Rheumatoid arthritis (RA) is a common disease that affects about 1% of the population worldwide. Women are affected almost 3 times as often as men. The prevalence increases with advancing age, and 4% to 6% of the white population older than 65 years may have RA. Although the cause is unknown, evidence suggests an association between severe RA and HLA, particularly to alleles coding for a shared epitope on the HLA-DRB1 molecule.

Major features of active disease include symmetrical polyarthritis with joint swelling and tenderness and morning stiffness lasting for an hour or longer. Subcutaneous nodules, presence of rheumatoid factor (in about 80% of patients with RA), and radio graphically evident erosions or juxta-articular osteoporosis in or adjacent to the involved joints are further characteristics of RA.

The onset and clinical course of RA are variable. Gradual onset is most common. About 20% of patients will have a monocyclic course, which will abate within 2 years, whereas the rest will have a polycyclic or progressive course.¹ The long-term prognosis of patients with abrupt onset of disease is similar to that for patients with gradual onset of disease.²

Rheumatoid arthritis is one of the most common causes of disability. After 12 years of disease, more than 80% of patients with RA are partially disabled, and 16% are completely disabled.³ Life expectancy is shortened by an average of 7 years in men and 3 years in women, an outcome equivalent to the increased mortality of patients with Hodgkin disease, diabetes, and stroke.⁴ Factors contributing to the poor prognosis include the presence of extra-articular disease and infections, as well as complications of treatment such as gastrointestinal (GI) toxic effects of nonsteroidal anti-inflammatory drugs (NSAIDs).

MANAGEMENT PRINCIPLES

The goals of therapy for RA are to alleviate pain, control inflammation, preserve the ability of the patient to function in activities of daily living and work, and prevent joint destruction. Appropriate and timely therapeutic intervention after accurate diagnosis diminishes not only the symptoms but also the progress of RA. The primary care physician has a crucial role in this process by early recognition of the symptoms of RA, leading to its diagnosis and use of the resources necessary to establish a successful treatment program to achieve these goals, and by participating in the ongoing management of the patient with RA.Early in the course of RA, education on the disease and vocational, lifestyle, and family counseling must be provided. Patients are best served by a multidisciplinary team that includes a rheumatologist and other specially trained medical personnel, including nurses and occupational and physical therapists skilled and knowledgeable about RA. Physical modalities such as joint protection, orthotics and other adaptive devices, and exercises improve the symptoms, function, and well-being of the patient. Adequate rest reduces the fatigue associated with active RA, and resting the involved joints lessens the symptoms of inflammation.

THERAPY

Nonsteroidal anti-inflammatory drugs reduce inflammation and help relieve pain but seldom completely eliminate signs and symptoms of active arthritis. They inhibit 1 or both types of cyclooxygenase (COX). Cyclooxygenase-1 is constitutively expressed in the GI mucosa, kidneys, platelets, and vascular endothelium. Cyclooxygenase-2 is functionally expressed and promotes the elaboration of prostaglandins in inflamed tissues.

Selective blockage of COX-2 may lead to an improved safety profile for these agents. Celecoxib and rofecoxib are the first such agents available in the United States that selectively block COX-2. Rofecoxib is withdrawn from the market due proven increase in cardiac risk.  Of importance, the efficacy of these COX-2 inhibitors does not differ substantially from that of conventional NSAIDs. Their putative advantage is principally because of a reduced rate of adverse events, especially upper GI bleeding.⁵ Cyclooxygenase-2 inhibitors should be considered in patients at high risk of GI bleeding, including those older than 65 years and those with a previous history of GI bleeding. Despite advantages, these drugs may be associated with important adverse reactions, including allergy and fluid retention, and like other NSAIDs should be used with caution in patients with renal insufficiency.

