Myth: “Vitamins and Natural Remedies can cure/heal Cushing’s”

Posted on July 2, 2015 by MaryO

myth-busted

 

More from Dr. Karen Thames:

Myth: “Vitamins and Natural Remedies can cure/heal Cushing’s”

Fact: Do you know how many people have told me that if I just “juice”, I will be cured from Cushing’s or Adrenal Insufficiency?! I appreciate the sentiment, but the sad reality is that no amount of juicing and no vitamin will cure Cushing’s. Some Cushing’s patients do take vitamins, some do eat raw food or paleo diets, and some even juice. However, this is just a lifestyle choice and not an attempt to cure Cushing’s. I must admit that when you have such a dreadful disease, you do sometimes take desperate measures to heal yourself. Perhaps, doing acupuncture or some other form of natural healing technique seems attractive at times. Take it from a person who has had acupuncture, seen many natural doctors, juiced, took vitamins, ate a raw food diet, and yes, I EVEN did a series of colonics! If you have ever had colonics, you know that it brings new meaning to the phrase, “no pain, no gain!”

Seriously, this is all before I knew I had Cushing’s. I watched as every person who administered the different kinds of treatment scratched their heads as I continued to gain weight, eventually at a rate of 5 pounds per week! They couldn’t believe that I was actually still gaining weight. Their natural and not surprising response, of course, was to project blame onto me. “Karen, there is NO way you are following protocol! You MUST be lying on your food log!” What we all didn’t realize is that I was suffering from a life-threatening illness called Cushing’s Disease that caused morbid obesity in me and that none of those “remedies” would EVER work!

Now, I have already been in Twitter wars over this topic. Someone tried to tell me that a raw food diet will “cure Cushing’s” and then she told me that I am “ignorant and in denial”! She proceeded to tell me that her daughter, though she had surgery to treat Cushing’s, was REALLY cured because of changing her diet. She also told me that the daughter, who had her Adrenal Glands removed, didn’t need steroids. Listen folks, this is VERY dangerous! I have no adrenal glands and I NEED steroids! Cortisol is life sustaining and you will die without it! I fully expect that someone will argue this point until the cows come home. It doesn’t matter. It won’t change the facts. Cushing’s is caused by excess cortisol in the body. The ONLY treatment is to target the source of the excess cortisol (i.e.brain tumor, adrenal tumor, ectopic tumor, or prolonged steroid use for another disease). Targeting the source is the first line of treatment. Cushing’s Syndrome/Disease will lead to death if not treated properly! #BattlegroundDiagnosis

Disclaimer: I am not a medical doctor. Please seek the advice of a medical professional if you have questions or need further assistance.

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ALD403 (migraine drug) and ALD1613 (for Cushing’s disease)

Posted on July 2, 2015 by MaryO

As it moves into crucial Phase 3 drug trials for its flagship migraine treatment, Bothell-based Alder Biopharmaceuticals (Nasdaq: ALDR) is looking to raise a lot of cash.

Alder is offering up to $200 million shares of its common stock, according to SEC filings.

The company plans to use the money to develop its drugs ALD403 (its migraine drug) and ALD1613 (for Cushing’s disease), conduct clinical trials and commercialize these drugs. Funds will also go toward “general corporate purposes,” which might include the acquisition or licensing of other products, businesses or technologies, according to those filings.

From http://www.bizjournals.com/seattle/blog/health-care-inc/2015/06/alder-biopharmaceuticals-sets-out-to-raise-200m-to.html

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An Open Label Study to Assess the Safety and Efficacy of COR-003 (2S, 4R ketoconazole) in the Treatment of Endogenous Cushing’s Syndrome

Posted on July 1, 2015 by MaryO
RESEARCH STUDY SUMMARY

An Open Label Study to Assess the Safety and Efficacy of COR-003 (2S, 4R ketoconazole) in the Treatment of Endogenous Cushing’s Syndrome

PURPOSE

The primary objectives of this study are to evaluate the efficacy of ascending doses of COR-003 in subjects with elevated levels of cortisol due to endogenous Cushing’s Syndrome by assessment of reduction in Urinary Free Cortisol (UFC) concentrations and to identify the range of safe and effective doses of COR-003 that reduce mean UFC concentrations ≤ULN (upper limit of normal) of the assay at month 6 of the maintenance phase of dosing without a prior dose increase in that phase.

