Regular physical activity helps improve your overall health and fitness, and reduces your risk for many chronic diseases.

Fitting regular exercise into your daily schedule may seem difficult at first, but the 2008 Physical Activity Guidelines for Americans are more flexible than ever, giving you the freedom to reach your physical activity goals through different types and amounts of activities each week. It’s easier than you think!

Children and adolescents should do 60 minutes (1 hour) or more of physical activity each day.

Choosing an Eating Plan to Prevent Weight Gain

So, how do you choose a healthful eating plan that will enable you to   maintain your current weight? The goal is to make a habit out of choosing   foods that are nutritious and healthful.

If your goal is to prevent weight gain, then you’ll want to choose foods   that supply you with the appropriate number of calories to maintain your   weight. This number varies from person to person. It depends on many   factors, including your height, weight, age, sex, and activity level.

Get Moving!

In addition to a healthy eating plan, an active lifestyle will help you   maintain your weight. By choosing to add more physical activity to your day,   you’ll increase the amount of calories your body burns. This makes it more   likely you’ll maintain your weight.
Although physical activity is an integral part of weight management, it’s   also a vital part of health in general. Regular physical activity can reduce   your risk for many chronic diseases and it can help keep your body healthy   and strong.

Self-monitoring

You may also find it helpful to weigh yourself on a regular basis. If you   see a few pounds creeping on, take the time to examine your lifestyle. With   these strategies, you make it more likely that you’ll catch small weight   gains more quickly.

Ask yourself—

• Has my activity level changed?
• Am I eating more than usual? You may find it helpful to keep a   food diary for a few days to make you more aware of your eating choices.

If you ask yourself these questions and find that you’ve decreased your   activity level or made some poor food choices, make a commitment to yourself   to get back on track. Set some reasonable goals to help you get more   physical activity and make better food choices.

It’s natural for anyone trying to lose weight to want to lose it very   quickly. But evidence shows that people who lose weight gradually and   steadily (about 1 to 2 pounds per week) are more successful at keeping   weight off. Healthy weight loss isn’t just about a “diet” or “program”. It’s   about an ongoing lifestyle that includes long-term changes in daily eating   and exercise habits.

To lose weight, you must use up more calories than you take in. Since one   pound equals 3,500 calories, you need to reduce your caloric intake by 500—1000 calories per day to lose about 1 to 2 pounds per week.¹

Once you’ve achieved a healthy weight, by relying on healthful eating and   physical activity most days of the week (about 60—90 minutes, moderate   intensity), you are more likely to be successful at keeping the weight off   over the long term.

Losing weight is not easy, and it takes commitment.

Even Modest Weight Loss Can Mean Big Benefits

The good news is that no matter what your weight loss goal is, even a   modest weight loss, such as 5 to 10 percent of your total body weight, is   likely to produce health benefits, such as improvements in blood pressure,   blood cholesterol, and blood sugars.²

For example, if you weigh 200 pounds, a 5 percent weight loss equals 10   pounds, bringing your weight down to 190 pounds. While this weight may still   be in the “overweight” or “obese” range, this modest weight loss can   decrease your risk factors for chronic diseases related to obesity.

So even if the overall goal seems large, see it as a journey rather than   just a final destination. You’ll learn new eating and physical activity   habits that will help you live a healthier lifestyle. These habits may help   you maintain your weight loss over time.

In addition to improving your health, maintaining a weight loss is likely   to improve your life in other ways. For example, a study of participants in the National Weight Control Registry  found that those who had maintained a significant weight loss reported   improvements in not only their physical health, but also their energy   levels, physical mobility, general mood, and self-confidence.

How can I tell if I’m at a healthy weight?

Adult Body Mass Index or BMI

One way to begin to determine whether  your weight is a healthy one is to calculate your “body mass index”  (BMI). For most people, BMI is a reliable indicator of body fatness. It is  calculated based on your height and weight.

Determine your BMI by finding your height and weight in this BMI Chart

• If your BMI is less than 18.5, it falls within the   “underweight” range.
• If your BMI is 18.5 to 24.9, it falls within the “normal” or   Healthy Weight range.
• If your BMI is 25.0 to 29.9, it falls within the “overweight”   range.
• If your BMI is 30.0 or higher, it falls within the “obese”   range.

“Underweight”, “normal”, “overweight”, and “obese” are all labels  for ranges of weight. Obese and overweight describe ranges of weight that are  greater than what is considered healthy for a given height, while underweight  describes a weight that is lower than what is considered healthy. If your BMI  falls outside of the “normal” or Healthy Weight range, you may want to talk to  your doctor or health care provider about how you might achieve a healthier  body weight. Obesity and overweight have been shown to increase the likelihood  of certain diseases and other health problems.

At an individual level, BMI can be used as a screening tool  but is not diagnostic of the body fatness or health of an individual. A trained  healthcare provider should perform appropriate health assessments in order to  evaluate an individual’s health status and risks.

Waist Circumference

Another way to assess your weight is to measure your waist size. Your   waistline may be telling you that you have a higher risk of developing   obesity-related conditions if you are:

• A man whose waist circumference is more than 40 inches
• A non-pregnant woman whose waist circumference is more than 35   inches

Excessive abdominal fat is serious because it places you at greater risk   for developing obesity-related conditions, such as Type 2 Diabetes, high   blood cholesterol, high triglycerides, high blood pressure, and coronary   artery disease. Individuals who have excessive abdominal fat should consult   with their physicians or other health care providers to develop a plan for   losing weight.

The key to achieving and maintaining a healthy weight isn’t about short-term dietary changes. It’s about a lifestyle that includes healthy eating, regular physical activity, and balancing the number of calories you consume with the number of calories your body uses.

Staying in control of your weight contributes to good health now and as you age.

