- 1. Gell, P. G. H. (1965) Auto-Allergy in Collagen Disease and Related States. Symposium on Advanced Medicine, p.p 45-51. Pitman Medical Publishing Co. Ltd.
- 2 . Hartford (1959), The Practitioner, 183, 461.
Before beginning this lecture I should like to take this opportunity of thanking Dr. Engel and his staff for the great pleasure he has given us and the hospitality we have received in this marvellous setting of Deeside, and, of course, the weather has been marvellous, showing us the scenery to the very best advantage I’m afraid I have never lived in a community of this kind before, but I doubt if I would be able to endure working in such an atmosphere as you have here. I’d be worried about the high concentration of disease complexes which are present, and the effects that this must have on healthy people and also on the other disabled people in the camp. The other factor which probably affect me more than any other would be the lack of challenge to the inmates of any closed community of this kind, and I wondered whether this might not account for the complaint that homoeopathic results were less satisfactory on patients living within the community when one compared them with the effects which the same doctors achieve with patients living outside.
This may tie up with remarks which Dr. Priestman made when she was talking about the two children brought up in America in Stanhope Community; when they left this they were weak and contracted many of the illnesses which children normally brought up escaped.
However, be that as it may, we may now turn to the question of rheumatology, and here I would like to enter the more practical plane. We have heard a lot about the philosophical aspect of medicine, and I do not wish in any way to detract from the value of this, but I wish, in this talk, to disregard two factors—the doctor-patient relationship and the philosophical aspects. This is not because I feel they form an unimportant part in the management of the patient—they are important—but because they are applicable to every good physician’s care and I feel that we must compare our expertise with good physicians and not just with the average. Homoeopathy, I am certain, on purely pharmacological grounds is an entity in its own right and can match the advantages of any other form of therapy. In fact, I would go further in saying that it is the only definitive method of medicine which attempts to cure a patient based, as I see it, on drugs producing a stimulus to which he reacts; it is this reaction that produces our cures.
Rheumatoid arthritis was first put on the map in 1858 by Sir Archibald Garrod. He first used the term and this is the first reference that one can find in the literature. It is odd, I think, that no cases were noted earlier than this; although patients with ankylosing spondylitis and with oesteoarthritis were well known through the ages from postmortem examinations on physical remains and/or from artist’s drawings and reports by acute observers, there is no reference until 1858 of anything like rheumatoid arthritis. One wonders why this is so. Perhaps Ralph Twentyman may have some explanation. It is impossible to tell. But it is, I feel, merely a confirmation of Hahnemann’s idea of chronic disease. It may have different manifestations but the chronic “miasm” exists permanently and has existed over the years; its appearance in clinical syndromes is merely being modified by the patient’s own resistance; by his deviation from health.
Now we may turn to the actual pathology of rheumatoid arthritis. When a patient comes into the consulting room, what is it in fact we see? I would like to suggest to you that what we see in the ill patient in the consulting room is the reaction of a healthy host to some form of agent which produces this disease. This agent may be bacterial, it may be emotional or it may be physical in nature, but it assaults the healthy host. To this assault the host reacts and produces the patient who walks into our consulting room. There is, however, a delay. There must be this delay in the host reaction. The attacker, as we know, always has the advantage and the defender is at a disadvantage, and there is no difference in this instance. The host is at a disadvantage and any measures which he takes are secondary to the initial onset. This must surely mean that the host’s defence and reaction are incomplete. Could this not explain Hahnemann’s idea of chronic disease being an imperfect response? I suggest that it is and that it is this delay which ensures that chronic disease will persist and the body will never be able to throw it off. It would well account for Dr. Twentyman’s reference to the ageing diseases which he encounters in the outpatient clinics at the hospital. These are end results of an imperfect host response to disease.
What is the pathology of the patients who present with rheumatoid arthritis? We have what has come to be called the immune response. This consists of an outpouring of polymorphs, lymphocytes, mast cells and the proliferation of synovial cells. We have oedema with vascular congestion associated with the outpouring of these cells and it is these plasma cells which produce the rheumatoid factor which is responsible for the local joint problems in rheumatoid arthritis.
