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Various causes of Cushing's syndrome is caused by excessive secretion of adrenal glucocorticoids and disease caused by the general term, which by the pituitary adrenocorticotropic hormone (ACTH) secretion of the most common diseases caused by hyperthyroidism, ie Cushing's disease (CD). Diagnosis and treatment of Cushing's syndrome focus of attention for the physician, the results of recent research report after another.Obesity: screening test should not be extensively
Cushing's syndrome in obese or overweight population incidence is not clear.
American scholar Bede (Baid) and other selected 369 overweight or obese patients (selected by at least two other features of Cushing's syndrome), are to be 2 to 3 the following checks: 24-hour urine cortisol, late night salivary cortisol test or 1 mg dexamethasone suppression test (DST). If abnormal, repeat the inspection and (or) line of dexamethasone - corticotropin releasing hormone (CRH) test, 1 mg DST were abnormal and the lower level of the body received dexamethasone 2 mg DST. Results, in addition to obesity, the patients an average of 5 to 6 features of Cushing's syndrome (such as drowsiness, sanguine face, irritability, abnormal body fat distribution), but no patients were diagnosed with Cushing's syndrome. Upon completion of three examinations, the examination of the specific exclusion of Cushing's syndrome are as follows: 24 hour urinary cortisol was 96%, 1 mg DST was 90%, by radioimmunoassay and liquid chromatograp


hy - tandem mass spectrometry saliva cortisol was 84% and 92%, any two tests combined specificity of 84% to 90%.
The research suggests that obesity and overweight in the population, the incidence of Cushing's syndrome is not high, the possibility of false-positive screening test, so Raed obesity and overweight is not recommended for widespscreening of the population of Cushing's syndrome.After the discovery of adrenal incidentaloma should be checked whether the secretion of hormones, especially cortisol, aldosterone, and catecholamines. Screening for Cushing's syndrome can be based on the following 2 points, that is, and in the application of excessive cortisol secretion after dexamethasone were not significantly inhibit the secretion. Salivary cortisol (SaC) and good correlation between free cortisol, stress testing can be avoided interference, better than in the serum cortisol (SeC).
German scholars under Ziba (Deutschbein), etc. In 2001 -2006 cortisol adenoma in 38 patients (CPA) patients, 18 healthy control patients and 48 patients (13 patients with aldosterone adenoma, 16 cases of pheochromocytoma , 19 cases of non-functioning adenomas), low-dose DST line after 11 pm ~ 8 am determined SaC and SeC. The result is to cortisol break point, and SeC (115 nmol / L) compared to, SaC (4.8 nmol / L) slightly higher specificity (63% vs. 69%), sensitivity was similar (both 97%) ; in DST after the break point with the SeC (94 nmol / L) compared to, SaC break point (3.7 nmol / L) was slightly lower specificity (88% vs. 83%), sensitivity was similar (both 97%), DST After the diagnostic specificity of detection of cortisol were higher than the night cortisol.
The study confirmed that, SaC screening of Cushing's syndrome is similar to the accuracy and SeC, DST cortisol specificity than after late-night cortisol.Desmopressin (DDAVP) test is recommended for the identification of CD and leave the state of Cushing (PC), but there are still controversial.
Italian scholar Umatilla Brazil (Tirabassi) 52 patients with CD and other selected patients, 28 cases of PC patients and 32 control subjects, the DDAVP test. The basis of serum cort 331 nmol / L and DDAVP stimulated ACTH increases the absolute value 4 pmol / L can be diagnosed as CD, have a negative diagnosis is excluded. DDAVP test in diagnosis of CD was 90.3% sensitivity and specificity of 91.5%. With the DST and midnight serum cortisol compared to late night, DDAVP test may better identify urinary free cortisol was elevated in the CD. This method can identify the PC with the following diseases: moderate urinary free cortisol CD (sensitivity 86.9%, specificity 92.8%); DST serum cortisol levels after the middle of the CD (86.6% sensitivity and specificity 92.8%); moderate levels of serum cortisol at midnight CD (sensitivity 100%, specificity 92.8%).