Glucocorticoids are the most potent suppressors of inflammation and may be needed to control severe polyarticular disease until disease-modifying antirheumatic drugs (DMARDs) have been added and become effective. At that point, the glucocorticoids should be tapered and discontinued. Glucocorticoids should not be used alone in the management of RA. Oral prednisone or an equivalent is given in dosages typically ranging between 2 and 15 mg/d, often in divided doses (eg, 2 mg twice a day). A split-dosing regimen is frequently necessary because the anti-inflammatory effect is relatively short. It is preferable, but often not possible, to avoid long-term glucocorticoid therapy in patients with RA because of the well-appreciated adverse effects of these drugs. Systemic extra-articular manifestations such as rheumatoid vasculitis may require treatment with initial prednisone dosages of 40 to 60 mg/d, tapering according to response.⁶ Intra-articular injection of glucocorticoids is an effective means for reducing pain and inflammation in individual recalcitrant joints.

Disease-modifying antirheumatic drug therapy is associated with reduced morbidity and mortality in patients with RA.⁷ It should be used when the diagnosis of RA has been established and before erosive change appears. Disease-modifying antirheumatic drugs are usually given with NSAIDs and glucocorticoids, if needed. The DMARDs currently in use are listed in Table 1. The mechanism of action of most of these agents is diverse and to a variable extent overlapping. For many of the agents, the mechanism of action is defined incompletely, whereas for some, including the new class of tumor necrosis factor (TNF) blockers, it is better understood.

For patients with mild disease, hydroxychloroquine is often the first drug of choice because of ease of use and its favorable toxicity profile. Retinopathy due to hydroxychloroquine rarely develops when appropriate dosages are used. The onset of antirheumatic disease activity occurs in about 3 to 4 months in almost 50% of patients, although 6 months may be needed for the full benefit to be realized. For patients with moderately active or severe newly diagnosed disease, methotrexate or sometimes sulfasalazine is a preferred initial choice. In patients with continuing active established disease, methotrexate may be used in combination with other agents including hydroxychloroquine, sulfasalazine, or both or cyclosporine, azathioprine, and the more recently available DMARDs.⁹

For patients with acute and severe disease, a combination of DMARDs, prednisone, and an NSAID may be initiated; the dose of prednisone should be tapered during the ensuing weeks to months as disease control improves.

Because of its favorable efficacy and toxicity profile, methotrexate is regarded by many rheumatologists as the anchor therapy for RA. The initial dosage is usually 7.5 to 10.0 mg/wk, titrated upward to an average dosage of 12.5 to 15.0 mg/wk, although dosages of 20 to 30 mg/wk (if tolerated) may be necessary to realize this drug’s therapeutic potential before the response is deemed “inadequate.” Methotrexate may be given in tablet or liquid form; the liquid form is substantially less expensive than tablets, and injection may be associated with less stomatitis and GI upset. Appropriately managed, methotrexate can be used effectively for long periods to control RA. Although generally well tolerated, methotrexate can cause GI upset and hepatotoxicity including liver fibrosis and cirrhosis. Concomitant alcohol use is an important risk factor for methotrexate-related hepatotoxicity, and thus alcohol should not be used by patients taking this drug. Methotrexate can also cause a syndrome of pulmonary hypersensitivity manifested by dyspnea, cough, and fever and should not be used in patients with hepatic or renal insufficiency or severe lung disease. Supplemental folate (usually 1 mg/d) seems to reduce the occurrence of other adverse effects, including stomatitis, hair thinning, and bone marrow suppression. In patients taking methotrexate, physicians should avoid prescribing antifolate drugs such as sulfamethoxazole for sinusitis or cystitis, which may precipitate pancytopenia.

Use of DMARDs has substantially improved disease control and the long-term outlook for patients with RA. Their use may be associated with a lower incidence of extra-articular disease manifestations such as systemic vasculitis. In a series of more than 3000 patients monitored for up to 20 years, patients who had received DMARD therapy had a 30% reduction in long-term disability and improvement in survival compared with patients who had received NSAIDs alone.⁷ Despite these successes, major challenges exist. For example, DMARDs are becoming more accepted among practicing physicians and their patients¹⁰ however, adverse effects or failure of the drug to produce long-term disease control often leads to a change in DMARD treatment.

To improve disease control, therapies that contain combinations of DMARDs are often used. About 50% of patients with RA treated by rheumatologists are prescribed combination therapies with either 2 or 3 DMARDs. The combination of methotrexate, hydroxychloroquine, and sulfasalazine is among the most popular regimens. Methotrexate is often combined with other DMARDs including cyclosporine, but many other combinations of DMARDs have also been used.