Following on this cellular exudate we have a fibroblastic proliferation with new blood vessel formation which forms over the cartilage of the joints and eventually leads to its destruction. This lysis occurs from enzymic action within the destroyed polymorphs and lysosomes. There are two aspects of this. One is the hyaluronidase-like substance which destroys the cartilage and the second is a protease-like substance which tackles the collagen fibres. The late result, of course, of these changes is fibrotic ankylosis. We see here the clinical rheumatoid which one would describe as the wet variety leading to the dry fibrotic type. It is interesting, I think, that the wet variety does appear to be associated with those patients who have been treated in orthodox circles with cortisone. The dry variety are those people who have been treated with gold injections. I wonder whether this would not give us some guide from the homoeopathic angle on the indications for the use of gold, or for the use of homoeopathically indicated cortisone.
The other feature in rheumatoid arthritis are the nodules. These occur widespread throughout the body, in joints, in muscles, in the heart, in pleura and in the lungs. Histologically these nodules consist of three separate zones. An inner necrotic zone of collagenous material. This gives the name collagen and is acellular. Surrounding this necrotic zone is the intermediate, highly cellular area with palisading of histiocytes and monocytes. Some of these have multinuclear centres, not unlike a form of giant cell which one sees in conditions like tuberculosis, but the linear palisading of these histiocytes is a characteristic feature of the rheumatoid nodule. In the peripheral area we have got evidence of chronic inflammation with granulation tissue, fibroblasts and lymphocytes.
The third type of lesion which one finds in rheumatoid arthritis is vasculitis. This takes two forms. One is a patchy diffuse inflammatory reaction with the invasion of monocytes in the adventitious or outer layers of the arteries. Occasionally one also finds the typical fibrinoid necrosis described for the nodules. The second variety is a diffuse non-inflammatory hypertrophy of the intima with hyperplasia and occlusion of the lumen which leads to necrosis of tissues distal to the artery. This is the characteristic lesion of the digital arteries and is one of the most troublesome forms of rheumatoid arthritis. We therefore see in this pathological survey that all the tissues of the body are involved in the rheumatoid process. It is a total body involvement and not merely a, joint problem.
How do we tackle this from the homoeopathic point of view? How does the homoeopathic approach differ from the orthodox approach? Ours, I hold, is as follows. We have seen the wet type of reaction in rheumatoid arthritis, with the effusion, with the outpouring of polymorphs, lymphocytes, plasma cells, mast cells, with hyaluronidase and protease digesting enzymes. This is rheumatoid arthritis. Do we have a drug which can match this? A drug, which when given to a healthy person will produce similar results? The answer is yes—Apis. Apis as we know is a substance which contains histamine, bradykinase, hyaluronidase and two other factors, a haemolytic factor, a neurotoxic factor, and the non-specific anti-inflammatory agent. It is interesting that, following the selection of this remedy on purely homoeopathic grounds, subsequent investigations should reveal the presence of histamine, bradykinase and hyaluronidase in Apis, the sting of the bee. Therefore on pharmacological grounds Apis must be considered a legitimate drug which is homoeopathic to the inflammatory reactions of the rheumatoid variety.
Now, as you perhaps know already, there is a polypeptide 401, recently discovered in the bee sting. This is the most important anti-inflammatory agent yet found. The mode of action is not known, but it is certainly different from any other anti-inflammatory agent so far discovered. It is odd, is it not, that this substance, this most important anti-inflammatory agent, should have been discovered in association with’ those very chemicals which produce such a marked inflammatory reaction in normal tissues. What is it, in fact, in our potency of the bee sting that produces the homoeopathic effect? Is it substance 401 or is it the active effects of histamine, bradykinase and the haemolytic and neurotoxic substances? We may never know, but does it matter? I suggest to you that it does not matter because of the homoeopathic relationship. The toxic effects of Apis on a healthy person, that is the provings of Apis, are similar to pathological and clinical effects in disease. I suppose most of us use Apis mel. in our treatment. Now as you know this is a preparation of the whole bee which contains not only the venom but also incorporates any of the pollens which may well have been on the bee before it was macerated. This may well suggest that we should use Apis mel. in cases of more widespread allergic reaction and limit the use of the preparation of the venom itself (Apium virus) for such diseases as rheumatoid arthritis where allergic aspects are minimal.
