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Case V RA

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Armed with new regimens for established drugs and new agents that block the inflammatory cascade,rheumatologists are taking a more aggressive approach to RA. Early diagnosis and promp institution of disease-modifying drugs may minimize the progression of joint damage.
A middle-aged woman was referred to a rheumatologist for evaluation of hand and foot pain of two months'duration. She had noticed a gradual increase in pain and swelling in the proximal interphalangeal (PIP ) and metacarphal phalangeal (MCP ) joints of the hands and the metatarsal phangeal (MTP ) joints of the feet. She also experienced a progressive increase in morning stiffness,which now lasted as long as two hours and could be relieved somewhat by taking a warm shower and forcing herself to use her hands (e.g., preparing breakfast). Later in the day,activity made the pain worse. There was occasional discomfort and stiffness in her knees,but substantially less in her hands and feet.
The patient worked as a secretary fo many years but was now having difficulty performing her job. She had tried over-the counter ibuprofen and acetaminophen; neither provided significant relief.
She had no fever,ulcers,serositis,neurological disorder,renal disease,or photosensitivity. Her family and family history revealed no history of significant disease.
Examination of the hands revealed significant warmth and swelling in both wrists and a noticeable reduction in both flexion and extension. There was mild swelling of the PIP and MCP joints in a bilateral and symmetric distribution. Palpation of the forefoot produced a notable tenderness.
Laboratory studies showed a white blood count of 6,500/mm^3,with a differential of 59 % polymorphonuclear leukocytes and 31 % lymphocytes; hemocrit,38.3 %;platelet count,275,000/mm^3;blood urea nitrogen (BUN),11 mg/dl;seru creatinine,0.7 mg/dL;aspartate aminotransferase (AST).16 U/L. Assays for antinuclear antibody (ANA) and rheumatoid factor (RF) were negative. The erythrocyte sedimentation rate (ESR) was 39 mm/hr. A urinalysis was normal. This patient has rheumatoid arthritis.
Treatment: The patient was treated with oral methotrexate,7.5 mg once a week,and this dosage was titrated to 20 mg during the next three months. Her liver function test remained normal,and she reported no significant side effects. However,she experienced only mild change of symptoms.
The rheumatologist considered adding one of the newer antirheumatic agents (leflunomide,etanercept,or infliximab),but the patient's insurance company refused to pay for treatment with these agents until therapy with at least two of the established DMARDs had failed. Consequently,hydroxychoroquine and sufasalazine were added to her regimen. Within three months,she showed substantial improvement.
The patient,posed a bit of a diagnostic decision.  In spite of her clinical history and findings on examination,her serum was negative for both rheumatoid factor and antinuclear antibody.and it was not clear whether there were any abnormalities on x-ray.
The decision to start MTX at the first call was a judgement call. Another rheumatologist might have tried another ( prescription ) NSAID at full dosage,added a few milligrams of predisone each morning,and checked films of the hands and wrists for at least evidence of some tell-tale juxtra-articular osteoporosis. If the films were normal,a few weeks of a full-dose NSAID or low dose steriod,or both,would probably have been satisfactory.
With minimal changes on x-ray (i.e., mild osteoporosis) the rheumatologist might have started with hydroxoychloroquine because of its great safety (eye examinations are really all that is needed for sound follow-up) and relatively minimum side effects. If the films showed any evidence of erosion,or very active,MTX would be the choice,with rapid escalation of doseage as needed.
 Had hydroxychloroquine been started and found inadequate,methotrexate could have been added at any time,as could sulfasalazine,but methotrexate appears to be more effective.
Many rheumatologists prescribe folic acid whenever treatment with methotrexate is begun. It appears to improve safety with little or no loss of MTX efficacy ( 5 day rather the 7 day treatment proved more effective in research trials-folic acid-dilution concerns of MTX when used with folic acid )
The importance of educating the patient cannot be overemphasized,but in reality,limited time is a factor in modern day medicine. Cox-2 inhibitors are not more effective than non-selective NSAIDs,but they are thought to do less damage to the gastric mucosa.
One other interim strategy to keep in mind when one or two joints remain troublesome is to inject them with corticosteriods. These injections,which may be given once or twice,can provide excellent relief for many weeks or months.
