Systemic Diseases. New way of understanding etiology and pathogenesis.

Rheumatism

 

The term rheumatism, "the flow of liquid" in Greek, was coined by Dr.Galen, a Roman physician, approximately 1800 years ago. This seemingly unsuitable term, today, had originated from a prevalent then belief that four types of fluids circulate in the human body: blood, mucus, bile and black bile, which are sustained in a perfect ratio, and that all human diseases arise from disturbances in their ratio and interaction. At the time, the society’s elite were commonly suffering from gout (podagra) that mainly affected the big toe. Dr.Galen was a court physician and he frequently dealt with this disease. By using the term rheumatism,  Dr.Galen had characterized and described symptoms of podagra based on ideas adapted in the medical world at the time. Rheumatism with its characteristic symptoms as recognized by modern medicine could not have existed at the times of Dr.Galen because biological basis for the occurrence of systemic pathologies in the human body were nonexistent. At that time, the human body lacked the necessary features and biological basis for the onset of systemic diseases.

Besides, if rheumatism as the systemic disease had appeared 1800 years ago, it is logical to assume that all other disease of this group such as glomerulonephritis, systemic scleroderma, dermatomyositis, systemic lupus erythematosus, periarteritis nodosa, and others would have immediately followed it instead of emerging only nearly two millennia later.

Our humanity returned back to using this term only in 1835 when for the first time, Dr.Bouillaud, a French physician, described the symptom complex of a completely new disease, a disease that was fundamentally different from what was described and treated by Dr.Galen. Dr.Bouillaud called the newly brought to light disease in honor of Dr.Galen as rheumatism. This is how a new era unfolded in the history of our humanity and medicine, an era of the systemic pathologies that would rule over all the human diseases during the coming centuries. 

The pathocomplex process as the origin of rheumatism

However, during the last centuries, leukocyte defense mechanisms were subjected to change. Gradually, with the advent of high-molecular-weight antigens, body defense functions passed over to B-lymphocytes, primarily and protein or humoral immunity emerged to the first place. Immunoglobulin protein molecules, which previously floated freely through the bloodstream, now mostly remained fixated to the surface of B-lymphocytes and hunted for foreign pathogenic agents whilst circulating in the blood flow in such form. If until that time, antigen destruction was carried out mainly through phagocytosis, with humoral immunity, the process of defense shifted to the formation of immune complexes that are specifically directed at the destruction of large-molecular-weight protein molecules. Following antigen destruction, these immune complexes now had to be disassembled wherein B-lymphocyte cells were released one by one to continue performing their further defensive function. It is important to understand that lymphocytes are released from immune complexes when the number of B-lymphocytes exceeds the number of antigens. This means that after being released from an immune complex, B-lymphocyte cells must have time to circulate in the circulatory system independently. If the number of antigens, especially those of protein nature, exceeds the number of B-lymphocytes, B-lymphocytes cannot circulate independently after they are disassociated since they are compelled to immediately attack another antigen by forming a new complex. Consequently, В-cells, which are the primary elements of our body defense potential, are constantly confined in complexes and never get to circulate in our bloodstream in their free form. This continual process exerts excessive load on our immune system.

The primary cause of B-lymphocyte retention in immune complexes, even without taking into account the excessive number of antigens in today’s world, is a deficiency of factors required for the disassociation of these complexes and in fact, this is what creates the pathological basis for the development of systemic diseases.

When any living creature is subjected to changes in environmental conditions, its body undergoes corresponding transformations. This is a natural adaptive response of every organism. Our sudden alienation from our natural and familiar living conditions played a fateful role in the reorganization of our biology. Drastic biological, evolutionary and adaptive changes have unavoidably occurred following our sharp turn towards urbanization, as required by nature, leaving a permanent mark on all of our further existence. A consequence of these changes are the degenerative processes in organs charged with synthesizing substances required for the disbandment of immune complexes and therefore, the release of B-lymphocytes. For the first time in our life, our body encounters pathological immune complexes (pathocomplexes) that lost their physiological capability to disband due to a shortage of certain biochemical substances. While circulating in our bloodstream, the associated immune complexes attract other plasma elements, including erythrocytes, thrombocytes, as well as leukocytes and protein molecules, thus forming huge (in terms of biology) aggregates. One after another, large aggregates floating in the blood flow clog up the blood vessels and sparsely deposit on the serous membranes of various organs, triggering inflammation and hence, a completely new symptom complex of systemic pathologies. Thus, we encounter a new phenomenon in medicine, a phenomenon called the pathocomplex process.

