Alimentação e cálcio
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Transcript of Alimentação e cálcio
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Alimentação e cálcio: problemas e soluções
Para algumas pessoas aumentar a quantidade de cálcio na alimentação pode, por motivos vários, ser
considerado um problema. Mas para quase tudo existe uma solução!
PROBLEMA O QUE SIGNIFICA COMO SE MANIFESTA COMO SE
RESOLVE Intolerância à lactose
(déficite de lactase)
Dificuldade de digerir
o açúcar (lactose) dos
lacticínios por
deficiência no enzima
(lactase) que o digere
Dores abdominais, diarréia,
náuseas, meteorismo (gases)
quando ingere leite
Prefira os iogurtes
e os queijos (a
lactose já está
digerida)
Beba leite sem
lactose
Use leite de soja e
seus derivados
Hipercolesterolémia Colesterol aumentado Risco aumentado de
doenças cardiovasculares
Use produtos
magros ou meio-
gordos (a
quantidade de
cálcio é igual)
Obstipação Prisão de ventre A prisão de ventre pode seragravada pelo aumento do
cálcio na dieta
Beba mais águaComa mais frutas
e vegetais
Coma fibras
Faça exercício
Obesidade Use produtos
magros
Reduza o consumo
de gorduras e
hidratos de
carbono
Faça exercício
Litíase renal Cálculos (pedras)
renais
Formação de cálculos é
provocada por eliminarmuito cálcio na urina
(hipercalciúria) e não por
ingerir cálcio a mais
Beba mais água
Evite comermuitos alimentos
ricos em oxalatos
(p.ex. vegetais
verdes)
Outros cuidados alimentares para prevenir a osteoporose :
- Não consuma bebidas alcoólicas em excesso. O álcool é prejudicial para o fígado, para os ossos e favorece
as quedas.
- Consuma com moderação as bebidas ricas em cafeína (p.ex. café, refrigerantes de cola, bebidas
energéticas). A cafeína em excesso aumenta a excreção de cálcio na urina.- Não consuma mais proteínas (carne, peixe, ovos e leguminosas) do que as recomendadas na pirâmide
alimentar. Mas, se tem mais de 65 anos ou se teve uma fractura recente deve ingerir a dose máxima
recomendada.
- Reduza o sal da sua dieta. Para além de ser bom para os seus ossos será ainda melhor para o seu coração.
- A vitamina D também é importante para ter ossos saudáveis. Parte da vitamina D de que necessitamos é
fabricada pela nossa pele através da exposição solar e outra parte provêm da alimentação (p.ex.
lacticínios). Se tem mais de 65 anos, se sai muito pouco de casa e não apanha sol (embora 30 minutos por
dia de exposição solar o seja suficiente) deve ter mais cuidado com a alimentação ou falar com o seu
médico para saber se precisa de um suplemento de vitamina D, principalmente nos meses de Outono e
Inverno.
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Alimentos ricos em cálcio, com indicação dequantidade (mg)
Alimento Quantidade Cálcio(mg)
LEITE - Magro 200 mg 248
- Meio Gordo 200 mg 243- Completo (gordo) 200 mg 237- Em Pó 15 g 64- De Soja 200 mg 25IOGURTE MAGRO - Simples 150 g 278- Fruta 150 g 230GELADO MAGRO - Semifrio (3% gordura) 100 g 185- Duro (4% gordura) 100 g 117QUEIJO - Parmesão 50 g 643
- Cruyère, Emmenthal(45% gordura) 50 g 590
- Flamengo 50 g 386- Ilha 50 g 370- Fundido 50 g 300- Serra (60% gordura) 50 g 278- Brie (50% gordura) 50 g 200- Camembert (45%gordura)
50 g 190
- Mozzarela 50 g 143- Fresco Magro (2 - 4%gordura)
50 g 37
- Creme (60% gordura) 50 g 17OMOLETA DE QUEIJO - 1 ovo + 25 g de queijoflamengo
80 224
PIZZA DE QUEIJO ETOMATE
100 g 189
QUEIJADA 50 g 130PUDIM DE OVOSCASEIROS
100 g 95
FLOCOS DE AVEIA (semleite)
50 g 66
PÃO 50 g 54FRUTOS SECOS
- Figos 50 g 139- Amêndoas 50 g 134- Nozes 50 g 90- Damascos 50 g 45- Amendoins 50 g 29CHOCOLATE DE LEITE 100 g 220SARDINHAS FRSCAS (com espinhas) - Em óleo, só o peixe 50 g 195- Em tomate, só o peixe 50 g 150CAMARÕES GRANDES 100 g 150LARANJA 1 grande 58VEGETAIS FRESCOS (cozidos e secos
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Osteoporose e dores nas costas
Durante a maior parte do tempo a osteoporose não dá sintomas, mas quando já existem fracturas
vertebrais você pode começar a ter dores nas costas.
As dores nas costas provocadas pela osteoporose podem ser agudas ou crónicas e a maneira de lidar com
elas é diferente nos dois casos.
Dor aguda
A dor aguda nas costas é habitualmente provocada por uma fractura vertebral. Surge de forma súbita, é
muito intensa e incapacitante, mas dura pouco tempo, não mais de 2 ou 3 semanas. Para tratar esta dor é
necessário fazer analgésicos (medicamentos para as dores) e alguns dias de repouso, evitando as
actividades mais pesadas da vida diária
Dor crónica
A dor crónica resulta do esforço que é colocado nos músculos e ligamentos da coluna. Se já desenvolveu
uma corcundae tem menos altura, como consequência da osteoporose, isso é resultado de várias
pequenas fracturas, que muitas vezes podem até ter passado despercebidas. Estas alterações tornam maisdifícil manter a coluna vertebral direita, exigindo um maior esforço aos músculos e ligamentos. Este
esforço é a causa da dor crónica. A dor crónica pode durar meses. A sua intensidade pode até nem ser
muito grande, mas é muito incomodativa e pode dificultar as tarefas diárias. Nos períodos de agravamento
da dor deve fazer os analgésicos que o seu médico receitou. Não espere que a dor seja insuportável para
começar a fazer os medicamentos. Mais vale tomar regularmente um analgésico, evitando que a dor se
agrave.
Outras medidas simples como a aplicação de calor local, são úteis para aliviar as dores nas costas. A
mudança frequente de posição e a utilização de um bom suporte lombar (p.ex. uma almofada atrás das
costas quando está sentada) são outros exemplos de gestos simples que também podem ajudar.
A execução regular de exercícios que ajudam a fortalecer e a alongar os músculos das costas são muito
importantes para diminuir a dor crónica. Estes exercícios podem ser executados em casa, depois de serem
aprendidos com um terapeuta.
A execução das tarefas diárias de forma correcta é fundamental para evitar as dores nas costas e também
para evitar novas fracturas vertebrais.
Nos quadros seguintes pode ver alguns exemplos de como deve executar as suas tarefas e também de
alguns exercícios de fortalecimento e alongamento que pode executar em casa, depois de se aconselhar
com o seu médico.
