Cellular Cancer Therapy, part 6
Chapter 7: Hypoglycemia
Humoral equilibrium is maintained by the constant circulation, in our organism, of certain hormones that govern the reaction of the organ’s humors. This reaction directs the life activities of the cell depending, we could say, on this humoral reaction in health and sickness.
It has been demonstrated that the defective functioning of the endocrine glands results in physico—chemical modifications of the humors modifying, as a result, the interior functioning of the cell. The vago—sympathetic system, functioning in harmony with this hormonal complex, regulates the equilibrium.
The humor regulating hormone par excellence is insulin. The intravenous injection of insulin produces the phenomena of hypoglycemia more rapidly and more intensely than through other ordinary means, where all of the phenomena appear almost simultaneously. For the reasons that we will deal with below, we have almost always administered medication in this way.
Sensitivity is always variable even in the same individual, but in any case such variations are always within the description that we will present of hyperacute hypoglycemia. This variability fluctuates according to the reserves of glucose in the organism. In an individual who has received injections of insulin and whose reserves of glucose have been depleted by them, the hypoglycemic symptoms appear in less time than in the first doses and with smaller quantities of insulin. In these cases, more sugar is always necessary to make the symptoms disappear. All of those facts, observed in several hundred cases, confirm the theory that the symptoms are chiefly due to the lack of glucose in the organism, though we can add other phenomena such as the probable intoxication with lactic acid, which is one of the forms of glucose breakdown.
In the course of our investigations, we have had the opportunity to observe three patients who died, where rigor mortis set in quickly, this being explained only by the action of lactic acid in the muscles.
From that which has been said, we can conclude by saying that the accidents of hypoglycemia are due, chiefly, to the lack of blood glucose, to the excess of lactic acid, and to other products of cell combustion. As a consequence, we have to refer the hypoglycemic symptoms to these factors.
Among the main factors that can always produce the same hypoglycemia, the individual’s age, his weight, and the glucose level in fasting are especially relevant. Certainly, the quantity of glucose stored in the form of glucogen in the liver and in the muscles are very important factors, but unfortunately are unmeasurable; it is probable that their quantity determines the intensity and the number of symptoms that will be present during hypoglycemia. Even so, the CNS and vago—sympathetic nervous system clearly influence the genesis of the symptomology of hypoglycemia; finally a group of hormonal elements that are closely related to insulin complete the symptomological description. Possibly this complex conglomerate which physiologically has not been able to be disentangled, can clear up for us the pathogeny of provoked hypoglycemia. The following description corresponds to an average, taken over a group of patients that have been treated for illnesses not closely related to diabetes.
There are very different ways of responding to the action of insulin; there are relatively insulin—resistant subjects who need greater quantities of insulin to produce the same symptoms; others, whose resistance causes late reaction; in these cases, with the same quantity of insulin, it takes much longer for the patient to manifest the symptoms, and thus they could also be considered insulin—resistant. There is another group whose symptoms are not very manifest; their glycemia level falls following the normal curve until its lowest point (below the half—way mark) and all of the symptoms appear suddenly, almost simultaneously. Finally there is a group with normal symptomology and reaction time but that, without further stimulation, regularizes its blood glucose level and as a result, the symptoms all disappear. In those patients it can be observed that the hemo—gluco—regulation system has carried out the organism’s defense against changes in the physico—chemical constants; this is the pure insulin—resistant group, though there are very few individuals who could be classified in it.
Investigators who support insulin—resistance have observed only diabetic patients in different states of glycemia; those vary, as is well known, according to the kind of food consumed before giving the injection of insulin; even so, the patient’s psychological state at the moment of administration also contributes to the variation.
