osteoporosis adapted and presented by: taraneh dormohammadi toosi, md assistant professor of...
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Osteoporosis
Adapted and presented by:Taraneh Dormohammadi Toosi, MD
Assistant professor of internal medicine Rheumatology
Tehran university of medical scienceValiasr hospita
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Definition
• A reduction in the strength of bone that leads to an increased risk of fractures
• Loss of bone tissue is associated with deterioration in skeletal microarchitecture
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Osteoporosis
• Prevalent – Postmenopausal women – Men and women • Underlying conditions • Major risk factors associated with bone
demineralization
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The World Health Organization (WHO) definition
• A bone density that falls 2.5 standard deviations (SD) below the mean for young healthy adults of the same (T-score of –2.5)
• Low bone density– A T-score <–1.0– Increased risk of osteoporosis– More than 50% of fractures among postmenopausal
women
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Epidemiology
• United States– 8 million women and 2 million
men have osteoporosis (T-score <–2.5)
– 18 million individuals have bone mass T-score <–1.0
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• The epidemiology of fractures – Follows the trend for loss of bone density– Fractures of the distal radius increase in frequency
before age 50 and plateau by age 60– Hip fractures double every 5 years after age 70
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• A hip fracture (50 years –old) – 14% for women – 5% for men
• Hip fractures – Deep vein thrombosis – Pulmonary embolism (20–50%) – Mortality rate between 5 and 20% (after surgery)
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• Multiple vertebral fractures – Height loss (often of several inches)– Kyphosis– Pain and discomfort – Thoracic fractures – Restrictive lung disease
• Lumbar fractures • Abdominal symptoms – Distention, early satiety, and constipation
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Risk factors for osteoporotic fracture
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Bone mass
• Genetic factors primarily determine peak skeletal mass and density
• Nutrition and lifestyle also play an important role in growth
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• Heritability – 50–80% for bone density and size
• Candidate genes – Vitamin D receptor– Type I collagen– The estrogen receptor (ER)– Interleukin 6 (IL-6)– Insulin-like growth factor I (IGF-I)]
• Genetic locus on chromosome 11 is associated with high bone mass
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• Families with high bone mass – Point mutation in LRP5 (low-density lipoprotein
receptor–related protein)
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Physiopathology
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Remodeling
• A process that results initially in bone resorption by osteoclasts, followed by a period of repair during which new bone tissue is synthesized by osteoblasts
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Bone remodeling has two primary functions1) Repair micro damage within the skeleton to maintain skeletal strength and 2) Supply calcium from the skeleton to maintain serum calcium
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Remodeling
• RANK ligand (RANKL) – The cytokine – Receptor activator of nuclear factor-kappa-B (NFκB)– A member of the TNF family– Secreted by osteoblasts
• RANK– The osteoclast receptor
• Activation of RANK by RANKL is a final common path in osteoclast development and activation
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Remodeling
• Osteoprotegerin– A humoral decoy for RANKL– Secreted by osteoblasts
• Modulation of osteoclast recruitment and activity appears to be related to the interplay among these three factors
• Additional influences – Nutrition (particularly calcium intake) – Physical activity level
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• After age 30–45– Resorption exceeds formation
• Exaggerated in women after menopause
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• Excessive bone loss – An increase in osteoclastic activity And/or – Decrease in osteoblastic activity
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Calcium Nutrition
• Peak bone mass may be impaired by inadequate calcium intake during growth
• During the adult phase of life– Insufficient calcium intake contributes to relative
secondary hyperparathyroidism – Increase in the rate of bone remodeling
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• PTH– Stimulates the hydroxylation of vitamin D in the
kidney– Increased levels of 1,25-dihydroxyvitamin D
[1,25(OH)2D] – Enhanced gastrointestinal calcium absorption– Reduces renal calcium loss
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• Total daily calcium intakes – The recommended daily required intake • 1000–1200 mg for adults
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Vitamin D