The study confirmed that even patients with mild Cushing's syndrome, multiple markers in the analysis of DDAVP test also can effectively identify CD and PC.21OHD treatment should be individualized
Congenital adrenal hyperplasia (CAH) is impaired cortisol biosynthesis, in which the 21-hydroxylase deficiency (21OHD) due to 95%. Current 21OHD (especially adult patients) treatment remains controversial. Through careful individual treatment of patients can occur from library welcomes the performance of their birth, sex, reach optimal bone health, patients can still benefit.
In 2008, Lawson - Wilkins (Lawson Wilkins) Pediatric Endocrine Society and the European Pediatric Endocrine Society have jointly issued a consensus statement for adult 21OHD. The consensus statements are based on retrospective evidence, still more prospective studies to explore new therapies.
Adult patients with classic 21OHD on the current treatment of choice tend to be more long-term corticosteroids (such as prednisone, prednisolone or dexamethasone), usually optional dexamethasone (375 ~ 500 g qn), but those who have requested birth of dexamethasone should be avoided, plus a small dose of hydrogen fluoride can be reduced glucocorticoid hydrocortisone dosage. Non-classical type of adult patients, male without treatment, women can use oral contraceptives and anti-androgen agents.
About 17 - hydroxyprogesterone, in order to avoid iatrogenic Cushing's performance, its level of control should not be too strict, for pediatric patients, 17 - hydroxyprogesterone levels of control in the 400 ~ 1200 ng / dl can be, but the adult patients control should be individualized, such as young women should be controlled at 800 ng / dl below which no testicular remnants of adrenal tissue of adult males should be controlled at 2500 ng / dl or less. Older 21OHD decreased bone mineral density in patients and should therefore be the prevention of osteoporosis, such as increased activity levels, taking calcium and vitamin D preparations.Cortisol is regulated by a central, obvious circadian rhythm of secretion of hormones. Conventional glucocorticoid replacement therapy does not mimic the circadian rhythms.
A sustained release of hydrocortisone on in healthy volunteers (n = 33) in the pharmacokinetic study showed that in 11 pm taking 15 ~ 20 mg, 7 am to take 10 mg of the drug model replicable cortisol secretion circadian rhythms. Sawyer Wilma (Somya Verma) and other reports to release hydrocortisone therapy CAH (n = 14) of the pharmacokinetic study and comparison with conventional hydrocortisone. 1 week in patients taking regular hydrocortisone (3 times a day, respectively, 10 mg, 5 mg and 15 mg), 1 month after the switch to sustained-release hydrocortisone (at 10 pm taking 30 mg). Result, conventional cortisol levels after hydrocortisone treatment appeared three peaks, and the application only after the release of hydrocortisone appeared in the 6 am one peak. After the release of hydrocortisone in the application of the afternoon (12 am ~ 8 pm) and night (8 pm ~ 4 am), the cortisol area under the curve was significantly lower than the conventional therapy group; at 4 am ~ 12 am, when the physiological of cortisol reached the highest value, slow-release hydrocortisone treatment group than in the conventional treatment group cortisol levels (P <0.001); release the afternoon of hydrocortisone treatment of blood 17 - hydroxyprogesterone, Androstene II ketones and higher ACTH levels, but 8 am 17 - OH progesterone levels were significantly lower than the conventional therapy group.
The study confirmed that the release of hydrocortisone can better control the s of the night adrenal androgen levels, but the night took a time unable to control the level of androgen afternoon, suggesting that early in the morning also have medications. The ideal treatment methods and long-term effect remains to be studied further.
CD residual disease: diagnosis, therapy should be individualizedResidual disease on the CD in the clinical assessment and treatment still is a difficulty. American scholar Lewis (Lewis) and other large-scale study conducted on the relevant systematic retable), that the existence of CD in patients with residual disease, first diagnosed, confirmed the diagnosis of CD, according to the severity of choosing the appropriate treatment program to continue Treatment should be individualized.



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