It is more common to observe individuals who are insulin—sensitive; that is in whom, with small doses of insulin, one can reduce the glycemia to less than half—of—normal over a normal period of time; others who with the same quantity of insulin manifest their symptoms quickly; and a third group which we can call the hypersensitive group. Those in this group show, with small doses of insulin and in a short time, all of the symptoms that correspond to much less than half—of—normal level glycemia with the proportional level of glycemia. A fourth group includes individuals in whom the symptoms that correspond to less than half—of—normal glycemia level appear quickly without, however, the actual level of glycemia having arrived at this point. Finally there are subjects who with small doses and in a short length of time have their glycemia fall below half—of—normal and show the corresponding symptoms. Administering glucose intravenously makes the glycemia rise to approximately two—thirds and five minutes later the corresponding symptoms disappear. However, this only lasts a few minutes, at which time the level falls back to half—of—normal with the return of the corresponding systems. These rapid increases and decreases repeat themselves up to five tines in the interval of approximately two hours, after which time the glycemia level rises to one equal to the patients described above (see Fig. 7.1).
For the classifications above, we have taken into consideration three factors: quantity of insulin, time until presentation of symptoms, and their intensity.
In spite of the observations that some investigators have made during experiments with animals, there do exist types that can be clearly classified and defined, similar to those described above.
The physiological glycemia of 82 mg/100 ml rises normally and without any clinical manifestations after the ingestion of glucose, reaching a peak thirty minutes later at 100 or 110 mg/100 ml, and returning to normal after approximately two hours. Frequently, after this time it dips below normal only to return soon thereafter to its initial level; not even traces of glucose are found in the urine during this short—lived hyperglycemia.
The hypo and hyperglycemia curves care very similar and agree with the physico—chemical phenomena already explained; both peak at about 35 minutes, and only differ in their mechanisms of production: to provoke hypoglycemia it is necessary to administer insulin intravenously and to induce hyperglycemia it suffices to ingest some glucose; in both the factors of age, weight, general state, etc. play a role.
If the blood sugar of an individual 35 years old and weighing 60 kilos, is made to fall below half—of—normal, we can observe that 21 minutes after the injection of insulin intravenously, sensations of hunger, thirst and slight asthenia begin almost simultaneously. These sensations are normally felt when an individual is lacking in energy—providing foods.
The energy—providing food par excellence is glucose; experimentally we have seen that the lack of glucose in the approximate proportion of 1/10 of the normal quantity produces these sensations. Therefore, hunger and thirst can be defined as general sensations that are caused by hypoglycemia when it is 1/10 below normal.
Besides these sensations, as a consequence of a more accentuated lowering of glucose in the blood, asthenia is felt, manifested by the lessening of visual acuity. We know that glucose is burnt up releasing H2O and C02, liberating a certain quantity of energy, which, according to the organ in which it is produced (heart, nervous system, etc.) can be mechanical, electrical, etc. According to this, one could conceive of the symptom asthenia as happening when the lack of glucose in a physiological quantity causes a smaller production of energy.
When the hypoglycemia is accentuated, the glucose or the muscular glucogen which had managed to maintain their normal quantities in the tissues begin to lessen as well, at which point manifestations appear that reveal the deficit of this indispensable element. Precisely the most delicate tissues (nervous system, endocrine glands, etc.) that are the first to manifest the need for energetic food, that is, glucose.
When this reduction is of approximately 20 mg, the following manifestations appear: profound asthenia, slight drowsiness, tachycardia, tachyapnea (increase of 10 or more heartbeats; 5 or more respirations per unit time), general excitation and peripheral vasodilation or vasoconstriction according to whether the individual is vaso or sympatheticotonic. The latter symptoms appear about 20 minutes after the former; with an even higher degree of hypoglycemia we observe the following symptoms: drowsiness, which had already begun, now appears more strongly; a slight, ephemeral rise in temperature, usually of about one degree, accompanied almost simultaneously by copious, generalized sweating; the arterial blood pressure rises approximately one half centimeter of mercury (Tychos sphygmomanometer) only for 3 or 4 minutes, after which it returns to normal, an unconscious or semicomatose hypoglycemic state begins, some reflexes begin to disappear (like the pupillar reflex, the tendonous, etc.); there is obvious bradycardia and e bradyapnea.
When the glycemia reaches half—of—normal, we can observe profuse sweating, waxy pallor; indifference; deep, tranquil sleep; loss of some reflexes, especially of the eye; and bradycardia or, in some patients, tachycardia and tachyapnea. These symptoms correspond to a state between semicomatose and comatose; certainly the hunger, thirst, and asthenia of the beginning have reached their maximum, causing autophagia which, in conjunction with the phenomena referred to above, make cell permeability optimal.
