TSH, temperature, pulse rate, and other indicators in hypothyroidism
甲状腺功能减退患者TSH、体温、脉搏等指标
by Raymond Peat
Each of the indicators of thyroid function can be useful, but has to be interpreted in relation to the physiological state.
甲状腺功能的每一项指标都是有用的，但必须与生理状态相联系。
Increasingly, TSH (the pituitary thyroid stimulating hormone) has been treated as if it meant something independently; however, it can be brought down into the normal range, or lower, by substances other than the thyroid hormones.
越来越多的人把TSH(垂体促甲状腺激素)当作一种独立的东西来对待;然而，除甲状腺激素外，其他物质也可以使其降至正常范围或更低。
“Basal” body temperature is influenced by many things besides thyroid. The resting heart rate helps to interpret the temperature. In a cool environment, the temperature of the extremities is sometimes a better indicator than the oral or eardrum temperature.
“基础”体温除了受甲状腺影响外，还受许多因素的影响。静息心率有助于解释温度。在寒冷的环境中，肢体温度有时比口腔或耳膜温度更能反映病情。
The “basal” metabolic rate, especially if the rate of carbon dioxide production is measured, is very useful. The amount of water and calories disposed of in a day can give a rough idea of the metabolic rate.
“基础”代谢率是非常有用的，特别是如果测量二氧化碳的产生率。一天中被消耗掉的水和热量可以粗略地反映新陈代谢率。
The T wave on the electrocardiogram, and the relaxation rate on the Achilles reflex test are useful.
心电图上的T波和跟腱反射测试上的松弛率是有用的。
Blood tests for cholesterol, albumin, glucose, sodium, lactate, total thyroxine and total T3 are useful to know, because they help to evaluate the present thyroid status, and sometimes they can suggest ways to correct the problem.
了解胆固醇、白蛋白、葡萄糖、钠、乳酸、总甲状腺素和总T3的血液测试是很有用的，因为它们有助于评估目前的甲状腺状况，有时它们可以建议纠正问题的方法。
Less common blood or urine tests (adrenaline, cortisol, ammonium, free fatty acids), if they are available, can help to understand compensatory reactions to hypothyroidism.
不太常见的血液或尿液测试(肾上腺素、皮质醇、氨、游离脂肪酸)，如果有的话，可以帮助了解甲状腺功能减退的代偿反应。
A book such as McGavack's The Thyroid, that provides traditional medical knowledge about thyroid physiology, can help to dispel some of the current dogmas about the thyroid.
麦加瓦克的《甲状腺》(The Thyroid)等书提供了有关甲状腺生理学的传统医学知识，有助于消除目前有关甲状腺的一些教条。
Using more physiologically relevant methods to diagnose hypothyroidism will contribute to understanding its role in many problems now considered to be unrelated to the thyroid.
使用更多与生理相关的方法来诊断甲状腺功能减退症将有助于理解它在许多目前认为与甲状腺无关的问题中的作用。
I have spoken to several people who told me that their doctors had diagnosed them as “both hypothyroid and hyperthyroid.” Although physicists can believe in things which are simultaneously both particles and not particles, I think biology (and medicine, as far as it is biologically based) should occupy a world in which things are not simultaneously themselves and their opposites. Those illogical, impossible diagnoses make it clear that the rules for interpreting test results have in some situations lost touch with reality.
我和一些人交谈过，他们告诉我，他们的医生诊断他们“甲状腺机能减退和甲状腺机能亢进”。虽然物理学家可以相信同时是粒子和非粒子的事物，但我认为生物学(和医学，就其生物学基础而言)应该占据一个事物本身和对立面不同时存在的世界。这些不合逻辑、不可能的诊断表明，在某些情况下，解释测试结果的规则与现实脱节。
Until the 1940s, hypothyroidism was diagnosed on the basis of signs and symptoms, and sometimes the measurement of oxygen consumption (“basal metabolic rate”) was used for confirmation. Besides the introduction of supposedly “scientific” blood tests, such as the measurement of protein-bound iodine (PBI) in the blood, there were other motives for becoming parsimonious with the diagnosis of hypothyroidism. With the introduction of synthetic thyroxine, one of the arguments for increasing its sale was that natural Armour thyroid (which was precisely standardized by biological tests) wasn't properly standardized, and that an overdose could be fatal. A few articles in prestigious journals created a myth of the danger of thyroid, and the synthetic thyroxine was (falsely) said to be precisely standardized, and to be without the dangers of the complete glandular extract.
直到20世纪40年代，甲状腺机能减退症都是根据症状和体征诊断的，有时还通过测量耗氧量(“基础代谢率”)来确认。除了引入所谓的“科学”血液测试，如血液中蛋白结合碘(PBI)的测量，还有其他原因使得甲状腺功能减退症的诊断变得吝啬。随着合成甲状腺素的引入，增加销售的理由之一是，天然甲状甲状腺素(通过生物测试精确地标准化了)没有适当地标准化，过量服用可能是致命的。一些有声望的杂志上的文章创造了一个关于甲状腺危险的神话，合成的甲状腺素被(错误地)说成是精确的标准化的，没有完全的腺体提取物的危险。
Between 1940 and about 1950, the estimated percentage of hypothyroid Americans went from 30% or 40% to 5%, on the basis of the PBI test, and it has stayed close to that lower number (many publications claim it to be only 1% or 2%). By the time that the measurement of PBI was shown to be only vaguely related to thyroid hormonal function, it had been in use long enough for a new generation of physicians to be taught to disregard the older ideas about diagnosing and treating hypothyroidism. They were taught to inform their patients that the traditional symptoms that were identified as hypothyroidism before 1950 were the result of the patients' own behavior (sloth and gluttony, for example, which produced fatigue, obesity, and heart disease), or that the problems were imaginary (women's hormonal and neurological problems, especially), or that they were simply mysterious diseases and defects (recurring infections, arthritis, and cancer, for example).
