (P < 0.001). Compared with controls, patients with active disease had a significantly increased prevalence of obesity, arterial hypertension, diabetes mellitus, hypercalciuria, hypocitraturia, and hyperuricosuria, significantly higher levels of serum and urinary cystine, urinary creatinine, urea, uric acid, potassium, calcium, phosphorus, and oxalate, significantly lower levels of urinary citrate levels. Compared with controls, patients cured from CD had a significantly increased prevalence of obesity, systemic arterial hypertension, and diabetes mellitus, whereas urinary citrate was significantly decreased. At multivariate analysis, a significantly increased risk to develop kidney stones was independently associated with urinary excretion of uric acid (odds ratio = 1.6, confidence interval = 1.0-2.5) and systemic arterial blood pressure (odds ratio = 2.6, confidence interval = 1.1-6.6). In conclusion, patients with active CD have an increased prevalence of nephrolithiasis compared with general population, which decreases but not disappears in patients successfully cured from the disease. This complication is likely caused by the synergic effect of different hypercortisolism-dependent metabolic and hemodynamic abnormalities, among which systemic arterial hypertension and excessive urinary uric acid excretion seem to play a pivotal role.
 ...
PMID:Nephrolithiasis in Cushing's disease: prevalence, etiopathogenesis, and modification after disease cure. 1272 57


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>