Rheumatism by Dr. Lance Christiansen
| Rheumatism by Dr. Lance Christiansen | |
| ICD-10 | M79.0 |
|---|---|
| ICD-9 | 729.0 |
| MeSH | D012216 |
Editor-in-Chief: Lance Christiansen, D.O.
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Overview
The following information concerning the chronic, inflammatory disease of rheumatism was obtained from reading countless texts, journal articles, and on-line sources during a career in medical science and especially during the last eight years during which time I have conducted a clinical, academic and epidemiological study of rheumatic fever. In addition, and perhaps the most important, was the information I learned from patients who had had rheumatic fever and later developed recurrent rheumatic fever.
Much of the medical knowledge I accumulated was during my medical education, but much more was developed and accumulated during a thirty-year career as a general practitioner in medicine. I owned my own clinic, examined and treated patients during 230,000 patient visits, accomplished at least 2000 house calls, and treated males and females, of all ages, for all diseases. At times, I treated family members for up to four generations. The continuity of medical care that I provided, in a semi-rural setting, enabled me to learn a great amount of medical information not written in typical medical texts. In addition, my clinic was located in an economically depressed area of S.W. Washington State, wherein there was a mini-epidemic of rheumatic fever during 2004-2006 and at least ten people, who were my patients, and who had chronic rheumatism, died of recurrent rheumatic fever. That experience, and the intellectual study that it stimulated, led to a epidemiological study wherein I traveled to twelve countries and visited hospitals, clinics and people on the street. All together, the experiences I have mentioned provided the knowledge to write this article.
Between 2002 and 2005 I conducted a three-year, clinical investigation in order to determine the true cause of most peripheral neuropathies since so many of my patients, through the years, failed to improve after they experienced spinal surgery. I eventually determined that the venerated, herniated spinal-disc concept was flawed, and most of the surgery accomplished for them was, I learned, usually mis-applied. Most patients had suspicious arthritis of the lumbar and cervical spine that featured osteophyte development and bulging, intervertebral spinal-discs, but I learned that typical MRI procedures did not have the resolution to "see" spinal nerve roots in an analytical fashion. Since the bulging intervertebral spinal-discs are attention-getting on MRI images, and because they do, occasionally, cause symptomatic, spinal nerve root compression, generalizing that almost all bulging intervertebral spinal-discs cause nerve root compression was a classic "red herring".
Just because individuals have arthritis of the spine does not mean that one of its features, bulging intervertebral spinal-discs, cause frequent, symptomatic, nerve-root compression. After I managed to determine the cause of the painful neuropathies, I learned that the same disease that causes the neuropathies also causes the arthritis to the spine; an anatomical feature of the spinal arthritis, herniated spinal discs, did not necessarily cause the painful neuropathies. There are occassional herniated spinal-discs that cause spinal nerve root compression, but surgery for them is very common.
Eventually, after a long, investigative period, I learned most patients neuroloical pain was caused by rheumatic, autoimmune-mediated, vasculitic neuropathy of the terminal nerves of the sacral plexus in the piriformis canal(deep in the buttock), concerning lumbosacral/buttock pain, and of the brachial plexus within the axillary canal(deep in the shoulder), considering shoulder/cervical pain. I learned that motion of the arm at the shoulder and of the the thigh at the hip, or an accident wherein either of the structures were stressed, would often cause or exacerbate the pain patients sensed. Patients felt pain in the lumbosacral region, because of centripetal referred pain from the distal sacral plexus, located deep in the buttock, and pain in the cervical region, because of centripetal referred pain from deep in the shoulder.
During the above investigation I attracted 700 miserable, painful patients who had chronic neurological pain. Eventually, I learned that they all had had meaningful, repeated Streptococcus pyogenes infections (tonsillitis, sinusitis, bronchitis, pharyngitis, otitis media, impetigo, and vaginitis) and many of them had, when they were younger, rheumatic fever or scarlet fever. Younger patients, born after 1970 had "flu-like" diseases with more mild symptoms and signs than accepted "Jones Criteria" standards for diagnosing rheumatic fever. I learned from information in Sir William Osler's text, Osler's Principles and Practice of Medicine, Twelfth Edition, (McCrea, T., Appleton-Century, 1935), that there are subacute and less than subacute states of rheumatic fever with more subtle systemic symptoms and signs of rheumatic disease.
