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A TSH test is done to find out if your thyroid gland is working the way it should. It can tell you if it’s overactive (hyperthyroidism) or underactive (hypothyroidism). The test can also detect a thyroid disorder before you have any symptoms. If untreated, a thyroid disorder can cause health problems. TSH stands for “thyroid stimulating hormone” and the test measures how much of this hormone is in your blood. TSH is produced by the pituitary gland in your brain. This gland tells your thyroid to make and release the thyroid hormones into your blood. The Test The TSH test involves simply drawing some blood from your body. The blood will then be analyzed in a lab. This test can be performed at any time during the day. No preparation is needed (such as overnight fasting). You shouldn’t feel any pain beyond a small prick from the needle in your arm. You may have some slight bruising. In general, there is no need to stop taking your medicine(s) before having your TSH level checked. However, it is important to let the doctor know what medications you are taking as some drugs can affect thyroid function. For example, thyroid function must be monitored if you are taking lithium. While taking lithium, there is a high chance that your thyroid might stop functioning correctly. It's recommended that you have a TSH level test before starting this medicine. If your levels are normal, then you can have your levels checked every 6 to 12 months, as recommended by your doctor. If your thyroid function becomes abnormal, you should be treated. High Levels of TSH TSH levels typically fall between 0.4 and 4.0 milliunits per liter (mU/L), according to the American Thyroid Association. Ranges between laboratories will vary with the upper limit generally being between 4 to 5. If your level is higher than this, chances are you have an underactive thyroid. In general, T3 and T4 levels increase in pregnancy and TSH levels decrease. Low Levels of TSH It's also possible that the test reading comes back showing lower than normal levels of TSH and an overactive thyroid. This could be caused by: Graves’ disease (your body’s immune system attacks the thyroid) Too much iodine in your body Too much thyroid hormone medication Too much of a natural supplement that contains the thyroid hormone If you're on medications like steroids, dopamine, or opioid painkillers (like morphine), you could get a lower-than-normal reading. Taking biotin (B vitamin supplements) also can falsely give lower TSH levels. The TSH test usually isn’t the only one used to diagnose thyroid disorders. Other tests, like the free T3, the free T4, the reverse T3, and the anti-TPO antibody, are often used too when determining whether you need thyroid treatment or not. Treatment Treatment for an underactive thyroid usually involves taking a synthetic thyroid hormone by pill daily. This medication will get your hormone levels back to normal, and you may begin to feel less tired and lose weight. To make sure you're getting the right dosage of medication, your doctor will check your TSH levels after 2 or 3 months. Once they are sure you are on the correct dosage, they will continue to check your TSH level each year to see whether it is normal. If your thyroid is overactive, there are several options: Radioactive iodine to slow down your thyroid Anti-thyroid medications to prevent it from overproducing hormones Beta blockers to reduce a rapid heart rate caused by high thyroid levels Surgery to remove the thyroid (this is less common) Your doctor may also regularly check your TSH levels if you have an overactive thyroid. From https://www.webmd.com/women/what-is-tsh-test
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The pituitary gland works hard to keep you healthy, doing everything from ensuring proper bone and muscle growth to helping nursing mothers produce milk for their babies. Its functionality is even more remarkable when you consider the gland is the size of a pea. “The pituitary is commonly referred to as the ‘master’ gland because it does so many important jobs in the body,” says Karen Frankwich, MD, a board-certified endocrinologist at Mission Hospital. “Not only does the pituitary make its own hormones, but it also triggers hormone production in other glands. The pituitary is aided in its job by the hypothalamus. This part of the brain is situated above the pituitary, and sends messages to the gland on when to release or stimulate production of necessary hormones.” These hormones include: Growth hormone, for healthy bone and muscle mass Thyroid-stimulating hormone, which signals the thyroid to produce its hormones