I. Background

• This report is on systemic lupus erythematosus (for shorthand, SLE or   lupus), and not on 2 other   types of lupus: discoid lupus (skin only), and drug-induced lupus   (temporary). (1,2)
• Lupus is a prototypical autoimmune disease with a wide array of   clinical manifestations (rash, photosensitivity, oral ulcers,   arthritis, pleuritis, pericarditis, kidney problems, seizures and   psychosis, blood cell abnormalities). It is characterized by the   production of antibodies to components of the cell nucleus. (1,2)
• Primarily a disease of young women. (1,2)
• Occurs from infancy to old age, with peak occurrence between   ages 15 and 40. (1,2)
• Females are affected far more than males (6-10:1). (1,2)
• Blacks (and possibly Hispanics, Asians, and Native Americans)   are affected more than whites. (1,2)
• Although there is a strong familial aggregation, the disease is   relatively uncommon and most cases are sporadic. (1,2)
• May occur with other autoimmune conditions (e.g., thyroiditis,   hemolytic anemia, idiopathic thrombocytopenia purpura). (1,2)
• Diagnosis can be very difficult. The gold standard is a   rheumatologist’s diagnosis. Even so, there is
  • Underdiagnosis because the presenting symptoms and signs   are often not specific. (1,2)
  • Overdiagnosis because doctors mistakenly use a positive   blood test (present in 5% of the healthy population) by itself to make a   diagnosis. (1,2)
• Accelerated atherosclerosis among these patients is a newly   recognized phenomenon responsible for premature mortality. (1,2)
• Treatment consists primarily of immunosuppressive drugs (e.g.,   hydroxychloroquine [Plaquenil] and corticosteroids [prednisone]). (1,2) In 2011 the FDA approved the first new drug for lupus  in more than 50 years—belimumab [BENLYSTA®].
• Morbidity and mortality may be related to late diagnosis,   problems in access to care, less effective treatments, and poor   compliance with therapeutic regimens. (1,2)

II. Prevalence

• Prevalence estimates vary widely, and range as high as 1,500,000 (Lupus Foundation of America). (3) A   recent study estimated a 2005 prevalence of 161,000 with definite   SLE and 322,000 with definite or probable SLE. (8)
• Congress  has funded CDC to conduct two population-based SLE registries with the primary purpose of generating better prevalence (and incidence) estimates for Caucasians and African Americans. One is in Michigan (Washtenaw and Wayne Counties) and the other is in Georgia (DeKalb and Fulton  Counties).  New registries in California (San Francisco and San Mateo Counties) and New York City (Manhattan) are funded to generate similar estimates for Hispanics and Asians.        The Indian Health Service is developing similar estimates for American  Indians/Alaska Natives.

III. Incidence

• National incidence data are difficult to obtain because onset is   difficult to determine (non-specific symptoms and signs) and the   required, resource-intense studies are done in small areas. (2)
• Existing estimates range widely, from 1.8 to 7.6 cases per   100,000 persons per year in parts of the continental United States. (2)
• Incidence rates in whites in Rochester, Minnesota (Mayo Clinic’s   Rochester Epidemiology Project) tripled from 1.5/100,000 in the   1950–1979 cohort to 5.6/100,000 in 1980–1992 cohort. (4)

IV. Mortality

• From 1979 to 1998, the annual number of deaths with lupus as the   underlying cause increased from 879 to 1,406. Crude death rates   increased with age (35% were in 15-44 year age group), among women   (5x higher than in men), and among blacks (3x higher than in   whites). Death rates were highest and increased the most over time   among black women aged 45-64 years. (5)
• An equivalent number listed lupus as a contributing cause   of death. (5)
• Causes of death are mainly active disease, organ failure (e.g.,   kidneys), infection, or cardiovascular disease from accelerated   atherosclerosis. (5)
• Among rheumatic conditions, lupus has a relatively high   mortality (14.5% of all rheumatic disease mortality in 1997). (5)
• At the same time, survival has been improving, suggesting that   more or milder cases are being recognized. (5)

References

1. Pisetsky DS, Buyon JP, Manzi S. Chapter 17. Systemic lupus   erythematosus. In: Klippel JH, Crofford LJ, Stone JH, Weyand CM.   Primer on the Rheumatic Diseases. Edition 12. Arthritis   Foundation, Atlanta, GA., 2001.
2. Rus V, Hajeer A, Hochberg MC. Chapter 7. Systemic lupus   erythematosus. In: Silman AJ, Hochberg MC (eds.) Epidemiology of the   Rheumatic Disease. 2nd edition. Oxford University Press, New   York, 2001.
3. Lawrence RC, Felson DT, Helmick CG, Arnold LM, Choi H, Deyo RA,   Gabriel S, Hirsch R, Hochberg MC, Hunder GG, Jordan JM, Katz JN,   Maradit Kremers H, and Wolfe F for the National Arthritis Data   Workgroup. Estimates of the prevalence of arthritis and other   rheumatic conditions in the United States: Part II. Arthritis Rheum   2008;58(1):26–35.
4. Uramoto KM, Michet CJ Jr, Thumboo J, Sunku J, O’Fallon WM,   Gabriel SE. Trends in the incidence and mortality of systemic lupus   erythematosus, 1950–1992. Arthritis Rheum 1999;42(1):46-50.
5. Sacks JJ, Helmick CG, Langmaid G, Sniezek JE. Trends in deaths   from systemic lupus erythematosus—United States, 1979–1998. MMWR 2002;51(17):371–374.
6. Lethbridge-Cejku M, Helmick CG, Popovic JR. Hospitalizations for   systemic lupus erythematosus in the United States: 1988–2000 (unpublished).
7. United States Bone and Joint Decade:  The  Burden of Musculoskeletal Diseases in the United States.  Rosemont, IL:  American Academy of Orthopaedic Surgeons;  2008.  Chapter 4.  Arthritis and Related Conditions.
8. Helmick CG, Felson DT, Lawrence RC, Gabriel S, Hirsch R, , Kwoh CK,   Liang MH, Maradit Kremers H, Mayes MD, Merkel PA, Pillemer SR, Reveille   JD, and Stone JH for the National Arthritis Data Workgroup. Estimates of   the prevalence of arthritis and other rheumatic conditions in the United   States: Part I. Arthritis Rheum 2008;58(1):15–25.
9. Sacks JJ, Luo Y-H, Helmick CG.  Prevalence of specific types of arthritis and  other rheumatic conditions in the ambulatory health care system in the United  States, 2001-2005.  Arthritis Care &  Research 2010;62(4):460-464.

I. Background

• Rheumatoid  arthritis (RA), an autoimmune condition, is a chronic inflammatory  polyarthritis (arthritis that affects 5 or more joints)(2).

