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Laboratory Medicine The Diagnosis of Disease in the Clinical Laboratory 2nd Edition
Laboratory Medicine The Diagnosis of Disease in the Clinical Laboratory 2nd Edition
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,Laboratory Medicine, NOTICE
Medicine is an ever-changing science. As new research and clinical
experience broaden our knowledge, changes in treatment and drug
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human error or changes in medical sciences, neither the authors nor the
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, a LANGE medical book
Laboratory Medicine
The Diagnosis of Disease
in the Clinical Laboratory
Second Edition
Edited by
Michael Laposata, MD, PhD
Chairman
Department of Pathology
University of Texas Medical Branch
Galveston, Texas
New York Chicago San Francisco Athens Lisbon Madrid
Mexico City Milan New Delhi Singapore Sydney Toronto
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,To Susan, with love
,Key Features of
Laboratory Medicine
A complete full-color guide to selecting the correct
laboratory test and accurately interpreting the
results—covering the entire field of clinical pathology
• 46 laboratory methods presented in easy-to-understand illustrations which include
information on the expense and complexity of the assays
• Features an easy-to-follow, consistent presentation for each disease discussed
• More than 200 tables and full-color algorithms encapsulate important information
and facilitate understanding
• Full-color blood-smear micrographs demonstrate common abnormal morphologies
of red blood cells
• Valuable learning aids in each chapter,
including learning objectives, chapter CHAPTER 10 Diseases of Red Blood Cells 231
outlines, and a general introduction
• Extensive table of Clinical Laboratory
Reference Values showing the conversions
between U.S. and SI units for each value
• An essential text for medical students
and residents studying clinical pathology,
medical technology students, and for
practitioners working in a clinical setting FIGURE 10–15 Peripheral blood smear from a
patient with large numbers of elliptocytes.
FIGURE 10–16 A peripheral blood smear stained with
Wright stain showing reticulocytes.
• This edition has been enhanced by coverage
of genetic test options that are now
commonly used in clinical practice.
Blood-smear micrographs demonstrate common
abnormal morphologies of red blood cells
FIGURE 10–17 A peripheral blood smear showing FIGURE 10–18 A peripheral blood smear from a patient
circulating nucleated red blood cells (arrowheads), as with stomatocytes.
well as Howell–Jolly bodies (arrows).
, CHAPTER 22 The Endocrine System 423
[–]
Hypothalamus
Thyrotropin-releasing
hormone (TRH)
[+]
[–]
Pituitary
Thyroid-stimulating
T3 200 tables and full-color algorithms
hormone (TSH) T4
[+]
Thyroid
rT3
T3 is primary
feedback stimulus
encapsulate important information
FIGURE 22–2 Hypothalamic–pituitary–thyroid interactions. [+] Stimulation; [−] inhibition.
426 CHAPTER 22 The Endocrine System
hormone replacement in hypothyroid patients. Third-generation assays are essential for monitor-
ing TSH suppression therapy in patients with a TSH-responsive thyroid tumor.