在1940年到1950年之间，根据PBI测试，甲状腺机能减退的美国人的估计百分比从30%或40%上升到5%，并且一直接近这个较低的数字(许多出版物声称只有1%或2%)。当PBI的测量被证明只与甲状腺激素功能有模糊的联系时，它已经被使用了足够长的时间，以至于新一代的医生被教导要忽视关于诊断和治疗甲状腺功能减退的旧观念。教它们告知患者,传统的症状被确定为1950年之前甲状腺功能减退的结果病人自己的行为(例如,懒惰和贪婪而产生疲劳,肥胖和心脏病),或者问题虚(女性荷尔蒙和神经问题,尤其是),或者它们仅仅是神秘的疾病和缺陷(例如，反复发生的感染、关节炎和癌症)。
As the newer, more direct tests became available, their meaning was defined in terms of the statistical expectation of hypothyroidism that had become an integral part of medical culture. To make the new TSH measurements fit the medical doctrine, an 8- or 10-fold variation in the hormone was defined as “normal.” With any other biological measurement, such as erythrocyte count, blood pressure, body weight, or serum sodium, calcium, chloride, or glucose, a variation of ten or 20 percent from the mean is considered to be meaningful. If the doctrine regarding the 5% prevalence of hypothyroidism hadn't been so firmly established, there would have been more interest in establishing the meaning of these great variations in TSH.
随着更新、更直接的检测手段的出现，它们的意义被定义为对甲状腺功能减退的统计预期，这已成为医学文化的一个组成部分。为了使新的TSH测量符合医学理论，将这种激素的8倍或10倍的变化定义为“正常”。对于任何其他生物测量，如红细胞计数、血压、体重或血清钠、钙、氯或葡萄糖，偏离平均值10%或20%被认为是有意义的。如果关于5%的甲状腺功能减退患病率的理论没有被如此坚定地确立，那么就会有更多的兴趣去确立TSH中这些巨大变化的意义。
In recent years the “normal range” for TSH has been decreasing. In 2003, the American Association of Clinical Endocrinologists changed their guidelines for the normal range to 0.3 to 3.0 microIU/ml. But even though this lower range is less arbitrary than the older standards, it still isn't based on an understanding of the physiological meaning of TSH.
近年来TSH的“正常范围”一直在下降。2003年，美国临床内分泌学会(American Association of Clinical endocrinology)将其指南的正常范围修改为0.3 - 3.0 microIU/ml。但是，尽管这个较低的范围不像旧的标准那么武断，它仍然不是基于对TSH的生理意义的理解。
Over a period of several years, I never saw a person whose TSH was over 2 microIU/ml who was comfortably healthy, and I formed the impression that the normal, or healthy, quantity was probably something less than 1.0.
在几年的时间里，我从未见过一个TSH超过2微iu /ml的人是舒适健康的，我形成的印象是，正常或健康的数量可能小于1.0。
If a pathologically high TSH is defined as normal, its role in major diseases, such as breast cancer, mastalgia, MS, fibrotic diseases, and epilepsy, will simply be ignored. Even if the possibility is considered, the use of an irrational norm, instead of a proper comparison, such as the statistical difference between the mean TSH levels of cases and controls, leads to denial of an association between hypothyroidism and important diseases, despite evidence that indicates an association.
如果病理上高TSH被定义为正常，那么它在诸如乳腺癌、乳房痛、多发性硬化症、纤维化疾病和癫痫等重大疾病中的作用就会被忽略。即使考虑到这种可能性，使用不合理的规范，而不是进行适当的比较，例如病例和对照组TSH平均水平之间的统计差异，也会导致否认甲状腺功能减退症与重要疾病之间存在关联，尽管有证据表明两者存在关联。
Some critics have said that most physicians are “treating the TSH,” rather than the patient. If TSH is itself pathogenic, because of its pro-inflammatory actions, then that approach isn't entirely useless, even when they “treat the TSH” with only thyroxine, which often isn't well converted into the active triiodothyronine, T3. But the relief of a few symptoms in a small percentage of the population is serving to blind the medical world to the real possibilities of thyroid therapy.
一些批评家说，大多数医生是在“治疗TSH”，而不是病人。如果TSH本身具有致病性，因为它具有促炎作用，那么这种方法并不是完全没用的，即使他们只用甲状腺素“治疗TSH”，而甲状腺素往往不能很好地转化为活性的三碘甲状腺原氨酸T3。但是，对一小部分人的一些症状的缓解，让医学界对甲状腺疗法的真正可能性视而不见。
TSH has direct actions on many cell types other than the thyroid, and probably contributes directly to edema (Wheatley and Edwards, 1983), fibrosis, and mastocytosis. If people are concerned about the effects of a TSH “deficiency,” then I think they have to explain the remarkable longevity of the animals lacking pituitaries in W.D. Denckla's experiments, or of the naturally pituitary deficient dwarf mice that lack TSH, prolactin, and growth hormone, but live about a year longer than normal mice (Heiman, et al., 2003). Until there is evidence that very low TSH is somehow harmful, there is no basis for setting a lower limit to the normal range.
TSH对除甲状腺外的许多细胞有直接作用，可能直接导致水肿(Wheatley和Edwards, 1983)、纤维化和肥大细胞增多。如果人们担心TSH“缺乏”的影响，那么我认为他们必须解释在W.D. Denckla的实验中缺乏垂体的动物的显著寿命，或者是天生垂体缺陷的矮小小鼠，它们缺乏TSH、催乳素和生长激素，但比正常小鼠多活一年左右(Heiman, et al.， 2003)。除非有证据表明非常低的TSH是有害的，否则没有基础来设定正常范围的下限。
Some types of thyroid cancer can usually be controlled by keeping TSH completely suppressed. Since TSH produces reactions in cells as different as fibroblasts and fat cells, pigment cells in the skin, mast cells and bone marrow cells (Whetsell, et al., 1999), it won't be surprising if it turns out to have a role in the development of a variety of cancers, including melanoma.
某些类型的甲状腺癌通常可以通过完全抑制TSH得到控制。由于TSH在不同的细胞中产生反应，如成纤维细胞、脂肪细胞、皮肤色素细胞、肥大细胞和骨髓细胞(Whetsell, et al.， 1999)，如果它被证明在各种癌症的发展中有作用，包括黑素瘤，那就不足为奇了。
Many things, including the liver and the senses, regulate the function of the thyroid system, and the pituitary is just one of the factors affecting the synthesis and secretion of the thyroid hormones.
很多东西，包括肝脏和感官，都在调节甲状腺系统的功能，而垂体只是影响甲状腺激素合成和分泌的因素之一。
A few people who had extremely low levels of pituitary hormones, and were told that they must take several hormone supplements for the rest of their life, began producing normal amounts of those hormones within a few days of eating more protein and fruit. Their endocrinologist described them as, effectively, having no pituitary gland. Extreme malnutrition in Africa has been described as creating “. . . a condition resembling hypophysectomy,” (Ingenbleek and Beckers, 1975) but the people I talked to in Oregon were just following what they thought were healthful nutritional policies, avoiding eggs and sugars, and eating soy products.