TO LEARN MORE

CW ID: 208654
Date Last Changed: June 25, 2015

Inclusion Criteria:

Subjects eligible for enrollment in the study must meet all the following criteria:

  • Male or female, ≥18 year of age
  • Confirmed diagnosis of persistent or recurrent CS (with or without therapy) or newly diagnosed disease, if they are not candidates for surgery. Subjects in whom surgery will be delayed beyond 5 months will be permitted to participate. CS will be defined according to the criteria in the guidelines for diagnosis of CS (Nieman 2008). Previous medical records will be collected and used to support the diagnosis. The diagnostic criteria for appropriateness of inclusion of each subject into the study will be reviewed by the Medical Monitor. Diagnosis of the disease will be based on the association of clinical features of endogenous CS (see Appendix G in clinical protocol), review of past medication history, excluding exogenous sources of glucocorticoids, and abnormal values from two of the three following tests:
    • Elevated 24-hour UFC levels ≥1.5X ULN of assay based on a minimum of 4 measurements from adequately collected urine. Urine may be collected on sequential days.
    • Abnormal DST: Elevated 8 AM serum cortisol ≥1.8 ug/dL (50 nmol/L) after 1 mg dexamethasone orally at 11 PM the evening prior (if not conducted already in the diagnostic workup of the subject within the previous 6 months; previous test results and details of conduct will need to be available; normal serum cortisol ≤ 1.4 ug/dL)
    • Elevated late night salivary cortisol concentrations (at least 2 measurements) >ULN at screening
    • [NOTE: For subjects with estimated glomerular filtration rate (eGFR as determined by MDRD equation >40 and <60 mL/min) a late night salivary cortisol test (≥2 measurements) MUST be conducted in addition to measuring UFC levels to demonstrate evidence of CS.]
  • Previously irradiated subjects will be allowed as long as the radiation treatment occurred ≥2 years ago and they do have stable UFC levels based on 24-hour urine collections for at least 6 months. The total number of previously irradiated subjects will not exceed 10.
    • In the vast majority of subjects treated with radiation, efficacy is observed in <2 years.
  • Confirmed diagnosis of persistent or recurrent endogenous hypercortisolemia as defined by UFC concentrations on repeated determinations (described in Inclusion #2) caused by either ACTH-dependent or ACTH-independent etiologies.
  • Subjects on treatment for CS for whom treatment has been inadequate or not well tolerated must agree to the following minimum washout periods as determined by the nature of their treatment before baseline assessments are performed for participation in this study:
    • Inhibitors of steroidogenesis: 2weeks; subjects on ketoconazole will be considered inadequately treated if they had failed to normalize UFC with a dose lower than or equal to 600 mg/day (also see Exclusion 7 below).
    • Dopamine agonists: bromocriptine (2 week), cabergoline (8 weeks)
    • Octreotide acetate LAR and lanreotide Autogel®: 12 weeks
    • Lanreotide SR/long-acting pasireotide: 8 weeks
    • Octreotide acetate (immediate release formulation) or short-acting pasireotide: 1 week
    • Mifepristone (RU 486): 4 weeks
  • Subjects on megasterol acetate (medroxyprogesterone acetate) must agree to a wash out of ≥6 weeks prior to receiving the first dose of the study medication.
  • Female subjects should be either post-menopausal, surgically sterile, or women of child-bearing potential (WOCP) with a negative serum beta human chorionic gonadotropin (ßhCG) pregnancy test prior to entering the study and who agree to use an acceptable method of contraception, for the duration of the study. Condoms will be considered an acceptable form of contraceptive.
  • 12-lead ECGs show no acute ischemia or clinically significant abnormality needing medical intervention
  • Ability to comprehend and comply with procedures
  • Agree to commit to participate in the current protocol
  • Subjects provide written informed consent prior to any study procedures being performed (all subjects should be able to understand the informed consent form and any other documents that subjects are required to read)

Exclusion Criteria:

Subjects will be excluded from the study if any of the following criteria are met:

