| <갑상선의 기능적 스케일-US Reference Ranges에 따름> http://www.wilsonssyndrome.com/WilsonsThyroidSyndrome.htm WTS참고
: TSH-TT4/TT3 넓게 분포되는 흩어진 패턴이 단순 갑상선 기능항진(TSH grade-3, TT4-TT3 +1/+2 )또는 단순 갑상선기능저하(TSH +4, TT4-TT3 -2/-3)의 패턴이요, 반면에 부신피로와 동반된 갑상선기능저하는 TSH 약간저하, TT4-TT3약간 더 저하되면서 그 흩어짐의 정도가 경미한 것이 특징임(TSH+2, TT4+1 TT3 0)
LABS TSH TT4 TT3
-5 0.0-0.5 0.0-4.5 0.0-60
-4 0.6 4.6-5.2 76-90
-3 0.7-0.8 5.3-6.1 76-90
-2 0.9-1.0 6.2-6.9 91-106
-1 1.1-1.2 7.0-7.4 107-119
0(정상) 1.3-2.0 7.5-8.1 120-125
+1 2.1-2.5 8.2-9.0 126-137
+2 2.6-3.5 9.1-10.2 138-152
+3 3.6-4.5 10.2-11.3 153-166
+4 4.6-5.4 11.4-12.4 167-180
+5 5.5-6.4 12.5-13.6 181-195
+6 6.5-7.6 13.7-14.8 196-210
+7 7.7-8.4 14.9-16.0 211-225
+8 8.5-9.9 16.1-99 226-999
"How To Get The Most From Your Thyroid Panel"
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--I get a lot of inquiries about the thyroid panel from practitioners all over the US, Canada, and the UK. Many doctors have asked me what tests they should put on their thyroid panels and what thyroid tests to put on their basic metabolic panel. My advise to all of you is this:
--Put TSH on your metabolic panel. Include Total T4 and T3. I'll be covering these tests later in the course.
Make sure you run the thyroid portion of the health appraisal questionnaire from my book "Signs and Symptoms Analysis from a Functional Perspective",
Make sure your patient has done the Basal Body Temperature Testing from my "In-Office Lab Testing System", and
Make sure you are using the latest optimal reference ranges for TSH.
I use the above as a "Gateway test" for running a comprehensive thyroid panel on my patients. By using three different diagnostic systems you can be very clear whether or not the thyroid needs further assessment.
#What are your latest optimal reference ranges for TSH
--It has been clear for a long time that TSH ranges have not really reflected the functional state of the thyroid. Most US labs have a normal TSH reference range of 0.5 to 5.5. In early 2001, the American Association of Clinical Endocrinologists stated: “Even though a TSH level between 3.0 and 5.0 is in the normal range, it should be considered suspect since it may signal a case of evolving thyroid under activity”.
--This was followed up by an interesting piece in the February 2002 issue of the Journal of Clinical Endocrinology and Metabolism, which said that among the disease-free population (those who do not have any presence of thyroid antibodies, or diagnosed thyroid disease), the mean TSH level is 1.5. This caused me to re-evaluate my TSH levels and to consider that optimal TSH levels are below 2 and that levels above that may represent hypothyroid function.
--When I see a TSH above 2 and the patient has other signs and symptoms of an under active thyroid I am more likely to order a comprehensive thyroid panel. I find the new reference range for TSH has made that test a lot more sensitive for primary hypothyroidism. It does however drop the specificity that we are actually dealing with an under active thyroid and not some other cause, which is why I rely on the other "gateway" tests described above.
#What tests should you have on your Comprehensive Thyroid Panel
--I usually request free levels of T4 and T3, which can help narrow down the cause of the problem as they are the best ways to measure actually active thyroid hormone, especially in people that are estrogen dominant.The Comprehensive Thyroid Panel can help uncover thyroid imbalances that often go undetected. The free T4 and T3 levels are ordered because they reflect the biologically active thyroid hormone, which increases the information we can get on thyroid metabolism, such as information on hypo and hyper thyroidism, altered peripheral conversion of T4 into T3, and auto-immune conditions that affect the thyroid.