• The natural  history of RA varies considerably with at least three possible disease courses (3-5):
  1. Monocyclic: Have one episode which ends within 2-5 years  of initial diagnosis and did not reoccur. This may result from early diagnosis  and/or aggressive treatment.
  2. Polycyclic: The levels of disease activity fluctuate over  the course of the condition
  3. Progressive: RA continues to increase in severity and is  unremitting
• Radiographic erosion is typically fastest in  the first year of disease (4).
• One natural history study found that 75% of  people with RA experienced remission within five years of diagnosis (5)

II. Diagnosis of RA

• Ideally, RA is diagnosed early — within 6  months of symptom onset — so that treatment can begin as soon as possible to  slow or halt disease progression.  Early  diagnosis is challenging because the symptoms of early RA can be non-specific (e.g.,  malaise, fatigue, weakness, muscle soreness, low-grade fever, weight loss) and  may actually be symptoms of other conditions (6).
• RA is diagnosed clinically, but classified  according to the 2010 American College of Rheumatology (ACR) and European  League Against Rheumatism (EULAR) classification criteria for rheumatoid  arthritis(7, 8).
• Prior to the 2010 criteria, the 1987 ACR criteria were the standard for  diagnosis and study of RA (http://www.rheumatology.org/practice/clinical/classification/ra/ra.asp)  (9). Comparison of the 2010 and 1987 criteria  indicate that the 2010 criteria are better at identifying people with early RA (7, 8).

III. Treatment

• Historically, treatment for most people started  with corticosteroids/non-steroidal anti-inflammatory drugs (NSAIDs), then slowly  progressed for fewer people to non-biologic disease-modifying antirheumatic  drugs (DMARDs) and finally progressed for even fewer people to biologic DMARDs if  people had not responded to the previous drugs.
• Today, a much more aggressive treatment  approach is advocated for people with RA, with prescription of non-biologic DMARDs  within three months of diagnosis to reduce disease activity and prevent joint  deformity. (10)
• Treatment guidelines have also changed with  the increasing array of biologic DMARDs available; in 2008, the American  College of Rheumatology updated RA medical management guidelines  (11).  These  guidelines describe which biologic DMARDs are indicated for specific RA disease  profiles (e.g., features such as diease activity, signs and symptoms, and  prognosis)
• The 2008 guidelines also recommend that treatment with nonbiologic and  biologic therapies should be acocmpanyied by non-medical interventsions  including physical and occupational therapy and anti-inflammatory pharmacologic  itnerventions (e.g., treatment with NSAIDs, intraarticular and oral  glucocorticoids) (11).

IV. Risk Factors

The etiology, or cause, of RA is unknown. Many cases are believed to result  from an interaction between genetic factors and environmental exposures.

Socio-demographics: The incidence of  RA is typically two to three times higher in women than men. The onset of RA,  in both women and men, is highest among those in their sixties(2)
Genetics: There is  longstanding evidence that specific HLA class II genotypes are associated with  increase risk.  Most attention has been  given to the DR4 and DRB1 molecules of the major histocompatability complex HLA  class II genes. The strongest associations have been found between RA and the  DRB1*0401 and DRB1*0404 alleles (12).  More  recent investigations indicate that of the more than 30 genes studied, the  strongest candidate gene is PTPN22, a  gene that has been linked to several autoimmune conditions(12).

Modifiable: Several  modifiable risk factors have been studied in association with RA including reproductive  hormonal exposures, tobacco use, dietary factors, and microbial exposures.

Smoking       Among these risk factors,  the strongest and most consistent evidence is for an association between smoking and RA.  A history of smoking is associated with a  modest to moderate (1.3 to 2.4 times) increased risk of RA onset (2). This relationship between smoking and RA is  strongest among people who are ACPA-positive (anti-citrullinated  protein/peptide antibodies), a marker of auto-immune activity (12).

Reproductive and  breastfeeding history       Hormones related to reproduction have been  studied extensively as potential risk factors for RA:

1. Oral  contraceptives (OC): Early studies found  that women who had ever used OCs had a modest to moderate decrease in risk of  RA (13, 14). The decreased risk has not confirmed in  recent studies (13, 15, 16).  The  estrogen concentration of contemporary OCs is typically 80-90% less than the  first OCs introduced in the 1960s (15), which may account for the lack of  association in recent studies (15).
2. Hormone  replacement therapy (HRT): There is mixed evidence of an association  between HRT and RA onset (15-19)
3. Live birth  history: Most studies have found that women who have  never had a live birth have a slight to moderately increased risk of RA (20-23).
4. Breastfeeding: Recent population based studies have found that RA is less common among  women who breastfeed (16, 24-26).
5. Menstrual history: At least two studies have observed that women  with irregular menses or a truncated menstrual history (e.g., early menopause)  have an increased risk of RA (16, 20). Because women with  polycystic ovarian syndrome (PCOS) have an icnreased risk of RA, the association  with an abberant menstrual history may result from PCOS (20).

V. Prevalence

• The prevalence of RA is believed to range  from 0.5-1.0% in the general population (2).  In  2005, an estimated 1.5 million US adults aged ≥ 18 (0.6%) had RA (27), a decrease from the previous 1990 estimate  of 2.1 million (28). Prevalence estimates derived from 2001-2005  US ambulatory health care system data estimated that 1.5 million US adults have  RA (29)
• In 1995 in the Rochester Epidemiology Project (Minnesota), the age-adjusted  prevalence of RA among women was 7.7 per 1000 compared with 4.4 per 1000 among  men).   By 2005, the prevalence among  women had increased (9.8 per 1000) but prevalence among men (4.1 per 1000) (30).

VI. Incidence

• The most recent US  data on the incidence of RA is from the Rochester Epidemiology Project, a study  that has provided the majority of population-based descriptive statistics on RA.  In 1995-2007, 41 per 100,000 people were  diagnosed with RA each year. Incidence rose with age (e.g., 8.7 per 100,000  people among those aged 18-34 compared with 54 per 100,000 among those aged ≥  85 years); incidence peaked among people aged   65-74 years (89 per 100,000) (all estimates age-adjusted to 2000 US  population). From 1995 to 2007, rates increased by 2.5% each year among women  but there was a small decrease (0.5%) among men (30).

