Rheumatism by Dr. Lance Christiansen

Jump to navigation Jump to search
Rheumatism by Dr. Lance Christiansen
ICD-10 M79.0
ICD-9 729.0
MeSH D012216

WikiDoc Resources for Rheumatism by Dr. Lance Christiansen

Articles

Most recent articles on Rheumatism by Dr. Lance Christiansen

Most cited articles on Rheumatism by Dr. Lance Christiansen

Review articles on Rheumatism by Dr. Lance Christiansen

Articles on Rheumatism by Dr. Lance Christiansen in N Eng J Med, Lancet, BMJ

Media

Powerpoint slides on Rheumatism by Dr. Lance Christiansen

Images of Rheumatism by Dr. Lance Christiansen

Photos of Rheumatism by Dr. Lance Christiansen

Podcasts & MP3s on Rheumatism by Dr. Lance Christiansen

Videos on Rheumatism by Dr. Lance Christiansen

Evidence Based Medicine

Cochrane Collaboration on Rheumatism by Dr. Lance Christiansen

Bandolier on Rheumatism by Dr. Lance Christiansen

TRIP on Rheumatism by Dr. Lance Christiansen

Clinical Trials

Ongoing Trials on Rheumatism by Dr. Lance Christiansen at Clinical Trials.gov

Trial results on Rheumatism by Dr. Lance Christiansen

Clinical Trials on Rheumatism by Dr. Lance Christiansen at Google

Guidelines / Policies / Govt

US National Guidelines Clearinghouse on Rheumatism by Dr. Lance Christiansen

NICE Guidance on Rheumatism by Dr. Lance Christiansen

NHS PRODIGY Guidance

FDA on Rheumatism by Dr. Lance Christiansen

CDC on Rheumatism by Dr. Lance Christiansen

Books

Books on Rheumatism by Dr. Lance Christiansen

News

Rheumatism by Dr. Lance Christiansen in the news

Be alerted to news on Rheumatism by Dr. Lance Christiansen

News trends on Rheumatism by Dr. Lance Christiansen

Commentary

Blogs on Rheumatism by Dr. Lance Christiansen

Definitions

Definitions of Rheumatism by Dr. Lance Christiansen

Patient Resources / Community

Patient resources on Rheumatism by Dr. Lance Christiansen

Discussion groups on Rheumatism by Dr. Lance Christiansen

Patient Handouts on Rheumatism by Dr. Lance Christiansen

Directions to Hospitals Treating Rheumatism by Dr. Lance Christiansen

Risk calculators and risk factors for Rheumatism by Dr. Lance Christiansen

Healthcare Provider Resources

Symptoms of Rheumatism by Dr. Lance Christiansen

Causes & Risk Factors for Rheumatism by Dr. Lance Christiansen

Diagnostic studies for Rheumatism by Dr. Lance Christiansen

Treatment of Rheumatism by Dr. Lance Christiansen

Continuing Medical Education (CME)

CME Programs on Rheumatism by Dr. Lance Christiansen

International

Rheumatism by Dr. Lance Christiansen en Espanol

Rheumatism by Dr. Lance Christiansen en Francais

Business

Rheumatism by Dr. Lance Christiansen in the Marketplace

Patents on Rheumatism by Dr. Lance Christiansen

Experimental / Informatics

List of terms related to Rheumatism by Dr. Lance Christiansen

Please Take Over This Page and Apply to be Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [1] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.

Overview

Rheumatism is a specific term for the chronic, systemic, inflammatory, autoimmune disease triggered by Streptococcus pyogenes infections. Acute rheumatism was the common term for rheumatic fever, the most elevated level of rheumatic autoimmunity, up through the early decades of the 1900's. High-grade rheumatic fever decreased in incidence, in modern western societies, secondary to improvements in living conditions including the development of antibiotics.

In 1931 Coburn in the USA and Collis in England determined, somewhat simultaneously that Streptococcus pyogenes caused rheumatic fever, but professional inertia being what it is, physicians did not completely adopt his theory until the late 1940's to early 1950's when rheumatic fever as a high-grade disease was becoming less and less common.