The systemic diseases that are currently considered to be induced by pathocomplex process are: rheumatism, systemic lupus erythematosus, dermatomyositis, periarteritis nodosa, glomerulonephritis, systemic vasculitis, arachnoiditis, endocarditis, Raynaud’s disease, pathocomplex induced diabetes, autoimmune thyroiditis, autoimmune hemolytic anemia, idiopathic thrombocytopenic purpura, chorea, multiple sclerosis, parkinsonism, Alzheimer’s disease, multiple myeloma, and even chronic lymphocytic leukemia and lymphogranulomatosis (Hodgkin’s disease) along with others.

The role of monocytes in the formation of clinical manifestations of the pathocomplex process

Monocytes, the most mysterious human blood leukocytes, first form in our body tissues and permanently fixate in them during our fetal development and first years of our life. The cells that in medical sciences and especially in histology are known as tissue macrophages are the same mysterious monocytes, fixated unto various tissues of our body. Virtually all our blood leukocytes have surface receptors (CDs – clusters of differentiation), which are also identical for other formed elements of the plasma. Some of B-cell receptors have structural similarities with receptors that are located on the surface of tissue macrophages. For this reason, the pathocomplexes that are circulating in the bloodstream can be attracted to these tissue macrophages that look to capture and fixate foreign substances in order to destroy them.

Every individual has his own specific map of macrophage disposition in his body depending on the script of his fetal development and first years of life. Tissue macrophages play the role of forming the symptom complex of the form of systemic disease that will manifest in the patient given the presence of a pathocomplex process. The primary areas of pathocomplex sedimentation are determined by the distinct distribution of macrophages, which in turn, determines which systemic disease’s symptom complex will predominate. Therefore, despite the fact that theoretically all diseases of this group are described as separate nosological entities, you can never observe an isolated picture of a single systemic disease in practice.

When tissue macrophages are mostly accumulated in the serous membranes of joints and joint sets, pathocomplexes primarily settle on these organs and trigger symptoms characteristic to rheumatism and rheumatoid arthritis. Predominant accumulation of macrophages in the skin and muscles leads to the sedimentation of pathocomplexes on these tissues, which triggers a systemic disease with a predominant symptom complex of either dermatomyositis or scleroderma, respectably. The same principle brings about glomerulonephritis (when pathocomplexes are mainly adsorbed by the kidneys), periarteritis nodosa (when pathocomplexes are mainly adsorbed by the blood vessels), multiple sclerosis, Parkinsonism, chorea (when pathocomplexes are mainly adsorbed by the brain tissue), etc. One of the serious diseases characterized by having dispensed symptoms of all systemic pathologies and failing to affect specific organs is systemic lupus erythematosus.

Despite the fact that all pathocomplex-induced diseases are manifestations of the same process, the map of tissue macrophage distribution is the determining factor in the proliferation of the symptoms of a particular systemic pathology. Exactly these macrophages define the area of lesion upon collagen outbreak.

Schematic representation of the development process of immunodeficiency
Schematic representation of the development process of immunodeficiency

Why is rheumatism accompanied by angina?

All systemic pathologies are accompanied by a partial or complete immunodeficiency. What is the source of this immune deficiency?

Leucocytes, especially lymphocytes are the primary defense factors of human immune system. During an immune reaction to antigens that have penetrated the body, B-lymphocytes are forced to join leucocytes, thereby forming immune complexes. For the time they are attached to the antigen to destroy it and until the immune complex is disbanded, B cells are temporarily neutralized.

The whole complex process that takes place with B-lymphocytes tends to resemble a situation that arises when two policemen handcuff themselves a criminal and thus become practically neutralized, unable to perform further defense actions until they are released from the handcuffs. Similarly, the B-cells form immune complexes by attaching to antigens and are released from these complexes only after their disbandment. Hence, once locked in the network of pathocomplexes, В-lymphocytes lose their defense abilities forever.