I conducted serology tests (ASO and Anti-DNase B titers) on over 100 patients and 70 were positive with elevated Streptococcus antibodies on one or more tests. Between the positive medical histories, the elevated serology tests, and those who had medical histories of "flu-like" diseases, chicken pox, measles, mononucleosis, and viral meningitis wherein the symptoms and signs were those of rheumatic fever, the great majority of the 700 patients, mentioned above, who had chronic neurological and arthritic pain, and other common diseases, were qualified to have had rheumatic fever. The septic responses were caused by rheumatic, systemic autoimmune inflammation and as time passed the autoimmune condition decreased, but it never disappeared. As the elevated rheumatic, autoimmune disease naturally decreased after infections by Streptococcus pyogenes patients maintained a low-level of rheumatic autoantibodies in their bodies and it caused chronic rheumatism. I learned that future, low-grade infections by Streptococcus pyogenes would cause an exacerbation in rheumatic stimulation establishing a chronic, waxing and waning autoimmune disease process: rheumatism.
Since Streptococcus pyogenes is endemic in human society, and a Russian Encyclopedia article (V. Nasonova & E. Talahaev) indicates that Streptococcus pyogenes is endemic in domestic animals, it seems that Streptococcus pyogenes causes a universal zooinosis, and therefore a, more or less, universal, chronic, inflammatory, autoimmune disease among most vertebrates, including humans: rheumatism.
As a reminder, the terms acute rheumatism, acute articular rheumatism, and rheumatic fever, all describe the same acute, high-grade autoimmunological disease caused from infections by Streptococcus pyogenes. There have been other more antiquated terms for rheumatic fever and sweating sickness and miliary fever. I have noted that the names of epidemics are often incorrect. For instance, in the mid-1800’s there were cholera epidemics in Buffalo, N.Y., but from their description they were caused by rheumatic fever. Rheumatic fever can cause gross gastrointestinal symptoms, for instance.
Current medical knowledge (Carapetis, JR.,et al., Lancet Jul 9-15; 366(9480): 155-68) indicates that an infection by a virulent strain of Streptococcus pyogenes, in a well rheumatically sensitized individual can cause the development of rheumatic fever, which is known to be an inflammatory, autoimmune disease process.
It has not been clinically recognized, however, that all infections by Streptococcus pyogenes cause an inflammatory autoimmune response and it slowly, but surely causes pathological damage to the body's tissues, and therefore organs, in a somewhat subtle, varying, but progressive fashion and causes, over time, the clinical signs and symptoms of rheumatism. Some of the more superficial clinical entities that are manifestations of rheumatism are: sciatica, carpal tunnel syndrome, ulnar neuropathy, meralgia paresthetica, De Quervain's tendonitis, Achilles tendonitis, olecrannon bursitis, rotator cuff abrasions and tears, and Dupuytren's contracture. One must remember, however, that rheumatism is a systemic disease process and all tissues, and therefore organs, are pathologically affected.
High-grade rheumatic fever decreased in incidence starting in the early 1900's, in modern, industrialized societies, secondary to the improvements in living conditions brought on by advances of the industrial revolution. Advances included larger homes that caused decreased crowding, smaller family size, more hygienic living habits, the common use of soap, home bathing facilities, clothes washers, dish washers, the pasturization of milk, and the use of antibiotics for respiratory infections starting in the 1930's. The environmental changes resulted in fewer and fewer Streptococcus pyogenes infections, and more importantly, perhps, infections with less virulence, so by 1970 high-grade rheumatic fever was a relatively rare disease in modern, developed countries.
