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BMD alone should not be used to define osteoporosis in a premenopausal woman but,
like fragility fractures, is an indication for further evaluation.
The etiology of low bone mass in premenopausal women may be related to failure to
attain expected peak bone mass, previous bone loss, or ongoing bone loss. It is possible
that the patient never achieved optimal peak bone mass or that insults to the skeleton
occurred in the past and are no longer active; this can best be confirmed by serial bone
density or biochemical markers of bone turnover.
Some women may have genetically determined low peak bone mass. Other women may
have accrued less bone than expected due to insults to the skeleton (eg, medications,
poor nutrition, estrogen deficiency) that occurred during adolescence and are no longer
present at the time of evaluation. In either case, these women should have stable BMD,
even though BMD is low. This is in contrast to women with continued declines in BMD
who may have an ongoing secondary cause. Serial BMD measurements, if available, are
helpful in making this distinction. If there is only a single measurement of BMD,
obtaining serum or urinary markers of bone turnover may provide useful information.
Specimens must often be collected fasting in the morning If markers of resorption are
elevated above the premenopausal range, ongoing bone resorption is more likely.
Adolescence and young adulthood are characterized by active bone modeling and
physiologic increases in markers of bone turnover. Additionally, elevated bone turnover
markers are expected after a recent fracture. Premenopausal women with bone fragility
and no identifiable etiology after extensive evaluation for secondary causes are said to
have idiopathic osteoporosis. In patients with a history of fragility fractures without a
known cause, iliac crest bone biopsy may be indicated to identify other sources of bone
fragility
Subcutaneous PTH (teriparatide) has been used successfully to prevent bone loss in
premenopausal women on gonadotropin-releasing hormone (GnRH) agonists for the
treatment of endometriosis , in premenopausal women taking glucocorticoids [47,48], in
premenopausal women with idiopathic osteoporosis [49], and in those with AN [50].
Additionally, a case series documented benefit in pregnancy-associated osteoporosis
[51]. Teriparatide is currently approved for the treatment of glucocorticoid-induced
osteoporosis. Teriparatide has been associated with osteosarcoma in rodent studies. Use
of this medication should be avoided in those at increased risk of osteosarcoma
(including those with Paget disease, prior radiation, growing bones (open epiphyses), or
unexplained elevation in alkaline phosphatase). Thus, this medication should be used
with great caution in young women, and use should be avoided in those with delayed
growth or open epiphyses.
SERMs such as raloxifene and tamoxifen should not be used to treat osteoporosis in
menstruating women, as they block estrogen action on bone, leading to further bone
loss.
Eliminating gluten from the diet of young women diagnosed with celiac disease leads
to marked improvement in BMD Parathyroidectomy in premenopausal women with
primary hyperparathyroidism results in improvement in BMD. Weight gain and
resumption of normal menstrual function appears necessary for skeletal recovery in
patients with Anorexia nervosa N (see "Anorexia nervosa: Endocrine complications and
their management"). However,
DIFFERENTIAL DIAGNOSIS . The main casue for steoporosis in post menop woemn
is loss of estrogen and with it increased bone resorbtion . Other causes of bone
fractures and reduced bone mineral density (BMD) include osteomalacia, malignancy
(eg, multiple myeloma), Paget disease, and hyperparathyroidism. Physical abuse should
always be considered a possibility Low BMD may also be seen in conjunction with
renal osteodystrophy in patients with decreased kidney function
Osteoporosis has no clinical manifestations until there is a fracture.Men may also have
symptoms of disorders that are known to cause osteoporosis, such as hypogonadism,
malabsorption, and hyperparathyroidism
There is an increased risk of fracture, particularly at the spine, hip, wrist, humerus, rib,
and pelvis. Age 50 years use the same classification of BMD to define osteoporosis
in men (age 50 and older) as in women ,a value for BMD 2.5 or more standard
deviations below the young healthy male reference mean (rather than female reference
mean). Age <50 years In men below age 50 years with low BMD (Z-score -2.0), we
diagnose osteoporosis if there is a history of a fragility fracture and, possibly, if other
risk factors for osteoporosis (such as glucocorticoid therapy, hypogonadism, or
hyperparathyroidism) are present.