一些脑下垂体激素水平极低的人，被告知他们的余生必须服用几种激素补充剂，在吃了更多的蛋白质和水果后的几天内，这些激素开始分泌正常数量。他们的内分泌学家说，实际上，他们没有脑下垂体。非洲的极端营养不良被描述为“造成……(Ingenbleek and Beckers, 1975)但我在俄勒冈州采访的人只是遵循他们认为健康的营养政策，不吃鸡蛋和糖，吃豆制品。
Occasionally, a small supplement of thyroid in addition to a good diet is needed to quickly escape from the stress-induced “hypophysectomized” condition.
偶尔，除了良好的饮食外，还需要补充少量甲状腺，以快速摆脱压力诱导的“垂体切除”状态。
Aging, infection, trauma, prolonged cortisol excess, somatostatin, dopamine or L-dopa, adrenaline (sometimes; Mannisto, et al., 1979), amphetamine, caffeine and fever can lower TSH, apart from the effect of feedback by the thyroid hormones, creating a situation in which TSH can appear normal or low, at the same time that there is a real hypothyroidism.
衰老、感染、创伤、皮质醇过量、生长抑素、多巴胺或左旋多巴、肾上腺素(有时;Mannisto, et al.， 1979)，安非他明，咖啡因和发烧可以降低TSH，除了甲状腺激素的反馈作用外，造成TSH出现正常或低的情况，同时存在真正的甲状腺功能减退。
A disease or its treatment can obscure the presence of hypothyroidism. Parkinson's disease is a clear example of this. (Garcia-Moreno and Chacon, 2002: “… in the same way hypothyroidism can simulate Parkinson's disease, the latter can also conceal hypothyroidism.”)
The stress-induced suppression of TSH and other pituitary hormones is reminiscent of the protective inhibition that occurs in individual nerve fibers during dangerously intense stress, and might involve such a “parabiotic” process in the nerves of the hypothalamus or other brain region. The relative disappearance of the pituitary hormones when the organism is in very good condition (for example, the suppression of ACTH and cortisol by sugar or pregnenolone) is parallel to the high energy quiescence of individual nerve fibers.
一种疾病或其治疗可以掩盖甲状腺功能减退的存在。帕金森氏症就是一个明显的例子。(Garcia-Moreno and Chacon, 2002:“……同样地，甲状腺功能减退可以模拟帕金森病，后者也可以掩盖甲状腺功能减退。”)
应激诱导的TSH和其他垂体激素的抑制使人想起在危险的高强度应激时发生在单个神经纤维中的保护性抑制，并可能涉及下丘脑或其他大脑区域的神经的这种“副产物”过程。当机体处于很好的状态时，垂体激素的相对消失(例如，糖或孕烯醇酮对ACTH和皮质醇的抑制)与个别神经纤维的高能量静止平行。
These associations between energy state and cellular activity can be used for evaluating the thyroid state, as in measuring nerve and muscle reaction times and relaxation rates. For example, relaxation which is retarded, because of slow restoration of the energy needed for cellular “repolarization,” is the basis for the traditional use of the Achilles tendon reflex relaxation test for diagnosing hypothyroidism. The speed of relaxation of the heart muscle also indicates thyroid status (Mohr-Kahaly, et al., 1996).
Stress, besides suppressing the TSH, acts in other ways to suppress the real thyroid function. Cortisol, for example, inhibits the conversion of T4 to T3, which is responsible for the respiratory production of energy and carbon dioxide. Adrenaline, besides leading to increased production of cortisol, is lipolytic, releasing the fatty acids which, if they are polyunsaturated, inhibit the production and transport of thyroid hormone, and also interfere directly with the respiratory functions of the mitochondria. Adrenaline decreases the conversion to T4 to T3, and increases the formation of the antagonistic reverse T3 (Nauman, et al., 1980, 1984).
这些能量状态和细胞活动之间的关联可以用来评估甲状腺状态，比如测量神经和肌肉的反应时间和松弛率。例如，由于细胞“复极化”所需要的能量恢复缓慢，所以松弛是迟缓的，这是传统使用跟腱反射松弛试验诊断甲状腺功能减退症的基础。心肌松弛的速度也表明甲状腺状态(Mohr-Kahaly, et al.， 1996)。
压力除了抑制TSH外，还以其他方式抑制甲状腺功能。例如，皮质醇会抑制T4向T3的转化，而T3负责呼吸产生能量和二氧化碳。肾上腺素除了能增加皮质醇的分泌外，还是脂质体，能释放脂肪酸，如果脂肪酸是多不饱和的，就会抑制甲状腺激素的分泌和运输，并直接干扰线粒体的呼吸功能。肾上腺素降低了T4向T3的转化，增加了拮抗逆转T3的形成(Nauman等，1980,1984)。
During the night, at the time adrenaline and free fatty acids are at their highest, TSH usually reaches its peak. TSH itself can produce lipolysis, raising the level of circulating free fatty acids. This suggests that a high level of TSH could sometimes contribute to functional hypothyroidism, because of the antimetabolic effects of the unsaturated fatty acids.
在夜间，肾上腺素和游离脂肪酸最高，TSH通常达到峰值。TSH本身可以产生脂解，提高循环中的游离脂肪酸水平。这表明，由于不饱和脂肪酸的抗代谢作用，高水平的TSH有时可能导致功能性甲状腺功能减退。
These are the basic reasons for thinking that the TSH tests should be given only moderate weight in interpreting thyroid function.
这些是认为TSH测试在解释甲状腺功能时只应给予适度权重的基本原因。
The metabolic rate is very closely related to thyroid hormone function, but defining it and measuring it have to be done with awareness of its complexity.
The basal metabolic rate that was commonly used in the 1930s for diagnosing thyroid disorders was usually a measurement of the rate of oxygen consumption, made while lying quietly early in the morning without having eaten anything for several hours. When carbon dioxide production can be measured at the same time as oxygen consumption, it's possible to estimate the proportion of energy that is being derived from glucose, rather than fat or protein, since oxidation of glucose produces more carbon dioxide than oxidation of fat does. Glucose oxidation is efficient, and suggests a state of low stress.
