Finally to be mentioned are the most complicated phosphorus compounds of the organism, the phosphoproteins (formerly nucleo albumins or phosphoglobulins). Apart from casein of milk and vitellin from the egg yolk, the nucleo-proteins come chiefly into consideration for the cell nuclei. The nucleic acid fraction of the nucleo-proteins is phosphorus containing. According to A.B. Macallum and J.B. Collip, the nucleus seems to be free from phosphate ions. Phosphorus is recognizable in the chromatin of the cell nucleus as well as in centrosomes. Youthful nuclei are phosphorus rich; later, with lessening of capacity for division, the phosphorus content markedly decreases. One also would not
go astray with the idea that the nuclear phosphorus content has a connection with growth and that this connection is also significant for the inheritable constitution.
No tissue is free from phosphorus. The heart is apparently the richest in phosphorus in the form of phosphatides in respect to the muscles. In the entire nervous system the P compounds are abundantly present. The liver is the richest of the parenchymatous organs.
An abundant use of phosphorus occurs in normal metabolism. The organic phosphorus compounds are excreted as inorganic phosphates, but inorganic phosphates have an important task in metabolic and energy changes.
While phosphorus is very easily oxidized in free air, the conditions for oxidation seem less favorable during and after resorption. This is because, in intoxication with large amounts, one finds phosphorus in the arterial blood and in the organs, especially in the liver, in an unbound form for several days. However, it may occur in the lowest step of oxidation in the expired air in that this shows luminescence. With intoxication with small amounts and fine division, the oxidation apparently proceeds rapidly so that no free phosphorus is found in the blood and the exhaled air does not show luminescence.
PHOSPHORUS POISONING
Phosphorus poisoning must be described here as the threatening background to the phosphorus picture. Phosphorus vapors release severe phenomena of irritation in the bronchial mucosa which leads rapidly to a pulmonary edema.
In one-half to twenty-four hours after the introduction of the poison the gastric symptoms usually appear. The patient vomits and has a burning pain in the epigastrium and the ejected material smells like phosphorus though later the material is more or less bilious.
Then follows, even after stronger doses, a two-to three day interval of comparative well being; indeed, one even speaks of euphoria. But still there appears a definite weakness with a nervous excitation and, three to four days after the ingestion, with the transient mental disturbances, the characteristic icterus appears. The epigastrium again becomes painful, the pains draw toward the right hypochondrium. One finds the liver enlarged and sensitive. Pains occur in all extremities; the patient becomes dejected, the pulse small, and the heart yields accessory sounds.
In the next few days the icterus increases, the liver definitely enlarges, though in some cases becomes smaller.
Then skin and mucous membrane bleeding begins. The vomiting reappears and bloody masses are evacuated; the gums, intestines and uterus bleed; the skin shows small petechia or extensive echymosis.
The blood pressure falls with increasing cardiac weakness. Slowing of the pulse is noted with the icterus and this may be maintained well into convalescence. In unfavorable cases the pulse rate is increased throughout the entire time. A high- grade tachycardia often appears antemortem. Fever up to 40O C is frequent.
In many cases the consciousness is clear up to shortly before death. In other cases, somnolence, delirium or convulsive attacks occur in the final twenty-four to forty-eight hours. In a case which survived, a paralysis was noted.
The urine decreases with the progression of the poisoning, and finally an almost complete anuria may exist. Bile pigments and bile acids are found in the urine. Urobilinogen is increased; in severe cases it may be diminished, the result of complete failure of the liver. Protein in moderate amounts is nearly always present. Casts, fatty casts, cellular detritus appear, and the urine usually contains moderate amounts of blood. Among 141 cases spontaneous glycosuria appeared in six, but an alimentary glycosuria could be provoked in 60 per cent of the cases.
The finding of a milk-like urine is perhaps traceable to free fat. Amino acids and peptone-like bodies and significant amounts of lactic acid are found and the excretion of ammonia can be considerably increased.