Let us take another drug, Urtica urens, the stinging nettle. This drug has been shown to contain acetylcholine, histamine and 5-hydroxytryptamine. Pharmacologists tells us that the stinging sensation
arises from the combination of an acetylcholine and histamine. You all know that Urtica urens is recommended in those patients with rheumatoid arthritis who have an urticarial reaction. These are substances which produce urticaria and therefore the use of Urtica urens must be homoeopathic. For myself, I have used Urtica urens as a general non-specific anti-inflammatory drug. It was used by Burnett in the treatment of gout as far back as the end of the last century. I have used it in such cases with some success. I have also used it in cases of migraine where, as you know, in the acute stage one may have no specific prescribing symptoms or indeed the patients may be so ill that they are unable to give you any prescribing symptoms. Under these circumstances it is often useful to use such a general non-specific remedy like Urtica urens and I think it is interesting that Burnett should have chosen it, on purely homoeopathic grounds, as a non-specific anti-inflammatory agent. In fact one could call it the homoeopathic antihistamine. I feel that insufficient attention is paid to such relatively simple remedies in the treatment of these diseases.
May we take now, more complicated varieties. I have already suggested the similarity of the tubercle of tuberculosis to the nodule of rheumatoid arthritis. It is interesting, I think, that in animal experiments it was impossible for the experimenters to produce rheumatoid arthritis in animals unless they had used an adjuvant, a foreign body, in addition to the other agents used. Such an agent was tuberculin. Could it be that Tuberculinum is one of the essential things to be used in the treatment and in the causation of rheumatoid arthritis? Could this explain why people have thought of a relationship with streptococci? Either may well be adjuvants in the causation of the disease and this being so may well give a homoeopathic guide to treatment, using at some stage either or Streptococcin. This, I think, is where Homoeopathy is so fortunate. We can make use of so many precipitating causes in choosing the drug for treatment.
Procainamide is a drug which on prolonged application produces lupus erythematosus. Has anyone used procainamide in the treatment of this very difficult and obstinate condition of lupus erythematosus? As yet I have not encountered a case, but I feel that when one does one must consider the use of procainamide in potency where there are no other prescribing symptoms.
The only other drug I would like to mention is triamcinolone and I would like to refer you to Dr. Priestman’s use of this drug in potency in a patient suffering from collagen disease. The patient suffered from flushing and sickness, with loss of weight, muscle wasting, osteoporosis, hypertension, gastric haemorrhage, bleeding tendencies in the skin, insomnia, psychotic episodes and he was running a low-grade pyrexia. These symptoms and the patient were encountered in 1959, when her Practitioner was lying open at an article by Hartford.2 This produced the homoeopathic picture of Dr. Priestman’s patient, and so similar was the condition, that she prescribed Triamcinolone in low potency. There ensued a reversal of the patient’s collagen type of disease, probably polyarteritis, to normal, and from being a deteriorating chronic invalid he was able to return to full duty. Modern pharmacological experiences, and orthodox literature, are of value even to an experienced homoeopath like Dr. Priestman.
This then is my conception of rheumatoid arthritis, and of the homoeopathic approach to the treatment of rheumatoid arthritis in particular. I hope I have been able to show how Homoeopathy differs from the orthodox management of patients, and why in 1974, almost two hundred years after Hahnemann commenced treating patients with Homoeopathy, it is still a very important form of therapy, nay, I say more, it is the only constructive form of therapy which so far exists.
I would like to close by quoting from a Dr. Gell.1 This is what he says: “Incidentally the lesion produced by antibodies and those by delayed reactivity are no doubt pathological deviants of physiological inflammatory responses and repair respectively. They are pathological deviants of normal physiological inflammation and repair”. Is this not the definition with which Hahnemann would have agreed had he still been alive, although 200 years elapsed since he enunciated his theory, of chronic disease being an imperfect vital response to infection.
We have recently carried out a survey of cases of rheumatoid arthritis at The Royal London Homoeopathic Hospital. To date we have 78 cases.
These have not been fully analysed as yet but the findings so far are to this effect. Some 43 have involvement of the upper extremities at onset and 18 of the lower. Morning stiffness is present in some 40 of these, with aggravation from cold and heat in 25 each. There is an equal distribution between the large proximal joints and the distal smaller joints-61 and 68 respectively. Depression was the most common mental condition present, being noted in 43 cases, with fear and anxiety in only 17. Now, how do these cases compare as regards severity? Some 50 had X-ray erosions, 46 were sera-positive and 50 had ESRs at one time or another over 20. Only 8 were anaemic, having haemoglobin values of less than 70 per cent.
Dr. Lester will be reviewing those cases more fully later and we hope to publish the findings in the JOURNAL.
Source: The British Homoeopathic Journal