In addition to hydroxychloroquine and methotrexate, other traditional DMARDs include penicillamine, gold, and sulfasalazine. Sulfasalazine was among the first drugs to be developed for the treatment of RA and may be chosen as the initial DMARD for patients with no allergy to sulfa, rather than hydroxychloroquine or methotrexate. The use of gold or penicillamine is seldom recommended because of the limited efficacy and the pronounced incidence of adverse effects associated with these drugs.

Three to 6 months may be needed before agents such as gold, hydroxychloroquine, and even sulfasalazine are effective. If the response is inadequate after 6 months of treatment, a second DMARD should be added or the DMARD regimen should be changed.

In the past year, 3 new DMARDs, etanercept, infliximab, and leflunomide, have been approved for the treatment of patients with RA.^11,12 Etanercept and infliximab are TNF-α antagonists that have powerful anti-inflammatory effects in patients with RA. Tumor necrosis factor is a potent inflammatory cytokine expressed in increased amounts in the serum and synovial fluid of patients with RA. It promotes the release of other proinflammatory cytokines, particularly interleukin (IL) 1, IL-6, and IL-8 and stimulates protease production. Etanercept consists of fusion monoclonal antibody composed of 2 identical chains of recombinant human TNF-α receptor fused with the Fc portion of human IgG1. In vitro it binds to soluble TNF. About 70% of patients receiving subcutaneous etanercept at dosages of 25 mg twice a week have substantial improvement in the extent of joint inflammation, often within 1 to 2 weeks after initiation of therapy. This improvement can be enhanced by combination with methotrexate. Adverse effects of etanercept are influenza-like symptoms and reactions at the injection site, which usually abate after the first few injections. The efficacy of infliximab, a recombinant TNF receptor fusion protein, seems to be roughly equivalent to that of etanercept. Infliximab is given intravenously once every 8 weeks, a regimen that may be more convenient for some patients. Potential long-term risks of these TNF-α antagonists have not been established. Infliximab may be associated with development of autoantibodies such as antinuclear antibodies. To date, neither drug has an increased risk of malignancy, autoimmune disease, or infection, issues that are the subject of ongoing postmarketing surveillance. The cost of these drugs is about $10,000 to $12,000 a year, generally higher for etanercept than infliximab. The available TNF-α antagonists should be considered in patients with recalcitrant disease not controlled by methotrexate.

Leflunomide is a pyrimidine synthesis inhibitor with clinical efficacy generally equivalent to methotrexate.¹³ Adverse effects reported include rash, alopecia, allergy, weight loss, thrombocytopenia, and diarrhea. Diarrhea often occurs early in the course of treatment and may abate, but discontinuation of the drug is necessary when the diarrhea cannot be ameliorated with dose reduction or concomitant use of antidiarrheal agents.

Serious extra-articular disease manifestations including vasculitis, scleritis, and recalcitrant serositis generally require systemic glucocorticoids and may necessitate the use of immunosuppressive agents such as cyclophosphamide. In my opinion, the only indication for cyclophosphamide in the treatment of RA is severe extra-articular disease, especially vasculitis.

Of importance, the decision about the use and aggressiveness of DMARD therapy should not be based solely on the presence or absence of the rheumatoid factor. Early in the course of RA, the rheumatoid factor may be absent, whereas in patients with established poly articular arthritis, absence of the rheumatoid factor is not invariably associated with mild disease and good disease outcome. Treatment must be tailored to the disease manifestations and needs of the individual patient. Consultation with a rheumatologist is helpful for patients who are pregnant or considering pregnancy because many antirheumatic drugs have severe fetal toxic effects including teratogenicity. Management suggestions for several clinical scenarios involving patients with RA are listed in Table 2.

When the symptoms of RA are well controlled, the glucocorticoids should be tapered, and the NSAIDs may also be tapered or used as needed. As a generalization, DMARD therapy should be continued indefinitely; however, if the patient does well and has no signs of active disease for at least 1 year, DMARD therapy could be carefully tapered. With combination DMARD therapy, one of the DMARDs could be tapered if the patient has been in remission for at least 6 months. Methotrexate can be considered as an “anchor” therapy and generally continue this drug for the longest period. Of note, less than 5% of patients with bona fide seropositive RA remain in long-term disease-free remission.

