alimentação e cálcio

8/8/2019 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.



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



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



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:



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.



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 ]



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 ]



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



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.)



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



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



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



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



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,



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.



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.



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



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.



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



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



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



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



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)



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



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



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



Interactions

None reported

Contraindications

Documented hypersensitivity; hypocalcemia

Precautions

Pregnancy



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.



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



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).



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:



- 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!

alimentação e cálcio

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