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Official reprint from UpToDate®

www.uptodate.com © 2022 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Clinical manifestations, diagnosis, and evaluation of

osteoporosis in postmenopausal women
Author: Harold N Rosen, MD
Section Editors: Clifford J Rosen, MD, Kenneth E Schmader, MD
Deputy Editor: Jean E Mulder, MD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: May 2022. | This topic last updated: Apr 27, 2022.

INTRODUCTION

Osteoporosis is characterized by low bone mass, microarchitectural disruption, and skeletal

fragility, resulting in decreased bone strength and an increased risk of fracture. Decreased bone
strength is related to many factors other than bone mineral density (BMD), including rates of
bone formation and resorption (turnover), bone geometry (size and shape of bone), and
microarchitecture ( picture 1).

The World Health Organization (WHO) has defined diagnostic thresholds for low bone mass and
osteoporosis based upon BMD measurements compared with a young adult reference
population (T-score). The majority of postmenopausal women with osteoporosis have bone loss
related to estrogen deficiency and/or age.

Early diagnosis and quantification of bone loss and fracture risk are important because of the
availability of therapies that can slow or even reverse the progression of osteoporosis.

The clinical manifestations, diagnosis, and evaluation of osteoporosis in postmenopausal

women will be reviewed here. The evaluation of osteoporosis in premenopausal women and
men and the treatment of osteoporosis are reviewed separately. (See "Evaluation and treatment
of premenopausal osteoporosis" and "Clinical manifestations, diagnosis, and evaluation of
osteoporosis in men" and "Overview of the management of osteoporosis in postmenopausal
women" and "Treatment of osteoporosis in men".)

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CLINICAL MANIFESTATIONS

Osteoporosis has no clinical manifestations until there is a fracture. This is an important fact
because many patients without symptoms incorrectly assume that they must not have
osteoporosis. On the other hand, many patients with achy hips or feet assume that their
complaints are due to osteoporosis. This is unlikely true in the absence of fracture. In
comparison, pain is common in osteomalacia in the absence of fractures or other bone
deformities. (See "Epidemiology and etiology of osteomalacia".)

● Vertebral fracture – Vertebral fracture is the most common clinical manifestation of

osteoporosis. Most of these fractures (approximately two-thirds) are asymptomatic; they
are diagnosed as an incidental finding on chest or abdominal radiograph ( image 1). The
clinical manifestations of symptomatic vertebral fracture, including height loss, are
reviewed separately. (See "Osteoporotic thoracolumbar vertebral compression fractures:
Clinical manifestations and treatment".)

● Other fractures – Hip fractures are relatively common in osteoporosis, affecting up to 15

percent of women and 5 percent of men by 80 years of age [1]. In addition, distal radius
fractures (Colles fractures) may occur. Colles fractures are more common in women
shortly after menopause, whereas the risk of hip fracture increases exponentially with
age. (See "Overview of common hip fractures in adults" and "Distal radius fractures in
adults".)

DIAGNOSIS

Osteoporosis is characterized by low bone mass, microarchitectural disruption, and increased

skeletal fragility. A clinical diagnosis of osteoporosis may be made in the presence of [2-4]:

● Fragility fracture, particularly at the spine, hip, wrist, humerus, rib, and pelvis

or

● T-score ≤-2.5 standard deviations (SDs) at any site based upon bone mineral density (BMD)
measurement by dual-energy x-ray absorptiometry (DXA) (see "Screening for osteoporosis
in postmenopausal women and men", section on 'Candidates for BMD testing')

As another means for diagnosis of osteoporosis in postmenopausal women, we agree with the
National Bone Health Alliance suggestion that a clinical diagnosis of osteoporosis may be made
if there is a clear elevated risk for fracture [3]. In the United States, for example, a clinical
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diagnosis of osteoporosis may be made when the FRAX 10-year probability of major
osteoporotic fracture (hip, clinical spine, proximal humerus, or forearm) is ≥20 percent or the
10-year probability of hip fracture is ≥3 percent [2,3]. (See "Osteoporotic fracture risk
assessment", section on 'Fracture risk assessment tool' and "Overview of the management of
osteoporosis in postmenopausal women", section on 'Fracture risk assessment'.)

All postmenopausal women with osteoporosis should have an evaluation to exclude causes of
low bone mass other than age and estrogen deficiency. (See 'Evaluation' below.)