代谢率与甲状腺激素功能密切相关，但在定义和测量代谢率时，必须意识到它的复杂性。
基础代谢率在20世纪30年代被广泛用于诊断甲状腺疾病，它通常是一种耗氧量的测量方法，是在清晨安静地躺在床上数小时不吃任何东西的情况下得出的。当二氧化碳的产生和氧气的消耗可以同时进行测量时，就有可能估计出来自葡萄糖而不是脂肪或蛋白质的能量的比例，因为葡萄糖氧化产生的二氧化碳比脂肪氧化产生的二氧化碳多。葡萄糖氧化是有效的，表明一种低压力状态。
The very high adrenaline that sometimes occurs in hypothyroidism will increase the metabolic rate in several ways, but it tends to increase the oxidation of fat. If the production of carbon dioxide is measured, the adrenaline/stress component of metabolism will be minimized in the measurement. When polyunsaturated fats are mobilized, their spontaneous peroxidation consumes some oxygen, without producing any usable energy or carbon dioxide, so this is another reason that the production of carbon dioxide is a very good indicator of thyroid hormone activity. The measurement of oxygen consumption was usually done for two minutes, and carbon dioxide production could be accurately measured in a similarly short time. Even a measurement of the percentage of carbon dioxide at the end of a single breath can give an indication of the stress-free, thyroid hormone stimulated rate of metabolism (it should approach five or six percent of the expired air).
甲状腺机能减退时肾上腺素含量很高会以多种方式增加代谢率，但会增加脂肪的氧化。如果测量二氧化碳的产生，代谢中的肾上腺素/应激成分将在测量中最小化。当多不饱和脂肪被调动时，它们的自发过氧化作用会消耗一些氧气，而不会产生任何可用的能量或二氧化碳，所以这是二氧化碳的产生是甲状腺激素活性的一个很好的指标的另一个原因。耗氧量的测量通常需要两分钟，而二氧化碳的产生也可以在同样短的时间内精确测量。即使是在一次呼吸结束时测量二氧化碳的百分比，也可以指示无压力的、甲状腺激素刺激的新陈代谢率(应该接近呼出空气的5%或6%)。
Increasingly in the last several years, people who have many of the standard symptoms of hypothyroidism have told me that they are hyperthyroid, and that they have to decide whether to have surgery or radiation to destroy their thyroid gland. They have told me that their symptoms of “hyperthyroidism,” according to their physicians, were fatigue, weakness, irritability, poor memory, and insomnia.
在过去的几年里，越来越多的人告诉我，他们有很多甲状腺功能减退的标准症状，他们是甲亢，他们必须决定是做手术还是放疗来破坏他们的甲状腺。他们告诉我，根据医生的说法，他们的“甲状腺机能亢进”症状是疲劳、虚弱、易怒、记忆力差和失眠。
They didn't eat very much. They didn't sweat noticeably, and they drank a moderate amount of fluids. Their pulse rates and body temperature were normal, or a little low.
他们吃得不多。他们没有明显的出汗，喝适量的液体。他们的脉搏率和体温正常，或略低。
Simply on the basis of some laboratory tests, they were going to have their thyroid gland destroyed. But on the basis of all of the traditional ways of judging thyroid function, they were hypothyroid.
Broda Barnes, who worked mostly in Fort Collins, Colorado, argued that the body temperature, measured before getting out of bed in the morning, was the best basis for diagnosing thyroid function.
仅仅是在一些实验室测试的基础上，他们的甲状腺就被摧毁了。但根据所有传统的判断甲状腺功能的方法，他们是甲状腺功能减退。
主要在科罗拉多州柯林斯堡工作的布罗达·巴恩斯(Broda Barnes)认为，早上起床前测量的体温是诊断甲状腺功能的最佳依据。
Fort Collins, at a high altitude, has a cool climate most of the year. The altitude itself helps the thyroid to function normally. For example, one study (Savourey, et al., 1998) showed an 18% increase in T3 at a high altitude, and mitochondria become more numerous and are more efficient at preventing lactic acid production, capillary leakiness, etc.
柯林斯堡地处高海拔地区，全年大部分时间气候凉爽。海拔本身有助于甲状腺的正常功能。例如，一项研究(Savourey, et al.， 1998)显示，在高海拔地区T3增加18%，线粒体变得更多，更有效地防止乳酸生成、毛细血管渗漏等。
In Eugene during a hot and humid summer, I saw several obviously hypothyroid people whose temperature seemed perfectly normal, euthyroid by Barnes' standards. But I noticed that their pulse rates were, in several cases, very low. It takes very little metabolic energy to keep the body at 98.6 degrees when the air temperature is in the nineties. In cooler weather, I began asking people whether they used electric blankets, and ignored their temperature measurements if they did.
一个湿热的夏天，在尤金，我看到几个明显甲状腺机能减退的人，他们的体温似乎完全正常，按照巴恩斯的标准，甲状腺机能正常。但我注意到他们的脉搏频率，在一些情况下，非常低。当气温在90度左右时，人体只需要很少的代谢能量就能保持在98.6度。天气转凉时，我开始询问人们是否使用电热毯，如果他们使用电热毯，我就忽略他们测量的温度。
The combination of pulse rate and temperature is much better than either one alone. I happened to see two people whose resting pulse rates were chronically extremely high, despite their hypothyroid symptoms. When they took a thyroid supplement, their pulse rates came down to normal. (Healthy and intelligent groups of people have been found to have an average resting pulse rate of 85/minute, while less healthy groups average close to 70/minute.)
脉冲频率和温度的结合比单独使用任何一种都要好得多。我碰巧看到两个人，尽管有甲状腺功能减退的症状，但他们的静息脉搏率长期极高。当他们服用甲状腺补充剂时，他们的脉搏降到了正常水平。(研究发现，健康和聪明人群的平均静息脉搏为85/分钟，而不健康人群的平均静息脉搏为70/分钟。)
The speed of the pulse is partly determined by adrenaline, and many hypothyroid people compensate with very high adrenaline production. Knowing that hypothyroid people are susceptible to hypoglycemia, and that hypoglycemia increases adrenaline, I found that many people had normal (and sometimes faster than average) pulse rates when they woke up in the morning, and when they got hungry. Salt, which helps to maintain blood sugar, also tends to lower adrenalin, and hypothyroid people often lose salt too easily in their urine and sweat. Measuring the pulse rate before and after breakfast, and in the afternoon, can give a good impression of the variations in adrenalin. (The blood pressure, too, will show the effects of adrenaline in hypothyroid people. Hypothyroidism is a major cause of hypertension.)