According to these symptoms, the lack of glucose is not only in the blood, but also in all of the organs without exception and all of the cells are in a cataclysmic state for lack of this element. Hypoglycemia has reached a point that the blood, in order to maintain its physico—chemical qualities, takes glucose from cells all over the body.
It is because of the lack of glucose in all of the cells, because of the excess work that is done to re—establish the physico—chemical equilibrium (PCE) and because of the accumulation of waste products that we see asthenia, drowsiness, the semicomatose or comatose state, the loss of reflexes, etc. which show that the CNS is being affected; one can infer that if the action has reached such a point as to show such serious manifestations in the CNS, then certainly each and every tissue of the organism will suffer the same effects, according to its physiological characteristics.
These facts prove that drowsiness is always produced by a lack of energetic foods for the neurons, glucose being the main or probably only source; even so, they prove that the accumulation of waste products originating in glucose combustion, contributes as well to the production of drowsiness, and that an increase in such products can lead to the symptoms of a comatose state (hypoglycemic coma is similar to others such as acetonic, uremic, etc.).
If the glucose level continues to decrease, the individual becomes deeply comatose: total disappearance of all reflexes, clonic convulsions begin, first myosis then mydriasis appear, cardiac asthenia is manifested by arrhythmia, the number and amplitude of the heartbeats diminishes, hypotension is such that the radial pulse is not perceptible; the respiratory rhythm is as in Cheyne Stokes respiration; the pallor is cadaveric and the temperature lower than normal; if, in such a state, the individual is not quickly attended to he will die in a few seconds.
We will see below that these concepts become clearer as they are explained, during the regression from the symptoms, in which consciousness is the first to return; the reflexes come back, though diminished in intensity and reaction time; drowsiness is slight; pulse and respiration rates are higher, with the qualities corresponding to this higher frequency. If the glycemia nears normal, we see that the pulse and respiration rates become normal, as when the individual is resting; the temperature returns to normal; the sweating, without disappearing is reduced considerably; the same happens to sensations of hunger and thirst. On the other hand, the drowsiness and asthenia maintain a certain intensity during two or more hours, during which the individual is more or less sleepy, in spite of normal glycemia, due probably to the slow recuperation of the nervous system.
There are patients in whom the glycemia still does not return to normal, remaining a few milligrams below, but always within normal limits.
The description above of hypoglycemia varies greatly depending on many factors, but we will only enumerate those with the most obvious influence. Infants and children are more susceptible to the action of insulin; from the age of two to 45 there is an inverse relationship, though with slight variations, i.e., according to the increase in age, the sensitivity to the hormone decreases. After this period, the individual seems markedly less sensitive to the action of insulin, but this lack of sensitivity is only apparent, as we will see below.
If insulin is injected in small doses so as to produce the sensation of hunger (a reduction of a tenth of the glucose), the action of the hormone obviously activates the catabolism of carbohydrates and the anabolism of the lipids, being that it is in the form of glycerides that the reserves are constituted, which is why subjects injected with small doses of insulin gain weight. On the other hand, we have observed that if the quantity of insulin increases in such a manner that it accelerates the respiratory and circulatory changes producing the symptoms mentioned above, it increases the consumption of oxygen and the release of carbonic anhydride, not leaving time for the formation of reserves; thus, besides the glucose, the reserve fats and proteins in the tissues are consumed. The action of insulin can even lead to critical autophagia.
If the quantity of insulin is so small as to cause only a five or ten percent decrease in the glycemia or if the organism takes better advantage of the double energetic potential of lipids, then the liver and probably the other organs will store in the form of glucogen the glucose that was in the blood stream (i.e., insulin has gluco—synthesizing effects in small doses); but if we produce a hypoglycemia such that besides the reserves of glucose of all the organs that contain it, the reserves of glucogen in the liver and other organs are used up, then insulin carries out its characteristic glucolytic, glucogenolytic or typically catabolic function.