Starting in the 1920's slowly, but then accelerating, especially in the 1950's, medical practice and education became conceptually segregated by means of specialty-organized, procedure-dominated concepts. By the turn of the century, 2000, even office calls by physicians had procedure codes mandated by government agencies. However, since acute rheumatic fever, and moreso, chronic rheumatism are both systemic disease processes with multitudes of target-organ manifestations they simply were not recognized, or ceased to be recognized, by the members of the specialty-oriented medical community. Even rheumatology was "elbowed" into dealing with connective tissue only! The medical paradigm, therefore, that developed simply never understood chronic rheumatism in a modern, etiological way even though all the elements of its understanding had been provided by investigators in prior eras, by microbiological breakthroughs, and by the initial insights made in autoimmune disease concepts.

Lesser levels of rheumatic autoimmunity were still propagated throughout human society, including modern western countries, since Streptococcus pyogenes infections still existed endemically within modern western countries and all other societies so they still caused pathological, rheumatic, systemic, inflammatory, autoimmune-mediated responses within "all" individuals in human society, but at a lesser level of intensity in modern western countries.

The clinical understanding of high-grade rheuamtic fever decreased so that, nowadays, the average physician has virtually no or little knowledge of it at this time, threrefore, the knowledge of the much lower grade, chronic rheumatic autoimmunity and its target-organ manifestations, is virtually null in modern western medicine.

Because of the belated full acceptance, by the medical community, of the cause of acute rheumatic fever, just as it was becoming less and less common in the late 1940's and 1950's, the wisdom concerning lesser, chronic levels of rheumatic autoimmunity never was established in modern medicine even though as early as the late 1700's the "clinical cause" of acute and chronic rheumatism was reasonably well known.

For instance, Galen, the famous Greek physician in the Roman period, who published over 66,000 pages of medical, philosophical, and scientific information, half of which has managed to survive since 200 AD, coined the word rheumatism. Rheum, in Greek, means to flow, or phlegm. The phrase "a defluxion of rheum" could be used. It was later connected with catarrh, influenza, or the grippe or other description of a respiratory disease. Galen knew, that when people developed contagions that caused the development of phlegm, or chronic phlegm development, they would also, eventually, develop chronic, painful problems that were part of the chronic disease of rheumatism. Arthritis, neuropathy (such as sciatica), angina, pericarditis, pleurisy, tendonitis, ligamentitis (for instance plantar fasciitis) are examples of modern names for target-organ manifestations of rheumatism.

The term "rheumatism" is still used in colloquial speech and in historical contexts, but it is no longer frequently used in medical or technical literature; it would be fair to say that there is no longer any recognized disorder simply called "rheumatism". The traditional term covers such a range of different problems that to ascribe symptoms and signs to rheumatism, would violate the artificially developed specialty structure that has developed in modern western medicine since the 1920's.

One of the first organizations that dealt with rheumatism, in the modern day, was the European League Against Rheumatism. Unfortunately, rheumatologists were shouldered out of dealing with infectious diseases, or problems of the body's organs, by the other specialty-segregated physician groups and so they deal with "connective tissue" even though they also, historically, have dealt with rheumatic fever, which is a high-grade, inflammatory, autoimmune-mediated, systemic disease process.

As a vestige of past wisdom, many individuals feel that arthritis, neuropathy, and tendonitis has something to do with rheumatism. For instance, during the early 1900's, in America, sciatica was termed sciatic rheumatism or hip gout, eczema of the hands was termed, salt rheum, and gout was termed, gouty rheumatism. Those who understood the collective wisdom of the time knew that the maladies described were part of the rheumatism complex. Old farmers, walking bent over with a cane often have said, "Oh, my rheumatism". Non-articular rheumatism, also known as soft tissue rheumatism, and which is now known as "fibromyalgia", was in prior eras known as "muscular rheumatism". Somewhat surprisingly that variously described condition is a dispersed sensory neuropathy: bilateral brachial plexitis and sacral plexitis that is made more symptomatic by use of the arms and legs. To understand the above pathophysiology an examiner must do an analytic neurological examination of the brachial plexus and the terminal nerves of the sacral plexus; they must "know" the location of the dermatomes of the body: in SPADES.

