GASTRO- INTESTINAL CANAL
The severe manifestation in the intestinal mucous membrane, particularly the large intestine in arsenic is explained most naturally by the capillary action. At the same time a cell damage due to excretion is to be considered just as in the kidneys.
The pseudomembranous deposits in the inflamed intestine consist of dead epithelial cells and hyaline droplets which are embedded in a congealed mass of transudate (pistorius, l.c.). In the small intestine only a hyperemia is found. The early vomiting even from parenterally introduced arsenic will be perceived as a reflex action of the excreted arsenic on the gastric wall. However an increased gastric secretion is observed from arsenic.
SKIN
An acute inflammatory manifestation in the skin can appear in the form of pemphigus and dermatitis herpetiformis. Arsenical therapy of the affections follows the simile rule. The skin manifestations in poisoning are likewise observed in animal experimentation, especially erythematous eruptions and falling out of hair. Of particular interest is the communication reported by Geyer on the so-called Reichen-steiner disease which is produced by drinking arsenic containing waters. It is expressed by melanosis and hyperkeratosis. These chronic actions appear only after prolonged use of the water, while people newly arriving in the district react with intestinal catarrh and other digestive disturbances in the first few weeks. The hyperkeratosis, like psoriasis and lichen on the other side form a well known indication for arsenic, not only in homoeopathy but also in non-homoeopathic dermatology.
The formation of pigment, arsenical melanosis, is individually very different. Wherever the arsenic solution comes into contact with the pigment cells, a pigmentation appears after an interval. This pigment consists of melanin. However there is probably a connection between the formation of pigment and adrenal injury arsenic.
CARCINOMA
The persistent injection of an alcoholic arsenic solution continued over months into the grey mouse leads to a keratotic flat epithelial cancer. In other cases injection of arsenic is without influence. In regard to the severe damages of coal workers Belgian students have found arsenic regularly up to 0.06 Percent of the final product of coal and likewise in aniline dyes. The experimentally produced tar carcinoma, however, can hardly be traced to coal arsenic since arsenic-free tar produces carcinoma. It is well known that since antiquity (in Egypt, India, Greece and later Arabia) arsenic has always been employed as a cancer remedy, especially by means of external application. Paracelsus states that the cause of cancer is “a natural arsenic” and therefore he employed realgar against foul ulcers. This use has continued to the present in the form of Zeller’s paste and Poljsak’s salve which has been tested and recommended by Aschner. Arsenical keratitis and arsenical melanosis have actually been suggested as internally produced precursors of carcinoma. Moreover the malignant lung tumors (lymphosarcoma) in arsenic workers are considered the result of arsenic action. Arsenic may also just as roentgen and radium rays produce cancer as well as heal it under certain conditions.
For explanation of the action of arsenic on carcinomatous tissue it may be recalled that a cell poison such as arsenic first destroys the cells least capable of resistance, for example carcinoma cells. The external application of arsenical pastes indeed depends upon the elective relation of arsenic to carcinomatous cells.
Sancyoshi found that arsenic acted particularly upon young markedly proliferating cells. Others have referred to the production of fever by arsenic. Fever as a sign of cell protein destruction can have significance for the melting down of carcinomatous tissue.
The consideration of the metabolic process in the cells leads deeper. O.Warburg has shown that carcinoma cells show an increase of the anoxybiotic fermentative process at the cost of the oxidative. A depression of oxygen consumption in the cells is also known of arsenic. The assimilative action of the usual arsenical medication in the first phase can be explained by this. But if the anoxybiotic cell process gains a definite preponderance so the cell process gains a definite preponderance so the cell chemistry becomes carcinoma-like and finally goes over to anoxybiotic cell destruction. Thus arsenic can favour the transformation and the destruction of cell in the sense of carcinoma and it will depend upon the dose and the existing state of reaction of the organism whether such a stimulation through arsenic will result favorably.
BONES
Concerning the influence of bone growth by arsenic the observations indicate entirely the same as they did with phosphorus. The growing animal fed with arsenic has more strongly developed bones. The cortex is thick, under the epiphysis is a compact bone layer, the arsenic stratum, exactly like phosphorus. The Haversian canals of the compacta, are smaller, the spongiosa is transformed into compact bone, and foot bones are transformed into solid bones. Lardeli also saw rabbits with a thickening of the cortex from Valsinestra spring water.