Rheumatoid arthritis is a serious disease. Follow-up early in the course of disease and in patients with poorly controlled disease should be every 2 to 6 weeks. Patients with well-controlled disease may be seen every 3 to 6 months. The primary care physician has an important role in the management of RA and can effectively guide and monitor routine therapy, with periodic consultation by a rheumatologist as needed. Assessment of disease activity and treatment efficacy is enhanced substantially with serial use of standard outcome measures, including duration of morning stiffness, severity of fatigue, presence and degree of joint pain and stiffness including joint counts, global and disease-specific health assessment instruments such as the modified Health Assessment Questionnaire, erythrocyte sedimentation rate, and radiographs of involved joints.

Appropriate medical care for patients with RA includes immunization and prompt treatment of infections. Patients with RA have a high risk of infections even if they are not taking DMARDs but particularly when they are taking immunosuppressive drugs. Several medications used to manage RA, including NSAIDs, cyclosporine, and glucocorticoids, may cause or exacerbate hypertension. Rheumatoid arthritis is associated with an increased incidence of pulmonary disease, and patients who smoke have an especially high rate of lung disease. In patients at high risk of GI bleeding, including elderly women and those with a previous history of GI bleeding, prophylaxis is achieved with agents such as proton pump inhibitors and misoprostol. As a general principle, use of NSAIDs should be avoided when possible and certainly discontinued when symptoms diminish. Virtually all patients with RA have or develop osteoporosis as a complication of the disease or its treatment. Adequate intake of calcium (1200-1500 mg/d) and vitamin D (400 IU/d) is important. In all patients receiving long-term corticosteroid therapy, including men, an antiresportive agent such as bisphosphonates or calcitonin should be considered. In postmenopausal women, estrogen replacement therapy or agents such as raloxifene may be considered. Finally, mouth and eye moisturization is necessary for patients with sicca complex symptoms.

Understanding the relationship of disease susceptibility and severity with genetic factors may provide an avenue for individualized treatment of patients with RA in the future. It may be possible to treat patients lacking genetic markers of severe disease with milder agents, while those with markers of severe disease may be treated more aggressively. More than 80 drugs are currently being developed for treatment of RA; thus, further advances in the management of the disease are forthcoming.

Questions About Treatment of RA

1. Which one of the following would be an acceptable therapeutic program for a patient with early mild RA?

1. Hydroxychloroquine with an NSAID
2. Hydroxychloroquine, methotrexate, and an NSAID
3. Methotrexate and prednisone at 5 to 15 mg/d
4. Etanercept and prednisone
5. Leflunomide and sulfasalazine

2. Which one of the following regimens would be appropriate for a patient with RA and new-onset systemic vasculitis?

1. Azathioprine, hydroxychloroquine, and prednisone at 10 to 15 mg/d
2. Prednisone, 20 mg/d, and methotrexate, 25 mg/wk
3. Prednisone, 40 to 60 mg/d, and cyclophosphamide
4. Cyclosporine and prednisone at 20 to 30 mg/d
5. Prednisone, 40 to 60 mg/d, and immunoabsorption column treatment

3. Which one of the following situations is not a relative contraindication to the use of etanercept?

1. Patient with history of tuberculosis exposure
2. Patient with history of lymphoma
3. Patient with active chronic infection
4. Patient with newly diagnosed RA
5. Patient with established RA receiving hydroxychloroquine and methotrexate

4. Which one of the following statements about the clinical course of RA is false?

1. The median life expectancy of patients with RA is the same as that for the general population
2. Most patients with RA have some disability after 12 years of disease
3. Predictors of poor outcome in patients with RA include the extent of radiographic erosions, female sex, and functional class
4. Patients in whom the rheumatoid factor is present have a worse prognosis than those with seronegative disease
5. Disease-free remission is unusual