Pain in the throat, dryness in the mouth, redness of the pharynx, catarrhal phenomena of the mucous membranes are observations which may be overlooked by virtue of the more severe symptoms.
In severe poisonings death usually occurs on the seventh to eighth day. In very rare cases improvement may occur after the icterus has appeared, and during convalescence a marked diuresis is noted.
In chronic poisoning one observes, outside of the still to be discussed necrosis of the jaw, pustular eruptions, eczema of the skin, falling out of hair. Individuals may complain of dryness of the throat and of cough. The tongue is coated; the appetite is poor; and the patient complains of gastric pains, tenesmus, hiccough, and meteorism. Vomiting occurs and the stools may be bile-containing and particularly bile-poor.
Pathologico-anatomically, in the lungs are observed traces of catarrhal inflammation, more rarely pneumonic foci; exudates, in the pleura; in the stomach, infarcts, bleeding into the lumen,
in the funds and the pars pylorica, pinhead to pea-sized ulcers; the mucous membrane is often swollen, hyperemic and hemorrhagic, the mucousa doubled or tripled in size, indurated with marked pigment deposit and flat ulcers. The interstitial tissue is overgrown and many times develops in thick, broad plaques. In the duodenum the solitary follicles and the glands of Brunner are swollen and in the lower intestinal segments inflammatory phenomena are found. The gastric and intestinal contents are usually bloody.
The severe alterations in the liver are observed early. The liver is usually enlarged, only rarely lessened in size. The liver cells for the most part remain but are filled with fat globules. The interlobar connective tissue is often diminished, but many times and particularly in chronic poisoning it is so markedly developed that one may speak of definite interstitial hepatitis. With time it may come to a smooth induration or form a luetic-like hepar lobatum with numerous, deeply penetrating tongues of scars and finally the classic cirrhosis of the liver with its resultant manifestations; venous hyperemia of the gastric and intestinal mucosa, indurative enlargement of the spleen, ascites, hydrothorax.
The spleen is frequently enlarged in acute poisoning as well.
The kidneys are swollen for the most part, the epithelium of the urinary tubules filled with numerous fat globules. Connective tissue overgrowth is observed here in many cases.
The heart is fatty to a marked degree, the muscle fibres are thickly filled with droplets. The walls of small blood vessels and capillaries are likewise involved and together with the reduced capacity for coagulation of the blood the already mentioned marked bleeding is explained. In poisoning before the menstrual period, the menstrual flow becomes profuse and large hematoma may form in the ovaries. Likewise, brain hemorrhages are frequent in poisonings before the period.
Repeatedly in animal investigations as well as in human poisonings, fat emboli have been observed particularly in the lungs and the kidneys.
The entire musculature, particularly that of the abdominal and thigh muscles, can show fatty changes.
Of the blood effects of subacute phosphorus poisoning, the long known and often confirmed lessened or absent coagulability is of special significance to us for the bleeding tendency of phosphorus. The depression of coagulation or the absence of it is associated with defects in the fibrinogen and the coagulation- promoting ferment.
The alkalescence of the blood in phosphorus poisoning is considerably reduced. This can be demonstrated titrimetrically as well as the through estimation of the CO2 content of the arterial blood. The diminution of alkalescence is the result of altered metabolism which is accompanied by an increased production of acids. Probably a decrease in the complement is associated with it as Ehrlich and Morgenroth found in the blood of poisoned animals.
The formed elements of the blood likewise undergo considerable alteration, in particular the erythrocytes. It is striking that the different species of animals react differently. Rabbits do not show definite influence; in pigeons there is a high-grade hemolysis; in men appears, partly a decrease, partly a sudden increase of erythrocytes and as high as eight million have been found. This increase was only transient for the most part and this has lent support to the otherwise not certainly determined concept that besides the increase of erythrocytes there is also an increased destruction. The leukocytes seem at first diminished, then slightly increased.
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,