• Optimal targets for serum 25(OH)D are >75 nmol/L (30 ng/mL)
• An intake of 800–1000 units/d
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• Estrogen deprivation– The life span of osteoblasts may be decreased– Longevity and activity of osteoclasts are increased
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Physical Activity• Inactivity such as prolonged bed rest or
paralysis, results in significant bone loss• Concordantly, athletes have higher bone mass
than does the general population
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Other Risk Factors
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Chronic Disease
• Hypogonadal states – Turner's syndrome – Klinefelter's syndrome– Anorexia nervosa – Hypothalamic amenorrhea – Hyperprolactinemia
• Endocrine disorders – Cushing's syndrome – Hyperparathyroidism – Thyrotoxicosis – Type 1 diabetes mellitus – Acromegaly Adrenal insufficiency
• Nutritional and gastrointestinal disorders – Malnutrition – Parenteral nutrition – Malabsorption syndromes– Gastrectomy– biliary cirrhosis Pernicious anemia
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• Rheumatologic disorders – Rheumatoid arthritis – Ankylosing spondylitis
• Hematologic disorders/malignancy – Multiple myeloma– Lymphoma and leukemia – Malignancy-associated parathyroid hormone (PTHrP)– Mastocytosis – Hemophilia – Thalassemia
• Selected inherited disorders– Osteogenesis imperfecta – Marfan's syndrome – Hemochromatosis – Hypophosphatasia – Glycogen storage diseases – Homocystinuria – Ehlers-Danlos syndrome – Porphyria– Menkes' syndrome – Epidermolysis bullosa
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• Other disorders – Immobilization – Chronic obstructive pulmonary disease– Pregnancy and lactation – Scoliosis – Multiple sclerosis – Sarcoidosis – Amyloidosis
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Medications
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• Cigarette Consumption– Toxic effects on osteoblasts – Indirectly by modifying estrogen metabolism– Intercurrent respiratory and other illnesses– Frailty– Decreased exercise– Poor nutrition– Need for additional medications • Glucocorticoids for lung disease
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Measurement of Bone Mass
• DXA is a highly accurate x-ray technique – Standard for measuring bone density – Usually are made of the lumbar spine and hip
• Portable DXA machines have been developed that measure the heel (calcaneus), forearm (radius and ulna), or finger (phalanges)
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• DEXA– Can not estimate the depth
or posteroanterior length of the bone
– Lower than average bone mineral density (BMD)
– Bone spurs• Falsely increase bone density of
the spine
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"Normal" values – T-scores• Compare individual results to those in a young population
that is matched for race and sex
– Z-scores • Compare individual results to those of an age-matched
population that also is matched for race and sex
– A T-score below –2.5 in the lumbar spine, femoral neck, or total hip is taken as a diagnosis of osteoporosis
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• CT – Spine – Hip– Three-dimensional – A true density – Analyze trabecular bone and cortical bone content
and volume separately• Expensive, involves greater radiation
exposure, and is less reproducible than DXA
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• US – Low cost and mobility– A screening procedure
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• The hip is the preferred site of measurement in most individuals
• In younger individuals such as perimenopausal or early postmenopausal women, spine measurements may be the most sensitive indicator of bone loss.
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When to Measure Bone Mass
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When to Treat Based on Bone Mass Results
• T-score ≤–2.5• Postmenopausal women with fracture risk factors – Age– Prior fracture– Family history of hip fracture– Low body weight– Cigarette consumption– Excessive alcohol use– Steroid use– Rheumatoid arthritis
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Assessment of fracture risk
• FRAX calculators (http://www.shef.ac.uk/FRAX/tool.jsp?
locationValue=9)
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Laboratory Evaluation• A general evaluation – Complete blood count– Serum and 24-h urine calcium– Renal and hepatic function
• An elevated serum calcium – Hyperparathyroidism – Malignancy
• A reduced serum calcium level – Malnutrition – Osteomalacia
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Laboratory Evaluation• A low urine calcium (<50 mg/24 h)– Osteomalacia, malnutrition, or malabsorption
• A high urine calcium (>300 mg/24 h)– hypercalciuria • A renal calcium leak• Absorptive hypercalciuria
– Idiopathic or associated – Increased 1,25(OH)2D in granulomatous disease
• Hematologic malignancies • Excessive bone turnover
– Paget's disease, hyperparathyroidism, and hyperthyroidism.