- Espinafres 100 g 600- Rama de Nabo (folhas ecaules)
100 g 168
- Couve Verde 100 g 160Brócolos 100 g 91Feijão de Soja 100 g 87Feijão Seco 100 g 45
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Cuidados posturais no seu dia -a-dia
A osteoporose torna os seus ossos mais frágeis, de tal modo que podem partir com um pequeno esforço
que não seria suficiente para partir um osso normal. Quando a sua postura não está alinhada
correctamente a sua coluna tem de suportar uma pressão maior. Consequências: mais esforço nos
músculos e ligamentos, mais dores nas costas e maior risco de fractura vertebral. Manter uma boa postura
quando está em pé, sentado ou quando se inclina ou estica é fundamental.Como verá nos exemplos que se
seguem, as regras básicas são:
- dobrar os joelhos e inclinar-se a partir das ancas, em vez de dobrar a partir da cintura.
- manter as costas direitas e bem apoiadas
- manter os braços junto ao corpo, repartir as cargas e usar os dois braços para pegar em objectos pesados.
De acrdo com a National Osteoporosis Founda tion (NOF), que reúne um grande número de pesquisadores
de diversas especialidades envolvidas com osteoporose, estas são as indicações formais para o estudo da
massa óssea:
todos os indivíduos com mais de 65 anos;
indivíduos com deficiência de hormônios sexuais;
mulheres na perimenopausa que estejam cogitando usar terapia de reposição hormonal, para auxiliar
essa decisão;
pacientes com alterações radiológicas sugestivas de osteopenia ou que apresentem fraturas
osteoporóticas;
pacientes em uso de corticoterapia crônica;
pacientes com hiperparatiroidismo primário;
pacientes em tratamento da osteoporose, para controle da eficácia da terapêutica.
Além dessas indicações, existem inúmeras outras condições clínicas que, por predisporem à perda óssea,
são consideradas fatores de risco e justificam a avaliação. Os fatores de risco são:
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Antecedente genético: inúmeros trabalhos observacionais demonstram a agregação familiar de menor
massa óssea e a concordância desse traço em gêmeos mono e dizigóticos. Cerca de 70 a 80% da variação
da densidade mineral óssea pode ser atribuída a fatores genéticos. Caucasianos e orientais apresentam
maior incidência de fraturas do que populações negras, assim como mulheres de qualque r raça em relação
aos homens. Desse modo, o antecedente familiar, particularmente materno, de fraturas osteoporóticas é
uma indicação para o exame.
Riscos ambientais: deficiências e/ou distúrbios nutricionais como baixa ingestão de cálcio, baixo peso,
dietas de restrição calórica, alcoolismo, excessos de sódio e proteína animal; consumo de cigarro;sedentarismo; longos períodos de imobilização.
Doenças crônicas: hipertiroidismo, tratamento do câncer diferenciado de tireoide com doses supressivas
de T4, hipercortisolismo, insuficiência renal crônica, hepatopatias, doença pulmonar obstrutiva crônica,
doenças de má absorção intestinal, hipercalciúria idiopática e artrite reumatoide. O risco de fraturas
também está associado a maior risco de quedas, principalmente em pacientes com déficit visual, de força
muscular no quadríceps e/ou cognitivo, alterações de marcha e disfunções neurológicas que afetem o
equilíbrio.
Uso crônico de drogas: a incidência de fraturas osteoporóticas em usuários de corticosteroides po r mais
de seis meses é de cerca de 30 a 50%. Mesmo doses pequenas de glicocorticoides, incluindo os inalatórios,podem causar perda óssea na maioria dos indivíduos. Outras drogas associadas à perda óssea são
ciclosporina, bloqueadores da secreção de gonado trofinas, heparina, anticonvulsivantes como hidantoína,
carbamazepina e fenobarbitúricos e os quimioterápicos. Drogas que provoquem hipotensão postural ou
alterações do equilíbrio, como anti-hipertensivos, barbitúricos, benzodiazepínicos e diuréticos, po dem
aumentar o risco de quedas.
emedicine.medscape.com
Introduction
Background
Osteoporosis is a systemic skeletal disorder characterized by decreased bone mass and deterioration of
bony microarchitecture. The result is fragile bones and an increased risk of fractures, even after minimal
trauma. Osteoporosis is a chronic condition of multifactorial etiology and is usually clinically silent until a
fracture occurs. Osteoporosis is a significant health problem in the United States and around the world.
Pathophysiology
Osteoporosis results from hereditary and environmental factors that affect both bone mass and bonequality. Traditionally, osteoporosis was described as type I (postmenopausal) or type II (senile).
Postmenopausal osteoporosis (PMO) is primarily due to estrogen deficiency; senile osteoporosis is
primarily due to an aging skeleton and calcium deficiency. However, it is increasingly recognized that
multiple pathogenetic mechanisms interact in the development of the osteoporotic state, regardless of
age.
Cortical and trabecular (cancellous) bone differ in architecture but are similar in molecular composition.
Bone consists of cells and an extracellular matrix with mineralized and nonmineralized components. The
composition and architecture of the extracellular matrix is what imparts mechanical properties to bone.
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Bone strength is determined by collagenous proteins (tensile strength) and mineralized osteoid
(compressive strength).[1 ]The greater the concentration of calcium, the greater the compressive strength.
Adult bone undergoes constant remodeling to maintain bone strength. Osteocytes, which are terminally
differentiated osteoblasts embedded in mineralized bone, direct the timing and location of remodelin g.
Osteoblasts not only secrete and mineralize osteoid but also appear to control the bone resorption carried
out by osteoclasts; thus, bone formation and resorption are coupled. Osteoclasts require weeks to resorb
bone, whereas osteoblasts need months to produce new bone. Therefore, any process that increases the
rate of bone remodeling results in net bone loss over time.[2 ]
Furthermore, in periods of rapid remodeling(eg, after menopause), bone is at an increased risk for fracture because the newly produc ed bone is less
densely mineralized, the resorption sites are temporarily unfilled, and the isomerization and maturation of
collagen is impaired. [3 ]
Molecular biologists have begun to elucidate the mechanisms of bone remodeling. For example, it is now
understood that the receptor activator of nuclear factor-kappa B ligand (RANKL)/receptor activator of
nuclear factor-kappa B (RANK)/osteoprotegerin (OPG) system is the final common pathway for bone
resorption. Osteoblasts and activated T cells in the bone ma rrow produce the RANKL cytokine. RANKL
binds to the RANK receptor expressed by osteoclasts and osteoclast precursors to promote osteoclast
differentiation. Osteoprotegerin is a soluble decoy receptor that inhibits RANK -RANKL by binding and
sequestering RANKL.
