34 Things You Need to Know About Arthri­tis

This painful joint dis­ease is ac­tu­ally a col­lec­tion of more than 100 ail­ments— and it af­fects peo­ple of all ages

Reader's Digest - - Contents - By sari harrar

This painful joint dis­ease is ac­tu­ally a col­lec­tion of more than 100 ail­ments— and it af­fects peo­ple of all ages.

Arthri­tis. If the word makes you think about older folks with creaky knees and jumbo bot­tles of ibupro­fen, you need an up­date. Arthri­tis now strikes an es­ti­mated 91 mil­lion Amer­i­can adults, ac­cord­ing to a new study, and 30 per­cent of them are ages 18 to 64. By far the most com­mon type, which af­fects 57 per­cent of Amer­i­cans with arthri­tis, is os­teoarthri­tis, fol­lowed by gout (27 per­cent of cases), pso­ri­atic arthri­tis (14 per­cent), and rheuma­toid arthri­tis (3 per­cent). There is no cure for any of them, but sci­ence has made sev­eral break­throughs in un­der­stand­ing how to treat the in­flam­ma­tion and pain that come with the con­di­tion as well as how to halt the un­der­ly­ing joint dam­age. The first line of de­fense: Ed­u­cate your­self.

OS­TEOARTHRI­TIS

(OA): Wear and tear of the car­ti­lage cush­ion be­tween joints that can of­ten cause—and in some cases re­sult from—chronic in­flam­ma­tion.

1 Old-fash­ioned X-rays are the best di­ag­nos­tic tool. A Wash­ing­ton Univer­sity study noted that X-rays can diagnose OA as ac­cu­rately as mag­netic res­o­nance imag­ing (Mri)—and they do it faster and more cheaply. Iden­ti­fy­ing arthri­tis early gives you time to turn to life­style changes (see page 111) be­fore ir­re­versible dam­age is done to your knees (the most com­mon pain point) or other joints. 2 The cus­tom­ary treat­ment for OA doesn’t re­pair joints. Up to 85 per­cent of os­teoarthri­tis suf­fer­ers try non­s­teroidal anti-in­flam­ma­tory drugs (NSAIDS) such as ibupro­fen. Though they can be ef­fec­tive at get­ting you through the day, says Kelli Allen, PHD, a re­searcher at the Thurston Arthri­tis Re­search Cen­ter, they don’t pro­tect joints from pro­gres­sive dam­age and may have se­ri­ous side ef­fects. 3 When peo­ple with os­teoarthri­tis used NSAID gels, drops, or patches, half said their pain fell by 50 per­cent or more over 12 weeks. Be­cause these ver­sions are rubbed onto your skin, less of the drug gets into your blood­stream, which re­duces the risk of gas­troin­testi­nal bleed­ing, heart prob­lems, and other side ef­fects. That said, do not use these top­i­cal treat­ments if you have kid­ney dis­ease or are also tak­ing oral NSAIDS. 4 A 2018 study of 240 os­teoarthri­tis pa­tients showed that those who took opi­oids were in slightly more pain af­ter a year than those who took non-opi­oid med­i­ca­tion. The re­searchers aren’t sure why, but given that these drugs can be very ad­dic­tive, they rec­om­mend against opi­oids.

5 Arthri­tis hurts your heart by con­tribut­ing to chronic in­flam­ma­tion, re­duc­ing phys­i­cal ac­tiv­ity, and in­creas­ing NSAID use—all fac­tors in car­dio­vas­cu­lar risk. All told, re­searchers es­ti­mate that OA boosts your odds for heart dis­ease by 24 per­cent. (Pso­ri­atic and rheuma­toid arthri­tis raise the odds even higher.)

6 Aus­tralian re­searchers who re­viewed the ev­i­dence for 20 topselling herbs and di­etary sup­ple­ments used to treat os­teoarthri­tis con­cluded that three—boswellia ser­rata ex­tract, pine bark ex­tract, and cur­cumin—are most ef­fec­tive in re­duc­ing in­flam­ma­tion and pain in the short term.

7 Cor­ti­sone in­jec­tions don’t help in the long term. “A sin­gle shot can ease pain,” says Ti­mothy Mcalin­don, MD, MPH, chief of rheuma­tol­ogy at Tufts Med­i­cal Cen­ter. But a re­cent study found that re­peated shots of cor­ti­sone, a steroid, not only didn’t con­trol pain but also ac­tu­ally led to more joint dam­age.

8 The jury is still out on other in­jectable treat­ments. Hyaluronic acid in­jec­tions are de­signed to add more shock-ab­sorb­ing fluid to joints, but re­search on their ef­fec­tive­ness is mixed. Sim­i­larly, new in­jecta­bles us­ing your own fat, bone mar­row, platelet-rich plasma, or stem cells prom­ise re­lief, but Dr. Mcalin­don says “the re­search isn’t suf­fi­cient to show if they ac­tu­ally work” to ease pain and re­build joints.

