Laboratory Investigation of Endocrine Disorders -  Bill Havard,  Michael R. Wills

Laboratory Investigation of Endocrine Disorders (eBook)

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2013 | 2. Auflage
126 Seiten
Elsevier Science (Verlag)
978-1-4831-8260-5 (ISBN)
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Laboratory Investigation of Endocrine Disorders, Second Edition serves as a basic guide to the available endocrine laboratory tests. This book discusses the developments in the understanding of the mechanisms involved in the pathogenesis of endocrine disorders. Organized into 9 chapters, this edition begins with an overview of the control of thyroid hormone secretion. This text then explains the role of hypothalamus in the control of the activities of the functionally distinct anterior and posterior lobes of the pituitary gland. Other chapters consider the disorders of calcium homeostasis and their investigation with specific reference to hypocalcemia and hypercalcemia. This book discusses as well the adrenal cortical function. The final chapter deals with the normal steady-state regulation of calcium, which includes diet, physiological mechanisms, and hormones. This book is a valuable resource for laboratory-based scientists, both the medical and the non-medical. Senior clinical students and medical practitioners will also find this book useful.
Laboratory Investigation of Endocrine Disorders, Second Edition serves as a basic guide to the available endocrine laboratory tests. This book discusses the developments in the understanding of the mechanisms involved in the pathogenesis of endocrine disorders. Organized into 9 chapters, this edition begins with an overview of the control of thyroid hormone secretion. This text then explains the role of hypothalamus in the control of the activities of the functionally distinct anterior and posterior lobes of the pituitary gland. Other chapters consider the disorders of calcium homeostasis and their investigation with specific reference to hypocalcemia and hypercalcemia. This book discusses as well the adrenal cortical function. The final chapter deals with the normal steady-state regulation of calcium, which includes diet, physiological mechanisms, and hormones. This book is a valuable resource for laboratory-based scientists, both the medical and the non-medical. Senior clinical students and medical practitioners will also find this book useful.

Front Cover 1
Laboratory Investigation of Endocrine Disorders 4
Copyright Page 5
Table of Contents 10
Preface to the Second Edition 6
Preface to the First Edition 8
Chapter 1. Thyroid disorders 16
Physiology 16
Specimens and normal range values 17
In vivo tests 20
Other tests 23
Diagnostic considerations 25
Chapter 2. Hypothalamic–anterior pituitary disorders 30
Physiology 30
Specimens and normal range values 31
Dynamic tests 35
Diagnostic considerations 38
Chapter 3. Hypothalamic–pituitary–adrenocortical axis 44
Physiology 44
Specimens and normal range values 45
Dynamic tests 46
Diagnostic considerations 56
Chapter 4. Hypothalamic–posterior pituitary disorders 59
Physiology 59
Specimens and normal range values 60
Diagnostic considerations 61
Chapter 5. Adrenal cortical disorders 67
Physiology 67
Specimens and normal range values 69
Diagnostic considerations 71
Chapter 6. Disorders of the adrenal medulla 76
Physiology 76
Specimens and normal range values 76
Diagnostic considerations 78
Chapter 7. Ovarian disorders 80
Physiology 80
Specimens and normal range values 84
Dynamic tests 86
Clinical considerations 89
CHapter 8. Testicular disorders 95
Physiology 95
Specimens and normal range values 97
Dynamic tests 98
Diagnostic considerations 99
Chapter 9. Disorders of calcium homeostasis 101
Physiology 101
Specimens and normal range values 105
Dynamic tests 112
Diagnostic considerations 112
Appendix 121

