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Cushing Syndrome And Diabetes

Management Of Hyperglycaemia In Cushings Disease: Experts Proposals On The Use Of Pasireotide - Em|consulte

Management Of Hyperglycaemia In Cushings Disease: Experts Proposals On The Use Of Pasireotide - Em|consulte

Received:3September2012; accepted:23October2012 Management of hyperglycaemia in Cushings disease: Experts proposals on the use of pasireotide Prise en charge de lhyperglycmie au cours de la maladie de Cushing: propositions dexperts pour lutilisation de pasirotide , J.Bertherat b , F.Borson-Chazot c , d , T.Brue e , P.Chanson f , C.Cortet-Rudelli g , B.Delemer h , A.Tabarin i , S.Bisot-Locard j , B.Vergs k aService endocrinologie, CHU Cte-de-Nacre, 14033 Caen, France bService des maladies endocriniennes et mtaboliques, hpital Cochin, 75014 Paris, France cHospices civils de Lyon, universit Lyon1, Lyon, France dInserm U 1052 CRCL, fdration dendocrinologie, groupement hospitalier Est, Lyon, France eService dendocrinologie, diabte et maladies mtaboliques, centre de rfrence des maladies rares dorigine hypophysaire DEFHY, CNRS, CRN2M UMR 7286, Aix-Marseille universit, hpital Timone, APHM, 13385 cedex 15 Marseille, France fService dendocrinologie et des maladies de la reproduction, hpitaux universitaires Paris-Sud, Assistance PubliqueHpitaux de Paris, 94270 Le Kremlin-Bictre, France gClinique Linquette, CHRU de Lille, 59037 Lille, France hService dendocrinologie-diabte-nutrition, hpital Robert-Debr, 51092 Reims, France iDpartement endocrinologiediabtologie et maladies mtaboliques, CHU de Bordeaux, USN du Haut-Lvque, 33604 Pessac, France jNovartis Pharma S.A.S, 92500 Rueil-Malmaison, France kService dendocrinologie, diabtologie et maladies mtaboliques, hpital du Bocage, CHU, 21000 Dijon, France Corresponding author. Tel.: +33 2 31 06 45 86; fax: +33 2 31 06 48 54. Cushings disease causes considerable morbidity and mortality, including cardiovascular, metabolic, respiratory and psychiatric complications, bone demineralization and increased susceptibility to infections. Metabolic Continue reading >>

Hypercortisolism - Other Types Of Diabetes Mellitus - Diapedia, The Living Textbook Of Diabetes

Hypercortisolism - Other Types Of Diabetes Mellitus - Diapedia, The Living Textbook Of Diabetes

Hypercortisolism refers to a range of conditions characterised by an excess of circulating corticosteroids. Endogenous hypercortisolism is known as Cushing's syndrome, and may arise from the adrenal cortex, e.g. because of an adrenal tumour, or may be secondary to overproduction of pituitary adrenocorticotrophic hormone (ACTH). The most common cause of hypercortisolism is, however, steroid therapy. Harvey CushingCushing's syndrome was first described in 1912 when the neurosurgeon Harvey Cushing described a patient known as Minnie G. She showed all the characteristic signs and symptoms of the syndrome, including hyperglycaemia. Since cortisone and adrenocorticotrophic hormone (ACTH) were unknown at the time, Cushing suggested a polyglandular disorder. The term Cushing's syndrome was coined by Fuller Albright in 1943 to designate the consequences of overproduction of a hormone affecting carbohydrate metabolism by the adrenal cortex. [1] In 1948 Lewis Sarett synthesised cortisone, which was then widely used without understanding of its potential adverse consequences. Two years later Van Seters demonstrated that Cushing's syndrome could also be induced by chronic treatment with glucocorticoids. [2] [3] Chronic treatment with glucocorticoids is the most common cause of hypercortisolism, whereas endogenous hypercortisolism (Cushing's syndrome) is a rare disease with an incidence of 1015 per million people per year. [4] Cushing' syndrome is usually due to a pituitary adenoma and is three to five times more common in women than in men. Hypercortisolism is associated with diabetes, obesity and hypertension, and should be considered in patients with these conditions, and in all those on steroid therapy. Some 20% of patients with Cushing's syndrome have a diagnosis of diabetes, b Continue reading >>