9 In­som­nia is an of­ten un­der­treated side ef­fect of arthri­tis, but there are fixes. Lack of sleep can in­ten­sify sen­si­tiv­ity to pain, a prob­lem for OA pa­tients, ac­cord­ing to a Johns Hop­kins Univer­sity study. Cog­ni­tive be­hav­ioral ther­apy, which helps peo­ple change the dis­torted think­ing that can worsen pain lev­els, has been shown to in­crease the amount of time os­teoarthri­tis suf­fer­ers slept—and pre­sum­ably decreased their pain.

10 A new de­vice called Coolief uses spe­cial­ized elec­trodes to send wa­ter-cooled ra­dio waves into the tis­sue around your knee, which tem­po­rar­ily de­ac­ti­vate nerves. Pa­tients re­ported greater, longer-last­ing pain re­lief (up to 12 months) with Coolief than with cor­ti­sone in­jec­tions.

11 Stem cells could save joints— some­day. Sci­en­tists have pro­grammed stem cells to grow new car­ti­lage on a 3-D tem­plate shaped like the ball of a hip joint. Us­ing gene ther­apy, they have also ac­ti­vated the new car­ti­lage to re­lease an­ti­in­flam­ma­tory mol­e­cules to fend off a re­turn of arthri­tis. But the stem cell ther­apy of­fered for knee os­teoarthri­tis in many clin­ics isn’t yet a proven cure.

RHEUMA­TOID ARTHRI­TIS

(RA): The im­mune sys­tem at­tacks the fluid that lu­bri­cates joints, caus­ing in­flam­ma­tion and de­stroy­ing car­ti­lage.

12 A new drug could pre­vent RA. Early re­sults from one study showed that for peo­ple with mild joint aches and high in­flam­ma­tion lev­els, one shot of rit­ux­imab cut the risk of de­vel­op­ing rheuma­toid arthri­tis in half. The drug blocks pro­duc­tion of com­pounds that trig­ger in­flam­ma­tion.

13 So could vi­ta­min D. In an­other study, re­searchers found that peo­ple with low blood lev­els of vi­ta­min D, which boosts im­mune func­tion, were at higher risk for RA. (One great free source of vi­ta­min D: sun­shine.)

14 It’s pos­si­ble to put rheuma­toid arthri­tis into re­mis­sion. While there’s no way to re­verse joint de­gen­er­a­tion, get­ting treated within six months of the on­set of pain and stiff­ness can curb symp­toms and pre­vent fur­ther dam­age. Un­for­tu­nately, a 2016 na­tional sur­vey found that it took peo­ple with RA four years and vis­its to at least three dif­fer­ent doc­tors to get a proper di­ag­no­sis.

15 Early arthri­tis clin­ics are show­ing great prom­ise. Fo­cused on treat­ing rheuma­toid arthri­tis pa­tients with a re­cent di­ag­no­sis, clin­ics have opened at the Univer­sity of Rochester Med­i­cal Cen­ter, Ore­gon Health and Sci­ence Univer­sity, and many pri­vate fa­cil­i­ties. In one study, 89 per­cent of RA suf­fer­ers treated at an early arthri­tis clinic got dis­ease-mod­i­fy­ing an­tirheumatic drugs (DMARDS) in three months, com­pared with 50 per­cent who got care else­where. The clinic’s pa­tients had higher re­mis­sion rates as a re­sult.

16 Menopause wors­ens the symp­toms of rheuma­toid arthri­tis. A 2018 study of 8,189 women in the jour­nal Rheuma­tol­ogy con­firms some­thing women with RA have long ex­pe­ri­enced: Joint de­gen­er­a­tion speeds up af­ter menopause. Early menopause can trig­ger the dis­ease too.

17 Rheuma­toid arthri­tis can raise your risk for cer­tain types of can­cer. Lung can­cer, lym­phoma, and mul­ti­ple myeloma are more com­mon in peo­ple with RA, partly due to in­flam­ma­tion and partly be­cause RA drugs sup­press the im­mune sys­tem.

18 One DMARD does not fit all. “DMARDS can put RA into re­mis­sion, but a drug may stop work­ing af­ter sev­eral years. Some peo­ple have to try sev­eral be­fore they find the one that works best,” says David Daikh, MD, PHD, out­go­ing pres­i­dent of the Amer­i­can Col­lege of Rheuma­tol­ogy.

19 Tu­mor necro­sis fac­tor (TNF) is an in­flam­ma­tory pro­tein re­spon­si­ble for pain and car­ti­lage de­gen­er­a­tion in RA, and drugs called TNF in­hibitors can some­times block it. And if one TNF in­hibitor—such as etan­er­cept (En­brel) or adal­i­mumab (Hu­mira)—doesn’t work, try an­other. In a re­cent study, 43 per­cent of pa­tients who didn’t re­spond to one type of TNF in­hibitor re­sponded pos­i­tively to a dif­fer­ent one. 20 Bi­o­logic drugs—such as etan­er­cept (En­brel), goli­mumab (Sim­poni), and adal­i­mumab (Hu­mira)—are en­gi­neered from hu­man genes. They work by tar­get­ing spe­cific parts of the in­flam­ma­tion process rather than sup­press­ing the im­mune sys­tem in gen­eral (as older DMARDS do), so they tend to have fewer side ef­fects. Un­for­tu­nately, they are also more ex­pen­sive than tra­di­tional med­i­ca­tions.