that govern metabolism and the body’s nervous system, among others Follicle-stimulating and luteinizing hormones for healthy reproductive systems (including ovarian egg development in women and sperm formation in men, as well as estrogen and testosterone production) Prolactin, for breast milk production in nursing mothers Adrenocorticotropin (ACTH), which prompts the adrenal glands to produce the stress hormone cortisol. The proper amount of cortisol helps the body adapt to stressful situations by affecting the immune and nervous systems, blood sugar levels, blood pressure and metabolism. Antidiuretic (ADH), which helps the kidneys control urine levels Oxytocin, which can stimulate labor in pregnant women The work of the pituitary gland can be affected by non-cancerous tumors called adenomas. “These tumors can affect hormone production, so you have too little or too much of a certain hormone,” Dr. Frankwich says. “Larger tumors that are more than 1 centimeter, called macroadenomas, can also put pressure on the area surrounding the gland, which can lead to vision problems and headaches. Because symptoms can vary depending on the hormone that is affected by a tumor, or sometimes there are no symptoms, adenomas can be difficult to pinpoint. General symptoms can include nausea, weight loss or gain, sluggishness or weakness, and changes in menstruation for women and sex drive for men.” If there’s a suspected tumor, a doctor will usually run tests on a patient’s blood and urine, and possibly order a brain-imaging scan. An endocrinologist can help guide a patient on the best course of treatment, which could consist of surgery, medication, radiation therapy or careful monitoring of the tumor if it hasn’t caused major disruption. “The pituitary gland is integral to a healthy, well-functioning body in so many ways,” Dr. Frankwich says. “It may not be a major organ you think about much, but it’s important to know how it works, and how it touches on so many aspects of your health.” Adapted from http://www.stjhs.org/HealthCalling/2016/December/The-Pituitary-Gland-Small-but-Mighty.aspx
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First published: 06 November 2021 https://doi.org/10.1111/cen.14617 Abstract Objective Ectopic Cushing′s syndrome (ECS) induced by medullary thyroid cancer (MTC) is rare, and data on clinical characteristics, treatment and outcome are limited. Design Retrospective cohort study in three German and one Swiss referral centres. Patients Eleven patients with MTC and occurrence of ECS and 22 matched MTC patients without ECS were included. Measurements The primary endpoint of this study was the overall survival (OS) in MTC patients with ECS versus 1:2 matched MTC patients without ECS. Results The median age at diagnosis of ECS was 59 years (range: 35–81) and the median time between initial diagnosis of MTC and diagnosis of ECS was 29 months (range: 0–193). Median serum morning cortisol was 49 µg/dl (range: 17–141, normal range: 6.2–18). Eight (73%) patients received treatment for ECS. Treatment of ECS consisted of bilateral adrenalectomy (BADX) in four (36%) patients and adrenostatic treatment in eight (73%) patients. One patient received treatment with multityrosine kinase inhibitor (MKI) to control hypercortisolism. All patients experienced complete resolution of symptoms of Cushing's syndrome and biochemical control of hypercortisolism. Patients with ECS showed a shorter median OS of 87 months (95% confidence interval [95% CI]: 64–111) than matched controls (190 months, 95% CI: 95–285). Of the nine deaths, four were related to progressive disease (PD). Four patients showed PD as well as complications and comorbidities of hypercortisolism before death. Conclusion This study shows that ECS occurs in advanced stage MTC and is associated with a poor prognosis. Adrenostatic treatment and BADX were effective systemic treatment options in patients with MTC and ECS to control their hypercortisolism. MKI treatment achieved complete remission of hypercortisolism and sustained tumour control in one treated case. 1 INTRODUCTION Medullary thyroid cancer (MTC) arises from calcitonin-producing parafollicular C-cells of the thyroid gland and accounts for 2%–5% of all thyroid malignancies.1 In about 25% of cases, MTC occurs in a hereditary manner as a part of multiple endocrine neoplasia type 2 (MEN2) caused by oncogenic germline REarranged during Transfection (RET)-mutations. Up to 65% of patients with the sporadic disease have somatic RET-mutations, among which RETM918T is the most common and associated with adverse outcome.2-5 At diagnosis, cervical lymph node metastases are present in about half of patients