In men with clinical manifestations of osteoporosis (low trauma fracture) or with low
bone mass by dual-energy x-ray absorptiometry (DXA) (T-score less than -2.0), an
initial evaluation for secondary causes of osteoporosis (such as renal or liver disease,
hyperparathyroidism, Cushing's syndrome, celiac disease and other forms of
malabsorption, or idiopathic hypercalciuria) should be performed.
Routine biochemical tests to uncover renal or hepatic disease, a complete blood count,
serum testosterone, calcium, alkaline phosphatase, 25-hydroxyvitamin D (calcidiol),
and 24-hour urine calcium and creatinine (table 3).
Other Parathyroid hormone Estradiol In adult men with acquired hypogonadism,
estrogen deficiency may contribute more to bone loss than does androgen deficiency,
particularly if levels are below 10 to 15 pg/mL Tissue transglutaminase antibodies to
screen for celiac disease We typically measure this in men who have a low 25-
hydroxyvitamin D level and/or low urinary calcium. Serum and urine protein
electrophoresis Markers of bone formation and resorption as serum bone-specific
alkaline phosphatase concentrations and urinary excretion of deoxypyridinoline 24-
hour urinary free cortisol Serum tryptase to screen for systemic mastocytosis if
fractures, unexplained osteoporosis, or bone pain. In rare cases, iliac crest bone biopsy
Treatment calcium (1000 mg/day in younger men, 1000 to 1200 mg daily in older men,
total diet plus supplement) and vitamin D (600 to 800 international units/day)
For the treatment of men with osteoporosis (T-score below -2.5 or fragility fracture)
who do not have symptomatic hypogonadism or in hypogonadal men in whom
testosterone therapy is contraindicated, we recommend pharmacologic therapy. For the
treatment of high-risk men with T-scores between -1.0 and -2.5, also suggest
pharmacologic therapy. Especially if a 10-year probability of hip fracture or combined
major osteoporotic fracture of 3.0 or 20 percent, respectively.
Guidelines suggest adding a pharmacologic agent with proven antifracture efficacy (eg,
a bisphosphonate or teriparatide) in hypogonadal men whose risk of fracture is felt to be
high High-risk groups might include men on high-dose glucocorticoids; men with
frequent falls; men who have had a recent fragility fracture, particularly if they have a
BMD T-score below -2.5 at any skeletal site; or men with T-scores below -3.5 or even
below -3 if they have other risk factors for fracture. Adding an established osteoporosis
therapy to testosterone should also be considered in hypogonadal men whose BMD T-
score is <-2.5 even after receiving adequate testosterone replacement therapy for two
years.
Choice of therapy Men seem to respond to available therapies in the same way that
women respond so that, for the most part (notable exceptions being male
hypogonadism), the approach to treating men and women with osteoporosis is quite
similar. Bisphosphonates are considered the treatment of choice such as weekly
alendronate or risedronate as initial therapy for most men . Men who have esophageal
disorders (achalasia, scleroderma involving the esophagus, esophageal strictures,
varices), gastrointestinal intolerance to oral bisphosphonates, or an inability to follow
the dosing requirements of oral bisphosphonates can be treated instead with
intravenous (IV) bisphosphonate therapy. Oral bisphosphonates should also be avoided
after certain types of bariatric surgery in which surgical anastomoses are present in the
gastrointestinal tract (eg, Roux-en-Y gastric bypass); IV bisphosphonates are acceptable
as long as vitamin D has been assessed and is in the normal range. Zoledronic acid (ZA)
is the only IV bisphosphonate that has demonstrated efficacy for fracture
Patients with kidney disease and estimated glomerular filtration rate (eGFR) >30 to 35
mL/min are managed similarly, as long as there are no accompanying biochemical
abnormalities (eg, hyperparathyroidism, hyperphosphatemia) that indicate the
coexistence of renal osteodystrophy. Bisphosphonates are generally not recommended
for those with eGFR below 30 to 35 mL/min.
Stopping therapy after three to five years (a "drug holiday") may be reasonable for
some men,. For men taking alendronate for five years or who received ZA once yearly
for three years, who have a stable BMD, no previous fragility fractures, and who are at
low risk for fracture in the near future, we suggest discontinuing the drug. BMD should
be monitored every two years after suspending therapy, and therapy should generally be
resumed if BMD declines significantly or if the patient develops a new fragility fracture.