In fact, when it is necessary to produce successive hypoglycemias, the quantity of insulin necessary decreases as the number of previous hypoglycemias produced increases, given that each of them has little by little depleted the reserves of glucogen. These facts confirm the observation that patients, during the repeated action of insulin, lose a noticeable amount of weight; this is due to the fact that the reserves of glycerides have little by little been consumed by the efficient consumption of the circulating glucose. The action of insulin on the metabolism of carbohydrates apparently makes the glucose—glucogen relation reversible.
If during the action of insulin or at the same time it is injected, the patient is given sugar, slight hypoglycemia is observed, and therefore the action of the hormone is only glucogen—synthesizing.
The function of adrenaline does not manifest itself when the reserves of glucogen have been depleted or almost depleted; in many patients in whom we have provoked hypoglycemias of less than half—of—normal, the administration of adrenaline in different doses has never been able to detain the grave symptoms of the moment. Because of this we can conclude that adrenaline has not been able to release the necessary glucose in the blood or that it has released so insufficient an amount that the symptoms continued.
The hemo—gluco—regulating function of these two hormones is only manifested ostensibly when their quantity varies within near normal limits. When the antagonistic action of adrenaline has to compensate for the energic action of insulin, it has to resort to other methods, because adrenaline alone is insufficient to carry out satisfactorily and according to the necessities of the moment its antagonistic functions.
Glucose is the only indispensable fuel which all of the cells of the organism use easily, and without which they cannot carry out their normal functions. Insulin is the hormone that maintains the glycemic index within certain limits compatible with cell life; in harmony with adrenaline, it keeps up the reserves of the organism not only in terms of carbohydrates, but also fats and proteins.
A third factor, the nervous system, affects this regulation. Even though until now its precise action has not been discovered, we believe that it is manifest. Remember that at the beginning of our exposition here, we pointed out that some patients have intense fear of the injection of insulin; when there is such an emotional state, the quantities of insulin necessary for producing the desired effect are smaller, as is the time required for the effects to appear. This demonstrates that the nervous system affects not only hyperadrenalinemia but also the general functioning of other hormones.
In fact, vago-sympatic tone has as its function the maintenance of the vital equilibrium in the whole organism, as well as the regulation of cell metabolism and the functioning of different organs.
Cells live in an environment that we can consider amphotropic; in it the active substances like insulin, adrenaline, the mineral ions, etc., some sympaticotropic, others vagotropic, are found in such proportions that the functional equilibrium of these two systems is assured by three major factors that, functioning in harmony, maintain this equilibrium: the endocrine secretions, vago and sympatotonic, the equilibrium of the reaction and the environment, and the ionic concentration of the plasma.
In a vagotonic state, the tissues are alkaline, they contain little calcium and a lot of potassium; the blood itself is more alkaline and contains less ionized calcium. In a sympatheticotonic state, the tissues and the blood are more acid, containing more calcium and less potassium. The increase in H+ ions is an effect of the calcium by excitation of the sympathetic system; on the other hand, the excitation of the vagosympathetic system produces OH— as an effect of the potassium.
To summarize, we can say that the excitation state of the vagal tone corresponds in general terms to an alteration in the ratio between K and Ca in favor of K, to an increase in cell permeability to hydration and glycemia. As we stated above, there are nerve centers that regulate all of these changes. The nervous stimulus is transmitted, partially, through the sympathetic nervous system, to the suprarenal capsules or to the isles of Langerhans.
Many books, of hundreds, even thousands of pages, have been written about cancer. Great researchers have produced many theories which fall apart in practice, and great doctors have written much without saying anything. Few are those who have really managed to follow the trails of the diagnosis and treatment of neoplastic diseases. During many years while the idea about writing a book about Donatian Therapy took root, we decided to finish it with a compendium of all of the existing treatments for neoplasias, and with a summary of the major neoplastic diseases, to describe simply what is known, what can be done, and what has been seen to work.
Any process that enters into a cause—effect relationship with the production of malignant neoplasias is called a carcinogenic factor. This implies the action of an external agent (virus, inhibited immunological reaction), adequate doses of this agent, internal susceptibility (immunological or hormonal deficiency, genetic anomalies, etc.), and the passing of relatively large periods of time.