--The other tests to have on your comprehensive thyroid panel might include anti thyroglobulin antibody studies and reverse T3 levels. Anti thyroglobulin antibody studies will give you important information on the thyroid gland itself and whether or not there is active cellular damage in the thyroid. Damage to the thyroid causes thyroid cellular contents to leak and causes antibodies to form, which are directly measurable. Reverse T3 levels can tell you whether or not there is a problem with peripheral conversion taking place.
#What are your reference ranges
--The reference ranges I am using at present are as follows:
TSH: 1.2 - 2.0 µIU/mL
Free T3: 2.3 - 4.2 pg/ml
Free T4: 0.7 - 2.4 ng/dl
Total T4: 6.0 - 12.0 mcg/dl
Reverse T3: 14.9 - 26.1 ng/dl
"Low Energy States- The Thyroid and Adrenal Connection Part I"
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--In the last lesson I looked at the concept of a Comprehensive Thyroid Panel. I have recently been looking at the whole concept of low energy states and the difficulty they pose for a practitioner. One of the most common chief complaints we face is fatigue and low energy and we need to be able to diagnose the exact cause of this state in our patients. We are also faced with cases of fibromyalgia, chronic fatigue syndrome, and other fatigue related conditions. These symptoms and other health problems we deal with are closely connected to a state of poor metabolism and low metabolic energy.
#What do you mean by "Low Energy States"
--The majority of the systems in our body rely on energy in the form of ATP (adenosine tri phosphate). Macromolecules are converted into ATP via glycolysis, the TCA cycle, and oxidative phosphorylation in the mitochondria, which produces ATP so our bodies can perform metabolic work. ATP is the universal "currency" of energy and is used by every cell in the body. When levels of ATP begin to fall below optimal levels physiological processes begin to function sub-optimally and we get the emergence of signs and symptoms.
--In the muscles this may cause easy tiring and even spasms, cramp, and pain. Muscles require ATP in order to relax.
--In the brain sub-optimal levels of ATP cause difficulties in thinking, cognitive dysfunction such as poor memory, and mood disorders such as depression.
--In the immune system this can manifest as asthma, allergies, frequent infections, and even cancer. There are few systems that are not affected and the difficulty is to find out what the cause is and not try and treat each system individually. This is especially true for our patients who may have been to visit many specialists and be on multiple drugs and alternative protocols to correct this problem.
#What causes Low Metabolic Energy
--If we are to back up and look at a hierarchy of systems we recognize that low metabolic energy must involve the thyroid, which acts as the metabolic accelerator in the body, the pituitary, which is the "master gland" that controls the ultimate activity of the thyroid, and the adrenal glands, which deal with stress in all its forms. These three glands play a huge role in the development of low metabolic energy states.
###The Thyroid
--The thyroid influences the rate of metabolism through the production of T4 from the thyroid and the peripheral conversion of T4 into the more metabolically active T3, which stimulates energy production on the cellular level via its ability to act as a "key" on cellular receptor sites and increase the production of ATP from the cell, or a molecule called Reverse T3 or rT3, which acts as a metabolic brake.
--The majority of T4 released by the thyroid is bound to a protein called thyroid binding globulin (TBG). Only about 0.03 - 0.05% of circulating T4 is in the free form. T4 is converted to T3, Reverse T3 or rT3, or is eliminated unconverted via conjugation, deamination or decarboxylation in the liver. It is estimated that about 70% of T4 produced in the thyroid is eventually deiodinated in peripheral tissues into either T3 or rT3 via deiodinase enzymes that cleave an iodine molecule from the quaternary form.
--T3 is the considered the most metabolically active thyroid hormone.
T3 is 4 -5 times more metabolically active than T4 and its systemic effects and half-life are shorter. Although some is produced in the thyroid, approximately 80 – 85% is produced outside the thyroid in peripheral tissues, primarily by conversion of T4 in the liver and kidneys. Within the liver and kidney, the enzyme responsible for the peripheral conversion of T3 is a selenium dependent enzyme called 5’-deiodinase. Similar to T4, the majority of T3 is in a bound form. Free T3 represents approximately 8 – 10% of circulating T3. Free T-3 is more available for tissue receptors and provides an accurate measurement for thyroid assessment than total T3 in patients that are estrogen dominant or on some form of estrogen replacement (birth control pills, HRT etc.).