• Longitudinal study  of RA incidence rates in the Rochester Epidemiology Project indicates that  incidence among women and men was highest at the beginning of the project in  1955 but declined to its lowest in the late 1980s/early 1990s.
• At least one study have found incidence to be the same regardless of the  definition (i.e., 1958 American Rheumatology Association, and 1987 American  College of Rheumatology definitions) (31).

VII. Lifetime risk

• The lifetime risk of rheumatoid arthritis in the Rochester Minnesota Mayo Clinic Population was estimated 4% among women and 3% among men (32).

VIII. Mortality and comorbidities

• In 1997, RA  accounted for 22% of all deaths due to arthritis and other rheumatic conditions  (33)
• Mortality has been  found to be increased among people with diagnosed RA in multiple studies.  Over the past half century, many studies have  found mortality to be increased in patients with established RA in comparison  with the general population (34)  Around 40% of all deaths in individuals with  RA are attributable to cardiovascular causes, including ischemic heart disease  and stroke. The most recent North American study of mortality among people with  RA, based on data from 1965–1990, found a standardized mortality ratio of 2.3  among people with RA compared to the general population (35), that is, people with RA are more than twice  as likely to die than people of the same age in the general population.
• Among people with RA, the presence of rheumatoid  factor (RF) and/or anti-citrullinated protein antibody (ACPA) are  potential markers of premature mortality (34).

IX. Co-morbidities

The four most common comorbidiities among  people with arthritis, in order of prevalence are the following:

• Cardiovascular disease (CVD), in partcular ischemic heart disease, is  more common among people with RA (34).  It  is unclear whether the risk of CVD precedes the disease onset or results from  the condition; a Rochester Epidemiology Project study found that people with RA  were more likely to have a hospitalizations because of myocardial infarction  prior to diagnosis  (34). However, two longitudinal cohort studies  have found no difference in presence of MI, congestive heart failure or angina  prior to diagnosis of RA (34).  People  with RA have greater evidence of subclinical atherosclerotic disease  (36), and risk of silent MI (37).
  It is unknown whether the increase in CVD  mortality is due to the disease, the risk factor profile of people with RA  (e.g., presence of hypertension, more likely to be smokers), or the effects of  the drugs used to treat the condition (36, 38).

• Infections, most commonly tuberculosis, are another  important and primary cause of death among people with RA may be responsible  for one-quarter of deaths among people with RA (37). It is unclear whether this increased  susceptibility arising from immunosuppression is due to the intrinsic immune  dysfunction in people with RA, the effects of the drugs used to treat it, or  both (36, 38).
• Mental health conditions: The high prevalence of anxiety and depression  has been documented in several clinical populations of people with RA. Both  conditions are associated with increased disease activity and decreased physical  function and adherence to medical and non-medical interventions (39-42).
• Malignancies: An increased incidence of  lymphoproliferative malignancies (such as leukemia and multiple myeloma) has  also been reported among people with RA. The cause of this increase is unknown (38).