The relationship between TSH and the thyroid hormones, particularly free T4, is an inverse
log-linear one, such that very small changes in free T4 result in large changes in TSH. Thus, TSH TABLE 22–1 Laboratory Evaluation of Patients for Thyroid Disease
is the most sensitive first-line screening test for suspected thyroid abnormalities. If the TSH is Laboratory Test Results Suggestive of Diagnosis in the Appropriate
Disorder Clinical Setting
within the normal reference range, no further testing is performed. If the TSH is outside of the
reference range, a free T4 is obtained. Hyperthyroidism
Graves disease TSH low; free T4 high; in some cases, T3 is elevated and free T4 is normal;
TRAbs or TSI elevated
Uptake into cells Toxic multinodular goiter TSH low; free T4 and T3 normal or high; normal or increased radioactive iodine
uptake; thyroid scan with multiple areas of increased uptake surrounded by
Oral intake Plasma producing thyroid homone Thyroidal suppressed uptake
of iodine iodide iodide
Toxic adenoma TSH low; free T4 and T3 normal or high; normal or increased radioactive iodine
uptake; thyroid scan with focal increased uptake in tumor surrounded by
Binding of iodide suppressed uptake in nontumor tissue
to thyroglobulin Subacute thyroiditis TSH low; free T4 and T3 high; increased; decreased radioactive iodine uptake
Painless thyroiditis TSH low; free T4 and T3 high; erythrocyte sedimentation rate normal;
Coupling of Monoiodotyrosine decreased radioactive iodine uptake
Proteases Thyroglobulin
iodotyrosines (MIT) and
Free T4 release T3 bound Hypothyroidism
diiodotyrosine
and T4 from T3 and T4 (DIT) residues on Hashimoto thyroiditis TSH high; T4 normal and then low, preceding a decline in T3; anti-TPO and/or
thyroglobulin
thyroglobulin antithyroglobulin antibody positive
Ablative hypothyroidism TSH high; free T4 and T3 low following procedure that ablates thyroid
Deiodination
Infantile hypothyroidism TSH high; free T4 low in a newborn or infant
Free T3 Thyroid hormones Euthyroid sick syndrome TSH normal to high; free T4 normal; T3 low; rT3 high; concentrations of TSH and
transported to tissues thyroid hormones vary throughout disease course
on thyroid-binding
rT3, reverse triiodothyronine; T3, triiodothyronine; free T4, free thyroxine; TSH, thyroid-stimulating hormone; TRAbs, TSH receptor
globulin (TBG), transthyretin, autoantibodies; TSI, thyroid-stimulating immunoglobulins.
Reverse and albumin Diverse metabolic
T3 (rT3) effects on target cells
may have exophthalmos, emotional changes, menstrual changes, and a fine tremor of the hands.
In the presence of a clinical history and physical examination consistent with hyperthyroidism,
Free T4
a diagnosis of hyperthyroidism (but not necessarily its cause) can be established by the demon-
stration of a low TSH level and a high free T4. In uncommon situations, only the total T3 level
FIGURE 22–3 The formation, secretion, and transport of thyroid hormones. is elevated and the serum free T4 is normal (T3 thyrotoxicosis). To determine the etiology of the
hyperthyroidism, additional testing is usually necessary. Graves disease, toxic multinodular goiter
(TMNG), and toxic adenoma account for the vast majority (>95%) of cases of hyperthyroidism. It
should be noted that diffuse or focal enlargement of the thyroid gland, also known as goiter, can
be associated with hyperfunction, normal function, and hypofunction of the gland.
Thyroid Storm
Thyroid storm is a relatively uncommon, but life-threatening manifestation of hyperthyroid-
ism caused by excess circulation of thyroid hormones. Symptoms of thyroid storm are similar,
Graves disease is a but much more severe than traditional hyperthyroidism, including a markedly high fever of
relatively common 105°F to 106°F, tachycardia, hypertension, and neurological and gastrointestinal abnormali-
hyperthyroid disorder ties. Thyroid storm is precipitated by acute illnesses such as sepsis, diabetic ketoacidosis, and
occurring more preeclampsia, as well as surgical or other diagnostic or therapeutic actions such as radioac-
frequently in women. tive iodine use, anesthesia, excessive thyroid hormone ingestion, or thyroid palpation. Thyroid
It is an autoimmune storm is associated with a high fatality rate if not identifi ed early. The diagnosis is based on the
disease caused by TSH presence of clinical signs and symptoms of severe hyperthyroidism in the context of a precipi-
receptor autoantibodies tating cause. In addition, marked elevations in free and total T4 are common in thyroid storm.
that bind to and stimulate Total T3 is unreliable in this setting because concomitant nonthyroidal illness (NTI) may cause
TSH receptors resulting in
T3 to decrease significantly.
autonomous production
of thyroid hormone.
Graves Disease
Graves disease is a relatively common hyperthyroid disorder occurring more frequently in
women. It has a familial predisposition. It is an autoimmune disease caused by TSH receptor
C H A P T E R
Breast
Karin E. Finberg 21
LEARNING OBJECTIVES
1. Learn the tissue- and serum-based biomarkers in breast cancer.
2. Understand how the individual biomarkers are used clinically.
CHAPTER OUTLINE
Introduction 413 Hereditary Breast and Ovarian
Breast Cancer 413 Cancer Syndrome 417
Laboratory Testing 414 Other High-penetrance Cancer
Tissue-based Biomarkers Predisposition Genes 418
in Breast Cancer 414 Li-Fraumeni Syndrome 418
Serum-based Biomarkers Cowden Syndrome 418
in Breast Cancer 416 Peutz-Jeghers Syndrome 419
INTRODUCTION
This chapter focuses on laboratory testing relevant to breast cancer. Infections of the breast are
included in Chapter 5.