Within the chapter on rheumatoid arthritis in Harrison's Principles of Internal Medicine, 16th Edition (Kasper,D., et al., McGraw-Hill, 2005) the author describes rheumatoid arthritis as a systemic, autoimmune disease (it is in the section of the text about autoimmune diseases), and in prior editions it indicates, that at times exacerbations appear sometime after a feverish affliction. In the edition mentioned above, the 16th Edition, the following is mentioned: "In approximately 10% of individuals the onset is more acute, with a rapid development of poly arthritis, accompanied by constitutional symptoms, including fever, lymphadenopathy, and splenomegally." It describes that rheumatoid arthritis, better termed rheumatoid disease, features arthritic aspects, vasculitis, neuropathy, and organ infarction, even myocardial infarction. At times, the text indicates,"Neurovascular disease presenting either as a mild distal sensory neuropathy or as mononeuritis multiplex may be the only sign of vasculitis." Anemia, subcutaneous nodules, and osteoporosis are concomitant features of rheumatoid arthritis. It mentions that pericarditis is found in 50% of individuals with rheumatoid arthritis at autopsy.

The connections, mentioned above, of an acute disease triggering vasculitis, arthritis, neuropathy, myocardial infarction, anemia, pericarditis, and osteoporosis describes many of the same causes of pain that are historically attributed to rheumatism. The acute disease process mentioned, is a mild case of acute rheumatic fever, the systemic, inflammatory, autoimmune disease process that post-dates, from a week to five weeks, the Streptococcus pyogenes infection that triggers the rheumatic, autoimmunological response.

Within the text, Rheumatic Fever and Streptococcus Infection (Massell, B., Harvard Press, 1997) the author indicates that fifty percent of Streptococcus pyogenes infections that trigger rheumatic fever have such mild symptoms and signs that patients do not remember them so it would not be surprising that those low-grade infections and the somewhat higher grade infections would be missed, forgotten, or just thought to be mild concomitant problems.

Individuals who develop high-grade rheumatic fever would seemingly represent a different, and separate, acute disease process, but it also has symptoms and signs of vasculitis, arthritis, pericarditis, subcutaneous nodules, and neuropathy also, but it has other more serious manifestations of acute rheumatism, for instance, rheumatic carditis, heart failure, cardiac arrhythmias, rheumatic encephalitis, kidney failure, etc., and those are the target-organ manifestations of acute rheumatism (rheumatic fever) on which modern physicians have focused.

Like most diseases, rheumatic fever (acute rheumatism) exists as lower-grade, more subtle disease phenomenon most of the time, and relatively rarely, except in certain, favorable epidemiological situations, does rheumatic fever exists in the high-grade state that has the symptoms and signs popularized by the Jones Criteria. Surprisingly, T.Ducket Jones, MD did not think that Streptococcus pyogenes was the cause of rheumatic fever even in the early 1950's, even though Alvin Coburn published a monologue that provided proof that it did, in 1931. To keep using the Jones Criteria, nowadays, is improper, I surely think. To think that rheumatic fever is mainly a cardiac disease is also a gross error: it is a systemic autoimmune disease process that in high grade cases has serious, somewhat focused, cardiac, autoimmunological sequela.

Frequently, the target-organ manifestations of rheumatic autoimmunity, rheumatism, clinically appear as seemingly isolated maladies. Examples of some of them are:

The rheumatic diseases including rheumatoid (rheumatic) arthritis, psoriasis and its arthritis, lupus erythematosis, Sjogren's syndrome, scleraderma, ankylosing spondylitis, dermatomyositis, myositis, Wegener's granulomatosis, and others. Osteoarthritis is simply rheumatic arthritis that appears due to an individuals stress on the meniscus, usually the medial meniscus, when they have more subtle signs and symptoms of rheumatoid (rheumatic) arthritis in other joints.