References

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2. Silman AJ, Hochberg MC. Epidemiology of the Rheumatic Diseases. 2nd ed. New York: Oxford University Press; 2001.
3. Pincus T, Callahan LF. What is the natural history of rheumatoid arthritis? Rheum Dis Clin North Am. 1993 Feb;19(1):123-51.
4. Graudal NA, Jurik AG, de Carvalho A, Graudal HK. Radiographic progression in rheumatoid arthritis: a long-term prospective study of 109 patients. Arthritis and rheumatism. 1998 Aug;41(8):1470-80.
5. Masi AT, Maldonado-Cocco JA, Kaplan SB, Feigenbaum SL, Chandler RW. Prospective study of the early course of rheumatoid arthritis in young adults: comparison of patients with and without rheumatoid factor positivity at entry and identification of variables correlating with outcome. Semin Arthritis Rheum. 1976 May;4(4):299-326.
6. Chan KW, Felson DT, Yood RA, Walker AM. The lag time between onset of symptoms and diagnosis of rheumatoid arthritis. Arthritis and rheumatism. 1994 Jun;37(6):814-20.
7. Aletaha D, Neogi T, Silman AJ, Funovits J, Felson DT, Bingham CO, 3rd, et al. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis and rheumatism. 2010 Sep;62(9):2569-81.
8. Neogi T, Aletaha D, Silman AJ, Naden RL, Felson DT, Aggarwal R, et al. The 2010 American College of Rheumatology/European League Against Rheumatism classification criteria for rheumatoid arthritis: Phase 2 methodological report. Arthritis and rheumatism. 2010 Sep;62(9):2582-91.
9. Arnett FC, Edworthy SM, Bloch DA, McShane DJ, Fries JF, Cooper NS, et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis and rheumatism. 1988 Mar;31(3):315-24.
10. American College of Rheumatology. Guidelines for the management of rheumatoid arthritis: 2002 Update. Arthritis and rheumatism. 2002 Feb;46(2):328-46.
11. Saag KG, Teng GG, Patkar NM, Anuntiyo J, Finney C, Curtis JR, et al. American College of Rheumatology 2008 recommendations for the use of nonbiologic and biologic disease-modifying antirheumatic drugs in rheumatoid arthritis. Arthritis and rheumatism. 2008 Jun 15;59(6):762-84.
12. Scott DL, Wolfe F, Huizinga TW. Rheumatoid arthritis. Lancet. 2010 Sep 25;376(9746):1094-108.
13. Brennan P, Bankhead C, Silman A, Symmons D. Oral contraceptives and rheumatoid arthritis: results from a primary care-based incident case-control study. Semin Arthritis Rheum. 1997 Jun;26(6):817-23.
14. Esdaile JM. Exogenous female hormones and rheumatoid arthritis: a methodological view of the contradictions in the literature. British journal of rheumatology. 1989;28 Suppl 1:4-10; discussion 8-23.
15. Doran MF, Crowson CS, O’Fallon WM, Gabriel SE. The effect of oral contraceptives and estrogen replacement therapy on the risk of rheumatoid arthritis: a population based study. J Rheumatol. 2004 Feb;31(2):207-13.
16. Karlson EW, Mandl LA, Hankinson SE, Grodstein F. Do breast-feeding and other reproductive factors influence future risk of rheumatoid arthritis? Results from the Nurses’ Health Study. Arthritis and rheumatism. 2004 Nov;50(11):3458-67.
17. Carette S, Marcoux S, Gingras S. Postmenopausal hormones and the incidence of rheumatoid arthritis. JRheumatol. 1989 07;16(7):911-3.
18. Koepsell TD, Dugowson CE, Nelson JL, Voigt LF, Daling JR. Non-contraceptive hormones and the risk of rheumatoid arthritis in menopausal women. IntJEpidemiol. 1994 12;23(6):1248-55.
19. Merlino LA, Cerhan JR, Criswell LA, Mikuls TR, Saag KG. Estrogen and other female reproductive risk factors are not strongly associated with the development of rheumatoid arthritis in elderly women. SeminArthritis Rheum. 2003 10;33(2):72-82.
20. Merlino LA, Cerhan JR, Criswell LA, Mikuls TR, Saag KG. Estrogen and other female reproductive risk factors are not strongly associated with the development of rheumatoid arthritis in elderly women. Semin Arthritis Rheum. 2003 Oct;33(2):72-82.
21. Pope JE, Bellamy N, Stevens A. The lack of associations between rheumatoid arthritis and both nulliparity and infertility. SeminArthritis Rheum. 1999 04;28(5):342-50.
22. Spector TD, Roman E, Silman AJ. The pill, parity, and rheumatoid arthritis. Arthritis Rheum. 1990 06;33(6):782-9.
23. Karlson EW, Mandl LA, Hankinson SE, Grodstein F. Do breast-feeding and other reproductive factors influence future risk of rheumatoid arthritis? Results from the Nurses’ Health Study. Arthritis Rheum. 2004 11;50(11):3458-67.
24. Brennan P, Silman A. Breast-feeding and the onset of rheumatoid arthritis. Arthritis Rheum. 1994 06;37(6):808-13.
25. Jorgensen C, Picot MC, Bologna C, Sany J. Oral contraception, parity, breast feeding, and severity of rheumatoid arthritis. AnnRheumDis. 1996 02;55(2):94-8.
26. Pikwer M, Bergstrom U, Nilsson JA, Jacobsson L, Berglund G, Turesson C. Breast feeding, but not use of oral contraceptives, is associated with a reduced risk of rheumatoid arthritis. Annals of the rheumatic diseases. 2009 Apr;68(4):526-30.
27. Helmick CG, Felson DT, Lawrence RC, Gabriel S, Hirsch R, Kwoh CK, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part I. Arthritis Rheum. 2008 Jan;58(1):15-25.
28. Lawrence RC, Helmick CG, Arnett FC, Deyo RA, Felson DT, Giannini EH, et al. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arthritis Rheum. 1998 May;41(5):778-99.
29. Sacks JJ, Luo YH, Helmick CG. Prevalence of specific types of arthritis and other rheumatic conditions in the ambulatory health care system in the United States, 2001-2005. Arthritis Care Res (Hoboken). 2010 Apr;62(4):460-4.
30. Myasoedova E, Crowson CS, Kremers HM, Therneau TM, Gabriel SE. Is the incidence of rheumatoid arthritis rising?: results from Olmsted County, Minnesota, 1955-2007. Arthritis and rheumatism. 2010 Jun;62(6):1576-82.
31. Dugowson CE, Koepsell TD, Voigt LF, Bley L, Nelson JL, Daling JR. Rheumatoid arthritis in women. Incidence rates in group health cooperative, Seattle, Washington, 1987-1989. Arthritis Rheum. 1991;34(12):1502-7.
32. Crowson CS, Matteson EL, Myasoedova E, Michet CJ, Ernste FC, Warrington KJ, et al. The lifetime risk of adult-onset rheumatoid arthritis and other inflammatory autoimmune rheumatic diseases. Arthritis Rheum. 2011 Mar;63(3):633-9.
33. Sacks JJ, Helmick CG, Langmaid G. Deaths from arthritis and other rheumatic conditions, United States, 1979-1998. J Rheumatol. 2004 Sep;31(9):1823-8.
34. ymmons DP, Gabriel SE. Epidemiology of CVD in rheumatic disease, with a focus on RA and SLE. Nat Rev Rheumatol. 2011;7(7):399-408.
35. Wolfe F, Mitchell DM, Sibley JT, Fries JF, Bloch DA, Williams CA, et al. The mortality of rheumatoid arthritis. Arthritis Rheum. 1994;37(4):481-94.
36. Wasko MC. Comorbid conditions in patients with rheumatic diseases: an update. CurrOpinRheumatol. 2004;16(2):109-13.
37. Boonen A, Severens JL. The burden of illness of rheumatoid arthritis. Clin Rheumatol. 2011 Mar;30 Suppl 1:S3-8.
38. Mikuls TR, Saag KG. Comorbidity in rheumatoid arthritis. RheumDisClinNorth Am. 2001;27(2):283-303.
39. Dickens C, McGowan L, Clark-Carter D, Creed F. Depression in rheumatoid arthritis: a systematic review of the literature with meta-analysis. Psychosom Med. 2002 Jan-Feb;64(1):52-60.
40. Minor MA, Brown JD. Exercise maintenance of persons with arthritis after participation in a class experience. Health education quarterly. 1993 Spring;20(1):83-95.
41. Odegard S, Finset A, Mowinckel P, Kvien TK, Uhlig T. Pain and psychological health status over a 10-year period in patients with recent onset rheumatoid arthritis. Ann Rheum Dis. 2007 Sep;66(9):1195-201.
42. Soderlin MK, Hakala M, Nieminen P. Anxiety and depression in a community-based rheumatoid arthritis population. Scandinavian journal of rheumatology. 2000;29(3):177-83.
43. Agency for Healthcare Quality and Research. HCUPnet. National and regional estimates on hospital use for all patients from the HCUP Nationwide Inpatient Sample (NIS). National statistics – principal procedure only. ICD-9-CM 714.0-714.9. 2011 [cited 2011 May 2011]; Available from: http://hcupnet.ahrq.gov/HCUPnet.jsp .
44. Schappert SM, Rechtsteiner EA. Ambulatory medical care utilization estimates for 2007. Vital Health Stat 13. 2011 Apr(169):1-38.
45. Hootman JM, Helmick CG, Schappert SM. Magnitude and characteristics of arthritis and other rheumatic conditions on ambulatory medical care visits, United States, 1997. Arthritis and rheumatism. 2002 Dec 15;47(6):571-81.
46. Gabriel SE, Crowson CS, Campion ME, O’Fallon WM. Direct medical costs unique to people with arthritis. JRheumatol. 1997;24(4):719-25.
47. Gabriel SE, Crowson CS, Campion ME, O’Fallon WM. Indirect and nonmedical costs among people with rheumatoid arthritis and osteoarthritis compared with nonarthritic controls. JRheumatol. 1997;24(1):43-8.
48. Maetzel A, Li LC, Pencharz J, Tomlinson G, Bombardier C. The economic burden associated with osteoarthritis, rheumatoid arthritis, and hypertension: a comparative study. AnnRheumDis. 2004;63(4):395-401.
49. Gabriel SE, Crowson CS, Luthra HS, Wagner JL, O’Fallon WM. Modeling the lifetime costs of rheumatoid arthritis. JRheumatol. 1999;26(6):1269-74.
50. Dominick KL, Ahern FM, Gold CH, Heller DA. Health-related quality of life among older adults with arthritis. Health QualLife Outcomes. 2004;2(1):5.
51. Yelin E, Lubeck D, Holman H, Epstein W. The impact of rheumatoid arthritis and osteoarthritis: the activities of patients with rheumatoid arthritis and osteoarthritis compared to controls. JRheumatol. 1987;14(4):710-7.
52. Yelin E, Henke C, Epstein W. The work dynamics of the person with rheumatoid arthritis. Arthritis Rheum. 1987;30(5):507-12.
53. Michaud CM, McKenna MT, Begg S, Tomijima N, Majmudar M, Bulzacchelli MT, et al. The burden of disease and injury in the United States 1996. Popul Health Metr. 2006;4:11.