Fragility fracture — A clinical diagnosis of osteoporosis may be made in the presence of a

fragility fracture, particularly at the spine, hip, wrist, humerus, rib, and pelvis, without
measurement of BMD. Fragility fractures are those occurring spontaneously or from minor
trauma, such as a fall from a standing height or less. Fragility fractures result from mechanical
forces that would not ordinarily result in fracture. Reduced bone density is a major risk factor
for fragility fractures.

The most common sites of fragility fracture are the spine (vertebral compression fractures), hip,
and wrist. Fragility fractures also occur at the humerus, rib, and pelvis. Certain skeletal
locations, including the skull, cervical spine, hands, feet, and ankles, are not associated with
fragility fractures. Stress fractures are also not considered fragility fractures, as they are due to
repetitive injury. (See "Overview of stress fractures".)

Bone mineral density — In the absence of a fragility fracture, BMD assessment by DXA is the
standard test to diagnose osteoporosis, according to the classification of the World Health
Organization (WHO) [2,5].

T-score — The WHO established diagnostic thresholds for BMD (by DXA) according to the SD
difference between a patient's BMD and that of a young adult reference population (T-score) (
table 1) [5].

● ≤-2.5 SD – A BMD T-score that is 2.5 SD or more below the young adult mean BMD is
defined as osteoporosis, provided that other causes of low BMD have been ruled out (such
as osteomalacia)

● -1 to -2.5 SD – A T-score that is 1 to 2.5 SD below the young adult mean is termed low bone
mass (osteopenia)

● ≥-1 SD – Normal bone density is defined as a value within 1 SD of the mean value in the
young adult reference population

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Individuals with T-scores of ≤-2.5 have the highest risk of fracture. However, collectively there
are more fractures in patients with a T-score between -1 and -2.5 because there are so many
more patients in this category [6]. (See "Overview of dual-energy x-ray absorptiometry".)

Z-score — The Z-score is a comparison of the patient's BMD to an age-matched population. A

Z-score of -2 or lower is considered below the expected range for age [7]. Thus, the presence of
Z-score values more than 2 SD below the mean should prompt careful scrutiny for coexisting
problems (eg, glucocorticoid therapy or alcoholism) that can contribute to osteoporosis. (See
'Additional evaluation' below.)

Applicability of WHO criteria — The World Health Organization (WHO) thresholds were
chosen based upon fracture risk in postmenopausal White women. Similar diagnostic threshold
values for men are less well defined, although for any given BMD, the age-adjusted fracture risk
is similar in men and women [8]. We agree with the International Society for Clinical
Densitometry (ISCD) recommendations for the application of the WHO classification in clinical
practice [7]:

● Postmenopausal women and men ≥50 years – The ISCD advises that the WHO criteria
be used in postmenopausal women and in men age 50 years and older.

● Premenopausal women and men <50 years – The ISCD advises that the WHO criteria
not be used in premenopausal women or men under age 50 years, because the
relationship between BMD and fracture risk is not the same in younger women and men.

● Children – The WHO classification should not be used in children (male or female under
age 20 years), and a diagnosis of osteoporosis cannot be made in a child based on
densitometric criteria alone. Z-scores, not T-scores, should be used, since it is not
appropriate to compare the BMD of someone who has not yet achieved peak bone mass
with that of an adult who has. Osteoporosis can be diagnosed in children based on the
presence of a vertebral compression fracture, or a Z-score <-2 in combination with a
significant fracture history (eg, two long bone fractures before age 10 years or three long
bone fractures before 19 years) [9].

Method of BMD measurement — Several different methods are available to measure bone
mineral density (BMD). DXA is the best available clinical tool for the diagnosis of osteoporosis
and monitoring changes in BMD over time. Detailed information about DXA is found elsewhere
(see "Overview of dual-energy x-ray absorptiometry"). Other methods of measuring BMD for
fracture risk assessment are reviewed separately. (See "Osteoporotic fracture risk assessment",
section on 'Methods of measurement of BMD'.)

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Site of measurement — In women who are candidates for BMD testing, we suggest DXA
measurements of the spine and hip because fractures at these sites have the greatest impact
on patients' health. Measurement of hip BMD also has the highest predictive value for hip
fracture. In addition, if pharmacologic therapy is planned, measurement of spine BMD is useful
as it shows less variability and can detect responses to therapy earlier than hip BMD. We make
the diagnosis according to the lowest T-score measured.

