Does anyone know anything about ppl with Cushing's Disease?
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When Cushing's is suspected, a dexamethasone suppression test (administration of dexamethasone and frequent determination of cortisol and ACTH levels) and 24-hour urinary measurement for cortisol have equal detection rates (Raff & Findling 2003). A novel approach, recently cleared by the US FDA, is sampling cortisol in saliva over 24 hours, which may be equally sensitive, as late night levels of salivary cortisol are high in Cushingoid patients. Other pituitary hormones may need to be determined, and performing physical examination directed for any visual field defect may be necessary if a pituitary lesion is suspected (which may compress the optic chiasm causing typical bitemporal hemianopia).\n\nWhen these tests are positive, CT scanning of the adrenal gland and MRI of the pituitary gland are performed. These should be performed when other tests are positive, to decrease likelihood of incidentalomas (incidental discovery of harmless lesions in both organs). Scintigraphy of the adrenal gland with iodocholesterol scan is occasionally necessary. Very rarely, determining the cortisol levels in various veins in the body by venous catheterisation working towards the pituitary (petrosal sinus sampling) is necessary.\n\n\nthis link has lots of information,,,hope your ok...god bless
665177
It's different for every patient. It's been 2 years since I was diagnosed and nothing yet for me.I'm on meds. Just type in facial lipostrophy in Google and you can read all about it.Hope this helps.
652385
This is a medical condition involving insufficiency of the adrenal glands, which after prolonged stress first try to compensate hormonally and eventually fail, leading to a life-threatening condition of Addison's Disease after going through the prior stages of Hypoadrenia and next to Hyperadrenia - http://www.royalrife.com/adrenal.html.\n\nRead more on adrenal glands and their impact on our health - http://www.drquinn-nd.com/dynamic_adrenal.html.\n\nIn Las Vegas, a local treating DC, Dr. Alex Bellinghausen, can test and diagnose this condition, and can then treat it.  You may contact Dr. Alex at Better Health Chiropractic at 702-382-4546 or 702-568-0000.  A page is under development, dedicated to Dr. Alex , and may be found on Very Important People.\n\nIt appears that traditional medicine does not recognize this disease often but the symptoms of it lead to other conditions which are life threatening... those they CAN treat.
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My boyfriend has it, and he's gone through a lot.  Many surgeries over the years (and he's only 29) and a rough childhood with teasing and hospital stays.  I think NF ultimately produces some incredibly brave people, who have been through a lot.  Right now we're dealing with a particularly difficult obstacle that NF has put in front of us.  What I think now is... I'm glad I've found people here talking about it and I hope awareness increases.  And, of course, I hope for a cure.
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One of the main symptoms of Polycistic Ovarian Syndrome (P.C.O.S.) is uncontrolled weight gain.  I put one website below, but I'm sure there are better ones.  \n\nThe main point I wanted to make to you is that you must see a very GOOD doctor about your condition.  He/She has to be skilled at managing your condition and this requires a good amount of knowledge of endocrine and thyroid issues.  If your GYN physician is managing your condition, make sure he or she is board-certified (check the medical board website for your state).  Also, if I were you, I might consider seeing an endocrinologist to either provide my primary treatment or to assist the GYN in providing the treatment.\n\nThere is a LOT of information on-line about the illness.  Try to find one that ends in .gov.  I put a link to a Medline article that looks that it came from the National Institutes of Health, so that might be the most trustworthy one.  \n\nOnce you have information, then you will know that they is nothing you can do to lose the weight except to get your thyroid and other hormone levels in check.  There are also new and recent studies finding that people who work the night shift (they focused on diabetics, but diabetics share some of the same issues) have more weight problems than people who work another shift.  Like I said, it was just one study, but it might be something you want to check out more later.\n\nTake care of yourself...