 The main concern is to be sure that no infection is in the joint. Sometimes, the second injection may prove less effective,but often,its a trial decision. Larger joint involve larger doses than smaller joints,and less frequency of repeat injection in the larger joints (i.e.,hip-knee vs fingers).

Two decades ago,the typical RA patient was kept on NSAID therapy until they showed evidence of joint damage or increased disease activity. During the last 10 to 15 years,however,rheumatologists have become more aggressive about starting DMARDs much earlier in the course of the disease. The principle agents used are hydroxychloroquine (HCQ),sulfasalazine (SSZ),and methotrexate (MTX). Gold salts while still available,are not often utilized, especially in their oral form. D-penicillamine has fallen out of favor, predominantly  because of its side effects. Other medications,such as cyclosporine,are generally reserved for combination therapy or refractory disease.
During the last 5 years,our therapeutic options increased significantly. The introduction of leflunomide (Arava).a pyrimidine synthesis inhibitor (suppresses cells that are rapidly dividing),has provided an alternative for patients who cannot tolerate methotrexate or provide another option.
Etanercept (Enbrel),a fusion protein that interrupts the inflammatory cascade by binding to tumour necrosis factor (TNF)-alpha,can be used in early disease or when conventional therapy do not work (limited by cost factor and insurance coverage). Another TNF-alpha inhibitor,infliximab (Remicade), would probably work very well in early disease,but currently its use is limited to refractory (people who do not respond to conventional therapy) cases,in which it is given in combination with traditional medications such as MTX (high cost).
Recently (2003)another TNF-alpha inhibitor Formerly known as DE27,now called Humira has been approved by the FDA for RA therapy. In the U.S.,the manufacturer,Abott Laboratory has introduced a promotional aspect to senior citizens on medicare whereby the drug is offered,free of charge. The manufacturer  estimates it will cost them 30 million per annum. Early clinical trial were conducted by Dr.Edward Keystone,researcher,scientist and rheumatologist of MT.Sinai  hospital,rheumatology division (Adelimumab). 
Kineret is a Il-1ra (interleukin family)inhibitor introduced in early 2002. It can be used with MTX,but currently,combination with other TNF inhibitor is not recommended because of recent clinical trials. Researchers believe the serious side effects may be dose related and they are working on the problem.
Both Remicade and Enbrel improve function,and there is good evidence they slow radiographic progression of RA(Arava also,but Arava might be more suitable for patients that cannot tolerate MTX). This would argue for their use early in the disease,especially in patients who seem likely to have a aggressive or a destructive course.
Traditional disease-modifying agents can also slow radioraphic progression,
however,and they are much less expensive then the newer agents. Consequenty,governments (provincial health plans have different guidelines in different provinces in Canada) and thrd-party payers impose restrictions on the use of the new biologic drugs. They may stipulate that patients must first be unresposive to as many as three traditional agents before they will pay for treatment with a TNF-alpha inhibitor.
These restrictions are being relaxed somewhat,slowly,as evidence of the new agents,efficacy and safety accumulates. Enbrel recently released a 5 year safety data,but drugs like methotrexate (what to expect-side effects-safety)-has a long track record.
For physicians whose choice of initial therapy is limited to traditional agents,the first question is whether to start with a single agent or combination therapy. Possible combinations include HCQ with SSZ or MTX,SSZ with MTX,or all three together.
The choice of initial therapy can be a difficult one. They do not want to administer more medication than is necessary,yet they want to be aggressive enough to improve function and prevent the development of radiographic destruction,therby ultimately minimzing functional impairement and keeping down the long-term cost of care.
At present the most common strategy is to start with methotrexate alone. However,to minimize the risk of hepatoxicity,the patient must agree not to consume alcohol (or to do so only very modestly). If a patient is not tolerant to MTX,Arava can be tried.
Most rheumatologists choose not to start treatment with HCQ monotheraphy (single),except perhaps in patients with mild disease. Physicians are beginnining to use,more and more,use of HCQ in combination with MTX or SSZ,then in the past. Another alternative would be to start with SSZ alone,but the approach is less common (increasing) in North America than in Europe.
In the past a typical RA patient's MTX doseage (7.5 mg orally once a week) would have been titrated up slowly over six months or even a year. Now rheumatologists tend to move much faster,starting with up to 10 mg per week and taking dose to as 20-25 mg a week within the first two to three months. In 1998 a clinical trial was conducted with subcutaneous MTX injection with a equivalent dose of 25 mg and they found it more efficacious on patients with less side effects.