Exterior factor + adequate dose + internal susceptibility + time = CANCER, in general irreversible with surgery, radiation therapy, and chemotherapy.
Several attractive theories have been put forth to explain immunological alteration as a notorious characteristic for the determination of whether or not a carcinomatose illness will progress.
However, the initial event in these mechanisms, is the impinging of an external agent on the gene and therefore, the creation of a foreign antigen. Tyler’s immunogenous theory sketches a convincing analogy between transplant sickness and cancer.
It is known that immunological responses are of two major kinds: cell responses and humoral responses. Cell responses are based on the action of lymphocytes and typically cause retarded hypersensibility, as in the tuberculin reaction and the rejection of grafts. Humoral responses are based on the action of immunoglobulins and make up, typically, the antibacterial and antiviral defenses.
The mechanism of graft rejection is important for explaining one basic factor that influences the metastasis of cancer.
The mechanism, in essence, is this: lymphocytes are constantly going in and out of the lymph nodes, through the lymphatic vessels and the bloodstream. When a sensitive lymphocyte encounters a foreign antigen, It begins to divide and proliferate. Therefore, according to Burnett’s clonal selection theory of acquired immunity, closeness of sensitive lymphocytes concentrate in a lymph node and its wells. If a specific tumoral antigen starts this process, the lymph nodes In that area grow and the rejection of the tumoral graft appears afterwards; later on general tumoral rejection begins, as the more distant lymph nodes develop sensitive lymphocytes. However, it is possible that the continuous massive development of the primary tumor dump into the blood and lymph an excessive amount of antigens which can suppress the clones of the sensitive lymphocytes. In this case, the lymph nodes get smaller, the immunity to the tumoral antigen disappears or is considerably diminished (immunological tolerance for cancer) and tolerance for the tumoral graft appears. The initial tumoral antigen is generally the viral DNA or RNA which has acquired greater molecular energy through changes of electron energy levels, usually because of interatomic overlap.
Applying this concept, it can be observed that cell immunity could prevent the tumoral graft, made up of cancerous cells, from "taking" in the beginning, but later it would "take" and permit the occurrence of metastasis.
As was already mentioned, benign tumors do not metastasize because of inhibition-by-contact in normal cells,’ which is not present in cancerous cells. It is a fact that clinical cancer only appears when the tumor can overcome the immunological defenses of the host organism.
At the cell level, the mechanism is easier to define. The DNA or RNA viruses that have been latent, sometimes for years, replace the normal genetic expression for the self-duplication of the cell DNA. The viral DNA, or sometimes the viral RNA, takes the place of the cell DNA, causing enzymatic deletions, damaging the mitochondrial system with subsequent! metabolic interference, this happening in the interior of the nucleus, between the nucleus and the cytoplasm, in the interior of the cytoplasm and intercellularly. New antigens are created with peculiar characteristics such as that of producing immunological tolerance, and thus are accepted as those of the cell’s immunological system. Some cells die as a consequence of these changes, but others survive, functioning as to-tally abnormal cells. The unchaining agent should be administered during critical periods of time and dosage, with the support of other carcinogenic factors or secondary promoting factors. The result will be a biophysical (alteration of the surface tension of the cell membrane), biochemical (alteration of the cell protein synthesis), enzymatic (enzymatic change by deletion and modifications of codons, cystrons (?) and triplets (?)), and metabolic (by elimination of negative feedback as well as inhibition by cell contact) overstimulation.
Rarely does the response come from 1OO% of the cells and it is very much conditioned by the tissue’s "base state." The conditioning histological promoting factors originate in an abnormal internal metabolic medium and show alterations ranging from hormonal imbalance to variation. in the mechanisms of oxygen transport, modifying the oxygen reduction potentials, changes in coenzymes, and an increase in mytotic excitation. However, in most circumstances a catalyst- will be an obligatory element in the process and this first change will be irreversible if there is no intervention to eliminate or modify it.
Afterwards time is needed for the carcinogenesis promoters to work so that through natural selection the formation of clones from carcinomatose cells can begin, proliferate and differentiate; this is uncontainable reproduction. At that point the protective mechanisms of the organism have been altered in such a way that they are almost totally different.