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All these quick-fixes for fat reminded us of DHEA, a wonder compound of the 1990s. DHEA (dehydroepiandrosterone) was supposed to be the Vise Grips of drugs. snake oil?Like the all-powerful super-pliers, it was expected to solve problems yet undiscovered. It was (to overstate it slightly) the cure for which there was no unsusceptible disease.\n\nIn studies over the past 10 years, this naturally occurring hormone prevented cancer and helped fight viruses, mostly in rodents. It restored vitality and libido to the aged and happiness to the depressed, and even slowed the tentacles of Alzheimer's disease. It made vaccines more effective in the elderly, and lowered bad (LDL) cholesterol, thus presumably protecting the heart and arteries.\n\nJust when we began hoping that DHEA would fight flab and change the oil in the old Chevy... along came evidence that DHEA could increase insulin sensitivity, a primary cause of adult-onset diabetes. This blood-sugar disorder affects about 14 million Americans, according to the American Diabetes Association.\n\nAnd it does seem that large doses of DHEA can help fight the bulge -- at least if you're a dog. In a study to be published in Obesity Research, University of Wisconsin-Madison scientists Ilene Kurzman and Gregory MacEwen fed a group of dogs a low-fat, high-fiber diet. Half of the dogs -- chosen at random -- also got a high dose of DHEA, but their identity was not known to the researchers during the study.\n\nDHEA worked: while the control dogs lost 5.5 percent of excess body weight per month, the group treated with DHEA lost 10 percent, says Kurzman.\n\nMeet the cure-all\nBut long before these results were due for publication, DHEA had gained a reputation as a cure-all. After Food and Drug Administration regulations were changed in 1994, it began appearing on drug store shelves as a "dietary supplement."\n\nYet despite years of study and a great deal of new enthusiasm, DHEA is not something that can be recommended for controlling obesity, or much else either. "I would not recommend it for weight loss," says MacEwen, a professor of veterinary medicine who's studied DHEA for almost a decade. "When you look at the rodent studies, you see that they were feeding it at about 0.1 percent of total diet."\n\nfat cell That's a lot -- about 100 times the dose per kilogram of body weight in the pills at your drugstore. (Dietary supplement pills are formulated to restore the DHEA level to what's in the blood of a 30-year-old.)\n\nFurthermore, as MacEwen points out, most of the obesity research has been done in mice and rats. "But a rodent is not a small human, and DHEA may have a totally different effect in people." Specifically, rodents normally have much less DHEA than humans do, so they're not necessarily a good species to test the effects of supplements.\n\nWhat do we know about DHEA?\nIt's a natural hormone produced by the adrenal gland (that's the little critter hitchhiking on the kidney). The concentration peaks in humans about age 25 -- (need we add at the time of peak health and vitality? OK, we added it).\n\nFrom that peak, blood levels decline at about 2 percent per year, raising the prospect that the hormone's disappearance could be linked to all sorts of problems of aging.\n\nLike "not getting it" about cyber-electro-funk music? No. Like decreased immune function, heart attacks, and gaining weight.\n\nIt's not known whether DHEA is actually a hormone, or just a precursor ("raw material") for the hormones testosterone and estrogen. If it's a precursor, then taking supplements could be dangerous -- since estrogen and testosterone can both speed the development of cancers. Indeed, MacEwen says, the only side effect seen in his dog study was an increase in aggressiveness, as the dogs "tended to take on male characteristics toward other dogs." And that's a sign that DHEA is being
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Treatment    Return to top \n\nTreatment for this disease concentrates on avoiding low blood sugar. Frequent feedings are needed during the day, especially foods that contain carbohydrates (starches). Neither fruit nor milk sugar can be adequately broken down in this disease, and are best avoided.\n\nOvernight fasting is avoided by continuous feedings (through a tube that goes through the nose into the stomach) of sugars or uncooked cornstarch. The tube can be put in at bedtime and taken out each morning. A medication called allopurinol, which can lower blood uric acid and decrease the risk for gout, is often used.