--Our energy systems need to not only turn energy production on but also switch it off. Throughout the day there are times when our systems require either more or less energy, depending on the level of activity. Short term control is governed by the conversion of T4 into active T3 for stimulating ATP production or into the molecule called Reverse T3 or rT3, which acts as a metabolic brake.
#Reverse T3
--Reverse T3 (rT3) is a metabolically inactive thyroid hormone. Small amounts of rT3 are made within the thyroid; however, 95% of rT3 is produced from peripheral conversion of T4. Reverse T3 is formed by the removal of a different iodine molecule from the quaternary structure of T4 than the one removed for T3 conversion. The enzyme responsible for this conversion is 5-deiodinase and is not believed to be dependent on selenium. Under normal conditions it has been estimated that 45 – 50% of the daily production of T4 is transformed into rT3. Reverse T3 can be seen as a sort of "blocker molecule" that fits in and occupies the T3 receptors on the cell membrane, but does not permit T3 to enter and increase energy production. It functions to slow down ATP synthesis within the cell.
--T3 is like the accelerator in your car and reverse T3 is more like the break. If there is a sudden need for less energy production, we make more rT3 from T4. If this reduced need for energy persists over months, we make less T4 by reducing the output of TSH from the pituitary. This leads to a situation of low normal TSH, which in turn reduces T4 production and produces a low normal level of T3. The body, in its infinite wisdom, wastes less effort in manufacturing thyroid hormone that will not be used.
###Adrenal Function
--What role, I hear you say, does the adrenal glands play in all of this The adrenal glands have many metabolic functions in the body. One of the most important of which is to help the body maintain stability and equilibrium in the face of both exogenous and endogenous stress. Stress comes in many forms and can be:
Emotional- family dysfunction, fear
Physical- injury, surgery, over exercise, chronic pain
Biological- chronic infections (epstein barr virus)
Metabolic- excess metabolic stimulation from hyperthyroidism, or early stage Hashimoto's thyroiditis
Chemical- exposure to toxicity, drugs, or heavy metals
Nutritional- excess yo-yo dieting, vitamin or mineral deficiencies, calorie deficiencies
The adrenals have a hard time interpreting "bad" stress as described above, or good stress such as the adrenaline rush of reeling in a big fish! The adrenals deal with stress through the production of cortisol and DHEA. We evolved to be able to use our adrenal glands to help us deal with short term stress. If we live in stress for long periods of time, we begin to lose the ability to keep up with the stress and begin to function as if the adrenals are fatigued. As the adrenals fatigue they go through a number of phases of fatigue. The first is marked by high cortisol and low DHEA output. In latter stages we see a generalized decrease in not only cortiosl and DHEA but also other adrenal hormones such as testosterone in both males and females, and aldosterone that regulates mineral metabolism. In response to the high levels of stress the hypothalamus will signal the pituitary to produce less TSH. The overall effect being a decreased production of T4 and a lowering of metabolic activity.
--In the early 1990s Dr. Wilson recognized a condition of low energy when he saw the condition where thyroid tests were normal but from a functional perspective the patient functions as if they were hypothyroid. This phenomenon used to be described as Euthyroid Sick Syndrome or Low T3 Syndrome, which describe a non-thyroidal illness marked by reduced peripheral 5’-deiodination conversion of T4 into T3 due to liver or renal dysfunction (Euthyroid Sick Syndrome) or stress, malnutrition, low calorie diets, lack of exercise etc. (Low T3 Syndrome). Dr. Wilson called this phenomenon Wilson's syndrome and went further by describing it as a condition in which the body increases reverse T3 output and gets "stuck" there indefinitely. The conditions that cause this pattern include increased exposure to stress, food and calorie deprivation, and yo-yo dieting, which sends our body into storage mode in the anticipation that calories will be hard to come by in the future.