Interference from osteophytes and vascular calcifications on the spine measurement are
common in aging women and interfere with the assessment of BMD at this site. In this setting,
measurement of hip BMD alone or hip and one-third radial site is sufficient.

In all studies, the risk for most fractures is inversely proportional to bone density [10-18]. Some
studies suggest that the risk for fracture at a particular site is best estimated by measuring
bone density at that site [19-22]. Other studies, however, have found that measurement of BMD
at any site predicts fracture risk at all sites equally well [23]. The preferred site for measurement
of bone density and the number of sites to measure are debatable, and it may vary according to
the clinical situation. The Fracture Risk Assessment Tool (FRAX) can improve the prediction of
fractures above that achieved by BMD. (See "Osteoporotic fracture risk assessment", section on
'Fracture risk assessment tool' and "Screening for osteoporosis in postmenopausal women and
men", section on 'Skeletal site to measure'.)

DIFFERENTIAL DIAGNOSIS

Decreased bone mass can occur because peak bone mass is low, bone resorption is excessive,
or bone formation during remodeling is decreased. All three processes are likely to contribute,
in varying degrees, to osteoporosis in individual patients. Most postmenopausal women with
osteoporosis, however, have either age- or estrogen deficiency-related bone loss due primarily
to excessive bone resorption.

Other causes of bone fractures and reduced bone mineral density (BMD) include osteomalacia,
malignancy (eg, multiple myeloma), Paget disease, and hyperparathyroidism. Most of these
diagnoses can be distinguished from estrogen deficiency-related osteoporosis by the clinical
history, physical examination, and laboratory testing. (See 'Evaluation' below.)

Physical abuse should always be considered a possibility in a patient with fractures, particularly
when the fracture burden exceeds what one would expect based on BMD, or when location of
fractures is atypical. (See "Elder abuse, self-neglect, and related phenomena", section on
'Warning signs'.)

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Low BMD may also be seen in conjunction with renal osteodystrophy in patients with decreased
kidney function [24-26]. It is difficult to distinguish low bone density due to osteoporosis from
low bone density due to any of the components of chronic kidney disease-metabolic bone
disease. The distinction may be made biochemically in most cases, but may sometimes require
bone biopsy. The diagnosis, evaluation, and management of osteoporosis in patients with
chronic kidney disease and the diagnosis and management of renal osteodystrophy and
secondary hyperparathyroidism are discussed in detail elsewhere. (See "Osteoporosis in
patients with chronic kidney disease: Diagnosis and evaluation" and "Bone biopsy and the
diagnosis of renal osteodystrophy" and "Management of secondary hyperparathyroidism in
adult nondialysis patients with chronic kidney disease" and "Management of secondary
hyperparathyroidism in adult dialysis patients".)

EVALUATION

The goal of the evaluation is to exclude causes of low bone mass other than age and estrogen
deficiency, such as osteomalacia, hyperthyroidism, and hyperparathyroidism, and to detect
potentially remediable causes or other contributing factors to osteoporosis ( table 2) [27-31].

Initial evaluation — The initial evaluation includes a history to assess for clinical risk factors for
fracture and to evaluate for other conditions that contribute to bone loss, a physical
examination, and basic laboratory tests.

● History and physical examination – Most of the conditions causing osteoporosis can be
excluded with a careful history and physical examination ( table 2). Lifestyle factors that
contribute to bone loss, including smoking, excessive alcohol, physical inactivity, and poor
nutrition, should be addressed. Height and weight should be measured.

A history of a fragility fracture is an important risk factor for a subsequent fracture

[10,32,33]. In women who have a vertebral fracture, approximately 19 percent will have
another fracture in the next year [32]. A meta-analysis of 11 cohorts (15,259 men and
44,902 women) showed that a previous fracture was associated with an increased risk of
any fracture compared with those without a prior fracture (relative risk [RR] 1.86, 95% CI
1.75-1.98) [34]. Thus, individuals with a history of a fragility fracture are a high-risk group
that requires evaluation and treatment. (See "Osteoporotic fracture risk assessment" and
"Overview of the management of osteoporosis in postmenopausal women" and
"Osteoporotic thoracolumbar vertebral compression fractures: Clinical manifestations and
treatment".)