Diabetes Mellitus Secondary To Cushings Disease

Diabetes Mellitus Secondary To Cushings Disease

Diabetes Mellitus Secondary to Cushings Disease Endocrinology Unit, Department of Medicine DIMED, University of Padua, Padua, Italy Edited by: Carla Giordano, Universit degli Studi di Palermo, Italy Reviewed by: Anton Luger, Medizinische Universitt Wien, Austria; Mauro Antonio Czepielewski, Universidade Federal do Rio Grande do Sul (UFRGS), Brazil; Rosario Pivonello, Universit degli Studi di Napoli Federico II, Italy *Correspondence: Mattia Barbot, [email protected] Specialty section: This article was submitted to Pituitary Endocrinology, a section of the journal Frontiers in Endocrinology Received 2018 Feb 13; Accepted 2018 May 14. Copyright 2018 Barbot, Ceccato and Scaroni. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. Associated with important comorbidities that significantly reduce patients overall wellbeing and life expectancy, Cushings disease (CD) is the most common cause of endogenous hypercortisolism. Glucocorticoid excess can lead to diabetes, and although its prevalence is probably underestimated, up to 50% of patients with CD have varying degrees of altered glucose metabolism. Fasting glycemia may nevertheless be normal in some patients in whom glucocorticoid excess leads primarily to higher postprandial glucose levels. An oral glucose tolerance test should thus be performed in all CD patients to identify glucose metabolism abnormalities. Since diabetes mellitu Continue reading >>

Cushing's Syndrome | Diabetes & Endocrinology

Cushing's Syndrome | Diabetes & Endocrinology

See your doctor if you have any of the signs or symptoms of Cushings syndrome. Cushings syndrome is caused by long-term exposure to too much cortisol. Cortisol is a hormone made in your body to protect your health. Too much cortisol, however, can cause health problems. Sometimes, long-term use of the steroid medicine cortisone can lead to Cushings syndrome. Sometimes, tumors can make chemicals that cause your body to make too much cortisol. Lab tests, including urine and blood tests, can show if you have Cushings syndrome and a possible cause of it. Imaging tests, such as an MRI or CT scan, may be used to check for tumors or other issues with the adrenal and pituitary glands the glands that help control cortisol levels in the body. Treatment depends on why your cortisol levels are too high. If you take the artificial hormone, cortisone, you may just need to take a smaller dose. If the cause is a tumor, surgery and other medical treatments may be necessary. If you take a steroid medicine, like cortisone, know the signs and symptoms of Cushings syndrome. If you have any of the signs and symptoms, see your healthcare provider. Early treatment may help prevent any long-lasting effects of the condition. If you use a steroid inhaler, rinse your mouth after breathing in the medicine. People who are obese and have type 2 diabetes have a higher risk of developing Cushings syndrome. They can lower their risk by: Getting recommended amounts of physical activity Continue reading >>

Cushing's Syndrome - Symptoms, Causes, Diagnosis & Treatment

Cushing's Syndrome - Symptoms, Causes, Diagnosis & Treatment

Using corticosteroids is the most common cause of Cushing's syndrome Cushings syndrome is a condition in which can occur if you have high levels of the stress hormone, cortisol, in your blood. Cortisol increases our blood pressure and blood glucose levels and diabetes is one complication which can result from untreated Cushings syndrome. Physical signs of Cushings syndrome may include: Fatty tissue building up typically around the waist, upper back, between the shoulders and the face. Slim arms and legs contrasting significantly with fat deposits around your middle Striae - red or purple stretch marks, which may resemble tiger stripes, commonly found on the abdomen, near the armpits or around the breasts and thighs Women may experience thicker than normal facial and body hair (hirsutism) and missed or irregular periods. Men may experience a loss of libido , difficulty achieving erections and loss of fertility. High blood pressure and high blood glucose levels ( hyperglycemia ) may commonly be experienced with Cushings syndrome. Usage of corticosteroids is the most common cause of Cushings syndrome. Corticosteroids are used to treat illnesses including: Doctors will prescribe the lowest effective dose to reduce the likelihood of complications, such as Cushings syndrome, developing. When Cushings syndrome results from steroid usage, this is known as iatrogenic Cushings syndrome. A less common reason for Cushings syndrome developing is known as endogenous Cushings syndrome, which is caused by the development of a tumour in the pituitary gland, one of your adrenal glands or one your lungs. Talk about Cushing's Syndrome in the Diabetes Forum A tumour in the pituitary gland is the more common cause for endogenous Cushings syndrome, accounting for about 7 out of 10 cases, and Continue reading >>