Faster dose escalation requires more frequent follow-up. Some physicians will try another approach. But they all look for abnormalities on liver function tests,mouth sores or ulcerations,significant fatigue,nausea,or discomfort during the first 24 hours after taking the drug.
Patients are asked to return two weeks (more or less)after first taking the drug,at which point the dose may be increased to 12.5 mg. Then they usually,return within four weeks. If they have had not a good response,the dose might be increased to 15 mg-17.5 mg. Four weeks after that,if patients still have not responded well enough,the dose may be increased to 20 to 25mg. But at that point,more than likely, subcutaneous injection of MTX will be introduced.
Clinical trials suggest that about 50 % of patients respond to methotrexate monotheraphy. Unfortunately,the average degree of improvement tends to be about 25 %. For example,the number of tender or swollen joints may decrease from 20 to 16,but there are always exceptions to the rule.
A few years ago,monotherapy was usually continued for six months to a year,and patients who had not responded might be switched to another drug. Today,if patients do not respond sufficiently to a adequate dose of medication, another DMARDs-HCQ,SSZ,or (if possible) Enbrel,Remicade,or Arava.
Arava is the least-cost wise of the new drugs,but is less efficacious of the other two-Enbrel and Remicade. Arava can stay in the body for up to 2 years after discontinuation of the drug A loading dose of 300 mg is given,100 mg for the first three day,at the start,and given in 10 or 20 mg ,tablet form,therafter.
The physician might consider switching to one of the newer agents,but if the patient has shown some improvement and has not been troubled by side effects,most rheumatologists will add rather then switch.
HCQ can be added at a doseage of 400 mg once a day or 200 mg twice a day. SSZ is usually added at a doseage of 500 mg once or twice a day, escalating to a total dose of 1 gm twice a day.
The escalation schedule traditionally recommended is for the patient to take one tablet a day for the first week,one tablet twice a day for the second week,one in the morning and two in the evening during the third week,one in the morning and two in the evening during the third week,and two tablets twice a day during the fourth week and thereafter.
For patients on combination therapy,physicians generally follow the same schedule for toxicity monitoring as with methotrexate.
They obtain a complete blood count and liver function test and look for myelosuppression. The other medications do not need to be monitored as frequently as methotrexate,but since the patient is in the office anyway,all the monitoring can be done at the same time.
If combination therapy does not produce substantial impprovement within three months,the physician has a good clinical basis to move to biologic (anticytokine) therapy,and hope there should be little difficulty in convincing a third party payer of the necessity of using these agents.
If a patient responds well to DMARD treatment,the physician should eventually think about reducing doseage or withdrawing the agents one by one. The goal is to provide just enough therapy to keep the disease under control,which drug is kept for maintenance purposes will depend on the rheumatologist and the patient.
Patients must undestand that current treatments can provide significant improvement,but complete relief is unlikely. Patients need to learn the importance of avoiding trauma or stress in involved joints and of physical and occupational therapy to improve structures around the joints to decrease pain and improve function.
Education about the disease and medication is also vital. Patients need to know the potential complications and toxicities of the drugs they are taking. They must be aware that some DMARDs take time to display their benefits,and be aware of a drug ,once efficacious,has become less effective. The bridge is usually low-dose glucocorticoid therapy (e.g.,up to 7.5 mg of predisone/daily).
Many RA patients are at risk of gastrointestinal complications from standard non-steriod drugs (NSAIDs). These patients tend to be older,have existing diseases such as diabetes,kidney,liver etc., and take glucocortoids and they may or may not have a history of coronary artery disease.
The cyclooxygenase (Cox-2) inhibitors ,since they appear to have a lower risk of gastrointestinal toxicity. The improved safety of these drugs shoud not be assuned to imply improved efficacy. No NSAID alone can alter the course of RA,they do not change radiographic progression or slow joint destruction.
For that reason,they should be used as adjuncts,never as monotheraphy. If a patient has heart problems,selection of NSAID may be important and that also applies to others, existing disease present,must be fully recognized and adjustments made in therapy.
