| Hypothyroidism |
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| Written by Administrator | |||||||||
| Tuesday, 07 March 2006 | |||||||||
Page 4 of 7 9. Glandular Fever. This is an often met with cause of failure of the thyroid/adrenal axis. Evidence has pointed to pituitary damage causing secondary hypothyroidism, but progressive loss of thyroid-producing cells within the thyroid has been noted. In either event, replacement is required. Discussion of failure of uptake at tissue level may be conveniently dealt with in the section below on therapeutic options. Consideration should now be given to the aims of replacement therapy. The overall purpose is to restore metabolism to normal, so as to eliminate all hypothyroid symptoms, and to secure a sense of normal well being. This implies that thyroid hormone levels in each and every cell are nominal; that all the exchange reactions are taking place, as they should be. Sadly, this ideal is at least as often as not, simply not reached, often by a long way. Residual tiredness, lack of drive, or depression is frequently admitted to. Menstrual dysfunction may remain a feature. Skin problems, fluid retention, digestive problems, or arthralgia may remain in some degree. Many patients will continue to complain of weight gain, or great difficulty in losing it, and receive scant sympathy. In this situation, the physician may estimate thyroid function by Free Thyroxine Index (Free T4), or Thyroid Stimulating Hormone (TSH) and be confronted by normal readings. It is the present writer’s view that these estimations may be seriously flawed, and their value fundamentally limited. The most popular, at the moment, is the TSH. This may be much affected by poor pituitary function itself due to hypothyroidism; it may be low or normal, rather than raised. The Free T4 test is subject to several errors. Poor tissue uptake is probably the most telling. If the actual use by the tissues is reduced by poor conversion of T4 to T3 (see below) and/or receptor block, then high or normal Free T4 blood tests will result. Haemoconcentration may be an additional factor. There can be no substitute for proper clinical appraisal. If the patient sounds and looks hypothyroid, then probably that is the problem, irrespective of pathological testing. The net result very much too often in clinical practice is to under-dose. To provide full remission of symptoms, the level in the tissues of thyroid hormone should be as high as possible, short of too much. (The patient/doctor monitoring to achieve this is described later). The situation is worsened by a tightly held misapprehension in many quarters that there are grave risks associated with overdose. These are largely apocryphal and must be corrected. Probably most widely held, is that thyroid overdose is bad for the heart. The risk is there if coronary artery insufficiency, previous M.l or incipient failure already compromises the heart; the risk of over working a damaged heart is obviously undesirable. The healthy heart will not be damaged by minor degrees of overdose, whether by accident or design; and is rarely much affected even by high levels of thyroid hormone, as in Grave’s Disease. Another anxiety is osteoporosis. There is a risk in sustained overdose, and untreated hypothyroidism, but this is still not certain. There is NO risk of osteoporosis in thyroid supplementation in correct, physiological doses obviously; and in any inadvertent minor overdose is rapidly detected by monitoring, and therefore of no consequence either. Suppression of the thyroid gland as a result of treatment is another frequently expressed anxiety. There is a sensitive negative feedback operating through the hypothalamus and the pituitary Overdose will suppress the thyroid; but this will come back to normal at once when the dose is adjusted. Not treating a patient with an under-active thyroid for tear of promoting further depression is quite unrealistic. Vague fears that thyroid is like "speed"; that any deliberate or accidental overrunning of the metabolism will result in early "burn out"; have been expressed. All that can be said is that is simply not true. The correct management of thyroid replacement requires a flexible approach; full explanation to the patient, and monitoring, relying as much on the patient’s assessment as the physician’s own clinical impression. One may often be obliged to deal with partial response to replacement therapy, with failure to respond to an increase of dose; and more wrongly, some symptoms of overdose on small levels of treatment. These will include raised pulse rate, tremor, breathlessness, headaches. Sometimes an encouraging response levels off and drops back. |
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| Last Updated ( Tuesday, 18 July 2006 ) | |||||||||



Hypothyroidism 