脉搏的速度部分是由肾上腺素决定的，许多甲状腺机能减退的人用非常高的肾上腺素分泌来弥补。我知道甲状腺机能减退的人容易发生低血糖，低血糖会增加肾上腺素，所以我发现很多人在早上醒来或者饿了的时候，脉搏都是正常的(有时比平均水平还要快)。盐有助于维持血糖，同时也会降低肾上腺素，而甲状腺机能减退的人往往很容易在尿液和汗液中失去盐。测量早餐前后和下午的脉搏频率，可以很好地反映肾上腺素的变化。(在甲状腺机能减退的人群中，血压也会显示肾上腺素的作用。甲状腺功能减退是高血压的主要原因。
But hypoglycemia also tends to decrease the conversion of T4 to T3, so heat production often decreases when a person is hungry. First, their fingers, toes, and nose will get cold, because adrenalin, or adrenergic sympathetic nervous activity, will increase to keep the brain and heart at a normal temperature, by reducing circulation to the skin and extremities. Despite the temperature-regulating effect of adrenalin, the reduced heat production resulting from decreased T3 will make a person susceptible to hypothermia if the environment is cool.
但低血糖也会降低T4到T3的转化，所以当一个人饥饿时，热量的产生往往会减少。首先，他们的手指、脚趾和鼻子会感到冷，因为肾上腺素或肾上腺素能交感神经活动会增加，通过减少皮肤和四肢的血液循环，以保持大脑和心脏处于正常温度。尽管肾上腺素有调节体温的作用，但如果环境较冷，T3降低所导致的产热减少会使人容易体温过低。
Since food, especially carbohydrate and protein, will increase blood sugar and T3 production, eating is “thermogenic,” and the oral (or eardrum) temperature is likely to rise after eating.
因为食物，尤其是碳水化合物和蛋白质，会增加血糖和T3的生成，所以吃东西是“生热的”，吃东西后口腔(或耳膜)的温度很可能会升高。
Blood sugar falls at night, and the body relies on the glucose stored in the liver as glycogen for energy, and hypothyroid people store very little sugar. As a result, adrenalin and cortisol begin to rise almost as soon as a person goes to bed, and in hypothyroid people, they rise very high, with the adrenalin usually peaking around 1 or 2 A.M., and the cortisol peaking around dawn; the high cortisol raises blood sugar as morning approaches, and allows adrenalin to decline. Some people wake up during the adrenalin peak with a pounding heart, and have trouble getting back to sleep unless they eat something.
血糖在夜间下降，身体依靠储存在肝脏中的葡萄糖作为糖原来提供能量，而甲状腺机能低下的人很少储存糖。因此，肾上腺素和皮质醇几乎一上床就开始上升，甲状腺机能减退的人，肾上腺素上升得非常高，肾上腺素通常在凌晨1点或2点左右达到峰值，皮质醇在黎明左右达到峰值;随着早晨临近，高皮质醇会提高血糖，导致肾上腺素下降。有些人在肾上腺素高峰时醒来，心脏怦怦直跳，除非吃点东西，否则很难再入睡。
If the night-time stress is very high, the adrenalin will still be high until breakfast, increasing both temperature and pulse rate. The cortisol stimulates the breakdown of muscle tissue and its conversion to energy, so it is thermogenic, for some of the same reasons that food is thermogenic.
如果夜间压力非常大，直到早餐前肾上腺素仍然会很高，体温和脉搏都会增加。皮质醇刺激肌肉组织的分解并将其转化为能量，所以它是产热的，这和食物产热的原因是一样的。
After eating breakfast, the cortisol (and adrenalin, if it stayed high despite the increased cortisol) will start returning to a more normal, lower level, as the blood sugar is sustained by food, instead of by the stress hormones. In some hypothyroid people, this is a good time to measure the temperature and pulse rate. In a normal person, both temperature and pulse rate rise after breakfast, but in very hypothyroid people either, or both, might fall.
吃完早餐后，皮质醇(和肾上腺素，如果皮质醇升高，但皮质醇仍保持高水平)将开始回到一个更正常、更低的水平，因为血糖是由食物而不是压力荷尔蒙维持的。对于一些甲状腺机能减退的人来说，这是测量体温和脉搏频率的好时机。对于正常人来说，早餐后体温和脉搏都会升高，但对于甲状腺功能极度低下的人，体温和脉搏都可能下降。
Some hypothyroid people have a very slow pulse, apparently because they aren't compensating with a large production of adrenalin. When they eat, the liver's increased production of T3 is likely to increase both their temperature and their pulse rate.
有些甲状腺机能减退的人脉搏很慢，显然是因为他们没有大量分泌肾上腺素来弥补。当它们进食时，肝脏增加的T3产量可能会增加它们的体温和脉搏。
By watching the temperature and pulse rate at different times of day, especially before and after meals, it's possible to separate some of the effects of stress from the thyroid-dependent, relatively “basal” metabolic rate. When beginning to take a thyroid supplement, it's important to keep a chart of these measurements for at least two weeks, since that's roughly the half-life of thyroxine in the body. When the body has accumulated a steady level of the hormones, and begun to function more fully, the factors such as adrenaline that have been chronically distorted to compensate for hypothyroidism will have begun to normalize, and the early effects of the supplementary thyroid will in many cases seem to disappear, with heart rate and temperature declining. The daily dose of thyroid often has to be increased several times, as the state of stress and the adrenaline and cortisol production decrease.
通过观察一天中不同时间的温度和脉搏频率，特别是餐前和餐后，有可能将压力的一些影响与甲状腺依赖的、相对“基础”代谢率分开。当开始服用甲状腺补充剂时，重要的是要将这些测量数据记录至少两周，因为这大概是甲状腺素在体内的半衰期。当身体积累了稳定的激素水平,并开始函数更充分,肾上腺素等因素,长期扭曲来弥补甲状腺功能减退会开始正常化,和早期补充甲状腺的作用将在许多情况下似乎消失了,随着心率和体温的下降。由于压力状态和肾上腺素和皮质醇的产生减少，甲状腺的每日剂量通常需要增加几倍。
Counting calories achieves approximately the same thing as measuring oxygen consumption, and is something that will allow people to evaluate the various thyroid tests they may be given by their doctor. Although food intake and metabolic rate vary from day to day, an approximate calorie count for several days can often make it clear that a diagnosis of hyperthyroidism is mistaken. If a person is eating only about 1800 calories per day, and has a steady and normal body weight, any “hyperthyroidism” is strictly metaphysical, or as they say, “clinical.”