Bone mass peaks by the third decade of life and slowly decreases afterward. The failure to attain optimal
bone strength by this point is one factor that contributes to osteoporosis. Therefore, nutrition and physical
activity are important during growth and development. Nevertheless, hereditary factors play the principal
role in determining an individuals peak bone strength. In fact, genetics account for up to 80% of the
variance in peak bone mass between individuals. [4 ]
Estrogen deficiency not only accelerates bone loss in postmenopausal women but also plays a role in bone
loss in men. Estrogen deficiency can lead to excessive bone resorption accompanied by inadequate bone
formation. Osteoblasts, osteocytes, and osteoclasts all express estrogen receptors. In addition, estrogen
affects bones indirectly through cytokines and local growth factors. The estrogen -replete state mayenhance osteoclast apoptosis via increased production of transforming growth factor (TGF) beta. In the
absence of estrogen, T cells promote osteoclast recruitment, differentiation, and prolonged survival via
interleukin [IL]1, IL-6, and tumor necrosis factor (TNF)alpha. T cells also inhibit osteoblast differentiation
and activity and cause premature apoptosis of osteoblasts through cytokines such as IL-7. Finally, estrogen
deficiency sensitizes bone to the effects of parathyroid hormone (PTH).
Calcium, vitamin D, and parathyroid hormone help maintain bone homeostasis. Insufficient dietary calcium
or impaired intestinal absorption o f calcium due to aging or disease can lead to secondary
hyperparathyroidism. Parathyroid hormone is secreted in response to low serum calcium levels.
Parathyroid hormone increases calcium resorption from bone, decreases renal calcium excretion, and
increases renal production of 1,25 -dihydroxyvitamin D (1,25[OH]2 D). It is this active hormonal form of
vitamin D that optimizes calcium and phosphorous absorption from the gut, inhibits parathyroid hormone
synthesis, and plays a minor role in bone resorption.
Vitamin D deficiency can result in secondary hyperparathyroidism via decreased intestinal calcium
absorption. Interestingly, the effects of parathyroid hormone and 1,25[OH] 2 D on bone are mediated via
binding to osteoblasts and stimulating the RANKL/RANK p athway. Osteoclasts do not have receptors for
parathyroid hormone or 1,25[OH] 2 D.[1 ]
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Endocrinologic conditions or medications that lead to bone loss (eg, glucocorticoids) can cause
osteoporosis. Corticosteroids inhibit osteoblast function and enhance ost eoblast apoptosis.[5
]Polymorphisms of IL-1, IL-6 and TNF-alpha, as well as their receptors, have been found to influence bone
mass. Other factors implicated in the pathogenesis of osteoporosis include polymorphisms in the vitamin D
receptor; alterations in insulin-like growth factor-1, bone morphogenic protein, prostaglandin E 2, nitrous
oxide, and leukotrienes; collagen abnormalities; and leptin -related adrenergic signaling.[2 ]
Osteoporotic fractures represent the clinical significance of these derangements in bone. Fractures occur
when bones fall under excess stress. Nearly all hip fractures are related to falls. [6 ]The frequency and
direction of falls can influence the likelihood and severity of fractures. The risk of falling may be amplified
by neuromuscular impairment due to vitamin D deficiency with secondary hyperparathyroidism or
corticosteroids. Vertebral bodies are composed primarily of cancellous bone with interconnected
horizontal and vertical trabeculae. Osteoporosis not only reduces bone mass in vertebrae but also
decreases interconnectivity in their internal scaffolding. [1 ]Therefore, minor loads can lead to vertebral
compression fractures.
International
Osteoporosis is estimated to affect over 200 million people worldwide. [8 ]An estimated 75 million people in
Europe, the United States, and Japan have osteoporosis. [9 ]
One in 3 women older than 50 years will eventually experience osteoporotic fractures, as will 1 in 5 men. [10
]By 2050, the worldwide incidence of hip fracture is projected to in crease by 240% in women and 310% in
men.[11 ]
Mortality/Morbidity
Osteoporosis is the most common human bone disease. In 2005, over 2 million osteoporosis -relatedfractures occurred in the United States. [12 ]Hip and vertebral fractures, in particular, are associated with
increased morbidity and mortality.
Hip fractures
y Hip fractures increase the one-year risk of death by 10-20%.[13,14 ]
y Patients with hip fractures incur decreased independence and a diminished quality of life. Only one
third of patients return to their prefracture level of function. [15 ]
y Among women who sustain a hip fracture, 50% spend time in a nursing home while recovering. In
addition, 1 in 5 patients with hip fractures requires long -term nursing home care.[7 ]
y Persons with a hip fracture are twice as likely to experience another fracture as persons withoutfractures. [16 ]
Vertebral fractures
y Vertebral fractures increase the 5-year risk of mortality by 15%.[17 ]
y Only one third of people with radiographic vertebral fractures are diagnos ed clinically.[18 ]
y Symptoms of vertebral fracture may include back pain, height loss, and disabling kyphosis.
y Compression deformities can lead to restrictive lung disease, abdominal pain, and early satiety.
y One in 5 postmenopausal women with a new vertebral fracture incurs another vertebral fracture
within one year. [19 ]
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Race
Whites (especially of northern European descent) and Asians are at an increased risk; however,
osteoporosis can occur in persons of all races and ethnicities.
Sex
y Overall, osteoporosis has a female-to-male ratio of 4:1.[7 ]
y Eighty percent of hip fractures occur in women.[20 ]
Age
y The frequency of postmenopausal osteoporosis is highest in women aged 50 -70 years.
y Senile osteoporosis is most common in persons aged 70 years or older.
y Secondary osteoporosis can occur in persons of any age.
y Ninety percent of hip fractures occur in persons aged 50 years or older. [20 ]
Clinical
History
Osteoporosis is typically asymptomatic until a fracture occurs. The history should focus on a thor ough
review of risk factors, which include the following:
y Age, sex, and race
y Family history of osteoporosis, particularly maternal history of fractures
y Reproductive factors, especially regarding early menopause and estrogen replacement therapy
y Lifestyle factors associated with decreased bone density
o Smoking
o Alcohol consumption
o Low levels of physical activityo Strenuous exercise (such as occurs in marathon runners) that results in amenorrhea
y Calcium and vitamin D intake
y History of low-trauma "fragility" fracture in patients aged 40 years or older (A fragility fracture is
defined as a fracture due to trauma that would not normally cause fracture [a force equal to or less
than that resulting from a fall from standing height].)
y Signs of vertebral fracture: Vertebral fracture may be asymptomatic. Patients with vertebral
fractures may note progressive kyphosis with loss of height. Some may report acute back pain after
bending, lifting, or coughing.
o The pain is located in the midthoracic to lower thoracic or upp er lumbar spine, where most
vertebral fractures occur.
o The pain is described variably as sharp, nagging, or dull; movement may exacerbate pain. Insome cases, pain radiates to the abdomen.
o Acute pain usually resolves after 4-6 weeks. In the setting of multiple fractures with severe
kyphosis, the pain may become chronic.