and distant metastases in around 10% of MTC patients.6 While the localized disease has a 10-year disease-specific survival (DSS) of 96%, 10-year DSS is only 44% in cases with distant metastases.7-9 Besides calcitonin and carcinoembryonic antigen (CEA), C-cells may also ectopically secrete corticotropin-releasing hormone (CRH) or adrenocorticotropic hormone (ACTH). Cushing's syndrome (CS) due to ectopic CRH or ACTH secretion induced by MTC is rare and data on clinical characteristics, treatment and outcome are limited and mostly from case studies. In a retrospective study of 1640 adult patients with MTC, ectopic Cushing's syndrome (ECS) due to ACTH secretion was reported in only 0.6% of patients, whereas previous studies reported a higher prevalence, possibly due to selection bias.10-12 ECS mostly occurs in metastatic cases and significantly impairs prognosis: around 50% of the mortality in patients with ECS has been attributed to complications of hypercortisolism.12 Diagnosis of ECS is difficult and includes a combination of clinical assessment, dynamic biochemical tests (e.g., 24 h urinary-free cortisol, midnight salivary cortisol, 1 and 8 mg dexamethasone suppression test), inferior petrosal sinus sampling (IPSS) and multimodal imaging.13 This retrospective study aims at describing clinical characteristics, treatment and prognosis of 11 patients with MTC and ECS at 3 German and 1 Swiss tertiary care centres and to illustrate effective treatment in this ultrarare condition. 2 PATIENTS AND METHODS 2.1 Setting This registry study was conducted as part of the German Study Group for Rare Malignant Tumours of the Thyroid and Parathyroid Glands. Data were obtained from records of patients diagnosed with MTC between 1990 and 2020 and concomitant ECS diagnosed between 1995 and 2020 in three German and one Swiss tertiary care centres. All patients provided written informed consent and the study was approved by the ethics committee of the University of Würzburg (96/13) and subsequently by the ethics committees of all participating centres. 2.2 Data acquisition Eligible patients were 11 adults with histopathological evidence of MTC and the diagnosis of ECS at initial diagnosis (synchronous CS) or during the course of disease (metachronous CS). This group was matched with 22 patients with histologically confirmed MTC without evidence of ECS by sex, age at MTC diagnosis (±5 years), tumour stage and calcitonin doubling time (CDT). The diagnosis of ECS was established by standard endocrine testing according to international guideline recommendations,14 local good clinical practice procedures and laboratory assays in participating centres. The primary endpoint of this study was the assessment of overall survival (OS) in MTC patients with ECS from the date of MTC-diagnosis and the date of ECS-diagnosis versus matched MTC patients without ECS (1:2 ratio). The secondary endpoints were assessment of progression-free survival (PFS) and efficacy of multityrosine kinase inhibitors (MKIs) treatment (based on routine clinical imaging in analogy to RECIST 1.0 and 1.1). Treatment and follow-up of patients were performed according to the local practice of participating centres. Efficacy was assessed locally by imaging (positron emission tomography/computed tomography [PET/CT], CT, magnetic resonance imaging [MRI] of the liver and bone scintigraphy) and measurement of serum calcitonin and CEA levels every 3–6 months. Clinical data were recorded by trained personnel at all sites. Tumour stage was defined according to the American Joint Committee on Cancer TNM classification, seventh edition,15 based on clinical and histopathological assessments. 2.3 Statistical analysis PFS and OS probabilities were estimated using the Kaplan–Meier method. The log-rank test was not used to test the difference between the study group and the control group due to the paired sample design. For the comparison of nonnormally distributed data, we used the Mann–Whitney U test. p Values less than .05 were considered statistically significant. Statistical analyses were performed with SPSS Version 26 (IBM). 3 RESULTS 3.1 Clinical characteristics of patients with ECS Eleven patients (five male and six female) with histopathological evidence of MTC with ECS in three German and one Swiss tertiary care centres were included. Twenty-two controls with histologically confirmed MTC without the diagnosis of ECS matched by sex, age at MTC diagnosis (±5 years), tumour stage and CDT were enroled. Baseline clinical characteristics of the study population and the control group are shown in Table 1. In patients with ECS, median follow-up from initial MTC diagnosis was 6.3 years (range: 0–17) and median follow-up from diagnosis of ECS 7 months (range: 0–110). Median age at initial diagnosis of sporadic MTC was 45 (range: 31–67, n = 7) and 52 years (range: 35–55, n = 3) for patients with germline RET mutant MTC. Read more at https://onlinelibrary.wiley.com/doi/10.1111/cen.14617 -