计算卡路里的作用与测量耗氧量大致相同，它可以让人们评估医生可能给他们的各种甲状腺检查。虽然每天的食物摄入量和代谢率都不同，但几天的大致卡路里含量往往可以清楚地表明甲状腺机能亢进的诊断是错误的。如果一个人每天只吃大约1800卡路里，并且体重稳定正常，那么任何“甲状腺机能亢进”都是严格意义上的形而上学，或者用他们的话来说，是“临床的”。
When the humidity and temperature are normal, a person evaporates about a liter of water for every 1000 calories metabolized. Eating 2000 calories per day, a normal person will take in about four liters of liquid, and form about two liters of urine. A hyperthyroid person will invisibly lose several quarts of water in a day, and a hypothyroid person may evaporate a quart or less.
在湿度和温度正常的情况下，人体每代谢1000卡路里，就会蒸发大约一升水。每天摄入2000卡路里，一个正常人会摄入约4升液体，并形成约2升尿液。甲状腺机能亢进的人每天会无形地失去几夸脱的水，而甲状腺机能减退的人可能蒸发掉一夸脱或更少的水。
When cells, because of a low metabolic rate, don't easily return to their thoroughly energized state after they have been stimulated, they tend to take up water, or, in the case of blood vessels, to become excessively permeable. Fatigued muscles swell noticeably, and chronically fatigued nerves can swell enough to cause them to be compressed by the surrounding connective tissues. The energy and hydration state of cells can be detected in various ways, including magnetic resonance, and electrical impedance, but functional tests are easy and practical.
当细胞由于代谢率低，在受到刺激后不能轻易恢复到完全充满能量的状态时，它们倾向于吸收水分，或者，在血管的情况下，变得过度通透。疲劳的肌肉明显膨胀，长期疲劳的神经膨胀到足以使其被周围的结缔组织压迫。细胞的能量和水化状态可以通过多种方法检测，包括磁共振和电阻抗，但功能测试是简单和实用的。
With suitable measuring instruments, the effects of hypothyroidism can be seen as slowed conduction along nerves, and slowed recovery and readiness for new responses. Slow reaction time is associated with slowed memory, perception, and other mental processes. Some of these nervous deficits can be remedied slightly just by raising the core temperature and providing suitable nutrients, but the active thyroid hormone, T3 is mainly responsible for maintaining the temperature, the nutrients, and the intracellular respiratory energy production.
有了合适的测量仪器，甲状腺功能减退的影响可以被视为减缓神经传导，减缓恢复和对新反应的准备。反应慢与记忆、感知和其他心理过程的慢有关。有些神经缺陷可以通过提高核心温度和提供适当的营养物质来轻微修复，但活跃的甲状腺激素T3主要负责维持温度、营养物质和细胞内呼吸能量的产生。
In nerves, as in other cells, the ability to rest and repair themselves increases with the proper level of thyroid hormone. In some cells, the energized stability produced by the thyroid hormones prevents inflammation or an immunological hyperactivity. In the 1950s, shortly after it was identified as a distinct substance, T3 was found to be anti-inflammatory, and both T4 and T3 have a variety of anti-inflammatory actions, besides the suppression of the pro-inflammatory TSH.
神经和其他细胞一样，随着甲状腺激素水平的适当提高，休息和自我修复的能力也会增强。在某些细胞中，由甲状腺激素产生的能量稳定性可以防止炎症或免疫机能亢进。20世纪50年代，T3被鉴定为一种独特物质后不久，又被发现具有抗炎作用，T4和T3除抑制促炎TSH外，还具有多种抗炎作用。
Because the actions of T3 can be inhibited by many factors, including polyunsaturated fatty acids, reverse T3, and excess thyroxine, the absolute level of T3 can't be used by itself for diagnosis. “Free T3” or “free T4” is a laboratory concept, and the biological activity of T3 doesn't necessarily correspond to its “freedom” in the test. T3 bound to its transport proteins can be demonstrated to enter cells, mitochondria, and nuclei. Transthyretin, which carries both vitamin A and thyroid hormones, is sharply decreased by stress, and should probably be regularly measured as part of the thyroid examination.
由于T3的作用受到多种因素的抑制，包括多不饱和脂肪酸、逆转T3、过量甲状腺素等，因此T3的绝对水平不能单独用于诊断。“游离T3”或“游离T4”是实验室概念，T3的生物活性不一定与试验中的“自由”相对应。T3与转运蛋白结合，可进入细胞、线粒体和细胞核。携带维生素A和甲状腺激素的转甲状腺素在压力下会急剧下降，应该定期进行甲状腺检查。
When T3 is metabolically active, lactic acid won't be produced unnecessarily, so the measurement of lactate in the blood is a useful test for interpreting thyroid function. Cholesterol is used rapidly under the influence of T3, and ever since the 1930s it has been clear that serum cholesterol rises in hypothyroidism, and is very useful diagnostically. Sodium, magnesium, calcium, potassium, creatinine, albumin, glucose, and other components of the serum are regulated by the thyroid hormones, and can be used along with the various functional tests for evaluating thyroid function.
当T3代谢活跃时，不会产生不必要的乳酸，所以血液中乳酸的测量是解释甲状腺功能的有用测试。在T3的影响下，胆固醇被迅速使用，自20世纪30年代以来，血清胆固醇在甲状腺功能减退症中明显升高，这在诊断上非常有用。钠、镁、钙、钾、肌酐、白蛋白、葡萄糖等血清成分受甲状腺激素调节，可与各种功能试验一起使用，用于评价甲状腺功能。
Stereotypes are important. When a very thin person with high blood pressure visits a doctor, hypothyroidism isn't likely to be considered; even high TSH and very low T4 and T3 are likely to be ignored, because of the stereotypes. (And if those tests were in the healthy range, the person would be at risk for the “hyperthyroid” diagnosis.) But remembering some of the common adaptive reactions to a thyroid deficiency, the catabolic effects of high cortisol and the circulatory disturbance caused by high adrenaline should lead to doing some of the appropriate tests, instead of treating the person's hypertension and “under nourished” condition.
刻板印象是很重要的。当一个非常瘦的高血压患者去看医生时，甲状腺功能减退可能不会被考虑;甚至高的TSH和低的T4和T3也可能被忽略，因为刻板印象。(如果这些检测结果在健康范围内，那么这个人就有被诊断为“甲状腺机能亢进”的风险。)但要记住甲状腺机能缺乏的一些常见适应性反应，高皮质醇的分解代谢影响和高肾上腺素引起的循环障碍应该导致做一些适当的测试，而不是治疗高血压和“营养不良”的情况。
REFERENCES
Clin Chem Lab Med. 2002 Dec;40(12):1344-8. Transthyretin: its response to malnutrition and stress injury. Clinical usefulness and economic implications. Bernstein LH, Ingenbleek Y.