21 Ge­netic pro­fil­ing could soon pin­point which drug classes or even in­di­vid­ual drugs will work for you. In a new mul­ti­site study pub­lished this May in the jour­nal Arthri­tis & Rheuma­tol­ogy, re­searchers an­a­lyzed joint tis­sue from 41 rheuma­toid arthri­tis pa­tients to de­ter­mine which gene vari­a­tions each in­di­vid­ual had and how they re­sponded to each type of drug. Next they hope to pre­dict which pa­tients will re­spond best to spe­cific drugs based on their ge­netic sig­na­ture, sav­ing time and money.

22 Nerve stim­u­la­tion could re­duce joint dam­age. In one small study, when pa­tients with rheuma­toid arthri­tis were zapped with mild elec­tri­cal cur­rent to the va­gus nerve (which passes through your neck to your ab­domen), the charge re­duced their lev­els of TNF, the same in­flam­ma­tory pro­tein tar­geted by TNF in­hibitors. Some also had less swelling and ten­der­ness.

PSO­RI­ATIC ARTHRI­TIS

(PSA): An au­toim­mune dis­ease in which the im­mune sys­tem at­tacks healthy joint tis­sue, PSA af­fects about 30 per­cent of peo­ple with pso­ri­a­sis, a con­di­tion marked by red, scaly patches on the skin.

23 PSA is not RA. Pso­ri­atic arthri­tis is of­ten mis­di­ag­nosed as rheuma­toid arthri­tis, but the cause and many treat­ments are dif­fer­ent. Un­til 2013, the med­i­ca­tions ap­proved by the FDA to treat pso­ri­atic arthri­tis were RA drugs. Since then, sev­eral new treat­ments for those with PSA have be­come avail­able.

24 Get­ting a timely di­ag­no­sis can pre­vent per­ma­nent joint dam­age. “In pso­ri­atic arthri­tis, ero­sive joint changes can be­gin within six months of first symp­toms,” says rheuma­tol­o­gist Ser­gio Schwartz­man, MD. “But for many peo­ple, there can be a five-year de­lay in re­ceiv­ing a di­ag­no­sis.” A grow­ing num­ber of com­bined der­ma­tol­ogy/rheuma­tol­ogy clin­ics may help re­verse the trend.

25 Pso­ri­atic arthri­tis suf­fer­ers are six times more likely to have the in­flam­ma­tory bowel dis­ease (IBD) known as Crohn’s dis­ease, ac­cord­ing to a study of more than 174,000 women. Chronic in­flam­ma­tion un­der­lies both Crohn’s and PSA, and some of the med­i­ca­tions used to treat arthri­tis may lead to or ex­ac­er­bate IBD symp­toms. (Other PSA drugs, though, can help IBD symp­toms.) Peo­ple with PSA are also at higher risk for di­a­betes, os­teo­poro­sis, kid­ney dis­ease, other au­toim­mune dis­eases, and many other con­di­tions.

GOUT

Caused by uric acid crys­tals in joints (most of­ten in the big toe). 26 The num­ber of peo­ple di­ag­nosed with gout dou­bled be­tween 1960 and 1990, and rates have risen about 25 per­cent since. The use of cer­tain med­i­ca­tions for high blood pres­sure—es­pe­cially loop and thi­azide di­uret­ics—are among the top rea­sons for the in­crease. Foods and drinks rich in com­pounds called purines (such as al­co­hol, ba­con, and sweets) also con­tribute to the for­ma­tion of uric acid crys­tals, as does be­ing over­weight and seden­tary.

27 Toma­toes, which can in­crease uric acid lev­els, could be a gout trig­ger for some peo­ple, a study from 2015 found. They were the fourth most com­mon food trig­ger af­ter seafood, al­co­hol, and red meat.

28 It Bears re­peat­ing: Cher­ries can lower the risk of a gout at­tack. In a 2012 study, re­searchers fol­lowed peo­ple with gout for a year and found that those who ei­ther ate fresh cher­ries or took cherry ex­tract through­out the year were 37 per­cent less likely to have re­cur­rent at­tacks.

29 Gout drugs can be ef­fec­tive, but they can also have draw­backs. In a 2018 study of more than 6,000 peo­ple with gout, those who took febux­o­stat were 34 per­cent more likely to die from heart dis­ease than peo­ple who took al­lop­uri­nol, an­other com­mon gout drug. But al­lop­uri­nol can cause liver prob­lems, while an­other older gout drug, colchicine, can cause se­vere di­ar­rhea.

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