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● Laboratory evaluation – We suggest that postmenopausal women with low BMD (T-score
below -2.5) and/or fragility fracture have the following basic tests ( table 3) [27,28,31,35]:

• Biochemistry profile (especially calcium, phosphorous, albumin, total protein,

creatinine, liver enzymes including alkaline phosphatase, electrolytes)

• 25-hydroxyvitamin D (25[OH]D)

• Complete blood count (CBC)

• If the diagnosis of osteoporosis is based upon the presence of a fragility fracture, we

also obtain a BMD measurement (dual-energy x-ray absorptiometry [DXA]), performed
on a nonurgent basis, for quantitative assessment of bone density and to monitor
response to therapy

Additional evaluation — The need for additional laboratory evaluation depends upon the
initial evaluation and Z-score ( table 3). Women who have abnormalities on initial laboratory
testing, suspicious findings on history and physical examination suggesting a secondary cause
of osteoporosis, or Z-scores ≤-2 may require additional evaluation to detect these secondary
causes ( table 2).

As examples:

● 24-hour urine for calcium and creatinine measurement is useful to assess for adequate
calcium intake and absorption in women with gastrointestinal disorders, such as
inflammatory bowel disease and celiac disease, or after gastrointestinal surgery, such as
gastrectomy or bariatric surgery. Assessment of urinary calcium is also necessary in
women with kidney stones, and it may be helpful in women with osteoporosis and no risk
factors beyond age to identify idiopathic hypercalciuria [36]. (See "Metabolic bone disease
in inflammatory bowel disease" and "Kidney stones in adults: Epidemiology and risk
factors", section on 'High urine calcium'.)

● A woman with unexplained anemia, vitamin D deficiency, and/or low urinary calcium
excretion should be tested for celiac disease. (See "Vitamin D deficiency in adults:
Definition, clinical manifestations, and treatment", section on 'Defining vitamin D
sufficiency' and "Diagnosis of celiac disease in adults" and "Epidemiology, pathogenesis,
and clinical manifestations of celiac disease in adults", section on 'Metabolic bone
disorders'.)

● Cancer or multiple myeloma should be considered in patients who also have

hypercalcemia, otherwise unexplained anemia, weight loss, or proteinuria. Measurement
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of serum and urine protein electrophoresis would be indicated in this case. (See "Multiple
myeloma: Clinical features, laboratory manifestations, and diagnosis".)

● Serum parathyroid hormone (PTH) should be measured in patients with hypercalcemia,

hypercalciuria, a history of renal stones, or osteopenia. (See "Primary
hyperparathyroidism: Diagnosis, differential diagnosis, and evaluation".)

● Urinary cortisol excretion should be measured if Cushing's syndrome is suspected and in

patients with unexplained osteoporosis and vertebral fracture since patients with
subclinical hypercortisolism (mild hypercortisolism without clinical manifestations of
Cushing's syndrome) are also at risk for low BMD and fractures. (See "Evaluation and
management of the adrenal incidentaloma", section on 'Subclinical Cushing's syndrome'
and "Establishing the diagnosis of Cushing's syndrome" and "Epidemiology and clinical
manifestations of Cushing's syndrome", section on 'Bone loss'.)

Bone turnover markers — We do not routinely measure markers of bone turnover (BTMs) in
postmenopausal women with osteoporosis. While the use of BTMs in clinical trials has been
helpful in understanding the mechanism of action of therapeutic agents, their role in the care
of individual patients is not well established. Potential roles of BTMs in clinical practice include
prediction of fracture risk, monitoring response to therapy, and improving compliance with
therapy. Biologic and laboratory variability in BTM values have confounded their widespread
use in clinical practice. This topic is reviewed separately. (See "Use of biochemical markers of
bone turnover in osteoporosis".)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Osteoporosis".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade
reading level, and they answer the four or five key questions a patient might have about a given
condition. These articles are best for patients who want a general overview and who prefer
short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more
sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading

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level and are best for patients who want in-depth information and are comfortable with some
medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print
or e-mail these topics to your patients. (You can also locate patient education articles on a
variety of subjects by searching on "patient info" and the keyword(s) of interest.)