y Coexisting medical conditions associated with bone loss (see Causes)
y Medications associated with bone loss (see Causes)
y Risk factors for falls in older patients
o Poor balance
o Orthostatic hypotension
o Weakness of the lower extremity muscles, deconditioning
o Use of medications with sedative effects
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o Poor vision or hearing
o Cognitive impairment
Physical
Patients with suspected osteoporosis should undergo a comprehensive medical examination. Areas of
concern include the following:
y Low body weight (body mass index <19 kg/m2
)y Signs that might indicate existing osteoporosis
o Kyphosis or dowager hump
o Point tenderness over a vertebrae or other suspected fracture site
y Signs that might indicate a secondary cause of osteoporosis (see Causes)
y Signs in older patients that may indicate increased fall risk
o Difficulty with balance or gait
o Orthostatic hypotension
o Lower-extremity weakness
o Poor vision or hearing
o Cognitive impairment
Causes
Primary causes
y Estrogen deficiency
y Changes associated with aging
Secondary causes - Up to one third of postmenopausal women, as well as many men and premenopausal
women, have a coexisting cause of bone loss. [21,22 ]
Risk factors for secondary osteoporosis
y Endocrine disorders -Hyperparathyroidism, hypogonadism, hyperthyroidism, diabetes mellitus,
Cushing disease, prolactinoma, acromegaly, adrenal insufficiency
y Gastrointestinal/nutritional conditions -Inflammatory bowel disease, celiac disease, malnutrition,
history of gastric bypass surgery, chronic liver disease, anorexia nervosa, vitamin D or calcium
deficiency
y Renal disease - Chronic kidney disease, idiopathic hypercalciuria
y Rheumatologic diseases -Rheumatoid arthritis, ankylosing spondylitis, systemic lupus
erythematosus
y Hematologic disease -Multiple myeloma, thalassemia, leukemia, lymphoma, hemophilia, sickle cell
disease, systemic mastocytosisy Genetic disorders -Cystic fibrosis, osteogenesis imperfecta, homocystinuria, Ehlers-Danlos
syndrome, Marfan syndrome, hemochromatosis, hypophosphatasia
y Other - Porphyria, sarcoid, immobilization, pregnancy/lactation, chronic obstructive pulmonary
disease (COPD), parenteral nutrition, HIV/AIDS
Medications known to cause or accelerate bone loss
y Corticosteroids - Prednisone ( 5 mg/d for 3 mo) [23 ]
y Anticonvulsants - Phenytoin, barbiturates, carbamazepine (These agents are associated with
treatment-induced vitamin D deficiency.)
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y Heparin (long-term)
y Chemotherapeutic/transplant drugs - Cyclosporine, tacrolimus, platinum compounds,
cyclophosphamide, ifosfamide, methotrexate
y Hormonal/endocrine therapies - Gonadotropin-releasing hormone (GnRH) agonists, luteinizing
hormone-releasing hormone (LHRH) analogs, depomedroxyprogesterone, excessive thyroid
supplementation
y Lithium
y Aromatase inhibitors - Exemestane, anastrozole
Differential Diagnoses
Hyperparathyroidism
Multiple Myeloma
Osteomalacia and Renal Osteodystrophy
Paget Disease
Workup
Laboratory Studies
Laboratory studies are used to establish baseline conditions or to exclude secondary causes of
osteoporosis.
y CBC count
y Serum chemistries including calcium, phosphate, creatinine, liver function tests, electrolytes: levels
of serum calcium, phosphate, and alkaline phosphatase are usually normal in persons with primary
osteoporosis, although alkaline phosphatase levels may be elevated for several months after a
fracture.
y Thyroid-stimulating hormone
y 25-hydroxyvitamin D [25(OH)D]
Other laboratory studies used to evaluate for secondary causes include the following:
y Twenty-four-hour urine calcium to assess for hypercalciuria
y Intact parathyroid hormone
y Testosterone level (in males)
y Sedimentation rate
y Urinary free cortisol and tests for adrenal hypersecretion
y Serum and urine protein electrophoresis
y Antigliadin and antiendomysial antibodies for celiac disease
y Serum tryptase, urine N-methylhistamine for mastocytosis
y Bone marrow biopsy if a hematologic disorder is suspected
Markers of bone turnover (both formation and resorption) may be elevated in high bone-turnover states
(eg, early postmenopausal osteoporosis) and may be useful in some patients for monitoring early response
to therapy. However, further study is needed to determine their clinical utility in osteoporosis
management. Some of these biochemical measures include the fo llowing:
y Bone formation markers - Bone-specific alkaline phosphatase, osteocalcin, type I procollagen
peptides
y Bone resorption markers - Urinary deoxypyridinoline and cross-linked N- and C-telopeptide of type I
collagen
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Imaging Studies
Dual-energy x-ray absorptiometry
Dual-energy x-ray absorptiometry (DXA) is the standard study used to establish or confirm a diagnosis of
osteoporosis, to predict future fracture risk, and to assess changes in bone mass over time. DXA is used to
calculate bone mineral density (BMD) at the hip and spine. Although measurement at any site can be used
to assess overall fracture risk, measurement at a particular site is the best predictor of fracture risk at that
site. Whenever possible, the same technologist should perform subseq uent measurements on the samepatient using the same machine. This method can be used in both adults and children. Factors that may
result in a falsely high bone density determination include spinal fractures, osteophytosis, and extraspinal
(eg, aortic) calcification.
The National Osteoporosis Foundation and the International Society for Clinical Densitometry (ISCD)
recommend that BMD be measured in the following patients:
y Women aged 65 years and older and men aged 70 years or older, regardless of clinical risk factors
y Younger postmenopausal women and men aged 50 -70 years with clinical risk factors for fracture
y Women in menopausal transition with a specific risk factor associated with increased risk for
fracture (ie, low body weight, prior low-trauma fracture, use of a high-risk medication)y Adults with fragility fractures
y Adults who have a condition (eg, rheumatoid arthritis) or who take a medication (eg,
glucocorticoids, 5 mg of prednisone daily for 3 mo) associated with low bone mass or bone loss
y Anyone being considered for pharmacologic therapy for osteoporosis
y Anyone being treated for osteoporosis (to monitor treatment effect)
y Anyone not receiving therapy in whom evidence of bone loss would lead to treatment
Bone density data from a DXA are reported as T-scores and Z-scores. T-scores represent the number of
standard deviations (SD) from the mean bone density values in healthy young adults, whereas Z -scores
represent the number of SD from the normal mean value for age - and sex-matched controls.
y Criteria by the World Health Organization (WHO) define a normal T -score value as within 1 SD of
the mean bone density value in a healthy young adult.
o T-score of -1 to -2.5 SD indicates osteopenia.
o T-score of less than -2.5 SD indicates osteoporosis.
o T-score of less than -2.5 SD with fragility fracture(s) indicates severe osteoporosis.
y For each SD reduction in BMD, the relative fracture risk is increased 1.5-3 times.
y The WHO BMD diagnostic classification should not be applied to premenopausal women, men
younger than 50 years, or children. Z -scores adjusted for ethnicity or race should be used, with Z-
scores of -2.0 or lower defined as "below the expected range for age" and those above -2.0 being
"within the expected range for age." The diagnosis of osteoporosis in these groups should not be
based on densitometric criteria alone.