Simultaneously with the above changes in the frequency of high-grade rheumatic fever, the citizens of modernized countries experienced a life-expectancy increase; in the USA the life expectancy increased from forty-seven in 1900 to about seventy-seven in 2000: an increase of about thirty years, which equates to an increase of 64% over a 100 year period. There has to be a logical reason for the increased longivity. The reason, mainly, was less Streptococcus pyogenes infections and lesser levels of rheumatic autoimmunity, including rheumatic fever, a disease that often caused the death of children and younger people, three to fifty years of age, and their decrease caused a remarkable increase in human longivity. There were other positive factors also, for instance, a better food supply, vaccines for other diseases, and improved medical care, especially supportive care and disease altering surgical procedures.
Rheumatic autoimmunity causes, initially and continually, an inflammatory vascular disease that results in inappropirate intra-arterial thrombosis especially at arterial bifurcations. The immune system reacts to localized intra-arterial thrombosis with a localized inflammatory response so that intra-arterial arteriosclerosis lesions develop. As Streptococcus pyogenes infections decreased, as mentioned above, fewer myocardial infarctions developed early in life and coronary artery disease became, to a great degree, a disease of older people in modernized portions of the world since it is caused by more subtle, chronic rheumatic autoimmunity: chronic rheumatism.
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 their theory until the late 1940's and the early 1950's when rheumatic fever, as a high-grade disease, was becoming less and less common, because of the above-mentioned improved living standards.
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 and by the 1960's most physicians were specialists and specialty practice settings and knowledge states were not conducive to an understanding of systemic diseases. 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.
Individuals in the various medical specialties concentrated on various target-organ manifestations of rheumatism and developed disease-altering treatments such as CABG, angioplasty/stent procedures and many other surgical procedures such as cholecystectomy and partial colectomy procedures for rheumatic, inflammatory, gall bladder disease and rheumatic ulcerative colitis/colonic polyposis/diverticulitis/redundent colon/Crohn's disease, respectively. In addition, many chemotherapeutic medications were developed and so the use of NSAIDS, Streroid anti-inflammatory medications, artery dilators, cancer chemotherapy drugs and countless other chemotherapeutic drugs became commonly used to alter the affects of chronic rheumatism on various organs or potentially on all organs as the prior-mentioned anti-inflammatories do. Both NSAIDS and steroid anti-inflammatory medications are used for acute, rheumatic fever, in addition.
During the development of "specialty medicine", it seems that rheumatology was "elbowed" into dealing with connective tissue only although most rheumatic syndromes such as rheumatoid arthritis, lupus erythematosis and psoriasis, for instance, are known to be systemic disease processes. The specialty-medicine paradigm that developed, since the 1920's, simply never provided a systemic disease concrept-base so chronic rheumatism has never been understood in a modern, etiological fashion even though all the elements of its understanding had been provided by investigators in prior eras, by the microbiological breakthroughs of the late 1800's through the early 1900's, and by the initial insights made in autoimmune disease concepts.
Even though high-grade rheumatic fever greatly decreased in incidence, from 1900 until 2000, lesser levels of rheumatic autoimmunity have still been propagated throughout human society, including modern developed countries, since Streptococcus pyogenes infections still exist endemically, but usually with less virulence, within the populations of all countries. Therefore, they still cause pathological, rheumatic, systemic, inflammatory, autoimmune-mediated responses within "all" individuals in human society, but at a lesser level of intensity in modern, developed countries.
The clinical understanding of high-grade rheuamtic fever (acute rheumatism) decreased in modern countries so that, nowadays, the average physician has virtually no, or little, knowledge of acute rheumatic fever at this time. Knowledge, therefore, of the much lower-grade, chronic, rheumatic autoimmunity and its more subtle, slowly-developing, target-organ manifestations has never been developed in modern medical science and along the way, rheumatism as a chronic disease concept, was dismissed as a serious medical subject, even though, as early 200 AD, certain knowledge concerning rheumatism was known, and in 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.
Within the first edition of the Encyclopedia Britannica(By a Society of GENTLEMEN of Scotland., In Three Volumes, Edinburgh: Printed for A.Bell and C. Macfarquhar; And fold by Colin Macfarquhar, at his Printing-office, Nicolson-stree, M.DCC.LXXI.), 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-1700'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 so upper respiratory diseases, even sore throats and tonsilitis, are not to be treated with antibiotics unless a positive quick strep test or culture is positive (even if those common tests are often inadequate or inconclusive). One must remember that when a physician is dealing with Streptococcus pyogenes infections one is dealing with a very important aspect of a patient's health.