Dr. Friedman is getting a lot of emails on booster shots versus third shots. Third shots are for immuno-compromised patients that the FDA is recommending for a small group of patients The FDA also has the intention to soon make booster doses widely available to all healthy individuals. I am writing to clarify the difference between booster shots and third doses. Third Doses for Immuno-Compromised Patients The purpose of a third dose of mRNA vaccine is to give immuno-compromised patients the same level of protection that two doses provide someone who has a normal immune system. It is recommended that the following people get a third dose Been receiving cancer treatment for tumors or cancers of the blood Received an organ transplant and are taking medicine to suppress the immune system Received a stem cell transplant within the last two years or are taking medicine to suppress the immune system Been diagnosed with moderate or severe immunodeficiency conditions (such as DiGeorge syndrome, Wiskott-Aldrich syndrome) An advanced or untreated HIV infection Been under active treatment with high-dose corticosteroids (> 20 mg of prednisone or 100 mg of hydrocortisone) or other drugs that may suppress immune response Dr. Friedman thinks it is unlikely that any of his patients have these conditions. Patients with Cushing’s syndrome, Addison’s, diabetes or thyroid disorders do not qualify. In contrast, a Booster Dose is for Patients With Healthy Immune Systems A booster dose—which is different from a third dose for immuno-compromised patients—is for healthy patients and is meant to enhance immunity and may protect against new variants of the virus. The Biden administration has announced that it intends to make booster doses available for people with healthy immune systems in September 2021, after they are authorized or approved by the FDA. This has not happened yet, but when it happens, Dr. Friedman would encourage his patients to get it. Dr. Friedman is expecting a booster shot against the Delta variant to be released in the fall of 2021 and would recommend that for his patients. Dr. Friedman wishes everyone to stay healthy.
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Updates on Treating Hypothyroidism Dr. Theodore Friedman will be giving a webinar on Updates on Treating Hypothyroidism. Topics to be discussed include: New articles showing patients prefer desiccated thyroid New thyroid hormone preparations Update on desiccated thyroid recalls New article on why TSH is less important than thyroid hormone measurements What is the difference between desiccated thyroid and synthetic thyroid hormones? Is rT3 important? Sunday • April 25• 6 PM PDT Via Zoom Click here to join the meeting or https://us02web.zoom.us/j/4209687343?pwd=amw4UzJLRDhBRXk1cS9ITU02V1pEQT09 OR +16699006833,,4209687343#,,,,*111116# Slides will be available before the webinar and recording after the meeting at slides Meeting ID: 420 968 7343 Passcode: 111116 Your phone/computer will be muted on entry. There will be plenty of time for questions using the chat button. For more information, email us at mail@goodhormonehealth.com
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Central hypothyroidism is prevalent in about 1 in 2 adults with Cushing’s syndrome, and thyroid function can be restored after curative surgery for most patients, according to study findings. “Our study findings have confirmed and greatly extended previous smaller studies that suggested a link between hypercortisolism and thyroid dysfunction but were inconclusive due to smaller sample size and short follow-up,” Skand Shekhar, MD, an endocrinologist and clinical investigator in the reproductive physiology and pathophysiology group at the National Institute of Environmental Health Sciences, NIH, told Healio. “Due to our large sample and longer follow-up, we firmly established a significant negative correlation between hypercortisolemia measures — serum and urinary cortisol, serum adrenocorticotropic hormone — and thyroid hormones triiodothyronine, free thyroxine and thyrotropin.” Shekhar and colleagues conducted a retrospective review of two groups of adults aged 18 to 60 years with Cushing’s syndrome. The first group was evaluated at the NIH Clinical Center from 2005 to 2018 (n = 68; mean age, 43.8 years; 62% white), and the second group was evaluated from 1985 to 1994 (n = 