5. Which one of the following statements about COX is true?

1. Cyclooxygenase-1 is constitutively expressed in the gastric mucosa, kidney, and platelets
2. Use of the currently available selective COX-2 inhibitors is safe in patients with renal failure
3. Currently available selective COX-2 inhibitors have been proved in multiple clinical trials to be safe in patients who are taking warfarin
4. Cyclooxygenase-1 is functionally expressed and promotes the elaboration of prostaglandins important in the inflammatory cascade
5. Selective COX-2 inhibitors are not associated with risk of GI bleeding Correct answers: 1. a, 2. c, 3. e, 4. a, 5. a

REFERENCES

1. Masi AT. Articular patterns in the early course of rheumatoid arthritis. Am J Med. 1983;75(suppl 6A):16-26.
2. Jacoby RK, Jayson MI, Cosh JA. Onset, early stages, and prognosis of rheumatoid arthritis. BMJ. 1973;2:96-100.
3. Sherrer YS, Bloch BA, Mitchell DM, Young DY, Fries JF. The development of disability in rheumatoid arthritis. Arthritis Rheum. 1986;29:494-500.
4. Mitchell DM, Spitz PW, Young DY, Bloch BA, McShane DJ, Fries JF. Survival, prognosis, and causes of death in rheumatoid arthritis. Arthritis Rheum. 1986;29:706-714.
5. Wolf MM, Lichtenstein DR, Singh G. Gastrointestinal toxicity of nonsteroidal antiinflammatory drugs. N Engl J Med. 1999;340:1888-1899.
6. Matteson EL, Conn DL. Extraarticular manifestations of rheumatoid arthritis. In: Weisman MH, Weinblatt ME, eds. Treatment of the Rheumatic Diseases. Philadelphia, Pa: WB Saunders Co; 1995:52-67.
7. Fries JF, Williams CA, Morfeld D, Singh G, Sibley J. Reduction in long-term disability in patients with rheumatoid arthritis by disease-modifying antirheumatic drug-based treatment strategies. Arthritis Rheum. 1996;39:616-622.
8. American College of Rheumatology Ad Hoc Committee on Clinical Guidelines. Guidelines for monitoring drug therapy in rheumatoid arthritis. Arthritis Rheum. 1996;39:723-731.
9. Borigini MJ, Paulus HE. Rheumatoid arthritis. In: Weisman MH, Weinblatt ME, eds. Treatment of the Rheumatic Diseases. Philadelphia, Pa: WB Saunders Co; 1995:31-51.
10. Ward MM, Fries JF. Trends in antirheumatic medication used among patients with rheumatoid arthritis, 1981-1996. J Rheumatol. 1998;25:408-416.
11. Weinblatt ME, Kremer JM, Bankhurst AD, et al. A trial of etanercept, a recombinant tumor necrosis factor recepton:Fc fusion protein, in patients with rheumatoid arthritis receiving methotrexate. N Engl J Med. 1999;340:253-259.
12. Moreland LW, Baumgartner SW, Schiff MH, et al. Treatment of rheumatoid arthritis with a recombinant human tumor necrosis factor receptor (p75)-Fc fusion protein. N Engl J Med. 1997;337:141-147.
13. Mladenovic V, Domljan Z, Rozman D, et al. Safety and effectiveness of leflunomide in the treatment of patients with active rheumatoid arthritis. Arthritis Rheum. 1995;38:1595-1603.

In order to develop what we call the "empathic position" a person has to develop to the "depressive position" -- in a nutshell what this means (via Melanie Klein's theory of Object Relations) is that someone who HAS attained this will be a "WHOLE" self.

We already looked at the negative mother in that last article, but let's look at some of the types of core woundings that can produce Narcissism.  Think about who Narcissus was in Greek Mythology.  Narcissus needs to "gaze" at himself, and also, likes to bask in the reflected gaze of others?  (Mirror) This is how NARCISSUS feels "alive."  Otherwise, there is NOTHING?

In other words a non-self.  This isn't a SELF that can be "empathic" because it never got there?

Developmentally.  In this election we have seen the long "service" careers of both Hillary and John McCain. What they both want to "serve" is the public?  They have EMPATHY!