● Basics topics (see "Patient education: Osteoporosis (The Basics)" and "Patient education:
Calcium and vitamin D for bone health (The Basics)")

● Beyond the Basics topics (see "Patient education: Osteoporosis prevention and treatment
(Beyond the Basics)" and "Patient education: Calcium and vitamin D for bone health
(Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

● Osteoporosis definition – Osteoporosis is characterized by low bone mass,

microarchitectural disruption, and skeletal fragility, resulting in decreased bone strength
and an increased risk of fracture. Decreased bone strength is related to many factors in
addition to bone mineral density (BMD), including rates of bone formation and resorption
(turnover), bone geometry (size and shape of bone), and microarchitecture ( picture 1).
(See 'Introduction' above.)

● Clinical manifestations – Osteoporosis has no clinical manifestations until there is a

fracture. Complications of fractures include pain, deformity, disability, and loss of height.
(See 'Clinical manifestations' above.)

● Diagnosis

• Fragility fracture – A clinical diagnosis of osteoporosis may be made in the presence

of a fragility fracture, particularly at the spine, hip, wrist, humerus, rib, and pelvis,
without measurement of BMD.

• DXA – In the absence of a fragility fracture, BMD assessment by dual-energy x-ray

absorptiometry (DXA) is the standard test to diagnose osteoporosis, according to the
classification of the World Health Organization (WHO) ( table 1). A DXA T-score ≤-2.5
is consistent with osteoporosis, whereas a T-score between -1 and -2.5 is low bone
mass (osteopenia). (See 'Diagnosis' above.)

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• High fracture risk – For patients without a history of fragility fracture and without a
DXA T-score ≤-2.5, a clinical diagnosis of osteoporosis may also be made if there is a
clear elevated risk for fracture. In the United States, for example, a clinical diagnosis of
osteoporosis may be made when the Fracture Risk Assessment Tool (FRAX) 10-year
probability of major osteoporotic fracture is ≥20 percent or the 10-year probability of
hip fracture is ≥3 percent. (See 'Diagnosis' above.)

● Evaluation – All postmenopausal women with osteoporosis should have a history,

physical examination, and basic laboratory evaluation. Initial laboratory studies should
include a complete blood count (CBC), biochemistry profile, and 25-hydroxyvitamin D
(25[OH]D). (See 'Evaluation' above.)

The need for additional laboratory evaluation depends upon the initial evaluation and Z-
score ( table 3). Women who have abnormalities on initial laboratory testing, suspicious
findings on history and physical examination suggesting a secondary cause of
osteoporosis, or Z-scores ≤-2 may require additional evaluation for these secondary
causes ( table 2). (See 'Additional evaluation' above.)

● Treatment – The treatment of osteoporosis in postmenopausal women is reviewed

separately. (See "Overview of the management of osteoporosis in postmenopausal
women".)

ACKNOWLEDGMENT

The UpToDate editorial staff acknowledges Marc K Drezner, MD, who contributed to an earlier
version of this topic review.

Use of UpToDate is subject to the Terms of Use.

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fractures in older women. J Bone Miner Res 1992; 7:633.
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34. Kanis JA, Johnell O, De Laet C, et al. A meta-analysis of previous fracture and subsequent
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GRAPHICS

Age-related loss of trabecular bone

Sequential trabecular loss as shown by histologic examination of bone specimens;

the vertical trabeculae are shown in yellow, the horizontal in blue-green.

(A) Normal 50-year-old male with an almost perfect continuous trabecular

network.

(B) 58-year-old male with thinning of the horizontal trabeculae and some loss of
continuity.

(C) 76-year-old male with continued thinning of the horizontal trabeculae and
wider separation of the vertical structures.

(D) 87-year-old female with advanced breakdown of the entire network showing
unsupported vertical trabeculae.

Panels C and D represent the degree of loss of bone mass and microarchitectural
deterioration that is generally defined as osteoporosis.

From: Mosekilde LI. Age-related changes in vertebral trabecular bone architecture—assessed by a new
method. Bone 1988; 9:247. Reprinted with permission from Pergamon Press.

Graphic 73327 Version 4.0

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Thoracolumbar vertebral compression fractures

Radiographic features of spinal osteoporosis include wedging of the

vertebra anteriorly with vertebral collapse (arrows), vertebral end-
plate irregularity, and general demineralization.