55; mean age, 37.2 years; 89% white). The first cohort was followed for 6 to 12 months to observe the pattern of thyroid hormone changes after surgical cure of adrenocorticotropic hormone-dependent Cushing’s syndrome. The second group underwent diurnal thyroid-stimulating hormone evaluation before treatment and during remission for some cases. Urinary free cortisol and morning thyroid hormone levels were collected for all participants. In the second group, researchers evaluated diurnal patterns of TSH concentrations with hourly measurements from 3 to 7 p.m. and midnight to 4 p.m. In the first group, adrenocorticotropic hormone and serum cortisol were measured. In the first cohort, seven participants were receiving levothyroxine for previously diagnosed primary or central hypothyroidism. Of the remaining 61 adults, 32 had untreated central hypothyroidism. Thirteen participants had free T4 at the lower limit of normal, and 19 had subnormal levels. There were 29 adults with subnormal levels of T3 and seven with subnormal TSH. Before surgery, 36 participants in the first group had central hypothyroidism. Six months after surgery, central hypothyroidism remained for 10 participants. After 12 months, the number of adults with central hypothyroidism dropped to six. Preoperative T3 and TSH levels were negatively associated with morning and midnight cortisol, adrenocorticotropic hormone and urinary free cortisol. In post hoc analysis, a baseline urinary free cortisol of more than 1,000 g per day was adversely associated with baseline and 6-month T3 and free T4 levels. In the second group, there were 51 participants not on thyroid-modifying drugs who had a thyroid function test 6 or 12 months after surgery. Before surgery, free T4 levels were subnormal in 17 participants, T3 levels were subnormal in 22, and TSH levels were in the lower half of the reference range or below in all but one participant. After surgery, two participants had below normal free T4, one had subnormal T3, and TSH levels were in the lower half of the reference range or below in 23 of 48 participants. Before surgery, there was no difference in mean TSH between daytime and nighttime. A mean 8 months after surgery, the second group had a normal nocturnal TSH surge from 1.3 mIU/L during the day to 2.17 mIU/L at night (P = .01). The nocturnal TSH increase persisted as long as 3 years in participants who had follow-up evaluations. “We found a very high prevalence of thyroid hormone deficiency that appears to start at the level of the hypothalamus-pituitary gland and extend to the tissue level,” Shekhar said. “Some of these patients may experience thyroid hormone deficiency symptoms, such as fatigue, depression, cold intolerance, weight gain, etc, as a result of systematic and tissue-level thyroid hormone deficiency. We also noted a strong correlation between hypothyroidism and hypogonadism, which implies that hypothyroid patients are also likely to suffer adverse reproductive effects. Thus, it is imperative to perform thorough thyroid hormone assessment in patients with Cushing’s syndrome, and thyroid hormone supplementation should be considered for these patients unless cure of Cushing’s syndrome is imminent.” Researchers said providers should routinely screen for hypothyroidism in adults with Cushing’s syndrome. Even after thyroid function is restored, regular follow-up should also be conducted. Further research is needed to investigate thyroid dysfunction in iatrogenic Cushing’s syndrome and the impact of these findings on euthyroid sick syndrome, Shekhar said. For more information: Skand Shekhar, MD, can be reached at skand.shekhar@nih.gov. From https://www.healio.com/news/endocrinology/20210208/thyroid-dysfunction-highly-prevalent-in-cushings-syndrome
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Thyroid cancer survival rates are 84 percent for 10 years or more if diagnosed early. Early diagnosis is crucial therefore and spotting the unusual signs could be a matter of life and death. A sign your thyroid cancer has advanced includes Cushing syndrome. What is it? What is Cushing syndrome? Cushing syndrome occurs when your body is exposed to high levels of the hormone cortisol for a long time, said the Mayo Clinic. The health site continued: “Cushing syndrome, sometimes called hypercortisolism, may be caused by the use of oral corticosteroid medication. “The condition can also occur when your body makes too much cortisol on its own. “Too much cortisol can produce some of the hallmark signs of Cushing syndrome — a fatty hump between your shoulders, a rounded face, and pink or purple stretch marks on your skin.” In a study published in the US National