With chronic treatment with aspirin or an regular NSAID (in some existing disease conditions,it may be wiser to use a standard NSAID like Naproxen), and add a gastroprotective agent (e.g.,misoprostol cytotec or a proton pump inhibitor).

 More Case Histories:
A elderly woman was referred to a rheumatologist for evaluation. She had a six-year history of bilateral pain in her knees and wrists. RA had been diagnosed four years earlier,and 3 years of treatment with low doses prednisone (5mg /day) and HCQ (plaquenil) had provided some improvment. She used no other medications. The patient complained of morning stiffness that lasted 45 minutes but felt her ability to function had not been significantly impaired.
However,during her most recent visit to her family physician,it had become apparent that she had occasional warmth,tenderness,and swelling in her second and third MCP joints bilaterally as well as her wrists and knees,and that she occasionally used wrist splints for pain relief. The physician realized that she might not be doing as well as she thought and refferred her for a possible adjustment in therapy.
Examination by the rheumatologist showed mild soft swelling and synovitis in both wrists. Their range of motion had decreased to 45 degree of flexion and 30 degree of extension. There was mild tenderness and swelling of the MCP and PIP joints bilaterally and evidence of mild effusions in the knees.
Laboratory studies showed a white blood count of 6,400/mm^3; hematocrit,39.17;platelet count,288,000/mm^3;BUN,13 mg/dL;serum creatinine,1.6 mg/dL;ALT,21 U/L;RF,negative;ESR,25 mm/hr.
X-rays showed extensive bony erosions in MCP joints as well as erosive disease involving carpel bones of the right wrist,distal ulna,and radius. In the left arm,there was foreshortening of the radius and significant erosion of the ulnar styloid.
This case illustrates why rheumatologists have become more rigourous in the follow-up of patients with RA. The patient thought that treatment had brought significant improvement,and her family doctor,and possibly a previous rematologist,had agreed. Because no one realized that her treatment was inadequate significant joint destruction had occurred.
The current evaluation provides clear-cut evidence that the patient's disease is still quite active,showing tender,swollen joints with reduction in range of motion,joint space narrowing,and erosion. The radiographic changes are fairly significant,they warn of potential future complications. Although the test for rheumatoid factor was negative,that is not always a predictor of long-term outcome. The ESR is still within the normal range,but that may be misleading. It is possible that the predisone and hydroxychoroquine  have been able to decrease the ESR without suppressing the disease.
Decision:,the addition of another medication should be considered. Sulfasalazine is out of the question because of the patient's sulfa allergy. The elevated serum creatinine level obviates methotrexate. She has slight renal impairement and using methotrexate,especially,at high doses,is not a option.. That limits the choices to lefluonomide (Arava)or etanercept. (Enbrel) Infliximab (Remicade)  is used in combination with methotrexate or sometimes another disease-modifying drug.

Treatment: The patient was started on leflunomide,at a loading dose of 100 mg a day for three days,and then a maintenance dose of 20 mg a day. She experienced mild diarrhea with the loading dose as instructed to take loperamide (1-3 mg) after each loose bowel movement. The diarrhea resolved over the following 10 days,and she had no further complications. Disease signs and symptoms improved during the next three months.
One possible strategy in this case would have been to replace HCQ with leflunomide. Since the patient pappears to have had some benefit from HCQ and has been tolerating it well.
Serious complications are rare with leflunomide,unless a underlying liver disease is present. The physician should be on the alert for rash,diarrhea or loose stools,and liver inflammation. The rashes tend to be reversible with either dose reduction or discontinuation of the medication. To monitor for liver inflammation,patients are asked to return in two weeks for liver function tests,and then every six to eight weeks thereafter. Rheumatologists often obtain intermittent complete blood counts to make sure there have been no decreases,although they are rare.
Diarrhea is among the most common complications of leflunomide,altered bowel function occurs in more than 33 % of patients. Diarrhea can develop at any point,but patients often experience it with the loading dose. It tends to be mild and self-limited and can be treated symtomatically with loperamide,in most cases.