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, more than trivially, 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, to maintain their specialty-mandated specialty status as experts at connective tissue diseases, do not generally deal with infectious diseases or problems of the body's organs even though they also, historically, have dealt with rheumatic fever, which is a high-grade, inflammatory, autoimmune-mediated, systemic disease process stimulated by Streptococcus pyogenes infections and that most of the rheumatic diseases are systemic in nature.
As a vestige of past wisdom, many individuals knew that arthritis, neuropathy, and tendonitis have 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 rheumatic, sensory neuropathy: bilateral brachial plexitis, sacral plexitis and at times femoral neuropathy 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, the terminal nerves of the sacral plexus, and the femoral nerve; 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 "NUT" of rheumatism is presented. The author following description: "Rheumatoid arthritis is a chronic multisystem disease of unknown cause." It seems that the disease, since it is multisystem in character, that it should, at least, be named rheumatoid disease. Further, 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, rheumatoid nodules, 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 a mild, 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, I surely think, a subacute case of rheumatic fever (the type Sir William Osler described in his famous text of 1935), 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, therefore, so it would not be surprising that those low-grade respiratory infections and the somewhat higher grade infections would be missed, forgotten, or just thought to be mild, pesky, previous or 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, fever, splenomegally, lynphadenopathy, other constitutional symptoms (signs and symptoms of SIRS) and neuropathy, but it has other more serious manifestations of acute rheumatism, for instance, rheumatic carditis, heart failure, cardiac arrhythmias, lassitude, stupor, coma, chorea, and seizures caused by rheumatic encephalitis, kidney failure, etc. Since rheumatic carditis is a life-threatening target-organ manifestation, and since it can cause acute rheumatic myocarditis, endocarditis, pericarditis and cardiac arrhythmias, most medical attention in rheumatic fever cases is, appropriately, given to the heart. Most modern attention given to rheumatic fever and its target-organ manifestations is focused on chronic cardiac valve disease and it is provided by cardiologists who specialize in disease altering procedures, but who rarely think about, or clinically deal with, acute, systemic, rheumatic, rheumatic fever. The rest of the target-organ manifestations of rheumatic fever have been, more or less, inappropriately disconnected from the acute, disease process.
Like most diseases, rheumatic fever (acute rheumatism) exists as a 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, who invented the Jones Criteria, 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, acute, somewhat focused, cardiac, autoimmunological target-organ manifestations.
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 individual's stress on their 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 nerves and the lateral femoral cutaneous nerves can be involved. Various cranial neuropathies such as trigeminal neuropathy (migraine headache), 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: Cancer of all tissue types are target-organ manifestations 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 rheumatic conditions such as dermatomyositis, lupus erythematosis, are also paraneoplastic conditions. I estimate that most individuals who develop cancer have, at least, rheumatoid (rheumatic) arthritis.
Vasculitides: Peripheral artery disease, carotid stenosis, aneurysm development, CVA's, and kidney vascular abnormalities are all caused by rheumatic vascultis, the primary lesion of rheumatism.
Central Neuropathies: autism, ADHD, depression, schizophrenia, manic-depressive illness, disassociative reactions, Tourette's syndrome (antisocial behavior, explosive personality, coprolallia, dysinhibition, stuttering/stammering, etc.) are some manifestations of "rheumatism of the brain", as it were termed in an earlier era.
Gastrointestinal system: 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 are examples.
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 valve syndrome, coronary artery disease, acute and chronic myocarditis (LVH, global cardiac enlargement, and decompensated enlarged heart), pericarditis, and cardiac arrhythmias are all caused by rheumatism. Coronary artery disease and another cardiac problems were termed, "rheumatism of the heart" a concept that was developed by David Pitcairn in 1788 (Rheumatic Fever and Streptococcus infection, cited above).
Kidney: rheumatic vasculitis leading to chronic rhenal failure, gout, and kidney stones.