1

Thyroid disorders


Publisher Summary


This chapter discusses thyroid disorders. The thyroid gland secretes its principal hormones, thyroxine (T4) and tri-iodothyionine (T3) into the circulation where they are associated with two proteins that bind them specifically. T3 is the metabolically active form of thyroid hormone. Both T4 and T3 are largely bound to plasma proteins. It is the free hormone that is metabolically active. Changes in the concentration of the serum binding protein will lead to parallel changes in the serum values of total thyroid hormones, but the free thyroid hormone values remain constant. Hypothyroidism is the clinical condition resulting from decreased circulating concentrations of free (unbound) thyroid hormones. Hypothyroidism is commonly caused by primary thyroid failure when serum thyrotrophin concentration is high because of a lack of negative feedback at the pituitary level by thyroid hormones. It can also be secondary to pituitary failure of thyrotrophin secretion when serum thyrotrophin values are usually low or just within the normal range. Hyperthyroidism is the clinical condition resulting from increased circulating serum concentrations of free thyroid hormones. Symptoms include weight loss, heat intolerance, tachycardia, and lid retraction. The main causes of hyperthyroidism are Graves’ disease, toxic multinodular goitre, toxic nodule, painless thyroiditis, and trophoblastic thyroid stimulating hormone syndrome, but the condition can be induced by over-treatment with thyroid hormones.

Physiology


The thyroid gland secretes its principal hormones, thyroxine (T4) and tri-iodothyionine (T3) into the circulation where they are associated with two proteins (the thyroxine-binding proteins) that bind them specifically. By paper electrophoresis the proteins appear between the α1 and α2 globulins (thyroxine-binding globulin (TBG)) and ahead of the albumin (thyroxine-binding prealbumin (TBPA)); in addition, a minor fraction of the hormone is bound to albumin itself. In the bound form, thyroxine and tri-iodothyronine are distributed throughout the extracellular fluid and are measurable by chemical or immunochemical assay.

T3 is the metabolically active form of thyroid hormone. Nevertheless T3 measurements cannot be substituted for T4 measurements in the clinical assessment of thyroid function for a number of reasons. Eighty per cent of the circulating T3 is derived from de-iodination of T4 by peripheral tissues so that T3 is only an indirect reflection of thyroid secretion. Stress, starvation and systemic illness decrease the rate of de-iodination so that the serum T3 level may be normal in the sick hyperthyroid patient. Furthermore the suppression of thyroid-stimulating hormone (TSH) is more dependent on circulating levels of T4 than of T3 so that in iodine deficiency, for example, the TSH may be raised because the circulating concentration of T4 is low but the patient is euthyroid because the levels of T3 are normal. Similarly, adequate T3 replacement therapy of the hypothyroid patient may not suppress TSH secretion in contrast to adequate T4 replacement therapy.

Both T4 and T3 are largely bound to plasma proteins. In the case of T4 99.95% is bound and with T3 99.5%. It is the free hormone that is metabolically active. Changes in the concentration of the serum binding protein will lead to parallel changes in the serum values of total thyroid hormones, but the free thyroid hormone values remain constant.

The control of thyroid hormone secretion is complex. A tripeptide thyrotrophin-releasing hormone (TRH) is synthesized and stored in the median eminence of the hypothalamus. It is released into the portal veins of the pituitary stalk. In the anterior pituitary it promotes pulsatile release of the glycoprotein TSH. It also promotes the release of prolactin although the physiological significance of this is at present unknown.

Thyrotrophin, the circulating concentration of which shows some nyctohemeral variation, stimulates most metabolic processes in the thyroid from iodide uptake to release of thyroid hormones. The mechanism is probably that thyrotrophin binds to a receptor site on the thyroid cell membrane and activates adenyl cyclase. This leads to a cyclic adenosine monophosphate (AMP) mediated activation of one or more enzymes ultimately leading to an increased release of T4 and T3 into serum.

In iodide deficiency states, and in conditions where thyroid throughput is accelerated, there is a relative switch in thyroid synthesis from the less active T4 to the more active T3. This could represent a control mechanism or could be explained on purely synthetic grounds since T3 contains one less iodine atom and is one step less complex than T4.