One of the attractive aspects of leflunomide is that dose escalation often is not required;the patient can simply be started at 20 mg a day. However,when leflunomide is given in combination with other drugs,it is preferable to give 100 mg daily for two days as a loading dose followed by 10 mg or 20 mg every other day. The dose can be increased later if necessary. Should toxicity develop,the medication can be withdrawn or the dose cut in half. Cholestyramine can be given to bind the leflunomide in the bowel and remove it from the body
The benefits of leflunomide often begin to appear within four weeks ( moreso with a loading dose-it appears),and most patients who are going to benifit will see it within 12 weeks. The drug is expected to improve function and impede radiofraphic progression. If it doesn't appear efficacious during that time period,it simply won't work ever, for that patient. Arava doesn't work for everyone.

The second case illustrates the problems that can occur if periodic x-rays are not obtained. In patients with any evidence of ongoing disease activity,a plain film of the most severely affected joints can be helpful. Had that been done, documentation of progressive joint destruction would have permitted far earlier intervention with aggressive therapy.
Usually,the patients who are most prone to joint destruction are rheumatoid-factor positive,this patient was not. Her hematocrit of 19.1 % is remarkably good for a patient with smoldering arthritis,but she may have been a smoker. Acute phase reactnts (white blood cell coun,platelets,ESR,and C-reactive protein ) may not be elevated in patients with active arthritis,especially in older patients. A sometimes useful strategy is to obtain and analyze synovial fluid,which should show features of disease activity. The method used is often a decision based on the patient symptoms and medical history.
Physicians have many patients to look after and are constantly bombarded by cost cutting measures by their peers,payees,and government,and sometimes, what should be done,is not done,in this pressure provoked and time-saving atmosphere. Some tests deemed unnecessary,or non-essential in one patient may make a world of difference in another.

A middle-aged man was referred by his family physician for evaluation of refractory rheumatoid arthritis ( can't toleraate conventional therapy) The patient complained of persistent pain and swelling to the joints of his hands and feet despite treatment with methotrexate.
Symptoms had begun three years earlier with swelling,significant pain, warmth, and erythema of the second PIP joint of the left hand. Not long afterward,the patient noted similar involvement of the PIP,MCP,and MTP joints occurred. Chronic pain and swelling of those joints was accompanied by 30 to 60 minutes of morning stiffness.
The family physician had initially prescribed NSAIDs,with only modest benefit. A year later,he was referred to a rheumatologist who prescribed methotrexate, initially at low doses and then rapid escalation to 20 mg a week,the patient experienced nausea,fatigue,and lack of energy for the next two to three days.
The rheumatologis switched from oral to subcutaneous MTX and added folic and folinic acid,but the patient remained unable to tolerate the higher doses.
Examination by the rheumatologist revealed marked bilateral synovitis and swelling of the PIP joints in a virtually symmetric pattern.
The second and third PIP joints in a virtually symmetric pattern. The second and third PIP joints showed the greatest involvement,with both swelling and mild deformity. There was also notable enlargement of the MCP joints,with mild ulnar deviation. Examination of the feet revealed mild tenderness and swelling of the MTP joints.
Laboratories studies showed a white blood count of 4,900/mm^3;hemocrit,34 %;platet count,197,000/mm^3;BUN,21 mg/dL;serum creatlinine,0.8 mg/dL; AST,27 U/L.;RF,positive;ESR,35 mm/hr;X-rays of the hands showed juxtra-articular osteopenia and small erosions of the second and fourth PIP joints on the left and of the third MCP joints bilaterally.
This case represents a situation that rheumatoligists unfortunately see all to often-a patient that has received a timely diagnosis and been given appropriate treatment but who neverthe less continues to have active disease. Although his disease showed some response to methotrexate,the limit of its usefulness clearly had been reached. Fatiegue and nausea are not uncommon with high doses of MTX, Swotching from oral to subcutneous administration often reduces the side effects and is more efficious,but not in this case.
Hence,this patient is an ideal candidate fpr anticytokine therapy. cytokines are involved in the inflammatory cascade of all autoimmune inflammatory conditions. Those considered the most important in mediating the swelling,pain,stiffness, and radiographic destruction are TNF-alpha and interleukin (IL-)-1. Etanercept and Remicade are TNF inhibitors,have different structures,but both bind to TNF-alfa,preventing it from binding to cell receptors.
Both etanercept and infliximab often dramatically reduce disease symptoms and signs after the first few injections. Dramatic reductions can occur during the first four weeks of therapy,and retardation of radiographic progression can occur within a year.