###Low Energy Due To Adrenals and Thyroid
--The basic pattern described by Dr. Wilson relates to the body producing less energy because it is trying to conserve energy. The body activates an ancient system for conserving energy in the face of potential famine. The problem is there's no famine! This pattern can best be called a Low Energy State due to the Thyroid. Dr. Bruce Rind (an MD in the Washington DC area) recognized that this only partly described the phenomenon and he went further in describing a second pattern that he called Low Energy State due to the Adrenals. In this state the body is trying to limit energy production because large amounts of energy are being poured into a body that cannot cope or manage so much energy. Some of the causes of low metabolic energy states are listed below.
#Causes of Low Metabolic Energy
--Based on the above explanation, some of the contributors of low metabolic energy include:
The thyroid gland cannot produce enough T4. The body is trying to produce less energy because it is trying to conserve energy.
Adrenal glands that are too weak to deal with the body's increased metabolic activity, which forces the body's energy production to slow down.
The actual chemical creation of ATP can be compromised by chemical interferences such as increased levels of metabolic toxins, a lack of essential ingredients (vitamins, minerals, essential fatty acids, and other accessory co-factors), inhibitory factors such as Trans fatty acids, or a general breakdown in the energy production system due to auto-immune disease or viral damage.
Imbalances in essential hormones such as Human Growth Hormone (HGH), Testosterone, Progesterone, or Estrogen.
Severe calorie restriction.
Nutritional deficiencies
Both Low Energy States due to Thyroid and Adrenals have low metabolic states and low body temperature. Some of the signs and symptoms are shared by both. However many are not.
###Summary of major contributors of low metabolic energy:
-The thyroid gland cannot produce enough T4. The body is trying to produce less energy because it is trying to conserve energy.
-Adrenal glands that are too weak to deal with the body's increased metabolic activity, which forces the body's energy production to slow down.
-The actual chemical creation of ATP can be compromised by chemical interferences such as increased levels of metabolic toxins, a lack of essential ingredients (vitamins, minerals, essential fatty acids, and other accessory co-factors), inhibitory factors such as Trans fatty acids, or a general breakdown in the energy production system due to auto-immune disease or viral damage.
-Imbalances in essential hormones such as Human Growth Hormone (HGH), Testosterone, Progesterone, or Estrogen.
-Severe calorie restriction.
-Nutritional deficiencies
When one or more of these factors begins to emerge we see the symptoms of low energy start to emerge.
###Some of the Symptoms of Low Energy States
Low Energy States in the body can produce a myriad of signs and symptoms that we must be aware of. Although many of these symptoms appear to be unrelated, they share a common root in a low metabolic energy.
--General Symptoms Low body temperature :General feeling of cold, Low energy, also described as fatigue Slow wound healing Difficulty gaining or losing weight
--Cognitive Function Mood disorders: depression, anxiety Cognitive problems: poor memory and focus Sleep problems: insomnia
--Cardiovascular Blood pressure abnormalities: high or low
--Raynaud's disease and capillary problems
--Neurological Increasing numbness in hands and feet
--Loss of senses: vision, smell, taste
--Gastrointestinal Tendency towards constipation Gas or bloating IBS
--Dermatological Tendency towards dry skin Acne Skin pallor Brittle hair
--Endocrine Infertility (both male and female) Menstrual irregularities and disorder Low libido
--Musculoskeletal Muscle weakness Joint pain and stiffness Fibromyalgia
---As you probably worked out the above list is a mix of symptoms of both low thyroid and low adrenal function. The diagnosis for these symptoms is low energy, the cause is due in most cases to either an adrenal or a thyroid abnormality. In order to get to the true cause of a patient's low energy state it is essential to be able to sort out a patient's symptomology in terms of the adrenal and thyroid function. Each of these dysfunctions have a unique symptomology profile that will help you key in to the causative factor.