When To Think Cushings Syndrome In Type 2 Diabetes

When To Think Cushings Syndrome In Type 2 Diabetes

When to think Cushings syndrome in type 2 diabetes ESTES PARK, COLO. Diabetes mellitus, osteoporosis, and hypertension are conditions that should boost the index of suspicion that a patient with some cushingoid features may in fact have endogenous Cushings syndrome, Dr. Michael T. McDermott said at a conference on internal medicine sponsored by the University of Colorado. An estimated 1 in 20 patients with type 2 diabetes has endogenous Cushings syndrome. The prevalence of this form of hypercortisolism is even greater estimated at up to 11% among individuals with osteoporosis. In hypertensive patients, the figure is 1%. And among patients with an incidentally detected adrenal mass, its 6%-9%, according to Dr. McDermott, professor of medicine and director of endocrinology and diabetes at the University of Colorado. "Endogenous Cushings syndrome is not rare. I suspect Ive seen more cases than Ive diagnosed," he observed. "Ive probably missed a lot because I failed to screen people, not recognizing that they had cushingoid features. Not everyone looks classic." There are three screening tests for endogenous Cushings syndrome that all primary care physicians ought to be familiar with: the 24-hour urine cortisol test, the bedtime salivary cortisol test, and the overnight 1-mg dexamethasone suppression test. "I think if you have moderate or mild suspicion, you should use one of these tests. If you have more than moderate suspicion if a patient really looks like he or she has Cushings syndrome then I would use at least two screening tests to rule out endogenous Cushings syndrome," the endocrinologist continued. The patient performs the bedtime salivary cortisol test at home, obtaining samples two nights in a row and mailing them to an outside laboratory. The overnight dexamet Continue reading >>

Cushing Syndrome | Johns Hopkins Diabetes Guide

Cushing Syndrome | Johns Hopkins Diabetes Guide

Hormonal disorder caused by prolonged exposure to high levels of glucocorticoids. May be due to exogenous glucocorticoids (iatrogenic) or endogenous hypercortisolism. May be ACTH dependent or independent. Cushing syndrome due to an ACTH-secreting pituitary adenoma is referred to as Cushing disease. More common in women particularly in reproductive age [7] Overt endogenous Cushing incidence in general population: 2.4 cases per 1 million persons per year with standardized mortality ratio of 3.8 for affected persons in Spain [11] Iatrogenic Cushing more common but measurements of incidence rate are imprecise. Approximately 25% of overweight, type-2 diabetes patients have impaired morning cortisol suppression after a low-dose overnight dexamethasone suppression test but do not necessarily have Cushing [9] . Most common hormonal abnormality in patients with adrenal incidentaloma. Detailed history to assess for any use of exogenous glucocorticoids (oral, topical, injection, inhaled). CYP3A4 inhibitors (especially ritonavir) inhibit glucocorticoid clearance and contribute to Cushingoid symptoms when taken with concurrent inhaled, oral or injectable steroids. Screening: late night salivary cortisol x 2, 24-hour urine free cortisol (UFC) x 2, low-dose dexamethasone suppression test (after 1mg dexamethasone at 11pm, normal 8AM cortisol < 1.8 mcg/dL) At least two clearly abnormal (e.g. UFC > 3 times upper limit of normal) tests using different test methods needed to establish diagnosis [1] . Use of estrogen containing OCPs can contribute to false positive dexamethasone suppression test due to increased cortisol binding globulin and may be discontinued prior to testing. After confirming hypercortisolism must measure ACTH to identify if ACTH dependent or independent. ACTH< 5 pg/mL Continue reading >>

Pathophysiology Of Diabetes Mellitus In Cushing's Syndrome.

Pathophysiology Of Diabetes Mellitus In Cushing's Syndrome.