Special Senses: cataracts, retinitis, iritis, keratokornus, uveitis, subconjuctival hemorrhage, decreased hearing, tinnitis, Menier's syndrome, phorias, tropias, and hyposmia are examples.
Skin: seborrheic keratosis, dermatitis, nevi, angiomas, purpura, urticaria, telangectasias, rosacea, erythroderma, poliosis, vitilago, spider nevi, petechiae, actinic keratosis, Stevens-Johnson syndrome, hypothetically, pityriasis rosea, palmar erythema, plantar erythema, dermographism and others.
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, are prophylactically treated with aspirin.
Since acute rheumatic fever causes a dampening of the protective 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, cited above. Tuberculosis, diptheria, cholera, whooping cough 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, herpex zoster, 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.
interested physicians should read articles and texts by Gene Stollerman, M.D. and Benedict Massel, M.D., two of the last physicians who treated many, patients who had rheumatic fever. Dr. Stollerman has written that physicians should treat patients with pharyngeal infections, after clinical inspection provides a reasonable adjudication that Streptococcus pyogenes could be the causual micorbiological agent, with penicillin. 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. One aspect of rheumatic encephalitis is Tourette's syndrome and one of its aspects is antisocial behavior. Our prisons are "filled" with hundreds of thousands of inmates, usually the poorer class of person, who is more likely to have experienced rheumatic fever, and many of them have organic mental problems caused by rheumatic encephalitis.
Since modern, specialty medicine "missed out" on recognizing rheumatism as an abiding, systemic, inflammatory disease that all humans develop, it evolved the concept that the target-organ manifestations of chronic rheumatism were independent idiopathic diseases. The semantic error of using the term disease, when the cause of a malady is not known, led, I surely think, to the general self-deception that physicians knew more about diseases than was true: they were dealing with syndromes, symptom and sign patterns, and not well defined diseases wherein their causes are known. 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 the descriptions of "diseases" that fill medical texts such as Harrison's Principles of Internal Medicine, 16th Edition, cited above, are really syndromes: symptom and sign patterns that commonly appear together. Medical science, has, therefore, for the last sixty years developed a multitude of disease altering treatments for various diseases and not curative treatments since the cause of a disease must be known before definative cures can be developed. Modern clinical trials are organized efforts to find a chemical that will alter, significantly, a syndrome for the better; not to cure a disease.
To better understand "where medical science is" at this time, an individual must understand the the scientific revolution of thought started in the modern era, about 1600, and that a modern approach to medical science was not possible without the insights first developed by Antony van Leewenhoek concerning microbiology. Progress was slow, thereafter, so that in 1850, just two long life-times ago, physicians did not know the cause of one disease so all treatments were disease altering. If a patient did not have a laceration, a fracture or a sprain, conditions wherein the cause was known, no curative treatments could be managed. Then the microbiological revolution started in Germany and France with the work of Pasteur, Henle, Koch, Ehrlich, and others. Their breakthroughs stimulated American medical science to become more academic. By the late 1930's sulfonamide and penicillin had been developed and their use was a great boon to physicians and patients alike. It seemed that there was not much further worry about infectious diseases and physicians and medical researches dropped their guard, understandibly.
Autoimmune concepts had been developed early in the 1900's, but the excitement over microbiology and antibiotics and the development of specialty, procedural medicine caused interest in immunology to wane. Interest in immunology re-developed in the 1970's and great progress has been made, but there have been few physicians on the street seeing patients of both sexes, of all ages, and for all diseases, who happened to practice in an area where rheumatic fever was active, and who could put the advances in immunology together, at least in a superficial fashion, with clinical medicine. I hope I have succeeded.
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
- ↑ Pennick, Nigel (1996). Celtic Sacred Landscapes. Thames & Hudson. ISBN 0-500-01666-6. P. 132.
External links
- BBC "Your Health" website on Arthritis and Rheumatism
- e-medicine article on Non-Articular Rheumatism
- List of plant species that have been recommended as treatments for rheumatism, from Dr Duke's Phytochemical and Ethnobotanical Databases
- Account of Rheumatism from the website of Retirement Matters Ltd of the UK