Since etanercept is injected subcutaneously,and this patient was already giving himself subcutaneous injections of MTX,etanercept is the logical choice for him. He still has to visit the physician for an educational session,however,during which a nurse shows him how to draw up the medication in a syringe,how to select and rotate injection sites,and how to give the injection. Potential complications are explained. He also watches an educational video produced by the manufacturer.
For patients who cannot or refuse to self-inject,infliximab is a more acceptable choice. The drug is given intravenously,so patients initially come to the government sponsored injection locations in Canada,if approved,for these medications,every two weeks,then every eight weeks for the infusion.

The patient was started on etanercept,25 mg subcutaneously twice a week. He experienced mild erythema,itching,and swelling at the injection site,but continued with treatment and within four weeks began to experience notable clinical improvement. Over time,injection site reactions became less frequent ,then ceased entirely. Follow up x-rays one year later showed stabilization of his disease.
Etanercept injection site reactions tend to be mild and self-limiting. Patients who continue the injections generally find that they will self-resolve.  Another potential side effect of etanercept is impaired eradiction of infection. Patients taking etanercept do not appear to have an increased risk of infection,but if a significant infection does develop,etanercept therapy should be stopped until it heals.
There have been some patients-typically those who are older or have comorbidities-who have had difficulty clearing an infection if they remain on etanercept. Some patients do not respond to biologic therapy,period.
Since this patient is still taking methotrexate,he requires regular liver function studies,and occasionally a complete blood count. Etanercept therapy does not require additional monitoring.
If a patient such as this shows a substantial response to therapy after six to nine months,one might consider reducing the methotrexate dosage from 20 mg to 15 mg a week or less,or even stopping it entirely. Withdrawal should be done slowly and carefully,over a period of six months,because is some patients, reduction of the methtrexate dosage results in disease exacerbation.
This case illustrates the special problems associated with MTX therapy. A trial of subcutaneous MTX can be valuable,because it often eliminates the gastrointestinal side effects seen with the oral route and,amazingly,is less expensive. (As noted the patient probably should have taking folic acid from the star tof MTX therapy.)
This patient is a fine candidate for etanercept;infliximab would be equally satisfactory. The safety record for both medications remains excellent,although there have been recent reports of reactivation of mycobacterial infections andmposibly,significant cytopenia. Neuropathies may also be an issue. Just how long etanercept should be continued is not known,but it appears clear that if the drug is withdrawn,the arthritis will flare.
The most formidle hurdle to management of arthritis in North America is cost. Insurance companies are,of necessity,wary of unlimited authorization of the newer medications. In Canada a few provincial formularies will approve biological therapy,while the majority,will not. In Ontario it is approved by "special access order",when conventional therapy proves ineffective.
It is becoming more clear that they are cost-effective-the follow-up expenses for a patient with improved function and less or no pain are significantly less. Furthermore,it is expected that with new technologies,production costs of these and other agents under investigation will be reduced, As time passes we will have a longer record of what these drugs can actually do and what to expect from them on a longer time basis. With,methotrexate,physicians know what it can do,and expect on a long term basis.
This is indeed a new era in the management of RA. But the government bureaucrats must get their health care in order that none that needs biological therapy is not denied treatment because of cost. For example in Canada,Remicade is approved for Chron's disease,but not for RA. HIV (aids)patients,high cost medication is paid by the government,but not RA. Special access plans is not the solution.

I want to tell a story about a survivor of RA.the name is unimportant,lets call him Tim,but his story might be of value to some. The lesson isn't always easily learned,Tim 35,began to cope when he learned to accept RA,he says,as "a part of me". It's not entirely me,and I'll never be free of it". But instead of "dissociating" when he has a lot of pain,instead of seeing his body as a enemy, he wants only to escape,Tim learned to stop turning out. He's come to understand his limitations and gain some control over his life again.
"I used to think I was just this person stuck in a crippled body",Tim says,"I'd try to disconnect myself from the neck up,all the time. I lived in a day-dream world,and the only time I was actually alive was when I was day-dreaming. I'd crawl into my own head,where I could run and play ball and do all those things I couldn't do in the real world. And that's where I liked to stay". the rest of the time,he endured a depression so black it came very near to being what a philosopher once called a "sickness unto death."