Peripheral Neuropathies: Sciatic back pain (sciatic, posterior femoral cutaneous, pudendal neuropathy), femoral neuroapthy, carpal tunnel syndrome, ulnar neuropathy, peroneal neuropathy, meralgia paresthetica, and tarsal tunnel syndrome. Fibromyalgia is a dispersed neuropathy of the bilateral brachial plexus and the terminal nerves of the sacral plexus. The femoral nerve and the lateral femoral cutaneous nerves can be involved. Various cranial neuropathies such as rheumatic, trigeminal neuropathy, Bell's palsy, hearing deficits, vertigo, and abnormalities of the motor nerves of the eye are all caused by rheumatic autoimmunity. When neuropathies present more severely they are more systemic in nature so they manifest as the syndromes of multiple sclerosis, Guillain-Barre' syndrome, and, hypothetically, amyotrophic lateral sclerosis.

Endocrinopathies: diabetes, Addison's disease, Cushing's syndrome, hypothetically, polycystic ovary disease, testicular failure, hypothyroidism, hypoparathyroidism, and pituitary abnormalities of various types.

Benign Tumors and cancer of various types. Yes, cancer of all tissue types is a target-organ manifestation of the systemic autoimmune disease of rheumatism. The rheumatic neuropathies often appear before, or concomitantly, with cancer and they are termed, in that case, paraneoplastic neuropathy. Often the neuropathy is sciatica. Ulcerative colitis, Crohn's disease, celiac disease, primary sclerosing cholangitis, and many other rheumatic conditions such as dermatomyositis, lupus erythematosis, are paraneoplastic rheumatic conditions. I estimate that most individuals who develop cancer have rheumatoid (rheumatic arthritis). It is common for those who have cancer to also have coronary artery disease or other cardiac problem. The reason is that they are all caused by the same underlying cause: rheumatic autoimmunity: rheumatism.

Central Neuropathies: autism, ADHD, depression, schizophrenia, manic-depressive illness, disassociative reactions, etc. are manifestations of "rheumatism of the brain".

Gastrointestinal target-organ maladies: ulcerative colitis, Crohn's disease, celiac disease, primary sclerosing cholangitis, pancreatitis, peptic ulcers, gastric ulcers (Helicobacter pylori is just an exacerbating problem with rheumatic vasculitis), esophagitis, peridontal disease.

Bursitis: olecrannon bursitis, pre-patellar bursitis, tibial tuberosity bursitis (house maids knee), and subacromial bursitis.

Tendinitis: tendonitis of the long head of the biceps, DeQuervains tendonitis, Achilles tendonitis, and rotator cuff abrasions, tears, etc. Ligamentitis such as plantar fasciitis, deltoid ligamentitis of the medial foot, etc.

Cardiological rheumatic problems: rheumatic cardiac valves, coronary artery disease, acute and chronic myocarditis (LVH, global cardiac enlargement, and decompensated enlarged heart), pericarditis, and cardiac arrhythmias.

Kidney: rheumatic vasculitis leading to chronic rhenal failure, gout, and kidney stones.

Special Senses: cataracts, retinitis, iritis, keratokornus, uveitis, subconjuctival hemmorage.

Skin: seborrheic keratosis, dermatitis, nevi, angiomas, purpura, urticaria, telangectasias, rosacea, erythroderma, poliosis, vitilago, spider nevi, petechiae, actinic keratosis, Stevens-Johnson syndrome, hypothetically, pityriasis rosea, and others.

Since modern, specialty medicine missed out on recognizing rheumatism as an abiding, systemic, inflammatory disease that all people develop, they evolved the concept that the target-organ manifestations of chronic rheumatism were independent idiopathic diseases. That semantic error, using the term disease, when the cause of the malady is not known, led, I surely think to the general self-deception that physicians knew more than was true: they were dealing with syndromes and not well defined diseases. Coronary artery disease is really coronary artery syndrome, for instance. Crohn's disease is really Crohn's syndrome and the list can go on and on since the great majority of "diseases" that fill medical texts such as Harrison's Principles of Internal Medicine are really syndromes: symptom and sign patterns that appear commonly.