WHO fracture risk algorithm[24 ]
This algorithm (www.shef.ac.uk/FRAX/) was developed to calculate the 10-year probability of a hip fracture
and the 10-year probability of any major osteoporotic fracture (defined as clinical spine, hip, forearm, or
humerus fracture) in a given patient. These calculations account for femoral neck BMD and other clinical
risk factors, as follows:
y Age
y Sex
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y Personal history of fracture
y Low body mass index
y Use of oral glucocorticoid therapy
y Secondary osteoporosis (ie, coexistence of rheumatoid arthritis)
y Parental history of hip fracture
y Current smoking status
y Alcohol intake (3 or more drinks per day)
This algorithm is useful in identifying patients with low bone mass (having T-scores in the osteopenicrange) who are most likely to benefit from treatment. The National Osteoporosis Foundation recommends
osteoporosis treatment in patients with low bone mass in whom a US -adapted WHO 10-year probability of
a hip fracture is 3% or more or in whom the risk for a major osteoporosis -related fracture is 20% or more.[7
]
Vertebral fracture assessment
Densitometric spine imaging can be performed at the time of DXA scanning to detect vertebral fractures.
Vertebral fracture assessment (VFA) is not available with all DXA machines. When available, VFA should be
considered when the results may influence clinical management of the patient. [25 ]
Radiography
Obtain radiographs of the affected area in symptomatic patients. Lateral spine radiography can be
performed in asymptomatic patients in whom a vertebral fracture is suspected, in those with height loss in
the absence of other symptoms, or in those with pain in the thoracic or upper lumbar spine.
y Radiographs may show fractures or other conditions such as osteoarthritis, disc disease, or
spondylolisthesis.
y Plain radiography is not as accurate as BMD testing. Approximately 30 -80% of bone mineral must
be lost before radiographic lucency becomes apparent on radiographs. [26 ]
Additional imaging modalities
y Quantitative CT scanning: This is used to measure BMD as a true volume density in g/cm 3, which is
not influenced by bone size. This technique can be used in both adults and children but assesses
BMD only at the spine. Other limitations include significant radiation exposure, high cost, and
possible interference by osteophytes.
y Peripheral DXA: This is used to measure BMD at the wrist. Peripheral DXA may be most useful in
identifying patients at very low fracture risk who require no furthe r workup.
y Quantitative ultrasonography of the calcaneus: This is a low-cost portable screening tool. This
method does not involve radiation but is not as accurate as other methods and cannot be used tomonitor the response to treatment because of its lack of precision.
Procedures
Undecalcified iliac bone biopsy with double tetracycline labeling is rarely necessary but may be considered
when no cause for osteoporosis is apparent, therapy is not eliciting a response, or osteomalacia is
suspected. Tetracycline double labeling is a process used to calculate data on bone turnover. In this
procedure, patients are given tetracycline, which binds to newly formed bone. This appears on biopsy
samples as linear fluorescence. A second dose of tetracycline is given 11 -14 days after the first dose; this
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appears on a biopsy sample as a second line of fluorescence. The distance between the two fluorescent
labels can be measured to calculate the amount of bone formed during that interval.
Histologic Findings
Histologic examination of osteoporotic bone may reveal generalized thinning of trabeculae and irregular
perforation of trabeculae, reflecting unbalanced osteoclast -mediated bone resorption.[20 ]
Treatment
Medical Care
Osteoporosis is typically asymptomatic until a fracture occurs. Patients identified as at risk for osteoporosis
(including children and adolescents) should undergo preventive measures, including adequate calcium
intake, vitamin D intake, and exercise. Counsel patients to avoid tobacco use. Identify and treat a lcoholism.
Protective measures should be taken in patients who must take glucocorticoids for other medical
conditions. These include using the minimum effective dose, discontinuing the drug as soon as possible,
and supplementing with calcium and vitamin D.
The National Osteoporosis Foundation recommends that pharmacologic therapy should be reserved for
postmenopausal women and men aged 50 years or older who present with the following:
y A hip or vertebral fracture (Vertebral fracture may clinical or morphomet ric [ie, identified on a
radiograph alone].)
y Other prior fractures and low bone mass (T -score between -1.0 and -2.5 at the femoral neck, total
hip, or spine)
y T-score less than -2.5 at the femoral neck, total hip, or spine after appropriate evaluation to exclude
secondary causes
y Low bone mass (T-score between -1.0 and -2.5 at the femoral neck, total hip, or spine) and
secondary causes associated with high risk of fracture (eg, glucocorticoid use or total
immobilization)
y Low bone mass (T-score between -1.0 and -2.5 at the femoral neck, total hip, or spine) and (1) 10 -
year probability of hip fracture of 3% or more or (2) a 10 -year probability of any major
osteoporosis-related fracture of 20% or more based on the US -adapted WHO algorithm[24 ]
Surgical Care
The goals of surgical treatment of osteoporotic fractures include rapid mobilization and return to normal
function and activities.
y Fixation and stabilization of hip or wrist fracture
y Vertebroplasty to reduce vertebral fracture associated pain
y Kyphoplasty to restore height or to treat the deformity associated with osteoporotic vertebral
fractures
Consultations
y Rheumatologist or endocrinologist to assist with management and determination of underlying
etiologies in complex cases
y Orthopedist to assist with fracture management
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Diet
Adequate calcium and vitamin D intake are important in persons of any age, particularly in childhood as
the bones are maturing. If dietary intake is inadequate, add supplements.
Calcium
y Premenopausal women and men younger than 50 years w ithout risk factors for osteoporosis
should receive a total of 1000 mg of calcium daily.y Postmenopausal women, men older than 50 years, and other persons at risk for osteoporosis
should receive a total of 1200-1500 mg of calcium daily.
y See the National Osteoporosis Foundation Web site for further calcium recommendations.
Vitamin D
y Adults younger than 50 years should receive 400 -800 IU of vitamin D 3 daily.
y All adults older than 50 years should receive 800 -1000 IU of vitamin D 3 daily.
y See the National Osteoporosis Foundation Web site for further vitamin D recommendations.
Activity
y Weight-bearing exercise has been shown to positively affect BMD. Regular exercise should be
encouraged in all patients, including children and adolescents (in order to strengt hen the skeleton
during the maturation process). Exercise also improves agility and balance, thereby reducing the
risk of falls.
y Physical therapists can assist in developing exercise regimens and instructing patients in proper
techniques.
Medication
Antiresorptive agents, including bisphosphonates, the selective estrogen-receptor modulator (SERM)raloxifene, calcitonin, denosumab, and one anabolic agent, teriparatide, are currently available for
osteoporosis treatment. All therapies should be given with cal cium and vitamin D supplementation. The
American College of Physicians reviewed the evidence and proposed guidelines for pharmacologic
treatments of osteoporosis. [27 ]
A combination of calcium and vitamin D supplementation can reduce fracture risk. [28 ]A meta-analysis was
performed to evaluate the efficacy of oral supplemental vitamin D in preventing nonvertebral and hip
fractures among individuals older than 65 years. The meta -analysis included 12 double-blind, randomized,
controlled trials of nonvertebral fractures (n=42,279) and 8 randomized controlled trials of hip fractures
(n=40,886) and compared oral vitamin D (with or without calcium) with either calcium alone or placebo.