Pathophysiology of diabetes mellitus in Cushing's syndrome. Department of Molecular and Clinical Endocrinology and Oncology, Federico II University, Naples, Italy. [email protected] Neuroendocrinology. 2010;92 Suppl 1:77-81. doi: 10.1159/000314319. Epub 2010 Sep 10. Cushing's syndrome is commonly complicated with an impairment of glucose metabolism, which is often clinically manifested as diabetes mellitus. The development of diabetes mellitus in Cushing's syndrome is both a direct and indirect consequence of glucocorticoid excess. Indeed, glucocorticoid excess induces a stimulation of gluconeogenesis in the liver as well as an inhibition of insulin sensitivity both in the liver and in the skeletal muscles, which represent the most important sites responsible for glucose metabolism. In particular, glucocorticoid excess stimulates the expression of several key enzymes involved in the process of gluconeogenesis, with a consequent increase of glucose production, and induces an impairment of insulin sensitivity either directly by interfering with the insulin receptor signaling pathway or indirectly, through the stimulation of lipolysis and proteolysis and the consequent increase of fatty acids and amino acids, which contribute to the development of insulin resistance. Moreover, the peculiar distribution of adipose tissue throughout the body, with the predominance of visceral adipose tissue, significantly contributes to the worsening of insulin resistance and the development of a metabolic syndrome, which participates in the occurrence and maintenance of the impairment of glucose tolerance. Finally, glucocorticoid excess is able to impair insulin secretion as well as act at the level of the pancreatic beta cells, where it inhibits different steps of the insulin secretion proce Continue reading >>

Management Of Diabetes Mellitus In Cushings Syndrome

Management Of Diabetes Mellitus In Cushings Syndrome

Management of Diabetes Mellitus in Cushings Syndrome Academic Unit of Diabetes and Endocrinology, University of Sheffield Room OU142, Floor O, Royal Hallamshire Hospital Active Cushings syndrome is associated with insulin resistance induced by the high and prolonged circulating level of glucocorticoids. In endogenous Cushings syndrome the overall incidence of diabetes mellitus and insulin resistance is very likely to be under-reported as not all patients are actively investigated with glucose tolerance tests. Whilst it is common clinical experience that management of diabetes mellitus is necessary in patients with Cushings syndrome there is a dearth of literature-based evidence to support which regimes are the most effective. Therefore, a pragmatic approach is necessary on an individualized patient basis, whereby patients are stratified according to the severity of their impaired glucose homeostasis. The most effective means of control of diabetes mellitus in a patient with active Cushings syndrome is to lower the levels of circulating cortisol. This may initially be achieved by using adrenal steroidogenesis blockade with drugs including metyrapone, ketaconazole, or, on occasion, mitotane. The rapid action of metyrapone is particularly suitable in this circumstance. Despite this, diabetes-specific therapy is often necessary and metformin and PPAR- agonists may be of use, but in the acute setting insulin therapy is frequently needed. Definitive management directed against source driving Cushings syndrome is often highly effective at either reducing the severity of diabetes, or allowing its complete resolution. Patients experiencing diabetes mellitus in the context of exogenously administered glucocorticoids may well require insulin therapy for the period that the high l Continue reading >>

Pathophysiology Of Diabetes Mellitus In Cushings Syndrome

Pathophysiology Of Diabetes Mellitus In Cushings Syndrome

Cushings syndrome is a rare clinical entity resulting from pathologic hypercortisolemia [1]. Patients may present along a spectrum of severity from classical signs and symptoms of cortisol excess to subclinical or entirely asymptomatic disease [13]. The most common endogenous causes are ACTH-producing pituitary adenomas, cortisol-secreting adrenal adenomas, and ectopic ACTH-secreting tumors [4, 5]. Arriving at an accurate diagnosis of the underlying etiology and initiating appropriate treatment in a timely manner are essential to preventing morbidity and mortality [6, 7]. Diagnostic evaluation requires a systematic approach and significant expertise [2, 4]. Although surgery is often the primary treatment modality, multispecialty care is often necessary for optimal outcomes [8]. The hormones produced by the adrenal gland have important effects on the bone both in physiological and pathological conditions. The role of cortisol secretion on the bone physiology during growth is not fully understood. During the adult life, the degree of the cortisol secretion, still in the normal range, seems to directly correlate with the bone mineral density in elderly individuals and in osteoporotic women. The overt and subclinical cortisol excess leads to an increased risk of fracture partially independent of the bone mineral density reduction and possibly related to a reduced bone quality. The individual sensitivity to cortisol due to the different polymorphisms of the glucocorticoid receptor (GR) or of the 11-hydroxysteroid dehydrogenase may modulate the effect of glucocorticoids (GCs) on the bone, thus explaining, at least in part, the wide interindividual variability of the skeletal consequences of the hypercortisolism. The adrenal androgens excess in congenital adrenal hyperplasia Continue reading >>