---The symptomology patterns of adrenal and thyroid dysfunction are about 90% opposite of one another. Recognizing this can have profound effects on the diagnosis and subsequent treatment of low energy states. There are of course non thyroid and non-adrenal causes of low energy, and there are a number of symptoms that are shared by both the adrenals and the thyroid (hair loss, poor memory, poor concentration and focus).
---Dr. Bruce Rind, a medical doctor who has pioneered much of this work, has made some interesting observations about the different symptomology presented by men and women:
"Women have a much higher ratio of low metabolic energy problems due to adrenal and thyroid dysfunction. The ratio is roughly 8:1."
"Light skinned individuals have a tendency towards weaker adrenals and dark skin individuals have a tendency towards weaker thyroids, while olive skinned individuals tend not to have weak adrenals or thyroids."
###Differentiating symptoms of Adrenal fatigue and low thyroid function.
The following is a summary of some of the most important differentiating symptoms of Adrenal fatigue and low thyroid function.
#differential S/SX between Thyroid(T) and Adrenal(A)
--Eyebrows Tend to lose outer 1/3 to 1/2 of the eyebrow
(T)Tend towards fullness Tissue under and around the eyes (A)Tend to have puffy eyes with bags underneath the eyes. Dark circles under eyes. More sunken than puffy.
--General body type
(T)Tendency towards weight gain. Weight can be global or localized. Weight is very hard to lose. (A)Tend to be thin and cannot gain weight easily
--Facial color
(T)Red and ruddy complexion (A)Pale color especially around the mouth
--Hair Tend towards coarseness.
(T)May be sparse. Tends to be thin and wispy. (A)Dry and may fall out easily.Sparse hair on forearms or lower legs.
--Skin Poor healing.
(T)Normal thickness though may easily bruise. (A)Dry and thin. May notice that the fingerprints are smoothed out. Look for longitudinal wrinkles over finger pads (Dr. Rind)
--Ligaments and general connective tissue
(T)Not that flexible. (A)Tend towards lax ligaments. May be "double jointed". may complain of joint sprain or strains.
--General state of fluids and secretions
(T)Skin tends towards the oily. Fluid retention common, especially in the pre-tibial area. (A)Tend towards dryness and cannot hold onto water well.
--Sensitivity to light
(T)Not really that susceptible to night blindness or light sensitivity. (A)Often have light sensitivity and tends towards night blindness. May report that they see a strong after image when a strong light is shone in face (Dr. Rind)
--General pain pattern
(T)May complain of muscle and/or joint pain esp. in feet or lower legs (A) May complain of headaches and/or migraines. Pain usually in muscles rather than joints, though can strain or sprain joints easily.
--Temperature patterns
(T)Tend towards a low body temperature usually below 97.6. The temperature is low, stable and does not fluctuate very much. May be in low 90's (A)Adrenal types are known as thermal chameleons as their temperature is never stable. Hot when it is warm and cold when it is cool. Cannot regulate temperature very well. The body temperature is low and usually below 97.6. The important part is that the temperature is low and always changing.
--Perspiration
(T)Tend to be more oily than sweaty. (A)In early stages of adrenal fatigue they may show marked perspiration. Cannot sweat in advanced stages.
--Mood Tendency towards depression.
(T)Little to no anxiety. (A)Tendency towards anxiety, panic attacks, and insecurity. Little to no depression.
--Stress
(T)tend to be able to tolerate a marginal amount of stress. (A)Cannot tolerate stress. It overwhelms their system.
--Sleep patterns
(T)Tend towards sleepiness and sleepy type of conditions (narcolepsy, sleep apnea, and waking unrefreshed) (A)Tend towards sleeplessness (insomnia, waking up at night unable to go back to sleep, waking unrefreshed.)
--Exercise tolerance
(T)Exercise tires them out. Can't exercise much. (A) Exercise causes fatigue. Body temperature drops after exercise (Dr. Rind)
--Orthostatic hypotesnion
(T)No (A)Yes
--BP Normal to very high.
(T)Poorly controlled by meds (Dr. Rind) (A)Tends to run low. Ranges from 110/70 to 80/50.