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Laboratory Evaluation
• Cushing's syndrome– Urinary free cortisol levels or a fasting serum cortisol
• Bowel disease, malabsorption, or malnutrition is suspected– Serum albumin, cholesterol, and a complete blood
• Asymptomatic malabsorption – Anemia
• Macrocytic—vitamin B12 or folate deficiency• Microcytic—iron deficiency
– Low serum cholesterol or urinary calcium levels
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Laboratory Evaluation
• Asymptomatic celiac disease – Antigliadin, antiendomysial, or transglutaminase
antibodies – Require endoscopic biopsy– A trial of a gluten-free diet can be confirmatory
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Laboratory Evaluation
Mastocytosis• Osteoporosis with • Rash, multiple allergies, diarrhea, or flushing, • 24-h urine histamine collection or serum
tryptase
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Laboratory Evaluation
• Myeloma – Bone pain – Punched-out lesions on radiography
• Serum and urine electrophoresis and evaluation for light chains in urine are required to exclude this diagnosis– A bone marrow biopsy
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Biochemical Markers
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Bone turnover markers
• Response to therapy • Long-term adherence to treatment• Monitoring the effects of 1-34hPTH
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• A decline in resorptive markers – After treatment with bisphosphonates or estrogen
• Less marked – After treatment with either raloxifene or
intranasal calcitonin
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Treatment
• Management of acute fractures • Treatment of the underlying disease• Education
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• Calcitonin – Reduce pain related to acute vertebral
compression fracture• Vertebroplasty or kyphoplasty– Percutaneous injection of artificial cement
(polymethylmethacrylate) into the vertebral body• Immediate pain relief
• Early mobilization is recommended
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Severe pain usually resolves within 6–10 weeks
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• Chronic pain – Abnormal strain on muscles, ligaments, and
tendons – Facet-joint arthritis – Thoracic and/or abdominal shape
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Treatment
• Education– Reduce the impact of modifiable risk factors
associated with bone loss and falling– Medications • Glucocorticoid
– As low as possible
• Levothyroxin
– Smoking cessation– Reducing risk factors for falling
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Nutritional Recommendations
• Calcium – Dairy products and other foods• Milk, yogurt, and cheese, fortified foods
– Calcium supplementation
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Calcium content
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• Calcium supplements containing carbonate are best taken with food since they require acid for solubility
• Calcium citrate supplements can be taken at any time
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Vitamin D
• Serum 25(OH)D consistently >75 μmol/L (30 ng/mL)
• Daily intakes – 200 IU for adults <50 years of
age– 400 IU for 50–70 years– 600 IU for >70 years
• Higher doses (≥1000 IU) – Elderly and chronically ill
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Other Nutrients
• Salt, high animal protein intakes, and caffeine may have modest effects on calcium excretion or absorption
• Adequate vitamin K status is required for optimal carboxylation of osteocalcin
• Cola intake is controversial – Reduced bone mass through factors that are
independent of caffeine
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Exercise
• Young individuals increases the likelihood that they will attain the maximal genetically determined peak bone mass
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Exercise
• Beneficial effects on neuromuscular function
• Improves coordination, balance, and strength
• Reducing the risk of falling– A walking program – Dancing, racquet sports, cross-
country skiing, and use of gym equipment
– At least three times a week
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Pharmacologic therapies
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Estrogens
• Reduce bone turnover• Prevent bone loss• Induce small increases in bone mass of the
spine, hip, and total body
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Estrogen effects
• The indirect estrogen actions primarily decrease bone resorption– Increasing IGF-I and TGF-β and – Suppressing IL-1 (α and β), IL-6, TNF-α, and
osteocalcin synthesis