A decrease or a termination in synthesis of substances required for the disbandment of immune complexes, partially or completely impedes the process of B-lymphocytes release. As a result, a huge number of B-lymphocytes remains locked in the networks of pathocomplexes in a neutralized state, deprived of the opportunity to perform their usual protective function. Based on the degree of pathocomplex formation, immunodeficiency manifests in either a partial form, as in systemic diseases such as rheumatism, systemic lupus erythematosus, systemic scleroderma or a complete form such as in Acquired Immunodeficiency Syndrome (AIDS). As a consequence of an immune deficiency induced by the pathocomplex process, multiple bacteria can penetrate through the biological gates of our body (upper respiratory tract and urogenital system) and cause inflammation of these organs.

Until recently and in most cases to this day, modern medicine practitioners consider that streptococcus, traces of which are detected in the blood of patients suffering from rheumatism, is the etiological factor of rheumatism. Direct cause and effect conclusions deduced from primitive observations are quite prevalent in medicine as in other fields of science. Accuse what you see: if you see streptococcus, then this is what triggers rheumatism. This is how the same pervasive and silly mistake as with cholesterol and triglycerides in cardiovascular diseases, sugar in diabetes and HIV in AIDS comes about. This is exactly why long-acting antibiotics such as bicillin are currently used for treating rheumatism and why temporary positive effects obtained are considered as the confirming factors for the proposed "theory". This misconception is further reinforced by the fact that fever and inflammatory process recur when antibiotics are cancelled. In reality, recurrence of infection and high fever as well as health aggravation in patients suffering from rheumatism that happens after termination of antibiotic treatment has a scientific explanation. Pathocomplex induced immune deficiency deprives the body of its capacity to fight with any pathogenic agent, including bacteria. As soon as antibiotic treatment is ceased, bacterial infections recur and each succeeding time, they recur with a growing threat of sepsis because regular use of antibiotics makes bacteria more tolerant and weakens immunity even further. Bacterial factors in the blood of patients suffering from systemic pathologies are merely a consequence of existing immune deficiency triggered by pathocomplexes rather than the cause of these diseases. For this reason alone, antibiotics will never permanently solve the problem of systemic pathologies, in particular, rheumatism, despite the fact that antibiotics do render a temporary improvement. They can only cope with one part of the problem and even here, they are incapable of doing it completely because other pathogenic agents in addition to bacteria settle in immune deficient body against which antibiotics are powerless. To treat the second part, namely the cause of immune system’s dysfunction that leads to the body’s vulnerability to all kinds of foreign substance intrusions, these drugs are completely powerless. This is why patients suffering from rheumatism, systemic lupus erythematosus, scleroderma, dermatomyositis, glomerulonephritis, periarteritis nodosa and other systemic abnormalities have high fever. Frequent angina, pneumonia, bronchitis, pyelonephritis, and even sepsis, which leads to endocarditis and myocarditis, are merely consequences of immune deficiency, the presence of which is characteristic to all pathocomplex diseases.

Treatment of systemic diseases

Is it the streptococcus or the pathocomplex process? What is the source of systemic diseases, after all? Treatment tactic and effectiveness of all collagens depends upon the resolution to this question. For half a century, the streptococcus has been dominating amongst "theories" explaining the etiology of diseases in this group and nonetheless, rheumatism is far from being over.

On the basis of a new approach to the etiology and pathogenesis of systemic pathologies, by applying the theory of the pathocomplex process, we offer a radical method of treatment that is capable of completely eliminating the source of these diseases found in the blood. However, unfortunately, the degenerative changes that have occurred in the course of the disease, such as joint deformations and pockets of scar tissue, are irreversibly. 

However, it is important to note that having removed the origin of the disease, the body’s dependence upon the use of exogenous corticosteroids that are generally used in the current medicine for the treatment of systemic diseases remains. According to the principle of feedback, the control system of endocrine gland hypophysis adjusts to the excessive amounts of exogenous corticosteroid in blood plasma during the use of hormonal preparations by sending a message to stop your endocrine glands to decrease their production giving the rise to endocrine gland dysfunction, mainly in the form of hypothyroidism. Due to long-term use of exogenous hormones, the organs that synthesize them, which in this case are the adrenal glands, can atrophy. Consequently, your body’s synthesis of hormones decreases or completely stops which then affects the future lives of former patients with systemic pathologies.

 

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