Specimens and normal range values


For all the thyroid hormone assays and antibodies 10 ml of venous blood should be sent to the laboratory in a sterile container.

Most of the in vitro tests attempt to measure the concentrations of the circulating thyroid hormones in the blood (T4 and T3). These hormones circulate in the plasma bound to proteins, particularly TBG. In the interpretation of laboratory results it is important to recognize those factors or diseases which may affect the concentration of TBG, and thus the assayed hormone concentration, although the actual amount of free hormone may not have changed.

Factors altering TBG are as follows:

Factors Reducing TBG

Nephrosis

Acromegaly

Corticosteroids

Malnutrition

Androgens and anabolic steroids

Old age

Factors Increasing TBG

Pregnancy

Oestrogens

Clofibrate (Atromid-S)

Phenothiazines

Factors Reducing Binding Capacity of TBG

Renal failure,

Drugs bound to TBG such as:

Salicylates

Phenytoin (Epanutin)

Phenylbutazone

Fenclofenac

Total serum thyroxine (T4)


The normal range of T4 for adults is 54–142 nmol/. Values up to 240 nmol/ are found in neonates, in pregnancy and in patients on the contraceptive pill; other than these variations there is little change with either age or sex.

The assay is useful in the diagnosis of both hyperthyroidism and hypothyroidism.

There are, however, a number of causes for a discrepancy between the measured serum T4 and the patient’s true thyroid status, as outlined below:

1. Change in serum concentration of TBG.

2. Drugs binding to TBG.

3. Disease states altering binding properties of TBG.

4. Conditions altering the ratio of T3 to T4, such as:

Iodine deficiency

Patients treated with T4

Patients treated with 131I

Patients with chronic thyroiditis

T3 thyrotoxicosis

Total serum tri-iodothyronine (T3)


The normal range of T3 for adults is 0.8–2.5 nmol/ with higher values being obtained in the neonatal period and in pregnancy. Males tend to have slightly lower levels than females. As with T4, values for T3 are affected, although to a lesser extent, by variations in the concentration of binding proteins.

The assay of T3 is of value in the special situation of a patient who is suspected of having T3-thyrotoxicosis when the T4 value may be normal. This situation is rare and represents less than 5% of all thyrotoxic patients in the United Kingdom.

Free binding capacity (FBC) (normal range 90–105%)


The abbreviation FBC should be used instead of the earlier term ‘T3 resin uptake’. This assay provides an indirect measurement of the unoccupied thyroxine-binding protein sites available in the patient’s serum. It does not give any information about total serum T3 value and is unaffected by iodine contamination. It should only be used in conjunction with a measurement of serum T4 to calculate the free thyroxine index.

Free thyroxine index (FTI) (normal range 53–142)


The FTI is obtained from the measurement of serum T4 and FBC. It is an attempt to obtain an indirect measurement of free thyroxine. The scientific validity of this index is debatable as the index is relative (results are related to a normal control) and is imprecise (containing two ratios). The FTI is of value in returning T4 results from euthyroid pregnant (or on the contraceptive pill) patients back to the normal adult range. Misleading results can occur, particularly in the thyroid assessment of elderly patients. The free thyroxine index is also less reliable in acute non-thyroidal illness, when it is often subnormal in the presence of a normal or even high free thyroxine level.

Thyrotrophin (TSH)


The reference range for normal adults varies slightly between centres but is usually from a lower detection limit of 1 mU/–6 mU/. Levels may be higher in neonates. A...

Erscheint lt. Verlag 22.10.2013
Sprache englisch
Themenwelt Sachbuch/Ratgeber Gesundheit / Leben / Psychologie Krankheiten / Heilverfahren
Medizin / Pharmazie Allgemeines / Lexika
Medizin / Pharmazie Medizinische Fachgebiete
ISBN-10 1-4831-8260-6 / 1483182606
ISBN-13 978-1-4831-8260-5 / 9781483182605
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