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SERMs
• Raloxifene, which is approved for the prevention and treatment of osteoporosis
• Tamoxifen, which is approved for the prevention and treatment of breast cancer
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Mode of Action of SERMs
• All SERMs bind to the ER, but each agent produces a unique receptor-drug conformation
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Bisphosphonates
• Alendronate and Risedronate
– Approved for the prevention and treatment of steroid-induced osteoporosis
– Approved for treatment of osteoporosis in men
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Mode of Action
• Impair osteoclast function • Reduce osteoclast number– Inducing apoptosis
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Calcitonin
• Approved by the FDA – Paget's disease– Hypercalcemia– Osteoporosis in women >5 years past menopause
• Not indicated for prevention of osteoporosis
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Mode of Action
• Suppresses osteoclast activity by direct action on the osteoclast calcitonin receptor
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Denosumab
• Given twice yearly/SC • Increase BMD in the spine, hip, and forearm • Reduce vertebral, hip, and nonvertebral
fractures
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• Denosumab was approved by the FDA in 2010 – Treatment of postmenopausal women who have a
high risk for osteoporotic fractures– Failed or are intolerant to other osteoporosis
therapy
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Mode of Action
• Fully human monoclonal antibody to RANKL• Inhibit its ability to initiate formation of
mature osteoclasts • Reducing the survival of the osteoclast• Serious adverse reactions – Hypocalcemia, infections, and dermatologic
reactions such as dermatitis, rashes, and eczema
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Parathyroid Hormone
• PTH also can exert anabolic effects on bone• Teriparatide has been approved for the
treatment of established osteoporosis in both men and women
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• 20 μg PTH(1–34) daily by SC injection reduced vertebral fractures by 65% and nonvertebral fractures by 45%
• Single daily injection given for a maximum of 2 years
• Increases in bone mass and mediates architectural improvements in skeletal structure
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• Side effects – Mild and can include muscle pain, weakness,
dizziness, headache, and nausea– Osteogenic sarcomas
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Mode of Action
• Direct actions on osteoblast activity• Stimulates IGF-I and collagen production and
appears to increase osteoblast number • Produces a true increase in bone tissue and an
apparent restoration of bone microarchitecture
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Fluoride
• Despite increments in bone mass of up to 10%, there are no consistent effects of fluoride on vertebral or nonvertebral fracture
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Strontium Ranelate
• Increases bone mass throughout the skeleton• Modestly antiresorptive while at the same
time not causing as much of a decrease in bone formation
• Small increased risks of venous thrombosis, seizures, and abnormal cognition
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Treatment Monitoring
• Consider BMD as a monitoring tool– Changes must exceed 4% in the spine and 6% in
the hip to be considered significant – The hip is the preferred site due to larger surface
area and greater reproducibility– BMD should be repeated at intervals >2 years
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Treatment Monitoring
• Biochemical markers of bone turnover – Determination should be made before therapy is
started and repeated ≥4 months after therapy is initiated
– A change in bone turnover markers must be 30–40% lower than the baseline
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• A generalized disorder of calcium, phosphate, and bone metabolism
• Increased secretion of PTH• Hypercalcemia and hypophosphatemia
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• The annual incidence – 0.2% in patients >60– Peak incidence between the third and fifth
decades
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Etiology
• Parathyroid tumors – Isolated adenomas – Hereditary syndromes such as MEN syndromes– Secondary to underlying disease• Excessive stimulation in secondary hyperparathyroidism
– Chronic renal failure– Lithium therapy
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Solitary Adenomas• A single abnormal gland –∼80% of patients– A benign neoplasm or adenoma – Rarely a parathyroid carcinoma