Tim sits angled uncomfortably into one end of the living room couch. His neck is painfully stiff;he doesn't turn his head if he can avoid it. There are scars visible on his left elbow and knee,below shirt-sleeves and shorts,evidence of two of five operations that have left him with artificial hips and a plastic knee. When he walks,his stride is laboured and out of site with his age. His hands,the knuckles deformed by disease,rest quietly in his lap as he brings back the years.
Recalling the past is a descent into darkness,and at times Tim's voice falters and his eyes mist. He agrees to to talk about this only after much soul-searching. The thought of exposing his pain,especially now that he hopes and believes the worst of it is behind him,wasn't easy.,but Tim feels a kind of obligation to speak. He believes that talking about his own experience of illness and depression might help other people get through theirs.
His story isn't unique,though it is wrenching. For more than twenty years,he's been taking a beating from arthritis and,emotionally,he's been down for the count more than once. What's important,though,is that he's gotten back on his feet. He knows he's never going to lick his arthritis,but he's learning to hold his own,with the RA and depression. And after everything he's been through,it feels like winning.
Tim was born in a Eas Coast mining village. It was there his ordeal began with a minor skiing accident,followed by the flu. In a way,he never recovered. In the next months,most of his joints became inflamed,and he was initiated into the harsh world of front-line anti-rheumatic drugs. He was eleven. Over the next few years,he went through "pure hell",a mental and physical anguish sometimes intensified by others' lack of understanding. During an arguement one day,another boy slapped Tim in the face. "It snapped my neck," he says,"and I blacked out. At that instant I realized how fragile I'd become. It hurt my neck,but it broke my heart. The whole illness hit me".
The disease went into remission for a few months,after knee surgery,and Tim thought he had it beat. Then it came back. This time he understood what was happening to him,he just totally gave up: " I lost all desire to live,Most of my prayers,for a whole year,were that I would die. The pain was excruciating. "This," he thought,"is how I'm going to spend the rest of my life".
At sixteen,both hips were replaced. Within months,the pain returned,and Tim drifted into alcohol and drug abuse. Can you imagine having RA and drug abuse,to cope with ? It's hell-triple trouble. "I felt like I was walking alone and looking into a window," he recalls,"like I never really belonged anywhere because I never had anyone my age to communicate with. No one at school was sick".
Tim turned eighteen. One day in early fall,he was home alone reading in front of the fireplace. "To this day," he says,"I don't know why this happened,but I got up to go to the kitchen. It'd just gotten dark,and I walked out to the porch and grabbed a budket. The next thing I know,I'm sitting in front of the fireplace again with my wrists split wide open and my hands in the bucket. When it dawned on me what I was looking at,it was like it wasn't even me that was there,I was just sitting there looking at my wrists with big gaping slashes in them and blood pouring into the bucket.
"I don't know where the knife came from. I phoned my brother,who lived next door,and told him,"you've got to come over. I did something really stupid. I slashed my wrists." When the reality of it started sinking in,I began to lose it. I could't believe I'd actually done it. the scary part was not realizing I had done it it till after the fact. I still don't recall actually doing it ".
Tim spiralled through most of the classic symptoms of depression,fellings of helplessness and isolation,lack of meaning and prolonged despondency,modd swings and emotional outbursts,sleep disorders and lack of appetiate,significant weight loss. Fuelled by drug abuse and alcohol,he developed a poor self-image and lost all will to live. His suicide attempt "was the climax to a steady decline in who I rhought I was. From the time I got sick until that point,the disease not only ate away at me physically but mentally as well. The only time I wasn't depressed was when I was stoned or drunk".
After the suicide attempt,a desparate cry for help,Tim was assigned a psychiatrist and admitted to hospital. It would be years filled with more suicidal thoughts,more despair and physical suffering,before he learned to accept the fact of his RA,and how to deal with depression in a real and lasting way.
Tim's arthritis didn't go away,but he go it under control. He got his weight up,got into better physical shape,and began trining for a career in computers. He took up some of the resposibility for his sister's children and developed a special relationship with an understanding woman. Most of the changes he was able to attribue to having "actually accepted the diseas as a part of life". Depression didn't vanish from his life,but he learned to handle it,rather than letting it handle him.
Tim in his youth didn't get the proper couseling,or medical help,that is available to-day. Everyone with RA doesn't suffer from depression.