Since acute rheumatic fever decreases the immune response, hypothetically the innate immune response, "other" infections often develop with acute rheumatic fever (as enumerated by Sir William Osler in his text, Osler's Principles and Practice of Medicine, Twelfth Edition (McRae, T., D. Appleton-Century Co., 1935). Tuberculosis,diptheria, cholera, and other diseases are mentioned. Chronic rheumatism also causes a decreased immune response and I surely hypothetically think that tuberculosis, MRSA, Streptococcal necrotizing fasciitis, erysipelas, Lyme disease, mononucleosis, AIDS, possibly Chigas disease and malaria, are all infectious disease process that take place more commonly in individuals who have high-grade rheumatic autoimmunity: rheumatism.

One can consider that rheumatic fever itself is also an acute aspect of rheumatism and its former name, acute rheumatism, more or less, defines that concept.

Although the above disorders usually are not thought to have much in common etiologically, they are all target-organ manifestations of one variable inflammatory, autoimmunological disease process: rheumatism. One cannot expect the eye to respond to a systemic disease as the plantar facia responds. One cannot expect the medial meniscus to respond to a systemic inflammatory disease as the hip joint responds. One should not expect the brain to respond to a chronic, inflammatory autoimmunological condition as the heart responds. All rheumatic conditions are inflammatory in nature and share two characteristics: they cause chronic (though often intermittent) pain, and they are difficult to treat. They are also, collectively, very common. Aspirin, other NSAIDS, and streroid antiinflammatory medications are used, however, to treat many of them and they "work" reasonably well if taken in adequate doses for protracted periods. Even coronary artery disease, and recently cancer, at times, is prophylactically treated with aspirin.

Within the first edition of the Encyclopedia Britannica, on page 124, under the chapter on medicine, under the paragraph, "Of the rheumatism", a description of acute rheumatic fever similar to that written by Thomas Syndenham is provided. It mentions fever, chills, rapid heart rate, fatigue, lassitude, gastrointestinal problems, the sciatic pain (lumbago), and migratory arthritis. It saliently mentions, "The proximate cause is the inflammation of the lymphatic arteries." Further, it mentions, "The chronic rheumatism is either the remains of a rheumatic fever, or a continuation of pains that proceeded at first from lesser but neglected colds." It appears, clearly, that physicians in the mid-1600's knew that repeated "...lesser but neglected colds." could cause the systemic disease of rheumatism, but in the modern day, pundits of evidence- based medicine (they gave up on scientific medicine, I surely think) pontificate to student-physicians that, all "colds" are caused by viruses and so upper respiratory diseases, even sore throats and tonsilitis, are not to be treated with antibiotics.

The above pundits should read articles by Gene Stollerman, M.D., one of the last physicians who treated many, individuals who had rheumatic fever and who has written that physicians should treat patients with pharyngeal infections, after inspection provides the thought, that Streptococcus pyogenes could reasonably be the causual micorbiological agent. No wonder the American population is becoming populated with millions of cases of fibromyalgia (muscular rheumatism), diabetes, sciatica, autism, MS, cancer, cardiac disease, psychological diseases, and other conditions.

Treatment

Since the etiolgy of rheumatism has not been known, individuals throughout history have used a great number of traditional and more modern treatments for the many symptoms of rheumatism. Modern medical treatment often consists of non-steroidal anti-inflammatory treatments and steroid anti-inflammatory treatments. Both are used for acute, rheumatic fever also. Treatment for the target-organ manifestations of rheumatism are as varied as cryotherapy for dermatological lesions, both cancerous and benign, surgical treatment for rheumatic arthritis as of the knees and fingers, tendonitis of the rotator cuff, and spinal surgery for heriated spinal-discs, which is usually inappropriate. Aaron Filler, M.D. (backpain-guide.com) accomplishes piriformis canal enlargement procedures to decrease the pressure on the terminal nerves of the sacral plexus and often has good results from his procedures when individuals experience recalcitrant sciatica.