\n\nSynonyms:\nvon Gierkes disease\nGlucose-6-Phosphatase Deficiency Glycogen Storage Disease\nType I Glycogenosis\nHepatorenal Glycogenosis\n\nIn Type I Glycogen Storage Disease, the enzyme glucose-6-phosphatase is defective in the liver, kidney, and small intestine, where it normally functions. However, the metabolic problem is centered in the liver.\n\nPatients with Type I GSD are unable to release glucose from glycogen. They cannot maintain their blood glucose levels and within a few hours after eating develop hypoglycemia (low blood sugar). The low levels of glucose in the blood of these patients often result in chronic hunger, fatigue, and irritability that is especially noticeable in infants. Symptoms of hypoglycemia only begin to appear when the interval between feedings increases and the infant sleeps through the night or when an illness prevents normal feeding routine. If the blood sugar falls to a low enough point, some patients may experience seizures. \n\nSince Type I patients are able to store glucose as glycogen but not release it normally, with time the stored glycogen builds up in the liver. Hormones, lactic acid, triglycerides, and other products are increased in the blood as the body attempts to raise blood sugar. Fats are stored in the liver along with the glycogen, which leads to enlargement of the liver. The liver does its many other functions normally, and there is not usually any evidence of liver failure. The kidneys are also enlarged due to glycogen accumulation. \n\nThe continued presence of low blood sugar eventually leads the body to experience severe biochemical abnormalities and delayed growth and development. Untreated patients may have muscle wasting and a buildup of body fat.\n\nWhen blood studies are done, it is discovered that there is usually a low blood sugar, elevated blood lactic acid, elevated cholesterol and other fats, and elevated uric acid concentration. High blood pressure has also been seen in a number of patients and when this occurs, appropriate treatment must be given.\n\nIn addition to the problems described above, patients with Glycogen Storage Disease Type Ib can develop frequent bacterial and fungal infections, due to abnormal functioning of the white blood cells. They may also develop chronic pancreatitis, chronic inflammatory bowel disease, and Crohn's disease. \n\nThe diagnosis of Type I GSD will always include blood studies, x-rays (including some of the kidneys), measurements, and ultrasound of the liver. Gene-based mutation analysis can be used to diagnose the majority of Type I patients, while liver biopsy analysis may be needed in some cases. \n\nThe treatments of Type I Glycogen Storage Disease are aimed at correcting the biochemical abnormalities and promoting growth and development. Current treatments consist of providing a continuous source of glucose by giving the patient glucose drinks frequently during the day and, in most cases, continuously overnight. Many medical centers have replaced these glucose feedings with uncooked cornstarch doses, mixed in water, Kool-Aid, or formula. \n\nLinks:\nvon Gierke Disease info from National Organization for Rare Disorders            [NORD]\nOMIM GSD Type I on Online Mendelian Inheritance in Man\n     searchable database\nGSD Type I from emedicine\nAmerican Liver Foundation information on Type I\nvon Gierke D
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I was on lexapro then seroquel then geodon, after weight gain creeping up for about year, all of a sudden I started rapidly gaining, like a pound or two a day, so I had to go off of the medication, I also started getting symptoms of diabetes and cushings syndrome, been off for three months now, lost the severe edema but weight loss is coming very slowly
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Insulin resistance, excessive androgen production, hypothyroidism, hyperprolactinemia, cushings disease.  I think I read that it is also caused from a genetic mutation Syndrome X.  Not for sure on the last one.
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I've been on some pretty heavy doses of steroids in the past, the toughest part is preventing yourself from eating everything in the house!  Try and cut down on the salt and processed foods (incredibly high in fat and salt).  Look for alternatives to flavour things like pepper, lemon juice, spices (I went through a Curry phase). This still may not prevent the typical symptoms of steroid use like Chipmunk cheeks and a round tummy, some people just exibit those symptoms.  Just keep an eye on your weight, try and eat healthy, and don't let Lupus stop you from being active.
