الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Despite the amazing medical development in various fields, there were things that happened and it is difficult to explain the mechanisms of their occurrence and their interpretation often depends on assumptions and hypotheses as autoimmune diseases, rheumatic diseases and others which can interfere in their occurrence many factors associated with human evolution and the surrounding environment. With the advances in the laboratory and imaging techniques in the endocrinological field, new emerging entities had been appearing on the medical arena. These entities encompass mild degrees of endocrine dysfunction. Their clinical significance was uncertain had led to controversy over the appropriateness of diagnostic and treatment strategies. The term subclinical would refer to the absent classical features of the wellknown endocrine diseases except for few nonspecific features or unsuspected complications which drive to search for solutions to these discovered disorders.
These disorders can affect any endocrine gland and they may represent the earlier stages of the classical endocrine diseases. They may be associated with some negative consequences on other body systems carrying the need to know more about these entities and trying to clarify some of the suggested solutions to deal with them.
The aim of this essay is discussion of various subclinical endocrine disorders (before appearance of overt clinical manifestations) and the role of management of these disorders for prevention of their possible harmful consequences.
Pituitary incidentalomas represent unsuspected abnormal radiological images discovered incidentally in the region of pituitary
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gland during routine investigations for other unrelated symptoms as persistent headache, recurrent dizziness and syncopal attacks. They attract attention to know their sizes and functional state. Their Surgical resection remain a solution, while trials of using dopamine agonist or somatostatin analogues still unsupported. Follow up is by MRI scan after 6 months in smaller tumours and one year in larger ones.
Subclinical Central diabetes insipidus is a hypothalamus-pituitary disease due to interference in synthesis, transport and/or release of vasopressin It may be the restriction of the damage process out of the secreting neurons so, new hormones still synthetized and released into circulation. Another cause is pregnancy which is associated with decreased threshold for thirst and AVP secretion and increased its clearance by vasopressinase of the placenta. Progesterone antagonize AVP. Its diagnosis is based on history of polyuria and measuring plasma Na, urine and plasma osmolality then proceeding to water deprivation test and desmopressin test. AVPcAb titer and MRI are used later for differentiation and tratification. Management aims to cambat the cause and to prevent progression to overt disease using isohormonal therapy, as DDAVP therapy.
Subclinical thyroid dysfunction is altered values of serum TSH hormone either increased or decreased with preservation of thyroid hormones within their reference ranges with no symptoms except some of their impact on other body systems.
Subclinical hypothyroidism is the presence of serum FT4 within normal ranges while serum TSH rises above 4.5 mIU/L and it is supposed that TSH is the moderator of the condition through its non-thyroidal receptors.The most common consequences are risk of progression to overt disease but it may predispose to diastolic
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hypertension, congestive heart failure, dyslipidemia, vascular dysfunction, ischaemic heart disease, myocardial infarction and aortic atherosclerosis. It should be confirmed by repeated measuring TSH, FT4 and TPO-Ab over 3-6 months to rule out transient causes then treating using levothyroxine using TSH values and presence of risk factors.
Subclinical hyperthyroidism is progressively decline in serum TSH until reaching very low undetectable values in the presence of normal thyroid hormones. Its consequences are more significant in post-menopausal women and elderly rather than younger individuals including reduction in BMD and increased risk of fractures and the risk of progression to overt disease. TSH, FT3 and FT4 should be repeated within 8-12 weeks to exclude transient causes then managing to restore euthyroidism and alleviate potential harms that it may exists
Normocalcemic primary hyperparathyroidism is abnormal elevations in serum parathyroid hormone but with normal serum calcium levels. The exact cause remains obscure but only some hypotheses about target organ(kidney and bone) or it may be the initial phase before evolution of hypercalcemic form.It may have a negative impact as bone metabolism dysfunction (BMD, osteoporosis, and even fractures) or kidney problems (nephrolithiasis) which was found in the discovered cases. Ruling out causes of secondary hyperparathyroidism is mainstep in diagnosis especially vitamin D insufficiency (values 20-30ng/mL) and reduced creatinine clearance (< 60 cc/min). There is lack of supporting data about the treatment options of such disorders. The use of estrogen, anti-reabsorptive drugs and calcinomimetics may cause some improvement especially in post-menopausal women.