Sphingolipids - Type 2 Diabetes, Metabolic & Cushing's Syndromes

Sphingolipids - Type 2 Diabetes, Metabolic & Cushing's Syndromes

Metabolic syndrome X and type 2 diabetes share many metabolic and morphological similarities with Cushing's syndrome, a rare disorder caused by systemic glucocorticoid excess. Pathologies frequently associated with these diseases include insulin resistance, atherosclerosis, susceptibility to infection, poor wound healing, and hypertension. The similarity of the clinical profiles associated with these disorders suggests the influence of a common molecular mechanism for disease onset. Interestingly, numerous studies identify ceramides and other sphingolipids as potential contributors to these sequelae. Herein we review studies demonstrating that aberrant ceramide accumulation contributes to the development of the deleterious clinical manifestations associated with these diseases. Metabolic syndrome X,[ 1 ] type 2 diabetes,[ 2 ] and Cushing 's syndrome[ 3 ] share a common set of pathogenic characteristics. A hallmark of these diseases is insulin resistance, i.e., when a maximal dose of the hormone is incapable of optimally eliciting its pleiotropic biological effects (e.g., stimulation of glucose uptake and glycogen, protein, and lipid synthesis in skeletal muscle). Other common disorders associated with these diseases include atherosclerosis, susceptibility to infection, poor wound healing, and hypertension. An enigma plaguing scientists has been to understand how these syndromes with markedly different etiologies share such a common clinical profile. Obesity predisposes individuals to both type 2 diabetes and metabolic syndrome X, but the mechanism by which increased adiposity induces defects in tissues other than adipose has remained elusive. A hypothesis gaining credibility is that increased deposition of lipid molecules in tissues not suited for fat storage, because Continue reading >>

Cushing[apos]s Syndrome And Diabetes

Cushing[apos]s Syndrome And Diabetes

Endocrine Abstracts (2015) 37 EP27 | DOI: 10.1530/endoabs.37.EP27 Said Azzoug, Leyla Rabehi, Sara Hannachi, Houda Medjdoubi & Farida Chentli Author affiliations View ePoster Download ePoster Endocrinology and Metabolic Diseases Department, Bab El Oued Hospital, Algiers, Algeria. Introduction: Cortisol has numerous actions on glucose metabolism and insulin action which explain the frequency of glucose abnormalities in Cushings syndrome (CS). The aim of our work was to assess the prevalence and characteristics of diabetes in CS. Material and methods: This is a retrospective study concerning 51 CS (44F/7M) in whom we looked for the presence of diabetes either by fasting glycaemia or 75 g oral glucose tolerance test. Thereafter, we looked for the characteristics of diabetes in CS. CS was secondary to Cushings disease in 82% and to adrenal adenoma in 18%. Results: 55% of patients have diabetes. Among diabetic patients, 39% have high blood pressure and 42% have a family background of diabetes. 40% of diabetics were treated with oral treatment, 25% with insulin and 35% were on life style therapy. Mean age was 31.9210.26 years; it was 31.6210.54 years in patients with diabetes vs 32.4510.04 years in patients without diabetes. Mean BMI was 31.477.33 kg/m2; it was 31.307.77 kg/m2 in patients with diabetes vs 31.896.47 kg/m2 in patients without diabetes. Diabetic retinopathy was present in 10% and diabetic neuropathy in 5%. After treatment of CS diabetes resolved in 40% and persisted in 60%. Conclusion: Diabetes mellitus is frequent in cortisol excess states, the high frequency of diabetes in our study may be explained by preexistent undiagnosed diabetes as diabetes persisted in 60% after resolution of CS. Continue reading >>