BREAST CANCER
Description
Cancers of the breast constitute a major cause of mortality in women of Western countries. In the
United States, the lifetime probability that a woman will develop breast cancer is 1 in 8. Breast
cancer accounts for 29% of new cancer cases and 14% of cancer deaths in American women.
About 1% of breast cancers occur in males. The risk of developing breast cancer is influenced by
several factors. These factors include increased age, family history of breast cancer (especially in
a first-degree relative), hormonal factors (early age at menarche, older age of menopause, older
age at first full-term pregnancy, fewer number of pregnancies, and use of hormone replacement
therapy), clinical factors (high breast tissue density and benign breast diseases associated with
atypical hyperplasia), obesity, and alcohol consumption. Since 1990, the mortality rate associated
Valuable learning aids are
with female breast cancer has decreased in the United States, a decline that has been attributed to
both therapeutic advances and early detection.
For localized breast cancer, primary treatment typically consists of either breast-conserving
surgery and radiation or mastectomy. Most patients with invasive breast cancer subsequently
included in each chapter
receive systemic adjuvant chemotherapy and/or hormone therapy, both of which have been
shown to reduce systemic recurrence and breast cancer-related mortality. However, the fact
that some patients who lack lymph node involvement are cured by the combination of sur-
gery and radiotherapy suggests that adjuvant treatment may not be necessary in all cases.
413
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, Contents
Authors xi
Preface xiii
Acknowledgments xv
Clinical Laboratory Reference Values xvii
1. Concepts in Laboratory Medicine 1 13. Diseases of White Blood Cells,
Michael Laposata, MD, PhD Lymph Nodes, and Spleen 317
Daniel E. Sabath, MD, PhD
2. Methods 13
Michael Laposata, MD, PhD, 14. The Respiratory System 339
James H. Nichols, PhD Alison Woodworth, PhD
Paul Steele, MD, & Thomas P. Stricker, MD, PhD 15. The Gastrointestinal Tract 351
3. Autoimmune Disorders Involving the Michael Laposata, MD, PhD &
Connective Tissue and Immunodeficiency D. Robert Dufour, MD, FCAP, FACB
Diseases 61 16. The Liver and Biliary Tract 357
Mandakolathur R. Murali, MD William E. Winter, MD
4. Histocompatibility Testing 17. Pancreatic Disorders 371
and Transplantation 83 David N. Alter, MD &
Yash P. Agrawal, MD, PhD & Michael Laposata, MD, PhD
Susan L. Saidman, PhD
18. The Kidney 385
5. Infectious Diseases 91 William E. Winter, MD
Eric D. Spitzer, MD, PhD
19. Male Genital Tract 397
6. Toxicology 159 Mark H. Wener, MD, ABIM, ABAI (CLI/DLI),
James H. Nichols, PhD, Sheila P. Dawling, PhD, Charles H. Muller, PhD, HCLD (AAB),
& Michael Laposata, MD, PhD & D. Robert Dufour, MD, FCAP, FACB
7. Diseases of Infancy and Childhood 185 20. Female Genital System 405
Paul Steele, MD Stacy E.F. Melanson, MD, PhD &
8. Blood Vessels 197 Ann M. Gronowski, PhD
Michael Laposata, MD, PhD 21. Breast 413
9. The Heart 209 Karin E. Finberg, MD, PhD
Fred S. Apple, PhD 22. The Endocrine System 421
10. Diseases of Red Blood Cells 221 Alison Woodworth, PhD, Vipul Lakhani, MD,
Daniel D. Mais, MD Samir L. Aleryani, PhD, C(ASCP), CLS (NCA),
FACB, & Michael Laposata, MD, PhD
11. Bleeding and Thrombotic Disorders 253
Elizabeth M. Van Cott, MD & Index 469
Michael Laposata, MD, PhD
12. Transfusion Medicine 291
Christopher P. Stowell, MD, PhD &
Jacqueline J. Haas, MD
ix
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