How we know their opponent does not have empathy?  We can look at the Jeremiah Wright thing for one thing.  As soon as the church he spent 20 years in wasn't going to be helping him, he just left it.  Someone with EMPATHY, would NOT have done this.

Here is why.  A person who had passed the Depressive stage of development would know that doing something like this would "HURT" the feelings of an old friend.  A child without empathy could tear the wings off a butterfly and laugh when it squiggled on the ground.  In other words, there is nothing THERE? On the inside to know that something wrong has been done? (Or something unethical).

A few articles back we were talking about Jung's typology, and the various types.  This is what a THINKING SENSATE would look like.  In other words, there is thinking, and there are sensations of pleasure?  But no FEELING or INTUITIVE parts of the personality.  The personality is like an egg, but with a hollow void inside.  The rest of us, have our feeling and intuitive feelings going.

Narcissism is not really a disorder that can be cured?  It is a Personality disorder.

The fragile "glue" that is holding the person together is like the egg shell?

How they behave is called "egosyntonic."  Meaning they cannot differentiate that they have done anything wrong?  In a healthy personality we have the "egodsytonic" which is the opposite thing.  This means, the person in the second category has the ability to understand there is something going on that feels "wrong" to them.  Let's use Depression as an example on this.  A person starts feeling "depressed"  for some reason.  They have the ability to realize that something is "wrong" with the way they normally feel, so they go to a doctor to "take care of it."

If we use WW2 as example here, it would have been the "egosyntonic" types who designed the gas chambers and decided to massacre all those people.  They wouldn't have seen anything "wrong" with what they did.  A Narcissist on a scale like this is capable of doing terrible things and not having a bad thought about it at all.  There is NO FEELING!

This is what the inferior introverted feeling function looks like.  There isn't a HEART, but there might be deep feelings twisting around in there, that are wounds based on what happened in childhood, in the object relations, good and bad mother, and environment.

These types can often be heads of corporations?  They have slick, shallow exteriors and oftentimes pass undetected unless they have done something wrong?  They can be extremely charming on the exterior.  Society itself, is going to notice the WRONGDOING, because most of society has a sense of something looking like a "red flag."  Because we are the 90% that got the "good enough mothering!" and so we all attained the "Depressive Position" as we were developing liitle children.

So, what kind of things cause a thing like this?

And what is inside the egg?  In terms of primitive repressed emotions.

Yikes, kiddos & pals...here we go!

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One thing about this whole election we have to view it as a generation of the walking wounded.  The electorate has witnessed the breakup of the nuclear family.  It could have been their own parents?  If you are looking at tail end baby boom demographics.

Unlike what happened to Bill Clinton when he tried to deny inhaling, we've had the last 8 years of a former coke addict reformed via religion.  You could think of half of this population as reformed addicts?  Also, you have the rise of big pharma to fill in where illegal drugs were once available.  How many cylinders are functioning in this group of people?  Interesting question.

You have a huge gay and lesbian population that is going to clash with the heterosexual religious right.  You have the baby boom with its new age spirituality.  You have the abortion question.  You have tremendous poverty all across the United States, the global wound of non-ecological thinking and the impending climate disasters.

Enter the Patriarchy.  The corrosive sexism witnessed in this campaign has shown feminists the terrific splits that have occurred for collective psyche in a post 1960's era.

One of the things I've thought about, in terms of my own life this election season is how many decisions I have had to live with because of the male psyche.  The reality for my generation of white married feminists is that if we wanted to keep the relationship we had to do what the man says.  Well, for me anyway.  The women had to defer to male authority once that golden band went on your left hand.

White feminists are used to white male supremacy, but black male supremacy?

Obama's camp has given this whole group of his age white women the finger!  Why?

Omnipotent narcissism.  It may be a model that works in a black cultural paradigm?  My sense is that in the quest for trancendence of "middle-classness" the ethos of the church the Obama's attended that there is no sense of a shared relationship between black and white feminist thought.

White women who have had to transcend white male patriarchal sexism, now have confronted an insulting black male sexist in this candidate!  To experiece sexism coming from one of our own age bracket in such a maligant manner?

It boggles the mind.