Somewhat commonly, initial therapy of the painful symptoms of rheumatism is to use analgesics, such as acetaminophen, and non-steroidal anti-inflammatory medications (NSAIDs), members of which are aspirin, ibuprofen, naproxen sodium, indomethocin, and diclofenac. Many others exist. Often, more efficacious analgesics are required and if individuals have meaningful pain, opiate analgesics have been safely used for hundreds of years.

If individuals know they have had rheumatic fever, prophylactic use of penicillin VK, G, or amoxicillin can be used to decrease the frequency of high-grade rheumatic fever, by decreasing meaningful Streptococcus pyogenes infections. Certain organizations are working on the development of a vaccine for Streptococcus pyogenes.

"Rheumatism" and weather

There has long been said to be a link between "rheumatic" pain and the weather. There appears to be no firm evidence in favour or against, but a 1995 questionnaire given to 557 people by R. Jamison and others at the Brigham and Women's Hospital's Pain Management Center concludes that "changes in barometric pressure are the main link between weather and pain. Low pressure is generally associated with cold, wet weather and an increase in pain. Clear, dry conditions signal high pressure and a decrease in pain"[2].

Within the first edition of the Encyclopedica Britannica, the following quote is provided: "The rheumatism chiefly attacks persons in the flower of their age, after violent exercise, or a great heat of the body from any other cause an, and then being too sudenly cooled." Within the text, Rheumatic Fever and Streptococcal Infection, cited above, the following is written: "Haygarth in 1805 was one of the earliest physicians to relate rheumatic fever to the throat when he noted that "persons who have been previously affected with the acute or chronical Rheumatism, the Gout, or sore throat, especially the first, are most liable to suffer attacks of this disease; and ought therefore to be particularly careful to avoid exposure to cold and moisture." In a study of 175 patients with acute rheumatism he observed that sixty-five of them ascribe their disease to "having caught a cold" and he expressed the opinion that the exciting cause was "exposure to cold and moisture.""

It is well known by mothers and physicians that respiratory diseases, colds, are more common in the autumn, winter and spring and those are the seasons when rheumatic fever is most common. In the above mentioned text, Rheumatic Fever and Streptococcal Infection, cited above, Bernard Schlesinger indicated, " It is no exaggeration to say that acute nasopharyngeal infection is the most serious menace to the rheumatic child with heart disease."

I do not think barometric pressure affects rheumatism's develoment, especially since it varies continually day in and day out and hour by hour, but cooler and damper weather affects the frequency of Streptococcus pyogenes infections. Damp weather is usually connected with lower barometric pressure and cooler weather often is connected with clear, high-pressure weather patterns. It is a sure fact that high altitude areas such as the Rocky Mountain area in the USA has an elevated frequency for the development of rheumatic fever cases for it was proved during the WW II period. Rheumatic fever, acute rheumatism, and therefore the development of chronic rheumatism is not limited, however, to any particular altitude or climate. The high-altitude area of Mexico features endemic rheumatic fever and I surely think that the great number of immigrants from Mexico, usually individuals from the more economically poor class, have been vectors for virulent strains of Streptococcus pyogenes and they have probably been one of the causes of the increased level of rheumatism as indicated by the increased incidence of fibromyalgia, explosive emotional behavior (Tourette's syndrome) in the United States.

Miscellany

A Trod in the West of England is a straight line or Fairy Path in the grass of a field with a different shade of green to the rest. People with rheumatism sought relief by walking along these tracks, though animals are thought to avoid them.[1]

References

  1. Pennick, Nigel (1996). Celtic Sacred Landscapes. Thames & Hudson. ISBN 0-500-01666-6. P. 132.

External links

Template:SIB



de:Rheuma it:Reumatismo he:שיגרון sl:Revmatizem ur:اشعالیت

Template:WH Template:WS Template:Jb1