Library of Medicine National Institutes of Health, thyroid carcinoma and Cushing’s syndrome was further investigated. The study noted: “Two cases of thyroid carcinoma and Cushing's syndrome are reported. “Both of our own cases were medullary carcinomas of the thyroid, and on reviewing the histology of five of the other cases all proved to be medullary carcinoma with identifiable amyloid in the stroma. “A consideration of the temporal relationships of the development of the carcinoma and of Cushing's syndrome suggested that in the two cases with papillary carcinoma these conditions could have been unrelated, but that in eight of the nine cases with medullary carcinoma there was evidence that thyroid carcinoma was present at the time of diagnosis of Cushing's syndrome. “Medullary carcinoma of the thyroid is also probably related to this group of tumours. It is suggested that the great majority of the tumours associated with Cushing's syndrome are derived from cells of foregut origin which are endocrine in nature.” In rare cases, adrenal tumours can cause Cushing syndrome a condition arising when a tumour secretes hormones the thyroid wouldn’t normally create. Cushing syndrome associated with medullary thyroid cancer is uncommon. The syndrome is more commonly caused by the pituitary gland overproducing adrenocorticotropic hormone (ACTH), or by taking oral corticosteroid medication. See a GP if you have symptoms of thyroid cancer, warns the NHS. The national health body added: “The symptoms may be caused by less serious conditions, such as an enlarged thyroid, so it's important to get them checked. “A GP will examine your neck and can organise a blood test to check how well your thyroid is working. “If they think you could have cancer or they're not sure what's causing your symptoms, you'll be referred to a hospital specialist for more tests.” Adapted from https://www.express.co.uk/life-style/health/1351753/thyroid-cancer-signs-symptoms-cushing-syndrome
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Dr. Friedman wants to update his patients about natural desiccated thyroid (NDT) recalls based on new information from the FDA. Dr. Friedman prescribes various thyroid hormone preparations to his patients with hypothyroidism. This includes natural desiccated thyroid (NDT) of which two preparations are WP Thyroid and Nature-Throid, both made by RLC Labs. On August 25, 2020, RLC Labs announced a voluntary, consumer-level recall of all lots of Nature-Throid and WP Thyroid tablets because some lots contain less than the required 90% of the active ingredient as determined by the FDA. The RLC spokesperson said to Dr. Friedman that one lot of WP Thyroid and 5 lots of Nature-Throid contained between 87% and 90% of the labeled amount of levothyroxine (T4) or liothyronine (T3). Recently the FDA announced which lots are recalled that are listed below. According to the recall, if a patient receives a sub-potent tablet, hypothyroid symptoms may not be controlled. To date, there have been no reports of adverse events related to this recall. Patients who have had an adverse event should contact RLC Labs. The lot numbers are listed on the bottles of Nature-Throid and WP Thyroid. With this information about which lots are recalled, Dr. Friedman is only recommended those taking the effective lots to discontinue them. Currently no lots of Nature-Throid and WP Thyroid tablets are commercially available, so a replacement with the same product is not an option. It is unknown how long it will be before Nature-Throid and WP Thyroid become commercially available. In September 2020, the FDA also announced that two lots (one of 15 mg and one of 120 mg) (see table) of NP Thyroid made by Acella Pharamceuticals were also recalled due to reduced potency between 87% and 90% of the labeled amount of levothyroxine (T4) or liothyronine (T3). Other lots are currently available. The lot numbers are not listed on the Acella product bottles, but the expiration dates are. If patient has one of the products with the expiration date listed, they can ask their pharmacy for the lot number. Dr. Friedman has several comments about these recalls. Dr. Friedman sees them as unfortunate, but still believes NDT is a good option for patients with hypothyroidism. The “subpotent” Nature-Throid, WP Thyroid and NP Thyroid pills are only slightly less potent than stated in that only the effective lots are between 87% and 90% of the T4 and T3 levels. For most patients, they will not have symptoms from these subpotent pills and if they are taking a lot that is subpotent, the dose can be adjusted based on laboratory levels at your next appointment with Dr. Friedman. According to Dr. Friedman, patients taking Nature-Throid and WP Thyroid with the subpotent lots have three options: 1) they can continue taking Nature-Throid and WP Thyroid knowing they may have a subpotent lot and knowing that they may not be able to get a refill at least temporarily. 