I. Background

• Also known as degenerative joint disease.
• Most common form of arthritis.
• Classified as: Idiopathic (localized or generalized) or   Secondary (traumatic, congenital, metabolic/endocrine/neuropathic   and other medical causes).
• Characterized by focal and progressive loss of the hyaline   cartilage of joints, underlying bony changes.
• Usually defined by symptoms, pathology or combination (1)
  • Pathology = radiographic changes (joint space narrowing,   osteophytes and bony sclerosis)
  • Symptoms = pain, swelling, stiffness
  • The American College of Rheumatoloty (ACR) has published clinical classification guidelines for OA of the hand, knee, and hip.

II. Prevalence

• Overall OA affects 13.9% of adults aged 25 and older and 33.6%   (12.4 million) of those 65+; an estimated 26.9 million   US adults in 2005 up from 21 million in 1990 (believed to be   conservative estimate) (2)
• Radiographic OA (moderate to severe)—prevalence per 100 (knee and hip may be   underestimated)
  • Hand = 7.3 (9.5 female; 4.8 male) (5)
  • Feet = 2.3 (2.7 female; 1.5 male) (2)
  • Knee = 0.9 (1.2 female; 0.4 male) (3)
  • Hip = 1.5 (1.4 female; 1.4 male) (2)
• Symptomatic OA—prevalence per 100
  • Hand = 8% (8.9% female; 6.7% male) 2.9 million adults aged   60+ years (5)
  • Feet = 2.0% (3.6 female; 1.6 male) aged 15–74 years (2)
  • Knee = 12.1% (13.6% female; 10.0% male) 4.3 million adults   aged 60+ years (3)
  • Knee = 16% (18.7% female; 13.5% male) adults aged 45+ years (4)
  • Data from Framingham OA Study reports similar rates:
    • Knee = 6.1% all adults > age 30 (6)
    • Knee = 9.5% (11.4 female; 6.8 male) ages 63-93 (6)
  • Hip = 4.4% (3.6% female; 5.5% male) adults ≥55 years of age (2)

III. Incidence

• Age and sex-standardized incidence rates of symptomatic OA:
  • Hand OA = 100 per 100,000 person years (7)
  • Hip OA = 88 per 100,000 person years (7)
  • Knee OA = 240 per 100,000 person years (7)
  • Among women:
    • Incident radiographic knee OA 2% per year (8)
    • Incident symptomatic knee OA 1% per year (8)
    • Progressive knee OA 4% per year (8)
• Incidence rates increased with age, and level off around age 80. (9)
• Women had higher rates than men, especially after age 50. (9)
  • Men have 45% lower incident risk of knee OA and 36% reduced   risk of hip OA than women. (10)
  • Prevalent knee OA, but not hip or hand OA, is significantly   more severe in women compared to men. (10)