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It would be life threatening. Look up Addison's Disease on the internet
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Background\n\nThis is a chronic and relapsing condition occurring within apocrine sweat glands, most commonly in women. Deep seated inflammatory nodules form in the axilla, groin, pubic region, and perineum. It is an androgen-dependent disorder and results from keratinous material occluding the sweat pores. There is an association with lithium therapy and Crohn's disease.\n\nEtiology\n\nHS often occurs in multiple members within families, suggesting a genetic predisposition (5). Various etiological agents have been associated. The increased incidence of HS in obese women with acne led to the theory of HS being associated with an hyperandrogenic endocrine disorder (6,7). One study did not find evidence for biochemical hyperandrogenism in women affected with HS (8). Thus, the role of androgens in HS is still not clear. Smoking (9), lithium (10) and oral contraceptives (11) may also be associated with HS, possibly as triggering factors. Nonetheless, the etiology of the disease is unknown. \n\nFrequency\n\nIn the US: In the United States, the prevalence of HS appears to be 1-2% in the general population. \n\nInternationally: The prevalence of HS appears to be 1% of the general population; it was 4% in a group of young adults who were treated at a clinic for sexually transmitted diseases. HS is probably more common than once thought, but the diagnosis is frequently ignored or missed. HS has a worldwide distribution, though hot, humid environments tend to support its development. \n\nMortality/Morbidity\n\nThe death rate is similar to that in the general adult population. \n\nAlthough rare complications of the disease are described, little is known about the typical effects of HS. HS is a chronic disabling disorder that relentlessly progresses and leads to keloids, contractures, and immobility; patients can become outcasts or at least have difficulty in making social contact. \n\nPathogenesis \n\nHistorically, apocrinitis was believed to be the defining histologic feature and pathogenetic mechanism of HS (12,13). Characteristic lobular abscesses in the apocrine gland, demonstrated histologically, seemed to further implicate apocrine gland involvement in the manifestation of disease (12-14). Recently, histological evidence points to HS being a follicular disease (1,15-19). Histological examination in the majority of specimens reveals follicular involvement, including poral occlusion and folliculitis (1). Apocrinitis as the dominant histological feature is found in only a small number of specimens (1,17). Furthermore, a paucity of apocrine glands was demonstrated in the genitofemoral region, one area commonly affected by HS (1). This finding supports the theory that apocrine gland inflammation is not the etiological and pathogenetic mechanism of HS, but rather a secondary manifestation of follicular involvement (1). \n\nClinical Features \n\nHS may arise singularly or multifocally in the genitofemoral, perianal and axillary areas (1-4). The lesions are painful and have a foul odor attributed to bacterial colonization. Erythematous dermal abscesses form that measure up to 2 cm in diameter. Untreated abscesses will gradually increase in size and may drain to the surface. The course of HS is chronic and remitting, with new abscesses arising in previously unaffected areas or in regions of past involvement. Scarring, fibrosis and sinus tract formations are manifestations of late disease. Strictures can occur secondary to sinus tracts; fistulas may also complicate HS. Squamous cell carcinoma is a rare sequella of longstanding HS (20-24). These cancers may be locally aggressive with distant metastases and a high mortality rate (25). \n\nRace/Sex/Age\n\nRace: Although many authors report no racial predilection, an increased incidence is observed in blacks, possibly because blacks have a greater density of apocrine glands compared with whites. \n\nSex: Although HS is widely considered to occur more frequently in females than in males, with
44127
My Dad had this. I think it depends on if other areas/organs are involved & how involved.  I hope the person who you are inquiring about will be okay. Originally that had told my Dad 2-15 years but it depends on many things.  Have you looked into the steroid treatments? You can look up the American Cancer Society online and see if there are any clinical trials of different things in your area.  Good Luck to you and yours.  God Bless.
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Cortisol causes hypercatabolism in certain parts of the body and not in others. Also, in iatrogenic Cushing's, the main culprit is artificial gluccocorticoids (of which there are several different types that may act on different body parts in different ways). I have seen patients on predinisone with very thin skin, muscle wasting, etc but with build up of body fat because gluccocorticoids stimulate glucconeogensis.
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You can write: \nBPEI Family Network \nSE 820 Meadow Vale Dr.\nPullman, WA  99163\nPhone: (509) 332 6628 USA\nOr email: Ischauble@gocougs.wsu.edu\nWEBSITE:\nhttp://freespace.virgin.net/andy.bowles/\nThey supply information and support to families affected with such disease.
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I haven't heard about that, but you might go to the Lupus Research Foundation's website (or that of another support group for lupus) to inquire.  They may be able to point you in the right direction.
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Yeah, my friend from HS had Lupus as did my suitemate in college.  Check out the following sites for more info.  Be strong!  =)