The results showed that nonvertebral fracture prevention with vitamin D is dos e-dependent, and a higher
dose reduced fractures by at least 20% in individuals aged 65 years or older. [29 ]
An additional meta-analysis (n=68,517) concluded that vitamin D alone is not effective in preventing
fractures, although, when administered with calcium, hip fractures and total fractures (and possibly
vertebral fractures) were reduced. The conclusions were based on 7 large studies that were randomized
with at least one intervention arm in which vitamin D was given and included analysis of fractures as an
outcome and at least 1000 participants. [30 ]
Bisphosphonates are the most commonly used agents for osteoporosis. Oral and intravenous options are
available. Trials have provided limited data about long-term treatment with bisphosphonates, and,
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recently, the optimal length of treatment with these medications has come into question. A patient's risk
of fracture can be used to help guide length of treatment. Patients at high risk may be continued on
bisphosphonates after 5 years; however, in some patie nts, especially those with a lower risk of fracture,
bisphosphonate treatment may be stopped. [31 ]
Raloxifene, a SERM first studied for breast cancer prevention, decreases bone resorption through actions
on estrogen receptors. Raloxifene may be most useful in younger postmenopausal women without severe
osteoporosis.
Teriparatide is currently the only anabolic agent in use for osteoporosis treatment. Bouxsein et al
retrospectively analyzed data from the Fracture Prevention Trial and the Multiple Outco mes of Raloxifene
Evaluation trial for the risk of new vertebral fractures adjacent to existing vertebral fractures in
postmenopausal osteoporotic women in patients on teriparatide or raloxifene. At baseline, 1226 untreated
postmenopausal women had 1 or more vertebral fractures. During the 2-year follow-up, 196 (16%) had a
total of 292 new vertebral fractures ; 47% of fractures were adjacent to a previously existing fracture.
Teriparatide reduced the risk of any new, new adjacent, and new nonadjacent verteb ral fractures by 72%,
75%, and 70%, respectively, compared with placebo, whereas raloxifene reduced the risk by 54%, 54%, and
53%, respectively, compared with placebo. [32 ]Teriparatide should be considered in younger and older
postmenopausal women with severe osteoporosis.
Calcitonin is an option for patients who are not candidates for other available osteoporosis treatments.
Denosumab, a humanized monoclonal antibody directed against receptor activator of nuclear factor -kappa
B ligand (RANKL), was approved by the US Food and Drug Administration (FDA) in June 2010. Denosumab
decreases bone resorption by inhibiting osteoclast activity. In a randomized placebo -controlled trial,
Cummings et al studied 7868 women aged 60 -90 years with osteoporosis who received either denosumab
60 mg SC or placebo every 6 months for 36 months. Compared with placebo, denosumab decreased the
risk of vertebral, nonvertebral, and hip fractures in women with osteoporosis. [33 ]Smith et al reported a
reduction in incident vertebral fra ctures when denosumab was used in 734 men receiving androgen -
deprivation therapy for prostate cancer compared with placebo. In the Smith study, denosumab
significantly increased lumbar spine, hip, femoral neck, and radial BMD.
[34 ]
Hormone replacement therapy (HRT) was once considered a first-line therapy for the prevention and
treatment of osteoporosis in women. Data from the Women's Health Initiative confirmed that HRT can
reduce fractures. However, HRT was associated with an increased risk of breast canc er, myocardial
infarction, stroke, and venous thromboembolic events. [35 ]HRT is approved for management of menopausal
symptoms and prevention of osteoporosis. It is no longer recommended as a treatment of osteoporosis in
postmenopausal women.
Evidence indicates that strontium ranelate (available in Europe) reduces the risk of fracture. Strontium is
not approved for the treatment of osteoporosis in the United States.
Bisphosphonate Derivative
Bisphosphonates are stable analogues of inorganic pyrophosphate. Bisphosphonates have a high affinity
for hydroxyapatite crystals, and by binding at sites of active bone resorption, these agents can inhibit
osteoclastic resorption. All oral bisphosphonates have a poor absorption and a bioavailability of less than
5%. Bone uptake is 20-80%, with the remainder being rapidly excreted through the kidney. [36
]Bisphosphonates are approved in the United States for the prevention and treatment of postmenopausal
osteoporosis, osteoporosis in males, and steroid -induced osteoporosis.
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Alendronate sodium (Fosamax); alendronate sodium/cholecalciferol (Fosamax Plus D)
Increases BMD at spine by 8% and hip by 3.5%.Reduces the incidence of vertebral fractures by 47% and
nonvertebral fractures by 50% over 3 y. Approved for treatment and pr evention of postmenopausal
osteoporosis, male osteoporosis, and steroid-induced osteoporosis. Tab is available with 2800 or 5600 IU
of vitamin D3 .Also available in PO solution taken weekly.
Dosing
Adult
Treatment: 70 mg PO qwk or 10 mg PO qd
Prevention: 35 mg PO qwk or 5 mg PO qd
Pediatric
Not established
Interactions
Coadministration with calcium-containing products and other multivalent cations decreases absorption
(separate dosing by 30 minutes); increased GI distress with aspirin, NSAIDs, or other GI irritants
Contraindications
Documented hypersensitivity; inability to stand or sit upright for at least 30 min; hypocalcemia; esophageal
abnormalities (eg, stricture, achalasia) that might delay esophageal emptying
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if
benefits outweigh risk to fetus
Precautions
Upper GI disease; renal insufficiency (CrCl <35 mL/min); treat disturbances of mineral metabolism; ensure
adequate vitamin D and calcium intake; discontinue if esophageal reaction (eg, dysphagia, odynophagia,
retrosternal pain, worsening heartburn) occurs; not for use in breastfeeding women
Risedronate sodium ( Actonel); risedronate sodium with calcium carbonate ( Actonel with calcium)
Increases BMD at spine by 5.4% and hip by 1.6%.Reduces vertebral fractures by 41% and nonvertebral
fractures by 39% over 3 y. Approved for treatment and prevention of postmenopausal osteoporosis, male
osteoporosis, and steroid-induced osteoporosis.
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Dosing
Adult
Treatment or prevention in women:
5 mg PO qd OR
35 mg PO qwk OR
75-mg tab PO on 2 consecutive days monthly OR
150-mg tab PO qmoTreatment in men:
35 mg PO qwk
Pediatric
Not established
Interactions
Coadministration with calcium-containing products and other multivalent cations decreases absorption
(separate dosing by 30 min); caution with aspirin, NSAIDs, or other GI irritants
Contraindications
Documented hypersensitivity; hypocalcemia; inability to stand or sit upright for at least 30 min
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if
benefits outweigh risk to fetus
Precautions
Upper GI disease; renal insufficiency (CrCl <30 mL/min); correct any preexisting hypocalcemia or other
mineral or bone disturbances prior to starting therapy; ensure adequate vitamin D and calcium intake;
discontinue if esophageal reaction (eg, dysphagia, odynophagia, retrosternal pain, worsening heartburn)
occurs; not for use in breastfeeding women
Ibandronate sodium (Boniva)
Increases BMD at spine by 5.7-6.5% and hip by 2.4-2.8%.Reduces vertebral fractures by 50% with
intermittent (non-daily) dosing over 3 y. No effects on reduction of nonvertebral fractures. Approved for
postmenopausal osteoporosis.