References

1. American Academy of Orthopaedic Surgeons.
2. Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the   prevalence of arthritis and other rheumatic conditions in   the United States. Part II. Arthritis Rheum 2008;58(1):26–35.
3. Dillon CF, Rasch EK, Gu Q, Hirsch R. Prevalence of knee   osteoarthritis in the United States: arthritis data from the Third   National Health and Nutrition Examination Survey 1991–1994. J   Rheumatol, 2006;33(11):2271–2279.
4. Jordan JM, Helmick CG, Renner JB, et al. Prevalence of knee   symptoms and radiographic and symptomatic knee osteoarthritis in   African Americans and Caucasians: The Johnston County Osteoarthritis   Project. J Rheumatol, 2007;34(1):172–180.
5. Dillon CF, Hirsch R, Rasch EK, Gu Q. Symptomatic hand   osteoarthritis in the United States: prevalence and functional   impairment estimates from the third U.S. National Health and   Nutrition Examination Survey, 1991–1994. Am J Phys Med Rehabil,   2007;86(1):12–21.
6. Felson DT, Naimark A, Anderson J, Kazis L, Castelli W, Meenan   RF.The prevalence of knee osteoarthritis in the elderly. The   Framingham Osteoarthritis Study. Arthritis Rheum.   1987;30(8):914–918.
7. Oliveria SA, Felson DT, Reed JI et al. Incidence of symptomatic   hand, hip, and knee osteoarthritis among patients in a health   maintenance organization. Arthritis Rheum 1995;38(8):1134–1141.
8. Felson DT, Zhang Y, Hannan MT, et al. The incidence and natural   history of knee osteoarthritis in the elderly. The Framingham   Osteoarthritis Study. Arthritis Rheum 1995;38(10):1500–1505.
9. Buckwalter JA, Saltzman C, Brown T. The impact of   osteoarthritis. Clin Orthoped Rel Res 2004:427S: S6–S15.
10. Srikanth VK, Fryer JL, Zhai G, Winzenberg TM, Hosmer D, Jones G.   A meta-analysis of sex difference prevalence, incidence and severity   of osteoarthritis. Osteoarthritis Cartilage 2005;13:769–781.
11. Sacks JJ, Helmick CG, Langmaid G. Deaths from arthritis and   other rheumatic conditions, United States, 1979–1998. J Rheumatol 2004;31:1823–1828.
12. Lethbridge-Cejku M, Helmick CG, Popovic JR. Hospitalizations for   arthritis and other rheumatic conditions: Data from the 1976   National Hospital Discharge Survey. Medi Care 2003;41(12):1367–1373.
13. Mehrotra C, Remington PL, Naimi TS, Washington W, Miller R.   Trends in total knee replacement surgeries and implications for   public health, 1990–2000. Public Health Rep 2005;120(3):278–282.
14. Mahomed NN, Barrett J, Katz JN Baron JA, Wright J, Losina E.   Epidemiology of total knee replacements in the United States   Medicare population. J Bone Joint Surg Am 2005;87(6):1222–1228.
15. Hootman JM, Helmick CG, Schappert S. Magnitude and   characteristics of arthritis and other rheumatic conditions on   ambulatory medical care visits, United States, 1997. Arthritis   Care Res 2002;47(6):571–581.
16. Hagglund KJ, Clark MJ, Hilton SA, Hewett JE. Access to   healthcare services among persons with osteoarthritis and rheumatoid   arthritis. Am J Phys Med Rehabil 2005;84(9):702–711.
17. Gabriel SE, Crowson CS, Campion ME et al. Direct medical costs   unique to people with arthritis. J Rheumatol 1997;24(4):719–725.
18. Maetzel A, Li LC, Pencharz J, Tomlinson F Bombardier C. The   economic burden associated with osteoarthritis, rheumatoid   arthritis, and hypertension : a comparative study. Ann Rheum Dis 2004;63(4):395–401.
19. Guccione AA, Felson DT, Anderson JJ, et al. The effects of   specific medical conditions on the functional limitations of elders   in the Framingham Study. Am J Pub Health 1994;84(3):351–358.
20. Michaud CM, McKenna MT, Begg S, Tomijima N, Majmudar M,   Bulzacchelli MT, Ebrahim S, Ezzati M, Salomon JA, Gaber Kreiser J,   Hogan M, Murray CJ. The burden of disease and injury in the United   States 1996. Popul Health Metr 2006;4:11. Available at   http://www.pophealthmetrics.com/content/4/1/11 (Accessed July, 19,   2007).
21. Felson DT, Zhang Y. An update on the epidemiology of knee and   hip osteoarthritis with a view to prevention. Arthritis Rheum 1998;41(8):1343–1355.
22. Felson DT. Risk factors for osteoarthritis. Clin Orthoped Rel   Res 2004;427S:S16–S21.
23. Rossignol M, Leclerc A, Allaert FA, et al. Primary   osteoarthritis of hip, knee and hand in relation to occupational   exposure. Occup Environ Med 2005;62:772–777.

Gout is a rheumatic disease resulting from deposition of uric acid crystals   (monosodium urate) in tissues and fluids within the body. This process is caused   by an overproduction or under excretion of uric acid. Certain common   medications, alcohol, and dietary foods are known to be contributory factors.   Acute gout will typically manifest itself as an acutely red, hot, and swollen   joint with excruciating pain. These acute gouty flare-ups respond well to   treatment with oral anti-inflammatory medicines and may be prevented with   medication and diet changes. Recurrent bouts of acute gout can lead to a   degenerative form of chronic arthritis called gouty arthritis.

I. Background

• Gout is an ancient and common form of inflammatory arthritis,   and is the most common inflammatory arthritis among men. Gout may   remit for long periods, followed by flares for days to   weeks, or can become chronic.
• Gout is caused by an uncontrolled metabolic   disorder, hyperuricemia, which leads to the deposition of monosodium   urate crystals in tissue. Hyperuricemia means too much uric acid in   the blood. Uric acid is a metabolic product resulting from the   metabolism of purines (found in many foods and in human tissue).  (1,   2)
• Hyperuricemia is caused by an imbalance in the production and   excretion of urate, i.e., overproduction, underexcretion   or both. Underexcretion is the most common cause, thought to account   for 80–90% of hyperuricemia. (3)
• Hyperuricemia is not the same as gout. Asymptomatic   hyperuricemia does not need to be treated.
• Risk factors for gout include being overweight or obese, having   hypertension, alcohol intake (beer and spirits more than wine),   diuretic use, and a diet rich in meat and seafood. (4,5,6)
• Weight loss lowers the risk for gout. (5,6)
• Gout can be viewed in four stages:
  • Asymptomatic tissue deposition occurs when people have no overt   symptoms of gout, but do have hyperuricemia and the asymptomatic   deposition of crystals in tissues. The deposition of crystals,   however, is causing damage.
  • Acute flares occur when urate crystals in the joint(s) cause acute   inflammation. A flare is characterized by pain, redness,   swelling, and warmth lasting days to weeks. Pain may be mild or   excruciating. Most initial attacks occur in lower extremities.   The typical presentation in the metatarsophalageal joint of the   great toe (podagra) is the presenting joint for 50% of people   with gout. About 80% of people with gout do have podagra at some   point. Uric acid levels may be normal in about half of patients   with an acute flare. Gout may present differently in the elderly,   with many joints affected.
  • Intercritical segments occur after an acute flare has subsided,   and a   person may enter a stage with clinically inactive disease before   the next flare. The person with gout continues to have hyperuricemia, which results in continued deposition of urate   crystals in tissues and resulting damage. Intercritical segments   become shorter as the disease progresses.
  • Chronic gout is characterized by chronic   arthritis, with soreness and aching of joints. People with gout   may also get tophi (lumps of urate crystals deposited in soft   tissue)—usually in cooler areas of the body (e.g., elbows, ears,   distal finger joints). (7,8)
• Gout is also associated with an increased risk of kidney stones. (9,10)
• The gold standard for diagnosing gout is aspiration and microscopic   analysis for urate crystals in joint fluid or a tophus. Urate   crystals are negatively birefringent under polarized light.   Infection must be ruled out. (7,11)
• The goals of treatment are to end the pain of acute   flares, and to prevent future attacks and the formation of tophi and kidney   stones. Therapy for acute flares consists of nonsteroidal   anti-inflammatory drugs, steroids, and colchicine.   Diet and lifestyle (weight loss, avoiding alcohol, reducing dietary purine intake) modifications may help prevent future attacks.   Changing medications (e.g., stopping diuretics) associated with hyperuricemia may also help.   Preventive therapy to lower blood uric acid levels in persons with recurrent acute flares or chronic gout   usually involves allopurinol or a new drug (febuxostat).