2) patients can be switched to Armour thyroid, NP thyroid or have a compounding pharmacy compound the equivalent dose using USP grade porcine powder. Please let Dr. Friedman’s office know if you would like to go on a different desiccated thyroid product (and which one) and what pharmacy you would like to use, 3) Dr. Friedman has a small supply of desiccated thyroid with no reclled lots that is available at his clinic for those in Los Angeles on the last Tuesday night of each month. He will not be able to mail desiccated thyroid. Please contact his office about this option. Patients with a subpotent lot of NP thyroid can have their pharmacy switch them to an unaffected lot at no charge. Patients do not need to contact Dr. Friedman, but if you have any questions or need to schedule an appointment with Dr. Friedman, please email us at mail@goodhormonehealth.com or schedule an appointment on his website at www.goodhormonehealth.com.
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Dr. Friedman prescribes various thyroid hormone preparations to his patients with hypothyroidism. This includes natural desiccated thyroid (NDT) of which two preparations are WP Thyroid and Nature-Throid, both made by RLC Labs. On August 25, 2020, RLC Labs announced a voluntary, consumer-level recall of all lots of Nature-Throid and WP Thyroid tablets because some lots contain less than the required 90% of the active ingredient as determined by the FDA. The RLC spokesperson said to Dr. Friedman that one lot of WP Thyroid and 5 lots of Nature-Throid contained between 87% and 90% of the labeled amount of levothyroxine (T4) or liothyronine (T3). The recall did not disclose which of the lots were affected and all lots are recalled, not just the affected lots. According to the recall, if a patient receives a sub-potent tablet, hypothyroid symptoms may not be controlled. To date, there have been no reports of adverse events related to this recall. Patients who have had an adverse event should contact RLC Labs. RLC Labs advised that patients should talk to their healthcare professional before they stop taking their Nature-Throid and WP Thyroid medicine. Consumers with questions about the recall can email RLC at recall@rlclabs.com or RLC Customer Service (877) 797-7997. Patients may return unexpired Nature-Throid and WP Thyroid tablets to their pharmacy who are legally required to refund the cost of the tablets. Currently no lots of Nature-Throid and WP Thyroid tablets are commercially available, so a replacement with the same product is not an option. It is unknown how long it will be before Nature-Throid and WP Thyroid become commercially available. Dr. Friedman has several comments about this recall. This is the second recall of desiccated thyroid as some lots of NP thyroid were recalled in May 2020. Dr. Friedman sees this as unfortunate, but still believes desiccated thyroid is a good option for patients with hypothyroidism. Secondly, the “subpotent” Nature-Throid and WP Thyroid pills are only slightly less potent than stated in that only a few lots are between 87% and 90% of the T4 and T3 levels. For most patients, they will not have symptoms from these subpotent pills and if they are taking a lot that is subpotent, the dose can be adjusted based on laboratory levels at your next appointment with Dr. Friedman. According to Dr. Friedman, patients taking Nature-Throid and WP Thyroid have three options: 1) they can continue taking Nature-Throid and WP Thyroid knowing they may have a subpotent lot and knowing that they may not be able to get a refill at least temporarily. 2) patients can be switched to Armour thyroid, NP thyroid or have a compounding pharmacy compound the equivalent dose using USP grade porcine powder. Please let Dr. Friedman’s office know if you would like to go on a different desiccated thyroid product (and which one) and what pharmacy you would like to use, 3) Dr. Friedman has a small supply of desiccated thyroid that is available at his clinic for those in Los Angeles on the last Tuesday night of each month. He will not be able to mail desiccated thyroid. Please contact his office about this option. Patients do not need to contact Dr. Friedman, but if you have any questions or need to schedule an appointment with Dr. Friedman, please email us at mail@goodhormonehealth.com or schedule an appointment on his website at goodhormonehealth.com.