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Dosing
Adult
Treatment or prevention in postmenopausal osteoporosis:
Oral: 150 mg PO qmo or 2.5 mg PO qd
Intravenous: 3 mg IV q3mo
Pediatric
Not established
Interactions
Multivalent cations (eg, calcium, aluminum, magnesium, iron) decrease absorption, administer at least 1 h
prior to vitamin and mineral supplements; NSAIDs may aggravate GI irritation
Contraindications
Documented hypersensitivity; uncorrected hypocalcemia; inability to stand or sit upright for at least 60 minfollowing drug administration
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if
benefits outweigh risk to fetus
Precautions
Upper GI disease; renal insufficiency (CrCl <30 mL/min); correct any preexisting hypocalcemia or other
mineral or bone disturbances prior to starting therapy; ensure adequate vitamin D and calcium intake;
discontinue if esophageal reaction (eg, dysphagia, odynophagia, retrosternal pain, worsening heartburn) or
severe musculoskeletal pain occurs; renal toxicity rarely reported with IV dose; not for use in breastfeeding
women
Zoledronic acid (Reclast)
Most potent bisphosphonate available. Increases BMD at spine by 4.3 -5.1% and hip by 3.1-3.5% compared
with placebo. Reduces the incidence of spine fractures by 70%, hip fractures by 41%, and non -vertebralfractures by 25% over 3 y. Approved for the treatment of postmenopausal osteoporosis.
Dosing
Adult
5 mg IV over 15 min once yearly
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Pediatric
Not established
Interactions
Aminoglycosides may enhance hypocalcemic effect of zoledronic acid; NSAIDs may enhance GI adverse
events; thalidomide may enhance adverse effects
Contraindications
Documented hypersensitivity; hypocalcemia
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Aspirin-sensitive asthma; concomitant cancer/chemotherapy/steroids or dental procedure in patients with
cancer may increase risk of osteonecrosis of the jaw; caution in renal insufficiency (CrCl <30 mL/m in);
correct preexisting hypocalcemia or other mineral or bone disturbances prior to starting therapy; ensure
adequate vitamin D and calcium intake; not for use in breastfeeding women
Hormone, Parathyroid
Teriparatide is a biological product that contains a portion of human parathyroid hormone. When given
intermittently, it increases bone remodeling with the net effect of increased bone mass and improved
skeletal microarchitecture. (This is in contrast to continuous exposure to parathyroid hormone, whichincreases bone resorption with a net effect of decreased trabecular bone volume). Teriparatide is
approved in the United States for postmenopausal osteoporosis and primary or hypogonadal osteoporosis
in men.
T eriparatide (Forteo)
Anabolic agent increases BMD at lumbar spine by 9-13% and hip by 3-6% compared with placebo. Reduced
the risk of spine fractures by 65% and nonspinal fractures by 54% in patients after an average of 18 mo of
therapy.Approved for postmenopausal osteoporosis and male osteoporosis.
Dosing
Adult
20 mcg SC qd
Pediatric
Not recommended
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Interactions
None reported
Contraindications
Documented hypersensitivity; increased risk for osteosarcoma (including those with Paget disease of bone
or unexplained elevations of alkaline phosphatase, open epiphyses, or prior radiation therapy involving
skeleton); children or growing adults; patients with bone metastases or history of skeletal malignanciesand those with metabolic bone diseases other than osteoporosis
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if
benefits outweigh risk to fetus
Precautions
Monitor for hypercalcemia; may cause orthostatic hypotension (particularly following first several doses),
dizziness, or leg cramps; therapy limited to 2 y owing to osteogenic sarcomas in rat studies
Selective Estrogen Receptor Modulator
Selective estrogen receptor modulators (SERMs) act as weak estrogens in some organ systems, while
acting as estrogen antagonists in others. Raloxifene is approved for the prevention and treatment of
postmenopausal osteoporosis.
Raloxifene (Evista)
Increases BMD at spine and hip.Reduces the incidence of spine fractures by 30 -55% over 3 y.
Most suitable in women <70 y at moderate risk for osteoporosis who have infrequent vasomotor
symptoms of menopause (eg, hot flashes) and who are at moderate-to-high risk for breast cancer.
Dosing
Adult
60 mg PO qd
Pediatric
Not recommended
Interactions
May antagonize warfarin; avoid with anion exchange resins (eg, cholestyramine); caution with other drugs
that are highly protein bound (eg, diazepam, diazoxide, lidocaine)
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Contraindications
Documented hypersensitivity; thrombophlebitis; pregnancy
Precautions
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
Not for use in premenopausal women; not recommended for use with concomitant estrogen replacement
therapy; discontinue 72 h before prolonged immobilization or surgery associated with thromboembolism
and resume once fully ambulatory; hepatic dysfunction; not recommended for use in breastfeeding
women
Calcitonin
This agent is a peptide hormone used to t reat and prevent osteoporosis in patients in whombisphosphonates and estrogen are contraindicated or not tolerated. It also has some analgesic effects in
patients with fractures.
Calcitonin (Miacalcin, Calcimar, Cibacalcin)
Increases BMD at lumbar spine by 1-1.5%. Reduced incidence of spine fracture by 33% in group receiving
200 IU/d. Available in parenteral and intranasal forms; however, intranasal form is more convenient and
better tolerated. Diminution of benefit may occur after 20 mo with parenteral f orm.
Dosing
Adult
200 IU (1 puff) qd in alternating nostrils
100 IU IM/SC qod
Pediatric
Not established
Interactions
May potentiate oral anticoagulants and oxyphenbutazone; may alter insulin effects
Contraindications
Documented hypersensitivity
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Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Perform periodic nasal examinations and discontinue if severe ulceration occurs with nasal spray use;monitor for hypocalcemic tetany initially and urine sediments over long term with injectable use;
hypocalcemia may occur (supplement with calcium and vitamin D); examine urine sediment during
prolonged therapy; caution in breastfeeding women
Estrogen Derivative
Estrogen is approved for the prevention of osteoporosis and relief of menopause -associated vasomotor
symptoms and vulvovaginal atrophy. The lowest effective dose at the shortest duration necessary should
be used. The FDA recommends that other approved nonestrogen treatments should be considered first for
osteoporosis prevention.
Estrogens (conjugated)
Contains a mixture of estrogens obtained exclusively from natural sources, occurring as the sodium salts of
water-soluble estrogen sulfates blended to represent the average composition of material derived from
pregnant mares' urine. Mixture of sodium estrone sulfate and sodium equilin sulfate.Contains, as
concomitant components, sodium sulfate conjugates, 17-alpha-dihydroequilenin, 17-alpha-estradiol, and
17-beta-dihydroequilenin.
Restores estrogen levels to concentrations that induce negative feedback at gonadotrophic regulatory
centers, which in turn reduces release of gonadotropins from pituitary.Increases synthesis of DNA, RNA,
and many proteins in target tissues.
Multiple aspects of menopause respond to estrogen replacement therapy, including vasomotor symptoms
and atrophic vaginitis. Also reduces bone resorption and may increase osteoblast activity.
Routinely prescribing conjugated estrogens to premenopausal women is not recommended. Use this
medication in postmenopausal women who are incontinent and who have had a hysterectomy. For
postmenopausal women with an intact uterus, cautiously recommend a short -term low-dose of Premarin,
with frequent monitoring.