My brother is Obama's age.  He also has a fragile shell based on abandonment issues by my mother and his father, but not quite the same...

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Dr. Mehta: Treating bone metastases

October 1, 2007

BY DR. NILESH MEHTA drnileshdmehta@gmail.com

I saw Mrs. S in my office after she was found to have bone cancer. Bone cancer is a very loosely used term by patients and their families, but it has very specific implications when physicians deal with it. Cancer can start in the bones, which is called "primary" bone malignancy, but the more common scenario is when patient's cancer spreads to the bones, referred to as "metastases." In the case of Mrs. S, when she first developed chest pain, her initial approach was to use Motrin for pain relief for a couple of weeks. Unfortunately, her pain did not subside. After she had X-rays and CAT scans to evaluate her discomfort, her primary doctor told her that she had a spot in her sternum (the bone in front of the chest). Further tests revealed that Mrs. S had lung cancer and it had spread to her sternum. Cancer patients with bone metastases often have significant discomfort and pain requiring pain medications and specialized care. These patients can also develop fracture of bones. They often require "spot" radiation to alleviate the pain and discomfort. Cancers that spread to the bones include breast, lung, multiple myeloma, prostate cancer etc. Fracture of long bones is also not uncommon in patients who have bone metastases. Treatment for patients with bone metastases includes pain medications, radiation therapy, chemotherapy, and bisphosphonates. Medications like Aredia or Zometa (bisphosphonates) are routinely utilized on a once-a-month basis to alleviate bone pain in patients. A new drug, Denosumab, is being studied and directly compared to a bisphosphonate-zoledronic acid (Zometa) in a group of cancer patients with bone metastases. We offer this clinical trial from Amgen to patients at our office, and we have enrolled over a dozen patients. Results of this trial will be available in the next three to four years. Osteoporosis is also a major public health threat affecting nearly 44 million Americans. Osteoporosis is not a cancerous condition but it is a process of aging when there is decreased bone mineral density. Osteoporosis should not be confused with bone metastases. Osteoporosis affects women as well as men. Several prevention and treatment strategies for osteoporosis are already in place for post-menopausal women and I would urge my readers to discuss this with their doctors. Intravenous Bisphosphonate therapy given once a year also was approved for osteoporosis in post-menopausal women. This osteoporos drug, zoledronic acid (Reclast, a new drug which has the same ingredient as Zometa) was found to have the potential to cut the risk of spine fractures by 70 percent and the chance of hip fractures by 41 percent. Reclast can cause an abnormal heart rhythm (atrial fibrillation) as a rare side effect. It is interesting to note that physicians will be using the same drug (zoledronic acid -- Zometa and Reclast) for patients who have osteoporosis and bone metastases, albeit on different schedules -- once a year for osteoporosis and once a month for cancer patients with bone metastases. With advances in medical therapy, doctors are finding new treatments for osteoporosis. Oncologists are also better equipped to handle patients with bone metastases. A lot of positive research is being done in bone health, osteoporosis, bone metastases and the future of these research endeavors is very bright. Dr. Nilesh D. Mehta is clinical associate professor at Rosalind Franklin University. Source: http://www.suburbanchicagonews.com/newssun/lifestyles/582102,5_5_WA01_MEHTA_S1.article

Di dunia, satu dari delapan perempuan akan terdiagnosa menderita kanker payudara selama masa hidupnya. Di Indonesia sendiri menurut Pita Pink, kanker payudara pada perempuan merupakan penyebab kematian nomor 2!!  setelah kanker leher rahim. Dan ternyata macam penyakit ini lebih dari satu, bisa dilihat disini.

Mungkin karena kanker ini tidak menunjukkan gejala apapun pada tahap awal sehingga orang ( perempuan) sukar untuk mengetahuinya. Sehingga penting bagi perempuan untuk melakukan pemeriksaan berkala secara teratur, baik pemeriksaan payudara sendiri (SADARI),  pemeriksaan pada profesional kesehatan atau mammografi. Artikel ini  dan ini menurut saya penting untuk dibaca perempuan (juga para suami). Ayo kita tingkatkan kewaspadaan terhadap kanker payudara!!