The first change in form that can be seen is dysplasia, and it is reversible. With the persistence of the situation described above, an in situ carcinoma develops; this may or may not be reversible. After 6-10 years (the average time for this change to happen in the cervix), clinical cancer appears. At this point, the tumor is found to be invading normal tissues; isolated or small groups of cells from these may be breaking apart, thus being apt to form embolisms. Whether these possibly embolizing cells or cell fragments will be strong enough to survive and develop into regional or distant metastases, will depend on the conditions they find in the different parts of the organism. When invasive cancer appears, the possibility of metastasis already exists, though in general it is necessary for several months or years to pass for this to happen. Invasive Cancer appears to need to "build up energy" to overcome the barriers that the body’s defense mechanisms put up to prevent metastasis. This interval, short or long, gives the doctor perhaps his only opportunity to control and cure carcionomatosis. Therefore, early diagnosis means the diagnosis of cancer before it has reached the stage of dissemination.
Ionizing radiation can also precipitate this stage, as can chemical carcinogens such as methylcolantrene, dimethylbenzanthrocene and benzopyrine.
People with very white, very thin and dry skin with abundant freckles, as those of Nordic or anglo-saxon descent, are often more cancer prone.
Basocellular carcinoma makes up 80% of the cancers of the skin and most often appears on the face (the upper half) and on the head. It never metastasizes. Macroscopically it consists of a pale, pearly white, node that grows slowly and at a later stage begins to ulcerate at its center. Afterwards it becomes intensely pigmented, like a melanoma.
The epidermoid or squamocellular carcinoma is less frequent, and appears on the inferior half of the face, the back of the hands, on the vulva and the glans. It grows more quickly than the basocellular carcinoma and metastasizes to the local lymph nodes. Macroscopically it also appears as a prominent node which is indistinguishable from the basocellular carcinoma. It may not develop a central ulceration but in later stages of development, may develop a peripheral serpiginous ulcer that bleeds at the touch, easily becomes infected and gives off a characteristic nauseating odor.
The carcinomas of basosquamous cells. This interesting variant is a mixture of both of those discussed above. Its clinical behavior is just like that of a basocellular carcinoma, and can be accurately diagnosed only by an experienced pathologist.
Frequency and distribution. Skin cancer makes up 18-20% of all cancers, but the large number of these cases that are treated without the aid of histological examination makes this difficult to determine with great accuracy. The ratio of men to women with this form of cancer is 2 to 1. About 20% of all the cancers that appear in men are -of the skin, second only to carcinomas of the digestive system, while 11% of the carcinomas in women are of cutaneous origin and rank fourth, after breast cancer, carcinoma of the digestive system, and cancer of’ the genitals.
Cause. The most important catalyst is the ultraviolet light from the sun. These radiations are absorbed by the epidermis producing miniscule, though very intense, burns. Progression towards cancer will depend on the accumulative effect of repeated exposure (not of isolated doses, though they may be very intense), on the thickness of the layer of keratin and on the quantity of melanin. These factors, however, become carcinogenic only in the context of cancer—susceptible terrain.
Kaposi hemorrhaging sarcoma: a rare cutaneous tumor which does not metastasize, though it can develop in several different sites at once. Its origin is still unknown.
Xeroderma pigmentosum: a hereditary disease causing hypersensitivity of the skin to all kinds of radiation, especially to sunlight.
Mycosis fungoides: a fatal, malignant disease that originates in the reticuloendothelial cells of the skin and, in advanced stages, involves the lymph nodes.
Precancerous lesions. The existence of these lesions is a controversial issue. In our view, there are no definitely precancerous lesions. The reason is obvious: either there is a confirmed cutaneous carcinoma or there is none, How is one to know which lesion may or may not produce skin cancer? In theory, any lesion might, though in practice none do. There is no cause and effect relation, this is simply a further, unnecessary complication of an already very complicated phenomenon.
Therefore, lupus vulgaris, bismuth, arsenic and mercury dermatosis, senile actinic keratosis, leukoplakia, and chronic diabetic or varicose ulcers are not and have never been precancerous. They are only cutaneous lesions that have the same probability of degenerating into cancer as a wart, a callus or a fistule.