Dosing
Adult
Prophylaxis: Initial, 0.3 mg PO qd given continuously or in cyclical regimens (25 d on, 5 d off); adjust to
lowest level that will provide effective control
Pediatric
Not established
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Interactions
May reduce hypoprothrombinemic effect of anticoagulants; coadministration of barbiturates, rifampin,
and other agents that induce hepatic microsomal enzymes may reduce estrogen levels; pharmacologic and
toxicologic effects of corticosteroids may occur as a result of estrogen-induced inactivation of hepatic P450
enzyme; loss of seizure control has been noted when administered concurrently with hydantoins
Contraindications
Documented hypersensitivity; known or suspected pregnancy; breast cancer; undiagnosed abnormal
genital bleeding; active thrombophlebitis or thromboembolic disorders; history of thrombophlebitis,
thrombosis, or thromboembolic disorders associated with previous estrogen use (except when used in
treatment of breast or prostatic malignancy)
Precautions
Pregnancy
X - Contraindicated; benefit does not outweigh ris k
Precautions
Certain patients may develop undesirable manifestations of excessive estrogenic stimulation, such as
abnormal or excessive uterine bleeding or mastodynia; estrogens may cause some degree of fluid
retention (exercise caution); prolonged unoppo sed estrogen therapy may increase risk of endometrial
hyperplasia
Monoclonal Antibody
Binds to RANKL, a transmembrane or soluble protein essential for the formation, function, and survival of
osteoclasts, the cells responsible for bone resorption.
Denosumab (Prolia)
Monoclonal antibody that specifically targets RANK ligand, an essential regulator of osteoclasts. Indicated
for prevention of fracture in postmenopausal women with osteoporosis and high fracture risk (ie, history
of osteoporotic fracture, failed other treatments).
Dosing
Adult
60 mg SC q6mo
Pediatric
Safety and efficacy not established
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Interactions
None reported
Contraindications
Documented hypersensitivity; hypocalcemia
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if
benefits outweigh risk to fetus
Precautions
Hypocalcemia must be corrected before initiating; hypocalcemia may worsen, especially in patients with
CrCl <30 mL/min or on hemodialysis; serious adverse reactions include hypocalcemia, serious infections
(including cellulitis), and dermatologic reactions (eg, dermatitis, rashes, eczema); common adverse effectsinclude back and musculoskeletal pain, extremity pain, hypercholesterolemia, and cystitis; bone t urnover
suppression; may increase risk for osteonecrosis of the jaw; pancreatitis reported in clinical trials
Patient Education
y Educate patients about osteoporosis and encourage them to follow preventive measures, including
adequate calcium and vitamin D intake, exercise, cessation of smoking, and moderation of alcohol
consumption.
y For excellent patient education resources, visit eMedicine's Bone Health Center; Eating Disorders
Center; Esophagus, Stomach, and Intestine Center; and Women's Health Center.
y Also, see eMedicine's patient education articles Understanding Osteoporosis Medications, AnorexiaNervosa, Inflammatory Bowel Disease, Menopause, and Hormone Replacement and Osteoporosis.
Miscellaneous
Medicolegal Pitfalls
Osteoporosis is a preventable disease with potentially devastating consequences. Failure to identify at -risk
patients, to educate them, and to implement preventive measures may lead to tragic consequences.
Special Concerns
y Recognize the increased mortality and morbidity associated with osteoporotic fractures.
y Many patients have a coexisting cause of bone loss. This should be investigated and treated.
y WHO criteria for T-scores should not be applied to premenopausal women, men younger than 50
years old, and children. Z-scores should be used for these individuals, and, in these cases, a
diagnosis of osteoporosis should not be based on densitometric criteria alone.
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Me
nop
us
Os dive ¡ s ¢ s sinais e sintomas que acompanham a menopausa (parada do fluxo menstrual), vemsendo estudadosdesde o século XV
£ £ £
¤
É um período com v¥
rios sintomas que estão sendo gradativamente decifrados e com isso diversas medidas j ¥ podem ser tomadas para melhorar a qualidade de vida das mulheres ¤
Os diversos sinais e sintomas que acompanham a menopausa(parada do fluxo menstrual), vemsendo estudados desde o século XV
£ £ £
¤
É um período com v ¥ rios sintomas que estão sendo gradativamente decifrados e com isso diversas
medidas j ¥ podem ser tomadas para melhorar a qualidade de vida das mulheres ¤
- Cli ¦
t§
̈ io: é o inicio do período que compreende alguns anos antes da parada do fluxo até alguns anos após
¤
- Menop us : última mestruação.
Co¦
o as mulheres entram na menopausa?
- A grosso modo, o aparelho reprodutor f eminino é formado pelos ov ¥ rios, o útero e as trompas © Os ov
¥ rios são os reponsavies pela produção dos hormônios.(estrógeno e progesterona) e também pela
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produção dos óvulos que são liberados mensalmentee se fecundados pelo espermatozóde darão origem a
uma nova vida.
Com o passar dos anos, a mulher di minui a produção dos hormônios, passa a não ovular; e com isso,
aparecem os ciclos irregulares e um gama de sintomas até a parada do fluxo.
Sintomas: são muito variáveis de pessoa para pessoa, de modo geral, compreendem: ondas de calor,
suores noturnos, fadiga, dores de cabeça, tontura, insônia, dores articulares, sintomas psíquicos que
também são frequentes, como: depressão, desânimo intenso, instabilidade emocional, irritação e baixa
auto-estima.
Isto não quer dizer que todas as mulheres nescessariamente terão estes sintomas, apenas que é
nescessário reconhecê-los para procurar ajuda do seu ginecologista que vai diagnosticar e melhorar muito
a passagem por este período da sua vida.
O que modifica no corpo com a menopausa?
-Pode-se observar um certo aumento de peso, com distribuição gordurosa maior na região da cintura
(barriga).
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O osso pode apresentar uma perda progressiva da massa óssea de + ou - 2 a 3% ao ano principalmente os
ossos da coluna e colo de femur, podendo levar ao quadro de osteoporos e.
O risco cardiáco pode estar aumentado com o aumento dos lípídes, hipertensão arterial. Perda damemória e maior relação com Alzeimer. Ressecamento vaginal com dor na atividade sexual e diminuição
da libido.
Existe tratamento?
- A menopausa é uma fase da vida e deve ser encarada como tal. Você não está e se você se cuidar bem,
não ficará doente.
Algumas dicas para isso são:
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- Qualidade de vida - cuide do corpo e da mente; faça exercícios; melhore seus hábitos alimentares.
Refeições leves e frequentes, coma mais carne branca, principalmente peixe, as vermelhas menos
gordurosas, aumente alimentos com cálcio (leite e derivados, brócolis, sardinha). Evite fumar e ingerir
álcool.
Tratamento : Existem várias maneiras de tratar sendo a escolha individualmente feita.
Pode-se optar por repor os hormônios perdidos, podem ser usados produtos sintéticos e naturais e drogas
não hormonais.
Procure o seu ginecologista e ele saberá escolher o melhor para você!