--GI
(T)Tend towards poor digestion but often say that it is good. (A)Hard time digesting protein due to low stomach acid or hypochlorhydria. May say that they have hyperacidity when it is clear that they tend towards a low gastric mucosal barrier, which causes gastric irritation. Better with supplements to protect mucosa such as DGL or cabbage extract.
--Bowel transit time
(T)Slow transit time leads to constipation. May actually be due to poor peristalsis. (A) Fast transit time causing an irritable bowel. Poor enzymatic digestion of food leads to a strong tendency to malabsorption. May do well with pancreatic enzyme supplementation.
--Food cravings
(T)Fat (A)Sweets
--Blood sugar regulation
(T)Tend towards high blood sugar (>100 mg/dl) (A)Tend towards low blood sugar and hypoglycemia. Lack of cortisol output to raise blood sugar via gluconeogenesis causes hypoglycemic crashes and a need for small meals.
--Immune function
(T)Tends towards infections due to underactive immune system. (A) tends towards allergies, sensitivities and autoimmune problems due to an over-reactive immune system.
### TERTROXIN™ =Liothyronine sodium 20mcg tablets
#Presentation
Small, white, biconvex, uncoated tablet, 5.6mm in diameter, engraved 'Tertroxin Glaxo' on one one side and scored on the other. Each tablet contains 20 micrograms (0.02mg) liothyronine sodium and complies with the specification for Liothyronine Tablet BP.
#Indications
Liothyronine sodium is indicated in the treatment of: coma due to myxoedema; management of severe chronic thyroid deficiency; hypothyroid states arising in treatment of thyrotoxicosis. Liothyronine sodium can also be used therapeutically in the treatment of thyrotoxicosis as an adjunct to carbimazole in order to prevent subclinical hypothyroidism developing during treatment. Liothyronine sodium may be preferred for treating severe and acute hypothyroid states because of its rapid, and more potent effect, but thyroxine sodium is normally the drug of choice for routine replacement therapy.
#Uses-Mode Of Action
Liothyronine (L-triiodothyronine) sodium is a naturally occurring thyroid hormone. Its biological action is qualitatively similar to that of thyroxine, but the effect develops in a few hours and disappears within 24 to 48 hours of stopping treatment.
TERTROXIN is particularly suitable for treating severe and acute hypothyroid states because of its rapid, intensive and short-lived effect.
#Pharmacokinetics-The following data apply to TERTROXIN Tablets.
Liothyronine is readily absorbed after oral administration. About 5% of endogenous organic iodine in the blood is in the form of liothyronine and normal plasma concentrations are about 70ng/mL. Liothyronine is highly bound in plasma but to a lesser extent than thyroxine. It has a plasma half-life of about 35 to 60 hours.
Liothyronine is widely distributed throughout the body tissues and fluids and is subject to enterohepatic circulation. It does not appear to cross the placenta or to be secreted into the breast milk.
Liothyronine is excreted mainly in the bile and faeces although iodide may be excreted in the urine.
*Dosage And Administration
Thyroid deficiency: Treatment of adults may be begun with 10 or 20mcg every eight hours increasing, if necessary, after one week to the usual recommended dosage of 60mcg daily in divided doses.
For children and elderly patients it is suggested that the initial dosage should be 5mcg daily. (To obtain small doses, tablets may be crushed and triturated with lactose for administration as a powder).
Liothyronine sodium should be given in divided doses two or three times daily.
Myxoedema coma: 60mcg may be given by stomach tube, then 20mcg every eight hours, although it is more usual to start treatment with intravenous liothyronine.
As therapy for thyrotoxicosis with carbimazole: In adults, 20mcg of liothyronine every eight hours.
#Contraindications
Hypersensitivity to any component of the preparation.
Liothyronine sodium is contraindicated in patients with cardiovascular disorders or angina of effort.
#Precautions
In severe and prolonged hypothyroidism there may be a decreased level of adrenocortical activity. When thyroid replacement therapy is instituted, metabolism increases at a greater rate than adrenocortical activity which can lead to adrenocortical insufficiency. Supplemental adrenocortical steroids may be necessary.