Endokrinologie. 1968;53(3):217-21.[Influence of hypophysectomy and pituitary hormones on dextran edema in rats] German. Boeskor A, Gabbiani G.
J Clin Endocrinol Metab. 2001 Nov;86(11):5148-51. Sudden enlargement of local recurrent thyroid tumor after recombinant human TSH administration. Braga M, Ringel MD, Cooper DS.
J Investig Med. 2002 Sep;50(5):350-4; discussion 354-5. The nocturnal serum thyrotropin surge is inhibited in patients with adrenal Incidentaloma. Coiro V, Volpi R, Capretti L, Manfredi G, Magotti MG, Bianconcini M, Cataldo S, Chiodera P.
Rev Neurol (Paris). 1992;148(5):371-3. [Hashimoto's encephalopathy: toxic or autoimmune mechanism?] [Article in French] Ghawche F, Bordet R, Destee A. Service de Clinique Neurologique A, CHU, Lille. A 36-year-old woman presented with partial complex status epilepticus. Magnetic resonance imaging with T2-weighted sequences showed a high-intensity signal in the left posterior frontal area. Hashimoto's thyroiditis was then discovered. The disappearance of the high-intensity signal after corticosteroid therapy was suggestive of an autoimmune mechanism. However, improvement could be obtained only with a hormonal treatment, which supports the hypothesis of a pathogenetic role of the Tyrosine-Releasing Hormone (TRH).
Am J Clin Nutr. 1986 Mar;43(3):406-13. Thyroid hormone and carrier protein interrelationships in children recovering rom kwashiorkor. Kalk WJ, Hofman KJ, Smit AM, van Drimmelen M, van der Walt LA, Moore RE. We have studied 15 infants with severe protein energy malnutrition (PEM) as a model of nutritional nonthyroidal illness. Changes in circulating thyroid hormones, binding proteins, and their interrelationships were assessed before and during recovery. Serum concentrations of total thyroxine and triiodothyronine and of thyroxine-binding proteins were extremely reduced, and increased progressively during 3 wk of refeeding. The T4:TBG molar ratio was initially 0.180 +/- 0.020, and increased progressively, parallel to the increases in TT4, to 0.344 +/- 0.038 after 21 days (p less than 0.025). The changes in free T4 estimates varied according to the methods used–FTI and analogue FT4 increased, dialysis FT4 fraction decreased. Serum TSH levels increased transiently during recovery. It is concluded 1) there is reduced binding of T4 and T3 to TBG in untreated PEM which takes 2-3 wk to recover; 2) there are methodological differences in evaluating free T4 levels in PEM; 3) increased TSH secretion appears to be an integral part of the recovery from PEM.
Neuroendocrinology. 1982;35(2):139-47. Neurotransmitter control of thyrotropin secretion. Krulich L. “The central dopaminergic system seems to have an inhibitory influence on the secretion of thyrotropin (TSH) both in humans and rats.”
Endocrinology 1972 Mar;90(3):795-801. TSH-induced release of 5-hydroxytryptamine and histamine rat thyroid mast cells. Ericson LE, Hakanson R, Melander A, Owman C, Sundler F.
Rev Neurol. 2002 Oct 16-31;35(8):741-2. [Hypothyroidism concealed by Parkinson's disease][in Spanish] Garcia-Moreno JM, Chacon J. Servicio de Neurologia, Hospital Universitario Virgen Macarena, Sevilla, Espana. [email protected] AIMS: Although it is commonly recognised that diseases of the thyroids can simulate extrapyramidal disorders, a review of the causes of Parkinsonism in the neurology literature shows that they are not usually mentioned or, if so, only very briefly. The development of hypothyroidism in a patient with Parkinson s disease can go undetected, since the course of both diseases can involve similar clinical features. Generally speaking there is always an insistence on the need to conduct a thyroidal hormone study in any patient with symptoms of Parkinson, but no emphasis is put on the need to continue to rule out dysthyroidism throughout the natural course of the disease, in spite of the fact that the concurrence of both pathological conditions can be high and that, in the same way hypothyroidism can simulate Parkinson s disease, the latter can also conceal hypothyroidism. CASE REPORT: We report the case of a female patient who had been suffering from Parkinson s disease for 17 years and started to present on off fluctuations that did not respond to therapy. Hypothyroidism was observed and the hormone replacement therapy used to resolve the problem allowed the Parkinsonian fluctuations to be controlled. CONCLUSIONS: We believe that it is very wise to suspect hypothyroidism in patients known to be suffering from Parkinson s disease, and especially so in cases where the clinical condition worsens and symptoms no longer respond properly to antiparkinsonian treatment. These observations stress the possible role played by thyroid hormones in dopaminergic metabolism and vice versa.
Endocrine. 2003 Feb-Mar;20(1-2):149-54. Body composition of prolactin-, growth hormone, and thyrotropin-deficient Ames dwarf mice. Heiman ML, Tinsley FC, Mattison JA, Hauck S, Bartke A. Lilly Research Labs, Corporate Center, Indianapolis, IN, USA. Ames dwarf mice have primary deficiency of prolactin (PRL), growth hormone (GH), and thyroid-stimulating hormone (TSH), and live considerably longer than normal animals from the same line.
(Lancet. 1975 Nov 1;2(7940):845-8.. Triiodothyronine and thyroid-stimulating hormone in protein-calorie malnutrition in infants. Ingenbleek Y, Beckers C.)
Am J Med Sci. 1995 Nov;310(5):202-5. Case report: thyrotropin-releasing hormone-induced myoclonus and tremor in a patient with Hashimoto's encephalopathy. Ishii K, Hayashi A, Tamaoka A, Usuki S, Mizusawa H, Shoji S.
Rev Neurol (Paris). 1985;141(1):55-8. [Hashimoto's thyroiditis and myoclonic encephalopathy. Pathogenic hypothesis] [Article in French] Latinville D, Bernardi O, Cougoule JP, Bioulac B, Henry P, Loiseau P, Mauriac L. A 49 year old caucasian female with Hashimoto thyroiditis, developed during two years a neurological disorder with tonic-clonic and myoclonic seizures and confusional states. Some attacks were followed by a transient postictal aphasia. Some parallelism was noted between the clinical state and TSH levels. Neurological events disappeared with the normalisation of thyroid functions. This association of Hashimoto thyroiditis and myoclonic encephalopathy has been rarely published. Pathogenesis could be double. Focal signs could be due to an auto-immune mechanism, perhaps through a vasculitis. A non-endocrine central action could explain diffuse signs: tonic-clonic seizures, myoclonus and confusional episodes.