The patient arrives at the doctor’s office with an already visible lesion. There is no necessity for complicated diagnostic methods; laboratory analysis and x-rays are not necessary. The Oncodiagnosticator is the ideal method, and the only one we feel is necessary.
To the list of diseases mentioned above, we can add: piogenous granuloma, sclerosing hemangioma, seborrheic keratosis, and caverous hemangioma.
Therapy. Donatian Therapy and electric fulguration (Hyfrecator).
MELANOMA: Makes up 1-2% of all cancers.
Cause: Biophysicochemical imbalance,
Pathology: Melanomas occur in all of the areas of’ the body covered with skin, and occasionally inside the mouth and the rectum. The most common areas are the back, the legs, the feet, the face and the anterior part of the scalp. Their classification according to the degree of dermal invasion, is directly related to the possibility of a cure.
1. Moles (by frequency)
2. Senile and sebborheic keratosis
3. Pigmented warts
4. Sclerosing Hemangioma
5. Intracutaneous and subungual hematomas (due to trauma)
6. "Coffee and milk" stains of neurofibromatosis
7. Piogenous granulomas
8. congenital verrucoid moles
The prognosis is excellent though almost all other oncologists hold the opposite opinion. We have achieved total cures of stage I and II in patients with melanomas (66 patients) and 40% in stage III (more than 5 years old).
This form of cancer has a peculiarity: its intermediary position between bucal and cutaneous carcinomas. These make up 1-2% of all cancers. Herpes virus (type I), traumatic ulcers, piogenous granuloma, and leukoplakia fall into this category, as well.
All of the cancers of the lip are squamocellular or epidermoid. The importance of this type of carcinoma is that it frequently metastasizes with great speed to the submental lymph nodes. We prefer Donatian therapy to ganglional dissection, and for these forms of cancer only use the former.
CANCER OF THE MOUTH including the tongue, the floor of the mouth, the gums, mucous membrane, and palate.
Frequency. Makes up 4-5% of all malignant tumors.
Cause. Intra and extracellular biophysicochemical alterations.
Factors leading to susceptibility. The habitual use of alcohol or tobacco products and a deficiency of B complex vitamins can lead to susceptibility.
Pathology. 92% of the malignant tumors of the mouth are of the squamocellular or the epidermoid type that have developed in the polystratified squamous epithelium the lines the inside of the mouth and pharynx. 4% of the tumors of the mouth are adenocarcinomas of the salivary glands.
There are three clinical varieties of the squamocellular bucal carcinoma: expophystic, verrucous and infiltrating. The first two have better prognoses than the third which unfortunately is the most frequent of the three.
Cancer of the mouth invades neighboring structures such as the gums, the palate, and the cheeks. When it infiltrates the muscles of the root of the tongue, or the pterygoid musculature, the situation is already grave and there is little that can be done.
Metastases occur in the majority of the cancers greater than 3 cm in diameter, through the lymphatic system that goes from the mouth to the neck. The first nodes to be affected by metastasis depend on the localization of the primary tumor.
In the case of cancer of the mouth, it is very important that the diagnosis be early. Initial signs are usually a hard plaque or node situated in general on one of the lateral edges of the tongue or on the floor of the mouth, and reddening that occurs in the case of leukoplakia.
A mass on the neck may constitute the first sign, from the point of view of the clinical examination (but not when the Oncodiagnosticator is used), though by the time such external signs appear, the disease will already have been present many years. Clinical examination should proceed by palpation of the floor of the mouth, the inside of the cheeks and the lateral edges of the tongue, especially the posterior portion of these edges. The tongue depressor should not be used, as it often hides the greater portion of tumoral lesions, especially when they are incipient and have not been ulcerated.
Differential Diagnosis. The mouth is where the greatest number of lesions can appear; these are the most frequent that can be confused with malignant neoplasias:
Treatment. We do not recommend surgery, and only use Donatian Therapy, because the mouth is anatomically very complicated and is used for speech. Surgery and radiation therapy cause mutilation and rarely achieve cures.