II. Prevalence

• A study of gout and kidney stones among male health   professionals showed that 5% of the 49,717 providing information   reported gout at baseline. [Data source: Health Professionals’   Follow-up Study; gout: self reported physician diagnosed. (10)]
• One study in a managed care population showed an increase in   prevalence of gout from 2.9 to 5.2 per 1000 enrollees in the time   period 1990 to 1999. For those under age 65, rates among men were 4   times those of women; over age 65 rates among men were 3 times   greater. Most of the increase occurred among enrollees over the age   of 65: among those over age 75, the prevalence increased (1990 to   1999) from 21 to 41 per 1000 enrollees. Among those 65 to 74,   prevalence increased from 21 to 31 per 100 enrollees. [Gout was   defined by ICD-9-CM codes 274xx or use of uric acid lowering drugs. (12)]
• One-year period prevalence estimates (“Have you or any member of   your household had gout within the past year?”) derived from the   NHIS were 0.94% for those 18 and older in 1996, thereby affecting   about 3.0 million adults in 2005. (18)
• Lifetime prevalence estimates (“Has a doctor ever told you that   you had gout?”) from NHANES III (1988-1994) were 2.6% overall for   those aged ≥20 years with a low of 400/100,000 in adults aged 20-29   years and a peak of 8,000/100,000 in adults aged 70-79 years, thereby affecting about 6.1 million adults in   2005. Gout was reported more often in men than in women overall, but   prevalence increased with age for both, especially for women after   menopause. (17)
• Both the above are likely overestimates because they are based   on self-reported data, but nationally gout appears to be increasing   in frequency, with one-year prevalence estimates up from 0.85% in   1998. (17)

References

1. Terkeltaub RA.Gout A. Epidemiology, pathology, and pathogenesis.   (Chapter 15) in Primer on the Rheumatic Diseases, 12th edition.   Klippel J (ed). 2001 Arthritis Foundation, Atlanta GA 30309.
2. Schumacher HR. Hyperuricemia and gout: a prevalent and chronic   disease. JointandBone.org. January 2005. accessed at info@JointandBone.org   July 27, 2005
3. Edward NL. Treating hyperuricemia in gout: a review of goals and   therapies. JointandBone.org. July 2005. accessed at info@JointandBone.org   July 27, 2005
4. Choi HK, Atkinson K, Karlson EW, Curhan G. Obesity, weight   change, hypertension, diuretic use, and risk of gout in men. Arch   Intern Med 2005;165: 742–748.
5. Choi HK, Atkinson K, Karlson EW, Willet W, Curhan G. Alcohol   intake and risk of incident gout in men: a prospective study. Lancet 2004;363:1277–12781.
6. Choi HK, Atkinson K, Karlson EW, Willet W, Curhan G. Purine-rich   foods, dairy and protein intake, and the risk of gout in men. N Engl J Med 2004;350:1093–1103.
7. Weaver AL. Diagnosing Gout. JointandBone.org. May 2005. accessed   at info@JointandBone.org July 27, 2005
8. Bieber JD, Terkeltaub RA. Gout. On the brink of novel   therapeutic options for an ancient disease. Arthritis Rheum 2004;50:2400–2414.
9. Kramer HM and Curhan G. The association between gout and   nephrolithiasis: The National Health and Nutrition Examination   Survey III, 1988–1994. Am J of Kid Dis 2002;40:37–42.
10. Kramer JH, Choi HK, Atkinson, K, Stampfer M, Curhan GC. The   association between gout and nephrolithiasis in men: The Health   Professionals’ Follow-up Study. Kidney International 2003;   64:1022–1026.
11. Terkeltaub RA Gout. N Engl J Med 2003. 349(17):1647–1655.
12. Wallace Kl, Riedel AA, Joseph-Ridge N, Wortmann R. Increasing   prevalence of gout and hyperuricemia over 10 years among older   adults in a managed care population. J Rheumatol 2004;   31:1582–1587.
13. Hochberg MC, Thomas J, Thomas DJ, Mead L, Levine DM, Klag MJ.   Racial difference in the incidence of gout. The role of   hypertension. Arthritis Rheum 1995;38(5): 628–632.
14. Arromdee E, Michet CJ, Crowson CS, O’Fallon WM, Gabriel SE.   Epidemiology of gout: Is the incidence rising? J Rheumatol 2002;29:2403–2406.
15. Sacks JJ, Helmick CG, Langmaid G. Deaths from arthritis and   other rheumatic conditions, United States, 1979–1998. J Rheumatol 2004;31(9):1823–1828.
16.                United States Bone and Joint Decade:  The  Burden of Musculoskeletal Diseases in the United States.  Rosemont, IL:  American Academy of Orthopaedic Surgeons;  2008.  Chapter 4.  Arthritis and Related Conditions.
17. Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the   prevalence of arthritis and other rheumatic conditions in   the United States. Part II. Arthritis Rheum 2008;58(1):26–35.
18. Sacks JJ, Luo Y-H, Helmick CG. Prevalence of specific types of arthritis and  other rheumatic conditions in the ambulatory health care system in the United  States, 2001-2005. Arthritis Care &  Research 2010;62(4):460-464.