Occult Cushings Syndrome In Type-2 Diabetes

Occult Cushings Syndrome In Type-2 Diabetes

Subclinical Cushings syndrome (SCS) caused by adrenal incidentalomas is frequently associated with overweight and insulin resistance. Metabolic syndrome X may therefore be a clue to the presence of CS. However, the incidence of CS in this situation remains unknown. We have conducted a prospective study to evaluate the prevalence of occult CS in overweight, type-2 diabetic patients devoided of specific clinical symptoms of CS. Two hundred overweight, type-2 diabetic patients, consecutively referred for poor metabolic control (HbA1C > 8%), were studied as inpatients. A first screening step was performed with the 1-mg overnight dexamethasone suppression test (DST) using a revised criterion for cortisol suppression (60 nmol/liter) to maximize the sensitivity of the procedure. A second confirmatory step of biochemical investigations (midnight plasma cortisol concentration, plasma cortisol circadian rhythm, morning plasma ACTH concentration, 24-h urinary free cortisol, and 4-mg iv DST) was performed in patients with impaired 1-mg DST. A third step of imaging studies was performed according to the results of second-step investigations. Fifty-two patients had impaired 1-mg DST. Among these, 47 were further evaluated. Thirty were considered as false positives of the 1-mg DST, whereas 17 displayed at least one additional biological abnormality of the hypothalamic-pituitary-adrenal axis. Definitive occult CS was identified in four patients (2% of the whole series) with Cushings disease (n = 3) and surgically proven adrenal adenoma (n = 1). Definitive diagnosis remains to be established in seven additional patients (3.5%) with mild occult CS associated with unsuppressed plasma ACTH concentrations and a unilateral adrenal tumor of 1029 mm in size showing prevalent uptake at radioch Continue reading >>

Cushing's Study Finds Oral Diabetes Therapy Limits Pituitary Tumor Growth - Cushing's Disease News

Cushing's Study Finds Oral Diabetes Therapy Limits Pituitary Tumor Growth - Cushing's Disease News

Metformin, an oral type 2 diabetes medicine, can promote cell death in tumors that cause Cushings disease and reduce the excessive production of the adrenocorticotroph hormone (ACTH) that underlies it, a study in mice cells reports. These findings suggest that metformin , a tablet, may offer a new way of treating the pituitary tumors that produce excess ACTH and cause Cushings disease. The research, Metformin suppresses growth and adrenocorticotrophic hormone secretion in mouse pituitary corticotroph tumor AtT20 cells , was published in Molecular and Cellular Endocrinology . The work was developed at The First Aliated Hospital of Chongqing Medical University in China. The most common cause of Cushings disease is pituitary adenoma a benign tumor in the pituitary gland, found behind the nose and near the underside of the brain which leads to overproduction of a hormone called ACTH. ACTH causes the adrenal glands, located on top of the kidneys, to make too much cortisol. Known as the stress hormone, cortisol has anability to increase blood-sugar levels, inhibit digestion, and halt immune activities all processes crucial to the body in times of stress. Cushings effects include metabolic and cardiovascular complications, bone alterations, kidney stones, autoimmune diseases, and susceptibility to opportunistic infections. Signifor (pasireotide, by Novartis ) is the only medicine approved by the European Medicines Agency and the U.S. Food and Drug Administration to treats adults with Cushings disease for whom surgery is not an option or whose disease failed to respond to surgery. While effective at reducing tumor size and ACTH secretion, 73 percent of patients in a Phase 3 trial experienced high blood sugar levels after taking Signifor. Some developed uncontrolled diabetes du Continue reading >>

Diabetes I And Cushing's Syndrome

Diabetes I And Cushing's Syndrome

D.D. Family type I, pumping Apidra in Accuchek Combo I have a question for you. The other day, there was a documentary on Cushing's Syndrome. It felt like I was facing myself, looking at that patient.... It made me sick to my stomach. For several years I have had many symptoms.... Does anyone recognize any of these or does anyone of you have Cushings? * lower back pain when bending or standing Thanks for thinking with me. I'm having a blood test soon, to check for Cushing's. Hope to get some response. Cathy, who loves to live, but who finds life pretty difficult some days D.D. Family T1 since 9/05, pump since 4/06, CGMS since 10/07 I have been diagnosed with Cushing's, and I have T2. I had chronic hives that I was given a lot of steroids to battle. Insomnia and diabetes are also complications of Cushing's. I had/have terrible insomnia. I have the opposit to cushings, I don't produce any steroids so have addison's disease. D.D. Family type I, pumping Apidra in Accuchek Combo thank you all for responding. I'm pretty anxious about this all. If there's a tumor in the brain, it means operation... I'm not really looking forward to that... Continue reading >>

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