• ∼15% of patients– All glands are hyperfunctioning
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Pathology
• Adenomas – Inferior parathyroid glands– 6–10% • Thymus, the thyroid, the pericardium, or behind the
esophagus
– Microscopic examination of biopsy specimens of several glands is essential
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Parathyroid carcinoma
• Not aggressive• More aggressive form– Distant metastases
• Lung, liver, and bone
• Hyperparathyroidism due to parathyroid carcinoma – More severe clinically– Calcium values of 3.5–3.7 mmol/L (14–15 mg/dL) are
frequent with carcinoma – Genetic basis of parathyroid carcinoma
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Signs and Symptoms
• One-half – Asymptomatic
• Kidney involvement– Deposition of calcium in the renal parenchyma • Decreased renal function and phosphate retention
– Recurrent nephrolithiasis• Urinary tract obstruction, infection, and loss of renal
function
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• Manifestations– Recurrent nephrolithiasis– Peptic ulcers– Mental changes– Extensive bone resorption– Milder form of the disease • Asymptomatic HPT
– Hypercalcemic parathyroid crisis• Occur abruptly • Marked dehydration and coma, so-called
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• Osteitis fibrosa cystica– 10–25% of patients in series reported 50 years ago
• Histologically– An increase in the giant multinucleated osteoclasts – Replacement of the normal cellular and marrow
elements by fibrous tissue• X-ray changes – Resorption of the phalangeal tufts – Subperiosteal resorption– Osteitis fibrosa cystica
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In symptomatic patients• Dysfunctions – CNS, peripheral nerve and muscle, gastrointestinal
tract, and joints also occur– Severe neuropsychiatric manifestations
• May be reversed by parathyroidectomy
• Neuromuscular manifestations – Proximal muscle weakness– Easy fatigability– Atrophy of muscles
• Complete regression of neuromuscular disease after surgical correction of the hyperparathyroidism.
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• Gastrointestinal manifestations – Vague abdominal complaints and disorders of the
stomach and pancreas– Duodenal ulcer• In MEN 1 patients
• Asympomatatic primary hyperparathyroidism – Biochemically confirmed hyperparathyroidism – The absence of signs and symptoms
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• Cardiovascular disease – Left ventricular hypertrophy, cardiac functional
defects, and endothelial dysfunction – Reversible after surgery
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• Diagnosis– PTH immunometric assays combined with
simultaneous blood calcium measurements
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Treatment
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Treatment
• Hyperparathyroidism– Surgical excision – Evidence favoring surgery, if medically feasible, is
growing • Concerns about skeletal, cardiovascular, and
neuropsychiatric disease, even in mild hyperparathyroidism
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• Preoperative 99mTc sestamibi scans with single-photon emission CT (SPECT) – Predict the location of an abnormal gland
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• A decline in serum calcium – Within 24 hours after successful surgery– Usually blood calcium falls to low-normal values
for 3–5 days • Acute postoperative hypocalcemia – Only if severe bone mineral deficits – Injury to all the normal parathyroid glands occurs
during surgery
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• Hypocalcemia – Muscle twitching– A general sense of anxiety– Positive Chvostek's and Trousseau's signs – Serum calcium consistently <2 mmol/L (8 mg/dL)
• Parenteral calcium replacement in symptomatic patient
• If symptoms worsen or if parenteral calcium is needed for >2–3 days, therapy with a vitamin D analogue and/or oral calcium (2–4 g/d) should be started
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• Hypoparathyroidism– Calcium falls to <2 mmol/L (8 mg/dL) And– Phosphate level rises simultaneously
• Unexpected hypocalcemia– Coexistent hypomagnesemia
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Surgery in asymptomatic patient
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Monitoring in asymptomatic patient
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Other Parathyroid-Related Causes of Hypercalcemia
• Lithium Therapy– Hypercalcemia in 10% of treated patients∼– Remitting and recurring when lithium is stopped
and restarted– Shift the PTH secretion curve to the right in
response to calcium