  • De novo Cushing´s disease AND a candidate for pituitary surgery
    • If surgery is to be delayed for >5 months, subjects may be allowed to participate in the trial while awaiting surgery, but must agree to complete this study prior to surgery.
  • Subjects treated with radiation within the previous 2 years.
    • In the vast majority of subjects treated with radiation, efficacy is observed in <2 years.
  • Characteristics of pseudo-CS (see Appendix H in clinical protocol)
  • Subjects with adrenal carcinoma
  • Body Mass Index (BMI) exceeding 50 kg/m2
  • Body habitus preventing repeated venipuncture as required by protocol
  • Subject is currently in another study or has received any investigational treatment (drug, biological agent or device) within 30 days or 5 half lives of screening, whichever is longer
  • History of significant abnormalities in liver function tests on ketoconazole; history of therapeutic response failure to ketoconazole as defined by lack of normalization of UFC at a dose greater than 800 mg/day; lack of therapeutic response failure at maximum dose of mitotane
  • Male and female subjects with QTc interval of >470 msec
  • History of Torsades des Pointes or ventricular tachycardia or ventricular fibrillation
  • Subjects with a non-endogenous source of hypercortisolemia such as exogenous source of glucocorticoids or therapeutic use of ACTH
  • History of malignancy, other than thyroid, early stage prostate, squamous cell and basal cell carcinoma, within 3 years prior to the initial dose of the study medication. Subjects with history of carcinoma must have a life expectancy of >1 year and must be on stable doses of their specific therapies. Subjects with early stage prostate cancer undergoing no treatment due to low grade potential may be enrolled.
  • Diagnosis of HIV
  • History of persistent uncontrolled hypertension (>210/110 mmHg) despite medical intervention
  • Subjects with hypercholesterolemia who are on current atorvastatin or simvistatin and not willing or unable to change to alternative therapies as noted (pravastatin, fluvastatin, and rosuvastatin) with 2 weeks of study screening
  • Subjects with T2DM or with a history of hyperglycemic episodes requiring repeated, frequent hospitalizations
  • Subjects with decreased renal function as defined by eGFR ≤40 mL/min, using Modified Diet in Renal Disease (MDRD) equation for estimating renal function (eGFR).
  • Any other clinically significant medical condition, as determined by the Investigator that precludes enrollment and participation in the study through completion (for example, New York Heart Association (NYHA) class III or IV congestive heart failure).
  • Known hepatic disease, other than mild to moderate hepatic steatosis consistent with fatty infiltration (non-alcoholic steatohepatitis [NASH]), with ongoing sustained biochemical activity (subjects with CS would be at risk for NASH)
  • History of recurrent gall stone attacks or pancreatitis
  • Positive for hepatitis B surface antigen (HbsAg) or positive hepatitis C test
  • Liver function tests (LFT) must not be above the following cut-offs at screening: ALT and/or AST >3.0X ULN, alkaline phosphatase (AP) >1.5X ULN and total bilirubin >ULN. If all LFTs are within normal limits (WNL) and total bilirubin is elevated, examination of direct and indirect bilirubin may be conducted. Subjects with indirect total bilirubin up to 3X ULN are presumed to have Gilbert’s syndrome and may be enrolled if all other LFTs are WNL.
  • Presence of any other clinically significant medical condition, as determined by the Investigator that would preclude the subject from being able to follow instructions or to perform the necessary procedures (for example, psychiatric instability or severe disability)
  • Compression of the optic chiasm
  • Abnormal free T4. Subjects with TSH
  • Excessive alcohol intake (>20 g per day for females (1.5 standard alcohol drinks) or >30 g per day for males (2.0 standard alcohol drinks) (a standard drink contains 14 g of alcohol: 12 oz of beer, 5 oz of wine or 1.5 oz of spirits) or drug abuse. (1.0 fluid oz (US) = 29.57 ml)
  • The subject is currently taking any H2 receptor antagonists or proton-pump inhibitors (which inhibit absorption of COR-003). Only over-the- counter liquid and tablet antacids are allowed which should be used in moderation and taken a minimum of 2 hours after dosing of COR-003.
  • The subject is receiving the following concomitant therapies:
    • Weight loss medications (prescription or over the counter)
    • Coadministration of COR-003 and drugs primarily metabolized by the cytochrome P450 3A4 enzyme system may result in increased plasma concentrations of the drugs that could increase or prolong both therapeutic and/or adverse effects. Therefore, appropriate dosage adjustments may be necessary.
    • Medications with metabolism largely mediated by CYP3A4 and a narrow therapeutic margin include: cyclosporine, midazolam, triazolam, alprazolam, digoxin, coumarin-derivatives, phenytoin, rifampin, erythromycin, clarithromycin, loratadine, astemizole, terfenadine, nicotinic acids, resins, orlistat, sibutramine, HIV protease inhibitors, thiazolidinodiones, aliskiren, and spironolactone.
    • A complete list of medications metabolized by or with an effect on cytochrome P450 3A4 is provided in Appendix K. Also see Section 10.2.
    • Coadministration of strong inducers or inhibitors of CYP3A4 enzyme system that may interfere with COR-003 and cannot be discontinued prior to the start of the study (see Appendix K for the list)
    • Statins other than pravastatin, fluvastatin and rosuvastatin
    • Following herbal medicines should be avoided: St John’s Wort, yohimbe and red rice yeast
    • Potent topical steroids, containing urea or salicylic acid, which are applied over 20% of the body
    • Inhaled steroid medications that exceed minimal to moderate use
    • Carbamazipine, fenofibrate, carbenoxolone
    • Excessive ingestion of genuine licorice
  • Pregnant or lactating women
  • Any other condition which would increase the risk of participation in the trial in the opinion of the Investigator