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(1865) English physician George Redmayne Murray was born. He is credited with pioneering the treatment of endocrine diseases, which include thyroid cancer.
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From http://www.cushie.info/index.php?option=com_content&view=article&id=1146:dr-theodore-F.-interviews&catid=10:media&Itemid=18 Theodore C. F., M.D., Ph.D. has opened a private practice, specializing in treating patients with adrenal, pituitary, thyroid and fatigue disorders. Dr. F. has privileges at Cedars-Sinai Medical Center and Martin Luther King Medical Center. His practice includes detecting and treating hormone imbalances, including hormone replacement therapy. Dr. F. is also an expert in diagnosing and treating pituitary disorders, including Cushings disease and syndrome. Dr. F.'s career reflects his ongoing quest to better understand and treat endocrine problems. With both medical and research doctoral degrees, he has conducted studies and cared for patients at some of the country's most prestigious institutions, including the University of Michigan, the National Institutes of Health, Cedars-Sinai Medical Center, and UCLA's Charles Drew University of Medicine and Science. Read Dr. F.'s First Guest Chat, November 11, 2003. Read Dr. F.'s Second Guest Chat, March 2, 2004. Listen to Dr. F. First Live Voice Interview, January 29, 2009. Listen to Dr. F. Second Live Voice Interview, March 12, 2009. Listen to Dr. F. Third Live Voice Interview, February 13, 2011. This post has been promoted to an article
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i read an article that was about the many different causes of empty sella one of them being thyroid cancer. it lead me to a link i will post here about an ectopic ACTH source in a vaginal lining malignancy. I have found in my own studies that it is beneficial to be vigilent about rooting out the source of our cushings. some doctors just want to offer multiple band aids. like in my case. doctors suggested removing my pituitary gland or my agrenal glands or trying to sustain me w/tons of insulin & hight blood pressure meds or ketoconazol. they did not get that i had 2 little ones to take care of. i wanted to stop my body from rotting. i knew i had little time left. i did not want agonizing prolongment. i wanted the SOURCE of the cushings hunted down & cut OUT of my body. in my hereditary type of cushings even removing a small portion (debulking) of the tumor, mass, cyst, watever your radiologist wants to call it, can save or add years to your life. it is hard to find such an agressive doctor. in my case it was my sisters who stood up to doctors. demanding they order a full body octreotide scan where they found the source of my cushings, a lung tumor that did not show up on other scans. the tumor can be ANYWHERE in your body. It will produce many different hormones not just ACTH. it can be the size of a spec of dust. Looking for these other tumor markers or hormones in 24hr urine catches besides just cortisol can put us closer to our cure. since i am posting a research link i picked this forum. if it is misplaced i apologize. please see this research link: http://lib.bioinfo.pl/pmid:9190988 our illness is not rare but doctors are not taught how to diagnose it. sometimes they need our help. we need to educate ourselves. my education on this website led to my cure. thank u MaryO for giving us this medium.