Not much use has been made of the possibility of using arsenic as a stimulus for the bone building process, like phosphorus and the phosphates up to the present. Still the similarity of the two chemical neighbors is worthy of note in this respect.
THEORY OF ARSENIC ACTION
Up to the present we have found extensive analogy between the action of arsenic on the organ cells and capillaries with that of phosphorus. One might imagine that the cell poisoning effect of arsenic, as with phosphorus, is combined with the regular oxidative cell metabolism. The depression of oxygen utilization of the red blood cells favors this as well as the stimulating action on assimilative processes. The destruction of cells, the splitting of protein, and the necrosis then could be an anoxybiotic process. The capillary poison effect does not oppose this idea, moreover, the inflammatory action on the capillaries can be conceived as a prestige of fatty degeneration and of a necrotizing end-effect on the vascular endothelium. The hypothesis of Binz and H. Schulz, that the cell damage occurs through the oxidation of arsenious acid to arsenic acid and again reversely by reduction of arsenic acid to arsenious acid, also by a change from oxygen consumption to oxygen yield, does not seem generally applicable, particularly since the oxidation from arsenious acid to arsenious acid, has not been proven in the organism up to the present. From the very slow excretion of arsenic out of the organism one might plausibly conclude that arsenic enters into a very firm compound with cell constituents and by transformation of this constituent the cell function was markedly influenced, indeed the entire cell was finally destroyed.
The apparently promoting action of arsenic proves to be the result of depressing or destructive influences; the increased assimilation probably results from depression of oxidation, the increased bone building, indeed in analogy to phosphorus, is probably an over-reaction to bone destruction. A stimulating action on the blood is still not confirmed experimentally, consequently it is also not explained. From the clinical use however such an end effect is not to be doubted.
Experimental knowledge is still too rudimentary to provide a detailed explanation of the effect mechanism of arsenic.
ACTION ON SINGLE CELLS
Some data have been secured on the actions of arsenic on bacteria and protozoa. They have become particularly important because of the attempts to obtain a parasitotropic sterilsatio magna by the aid of organic arsenical compounds an atoxyl, salvarsan, etc.
If at first we study the bacterial action of inorganic arsenic, then it is striking that the arsenic sensitivity with single types of bacteria is entirely different. Streptococci, cholera vibrio and typhoid bacilli are injured by very small amounts of arsenic while staphylococci, coli bacilli and proteus not only retain life with great concentrations but even thrive. We also see closely related types of bacteria are influenced entirely differently. We need merely assume that also in the organism the defense against the toxins or the decomposition products is favored in the same way in order to understand that in homoeopathy arsenic has proven itself much more useful in streptococcus sepsis, cholera and typhoid than in the suppurations or inflammations provoked by staphylococci and coli. In homoeopathy arsenic is not employed in the infectious diseases named because these organisms are arsenic sensitive, but the guiding line is the similarity between the responses of the organism, on any side to the particular organism, on the other to arsenic. If now the germ which is able to provoke a “morbus arsenicalis,” that is, produces effects similar to those of arsenic, is sensitive to arsenic even in the test tube, then there exists a probability of a deeper connection: the chemical affinity of the arsenic to the germ under the complicated conditions of the organism might prepare them, as an opsonin does, for the assault of body, cells, and on the other side it would be exactly the skin cell powers with an affinity for arsenic which would be stimulated; arsenic also acts in consequence to its affinity on both sides as a link of the attack.
Leeser, a Consultant Physician at the Stuttgart Homeopathic Hospital and a member of the German Central Society of Homeopathic Physicians, fled Germany in 1933 after being expelled by the German Medical Association. In England Otto Leeser joined the staff of the Royal London Homeopathic Hospital. He returned to Germany in the 1950s to run the Robert Bosch Homeopathic Hospital in Stuttgart, but died shortly after.
Otto Leeser wrote Textbook of Homeopathic Materia Medica, Leesers Lehrbuch der Homöopathie, Actionsand Medicinal use of Snake Venoms, Solanaceae, The Contribution of Homeopathy to the Development of Medicine, Homeopathy and chemotherapy, and many articles submitted to The British Homeopathic Journal,