Contact

Adrine Gdakian
UCLA School of Medicine
700 Tiverton Avenue, Factor Building Rm 9-240
Los Angeles, CA 90095
Phone: 310-825-5874
Fax: 310-206-5553

Jessica Rios-Santiago
Coastal Metabolic Research Center University Medical Center, Dept. of Endocrinology
3454 Loma Vista Rd.
Ventura, CA 93003
Phone: 805-658-8460
Fax: 805-658-8462

Betsy Parrott, RN, CCRC
Rhode Island Hospital, Hallett Center for Diabetes and Endocrinology
900 Warren Avenue, Suite 300
East Providence, RI 02914
Phone: 401-444-2091
Fax: 401-444-4921

Becky Wood, CCRP
Swedish Neuroscience Research
500 17th Ave
Professional Bldg 303
Seattle, WA 98122
Phone: 206-320-7115

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Moderately impaired renal function increases morning cortisol and cortisol levels at dexamethasone suppression test in patients with incidentally detected adrenal adenomas

Posted on June 26, 2015 by MaryO
Clin Endocrinol (Oxf). 2015 May 23. doi: 10.1111/cen.12823. [Epub ahead of print]
Olsen H1, Mjöman M2.

Author information

Abstract

OBJECTIVE:

Patients with incidentally detected adrenal adenomas may have subclinical hypercortisolism. We hypothesized that impaired renal function could lead to increased cortisol levels in these patients.

DESIGN:

Descriptive retrospective study of consecutive patients.

PATIENTS:

A total of 166 patients with incidentally detected unilateral adrenal adenomas were examined during 2008-2013.

MEASUREMENTS:

Levels of cortisol, ACTH and cortisol at 1 mg overnight dexamethasone suppression test (DST) were measured. The estimated glomerular filtration rate (eGFR) was calculated using the MDRD equation.

RESULTS:

Renal function was normal, mildly impaired, moderately impaired or severely impaired (eGFR >90, 60-90, 30-60 and 15-30 ml/min/1·73 m2 ) in 34, 54, 10 and 1% of the patients, respectively. Patients with normal and mildly impaired renal function had similar cortisol levels. Patients with moderately impaired renal function, compared to all the patients with eGFR >60 ml/min/1·73 m2 , exhibited increased cortisol (541 vs 456 nmol/l, P = 0·02), increased cortisol at DST (62 vs 37 nmol/l, P = 0·001), but similar ACTH levels (4·1 vs 2·9 pmol/l, P = 0·21). Patients with moderately impaired renal function thus exhibited cortisol at DST ≥50 nmol/l, more often than patients with eGFR >60 ml/min/1·73 m2 (76% vs 30%, P = 0·000), while the prevalence of ACTH below 2 pmol/l was similar (24% vs 31%, P = 0·51).

CONCLUSIONS:

Moderately impaired renal function increases cortisol and cortisol at DST in patients with adrenal adenomas, while mildly impaired renal function has no such effect. Cortisol level at DST ≥50 nmol/l therefore seems to have low specificity in diagnosing subclinical adrenal hypercortisolism, and an additional criterion, for example low ACTH, is required.

© 2015 John Wiley & Sons Ltd.

PMID:
26010731
[PubMed – as supplied by publisher]

From http://www.ncbi.nlm.nih.gov/pubmed/26010731

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Multiple aberrant hormone receptors in Cushing’s Syndrome

Posted on June 26, 2015 by MaryO
Eur J Endocrinol. 2015 May 13. pii: EJE-15-0200. [Epub ahead of print]
Multiple Aberrant Hormone Receptors in Cushing’s Syndrome.
El Ghorayeb N1, Bourdeau I2, Lacroix A3.

Author information

Abstract

The mechanisms regulating cortisol production when ACTH of pituitary origin is suppressed in primary adrenal causes of Cushing’s syndrome include diverse genetic and molecular mechanisms. These can lead either to constitutive activation of the cAMP system and steroidogenesis or to its regulation exerted by the aberrant adrenal expression of several hormone receptors, particularly G-protein coupled hormone receptors (GPCR) and their ligands.

Screening for aberrant expression of GPCR in BMAH and unilateral adrenal tumors of patients with overt or subclinical CS demonstrates the frequent co-expression of several receptors. Aberrant hormone receptors can also exert their activity by regulating the paracrine secretion of ACTH or other ligands for those receptors in BMAH or unilateral tumors.

The aberrant expression of hormone receptors is not limited to adrenal Cushing’s syndrome but can be implicated in other endocrine tumors including primary aldosteronism and Cushing’s disease. Targeted therapies to block the aberrant receptors or their ligands could become useful in the future.

PMID:
25971648
[PubMed – as supplied by publisher]

Filed under: adrenal, Cushing's, pituitary, Rare Diseases | Tagged: , , , , , , , , | Leave a comment »

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