-Thyroid replacement therapy may aggravate diabetes mellitus and result in an increase in dosage requirement of insulin or other antidiabetic therapy.
-In myxoedema, care must be taken to avoid imposing excessive burden on cardiac muscle affected by prolonged severe thyroid depletion.
-Special care is needed in the elderly and in patients with diabetes insipidus.
#Pregnancy And Lactation
-Pregnancy:.Tertroxin has been taken by a large number of pregnant women and women of childbearing age, without any form of definite disturbances in the reproductive process having been observed so far. Thyroid, hypo- or hyperactivity in the mother may however unfavourably influence the foetal outcome or well being.
-Lactation:.Liothyronine is excreted in breast milk in low concentrations and this may be sufficient to interfere with neonatal screening for hypothyrodisim.
#Side Effects
The following effects are indicative of excessive dosage, and usually disappear on reduction of dosage or withdrawal of treatment for a day or two. Anginal pain, cardiac arrhythmias, palpitation and cramps in skeletal muscle; also tachycardia, diarrhoea, restlessness, excitability, headache, flushing, sweating, excessive loss of weight and muscular weakness.
#Interactions
-Liothyronine sodium therapy may potentiate the action of anticoagulants.
-Phenytoin levels may be increased by liothyronine.
-Anticonvulsants such as carbamezapine and phenytoin enhance the metabolism of thyroid hormones and may displace them from plasma proteins.
-Initiation or discontinuation of anticonvulsant therapy may alter liothyronine dose requirements.
-If co-administered with cardiac glycosides, adjustment of dosage of cardiac glycoside may be necessary.
-Cholestyramine given concurrently reduces gastrointestinal absorption of liothyronine.
-Liothyronine increases receptor sensitivity to catecholamines thus accelerating the response to tricyclic antidepressants.
-A number of other drugs may affect thyroid function tests and this should be borne in mind when monitoring patients on liothyronine therapy.
-Co-administration of oral contraceptives may result in an increased dosage requirement of liothyronine sodium.
#Overdosage
Gastric lavage or emesis is required if the patient is seen within a few hours of taking the dose. In addition to exaggeration of side effects the following symptoms may been seen: agitation, confusion, irritability, hyperactivity, headache, sweating, mydriasis, tachycardia, arrhythmias, tachypnoea, pyrexia, increase bowel movements and convulsions.
-Treatment is symptomatic; tachycardia has been controlled in adults by 40mg doses of propranolol given every six hours.
#Pharmaceutical Particulars
Special precautions for storage Store at room temperature (below 25°C). Protect from light.
Shelf-life 36 months
Nature and Contents of Container Bottles of 100 tablets
Further Information :20 micrograms liothyronine is equivalent in activity to between 60 to 100 micrograms thyroxine or to 60mg Thyroid BP.
#Wt.reduction Schedule :
1>Cytomel 25mcg 3wk : Day1-3(1T) 4-6(2) 7-9(3) 10-12(4) 13-15(3) 16-18(2) 19-21(1)
2.Clenbuterol 20mcg 3wk : Day/Tab.1-2-3-4-5-6Tab(Day6/Day7)-7(8-12)-6(13-16)-5-4-3-2-1
#WTS control schedule..by LT3 20mcg Tid (AM6:00 PM2:00 PM10:00) : 30일 스케쥴..
:Day1-3(1T Tid까지)
-->4-6(2T Tid까지) :
-->7-9(3T Tid) : maintenance--hyperthyroidism Sx 확인되면3-3-2 for 3 days==> 3-2-2 for 3 days===> 2-2-2 for 3 days==>이후 이 패턴 그대로 줄여나간다.
##ana.ster.관련 제품은 다음과 같다. <생산취하품목제외> 삼일테스토정(삼일제약), 한국화이자 테포남성주(화이자), 예나스테론주(제이텍바이오젠), 안드로올테스토캡스 연질캅셀(한국오가논), 네비도주(한국쉐링, 테카듀라보린주(한화제약), 한서옥시메톨론정(한서제약), 한서옥산드롤론정(한서제약) 등
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제 목 : Fatigue and low Energy
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