J Clin Endocrinol Metab. 1992 Jun;74(6):1361-5. Fatty acid-induced increase in serum dialyzable free thyroxine after physical exercise: implication for nonthyroidal illness. Liewendahl K, Helenius T, Naveri H, Tikkanen H.
Adv Exp Med Biol. 1990;274:315-29. Role of monokines in control of anterior pituitary hormone release. McCann SM, Rettori V, Milenkovic L, Jurcovicova J, Gonzalez MC.
Acta Endocrinol (Copenh). 1979 Feb;90(2):249-58. Dual action of adrenergic system on the regulation of thyrotrophin secretion in the male rat. Mannisto, Ranta T, Tuomisto J. “….noradrenaline (NA) (1 h), and L-Dopa (1 h) were also effective in decreasing serum TSH levels….”
Endocrinology 1971 Aug;89(2):528-33. TSH-induced appearance and stimulation of amine-containing mast cells in the mouse thyroid. Melander A, Owman C, Sundler F.
Epilepsy Res. 1988 Mar-Apr;2(2):102-10. Evidence of hypothyroidism in the genetically epilepsy-prone rat. Mills SA, Savage DD. Department of Pharmacology, University of New Mexico School of Medicine, Albuquerque 87131. A number of neurochemical and behavioral similarities exist between the genetically epilepsy-prone (GEPR) rat and rats made hypothyroid at birth. These similarities include lower brain monoamine levels, audiogenic seizure susceptibility and lowered electroconvulsive shock seizure threshold. Given these similarities, thyroid hormone status was examined in GEPR rats. Serum samples were collected from GEPR-9 and non-epileptic control rats at 5, 9, 13, 16, 22, 31, 45, 60, 90, 150 and 350 days of age. Serum thyroxine (T4) levels were significantly lower in GEPR-9 rats compared to control until day 22 of age. GEPR-9 thyrotropin (TSH) levels were significantly elevated during the period of diminished serum T4. GEPR-9 triiodothyronine (T3) levels were lower than control throughout the first year of life. The data indicate that the GEPR-9 rat is hypothyroid from at least the second week of life up to 1 year of age. The critical impact of neonatal hypothyroidism on brain function coupled with the development of the audiogenic seizure susceptible trait by the GEPR-9 rat during the third week after birth suggests that neonatal hypothyroidism could be one etiological factor in the development of the seizure-prone state of GEPR-9 rats.
Przegl Lek. 1998;55(5):250-8. [Mastopathy and simple goiter–mutual relationships] [Article in Polish] Mizia-Stec K, Zych F, Widala E. “Non-toxic goitre was found in 80% patients with mastopathy, and the results of palpation examination of thyroid were confirmed by thyroid ultrasonographic examination. Non-toxic goitre was significantly more often in patients with mastopathy in comparison with healthy women, and there was found significantly higher thyroid volume in these patients.” Endocrinology. 1997 Apr;138(4):1434-9. Thyroxine administration prevents streptococcal cell wall-induced inflammatory responses. Rittenhouse PA, Redei E.
Eur J Appl Physiol Occup Physiol. 1998;77(1-2):37-43. Pre-adaptation, adaptation and de-adaptation to high altitude in humans: hormonal and biochemical changes at sea level. Savourey G, Garcia N, Caravel JP, Gharib C, Pouzeratte N, Martin S, Bittel J.
Endocrinol Jpn. 1992 Oct;39(5):445-53. Plasma free fatty acids, inhibitor of extrathyroidal conversion of T4 to T3 and thyroid hormone binding inhibitor in patients with various nonthyroidal illnesses. Suzuki Y, Nanno M, Gemma R, Yoshimi T.
Natl Med J India. 1998 Mar-Apr;11(2):62-5. Neuropsychological impairment and altered thyroid hormone levels in epilepsy. Thomas SV, Alexander A, Padmanabhan V, Sankara Sarma P. Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala, India. BACKGROUND: Neuropsychological impairment is a common problem in epilepsy which interferes with the quality of life of patients. Similarly, thyroid hormone levels have been observed to be abnormal in patients with epilepsy on various treatments. This study aimed to ascertain any possible correlation between neuropsychological performance and thyroid hormone levels among epilepsy patients. METHODS: Thyroid hormone levels, indices of neuropsychological performance and social adaptation of 43 epilepsy patients were compared with those of age- and sex-matched healthy control subjects. RESULTS: Epilepsy patients exhibited significantly (p < 0.001) lower scores on attention, memory, constructional praxis, finger tapping time, and verbal intelligence quotient (i.q.) when compared with controls. Their T3, T4 and Free T3 levels were significantly lower; and TSH and Free T4 levels were significantly higher than that of controls. There was no statistically significant correlation between the indices of neuropsychological performance and thyroid hormone levels. CONCLUSION: We did not observe any correlation between neuropsychological impairment and thyroid hormone levels among patients with epilepsy.
Crit Care Med. 1994 Nov;22(11):1747-53. Dopamine suppresses pituitary function in infants and children. Van den Berghe G, de Zegher F, Lauwers P.
Ned Tijdschr Geneeskd. 2000 Jan 1;144(1):5-8. [Epilepsy, disturbances of behavior and consciousness in presence of normal thyroxine levels: still, consider the thyroid gland] [Article in Dutch] Vrancken AF, Braun KP, de Valk HW, Rinkel GJ. Afd. Neurologie, Universitair Medisch Centrum Utrecht. Three patients, one man aged 51 years, and two women aged 49 and 52 years, had severe fluctuating and progressive neurological and psychiatric symptoms. All three had normal thyroxine levels but elevated thyroid stimulating hormone levels and positive thyroid antibodies. Based on clinical, laboratory, MRI and EEG findings they were eventually diagnosed with Hashimoto's encephalopathy, associated with Hashimoto thyroiditis. Treatment with prednisone in addition to thyroxine suppletion resulted in a remarkable remission of their neuropsychiatric symptoms. The disease is probably under-recognized.
Cell Immunol. 1999 Mar 15;192(2):159-66. Neuroendocrine-induced synthesis of bone marrow-derived cytokines with inflammatory immunomodulating properties. Whetsell M, Bagriacik EU, Seetharamaiah GS, Prabhakar BS, Klein JR.