Courtesy of Toledo Hospital.

Graphic 60593 Version 3.0

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Diagnostic categories for osteoporosis and low bone mass based upon BMD
measurement by DXA

Category Bone mass

Normal A value for BMD within 1.0 SD of the young adult female reference mean (T-score
greater than or equal to -1.0 SD).

Low bone mass A value for BMD more than 1.0 but less than 2.5 SD below the young adult
(osteopenia) female reference mean (T-score less than -1 and greater than -2.5 SD).

Osteoporosis A value for BMD 2.5 or more SD below the young adult female reference mean (T-
score less than or equal to -2.5 SD).

Severe A value for BMD more than 2.5 SD below the young adult female reference mean
(established) in the presence of one or more fragility fractures.
osteoporosis

BMD: bone mineral density; DXA: dual-energy x-ray absorptiometry; SD: standard deviation.

Data from: WHO scientific group on the assessment of osteoporosis at the primary health care level: Summary meeting
report, 2004. Geneva: World Health Organization, 2007.

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Causes of osteoporosis

Drugs Marrow-related disorders

Glucocorticoids Amyloidosis

Immunosuppressants (cyclosporine) Hemochromatosis

Antiseizure medications (particularly phenobarbital and Hemophilia

phenytoin)
Leukemia
Aromatase inhibitors
Lymphoma
GnRH agonists and antagonists
Mastocytosis
Heparin
Multiple myeloma
Cancer chemotherapy
Pernicious anemia
Endocrine disorders Sarcoidosis
Acromegaly Sickle cell anemia
Adrenal insufficiency Thalassemia
Cushing's syndrome
Organ transplantation
Eating disorders
Bone marrow
Endometriosis
Heart
Hyperparathyroidism
Kidney
Hyperprolactinemia
Liver
Hyperthyroidism
Lung
Hypogonadism (primary or secondary)
Miscellaneous causes
Diabetes mellitus
Ankylosing spondylitis
Gastrointestinal disease/nutritional disorders
Chronic obstructive pulmonary disease
Alcohol-related liver disease
Epidermolysis bullosa
Celiac disease
Idiopathic hypercalciuria
Chronic active hepatitis
Multiple sclerosis
Chronic cholestatic disease
Rheumatoid arthritis
Gastrectomy
Genetic disorders
Inflammatory bowel disease
Hypophosphatasia
Jejunoileal bypass
Osteogenesis imperfecta
Malabsorption syndromes
Homocystinuria due to cystathionine
Pancreatic insufficiency deficiency

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Parenteral nutrition

Primary biliary cholangitis

Severe liver disease

Vitamin D and/or calcium deficiency

GnRH: gonadotropin-releasing hormone.

Reproduced with permission from: Fitzpatrick LA. Secondary causes of osteoporosis. Mayo Clin Proc 2002; 77:453. Copyright
© 2002 Mayo Foundation.

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Laboratory evaluation for postmenopausal osteoporosis

Initial laboratory tests

Complete chemistry profile (including alkaline phosphatase)

Complete blood count

Calcium, phosphorus

25-hydroxyvitamin D

Additional laboratory tests if indicated

24-hour urine for calcium and creatinine

24-hour urine for free cortisol

FSH, LH

Prolactin

Magnesium

1,25-dihydroxyvitamin D

Intact PTH

TSH

Celiac screen

Serum protein electrophoresis/urine protein electrophoresis

Erythrocyte sedimentation rate

Rheumatoid factor

Ferritin and carotene levels

Iron and total iron binding capacity

Serum tryptase and histamine levels

Homocysteine

Skin biopsy for connective tissue disorders

COL1A genetic testing for osteogenesis imperfecta

Serum and urine bone turnover markers

FSH: follicle-stimulating hormone; LH: luteinizing hormone; PTH: parathyroid hormone; TSH: thyroid-
stimulating hormone.

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Contributor Disclosures
Harold N Rosen, MD No relevant financial relationship(s) with ineligible companies to disclose. Clifford J
Rosen, MD No relevant financial relationship(s) with ineligible companies to disclose. Kenneth E
Schmader, MD No relevant financial relationship(s) with ineligible companies to disclose. Jean E Mulder,
MD No relevant financial relationship(s) with ineligible companies to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.

Conflict of interest policy

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