- Email: [email protected]
Vitamin D Deficiency (Rickets)*
The Medical t:linics of North America March,1943
VITAMIN D DEFICIENCY"" (RICKETS) JOSEF WARKANY, M.D.t
RICKETS is a systemic disease brought about by' certain faulty living conditions which frequently accompany the "higher forills" of civilization. For its development two factors must concur: insufficient exposure to ultraviolet rays and an inadequate intake of vitamin D. Wherever living habits lead to the coexistence of these two factors, rickets appears in an endemic form in infants. If one of these etiologic factors is excluded, the disease does not develop. As soon as this fact was recognized and artificial sources of ultraviolet rays and the various forms of vitamin D became available, rickets in an endemic form disappeared in all civilized countries. The war and its consequences, such as disruption of lines of communication and of industrial production, make rickets once more a very real menace to children all over the world. Unless definite steps are taken to prevent it, the disease will again become prevalent. ETIOLOGY
Rickets may be considered a climatic disorder occurring chiefly in the temperate zones. There, especially during the winter, the amount of sunshine available is rather small, and infants born during the fall and early winter are not sufficiently protected by natural irradiation. In cold weather they are kept indoors the greater part of the time and during their short outings are so heavily dressed that they are only .. From The Children's Hospital Research Foundation and the Department of Pediatrics, College of Medicine, University of Cincinnati. t Assistant Professor of Pediatrics, University of Cincinnati College of Medicine; Attending Pediatrician in the Pediatric Division and Attending Physician in the Contagious Division of the Pediatric Service, Cincinnati General Hospital (Cincinnati, Ohio'). 361
362
JOSEF W ARKANY
slightly exposed to sunlight. Moreover, in cities dust, smoke, and the shadows cast by the buildings reduce the antirachitic potency of the sunlight and skyshine by filtering out the effective ultraviolet rays (wavelengths of 230 to 313 mp.). Ultraviolet rays are required for the conversion of provitamin D, which is always present in the infant's skin, into active vitamin D. If this endogenous vitamin D cannot be procured, an exogenous source must be made available in order that rickets may be prevented. The foodstuffs usually given to infants contain little vitamin D. Breast milk is a poor source of the vitamin. This may seem surprising, since we know that breast-fed children develop rickets less often than the artificially fed. Other protective factors not entirely known to us must operate to the benefit of the breast-fed child. Certainly breast feeding in itself cannot be considered a prophylactic measure, and the breast-fed child requires supplements of vitamin D. The same is true of the artificially fed child. Cow's milk, sugar, cereals and vegetables are not good sources of vitamin D. Butter and eggs, though richer in the antirachitic factor, cannot be considered protective in the amounts given to infants. It is imperative, therefore, to add -a more concentrated form of vitamin D to the diet of infants. This is to be found in the fish liver oils and their substitutes. Without such supplements an infant's diet should always be considered inadequate in vitamin D. Several predisposing factors play a role in the etiology of rickets. Rapid growth is one that deserves special mention. It is often thought that vitamin deficiencies occur chiefly in undernournished persons. So far as rickets is concerned, this is not true, as vitamin D is needed particularly by the rapidly growing organism, and infants who are otherwise in a good state of health and nutrition may develop marked signs of rickets. The predisposition of premature children is partly due to their rapid growth. In such children, however, the lack of mineralization of the skeleton, which normally progresses rapidly in the last few weeks of intra-uterine life, may also be an important rachitogenic factor. Vitamin D deficiency manifests itself in different ways at different ages, although
VITAMIN D DEFICIENCY
363
the rachitic process is basically the same in the different age groups. It has been suggested, therefore, that the terms "juvenile," "adult" and "senile rickets" replace the older terms "late rickets," "osteomalacia" and "hunger or war osteopathy." Since older persons are rarely completely deprived of ultraviolet light and dietary vitamin D, the late forms of rickets are seldom seen. In certain regions of China or India, however, endemic foci of rickets beyond infancy do exist. A deficiency of vitamin D manifests itself particularly during puberty, pregnancy and lactation. The late forms of rickets respond well to treatment with vitamin D. Negro children have a definite tendency to develop rickets. Whether this is due to the pigmentation of their skin or to the conditions under which they live has not yet been determined. A few rare conditions of disturbed mineral metabolism occur in which osseous changes simulating those of vitamin D deficiency appear. Vitamin D refractory rickets is due to a chronic hypophosphatemia of unknown etiology. In a number of cases, healing has been achieved with very large doses of vitamin D. Renal rickets is caused by an abnormal mineral metabolism due to insufficiency' of the kidneys. Vitamin D is of no avail in renal rickets. DIAGNOSIS
In the diagnosis of rickets, recognition of the early signs is of the greatest importance. Since they are often inconspicuous and may occur in otherwise healthy children, they may escape even the trained observer. Craniotabes, an important early symptom of rickets, should be looked for particularly in premature infants. A parchmentlike softness in the squama of the occiput or, less often, in the parietal bones indicates clearly the onset of the rachitic process. Healing of rickets leads to a rapid hardening of these spots. Softness of the borders of the large fontanelle and a delay in the decrease of its size may also become noticeable in early rickets. Moderately enlarged costochondral junctions may be palpable. Slight thickening of the wrists and ankles is suggestive of early rickets, but in this stage the swellings are usually covered by fat and therefore are not visible. Gen-
364
JOSEF WARKANY
eral irritability, marked perspiration of the skin of the head, . and flaccidity of the muscles are often present. The inorganic serum phosphorus may fall below 3.5 mg. per 100 cc. The roentgenogram is the best means by which an early diagnosis , can be made. The wrist reveals cupping and fraying of the distal end of the ulna at an early stage. Neither pa~n nor impairment of locomotion betray the onset of rickets. Advanced cases of rickets are easily recognized. The infant's head appears square and the frontal and parietal bones become prominent. Sometimes these prominences are separated from each other by grooves, which correspond to the sutures of the flat bones. The large fontanelle remains widely open even after the child is eighteen months old. Dentition is delayed and disorderly. The teeth are irregular in shape and position and there are defects in the enamel. The rachitic rosary becomes visible. Harrison's groove, a furrow that runs from the ensiform process around the lower aperture of the thorax, becomes visible along the attachments of the diaphragm. The normal curve of the ribs is interrupted in the region of the costochondral junction, and their cartilaginous portions and the sternum may protrude to form a "pigeon breast" or be depressed to form a funnel-shaped thorax. Deformities of the spine, such as kyphosis and scoliosis, may develop at this stage. They are serious symptoms since they generally persist after the rachitic process has been checked. The flaccid abdominal muscles yield to the intra-abdominal pressure and a "pot belly" develops. The rachitic pelvis is small, and its entrance is further narrowed by a forward projection of the promontory. The lower parts of the sacrum and the coccyx appear to be bent forward in the sagittal plane, thus narrowing the pelvic exit. In the female these changes, if they become permanent, add to the hazards of childbirth, since the disproportion between the size of the child and the narrowed pelvis may result in obstruction. In such cases unless an operation is performed, the death of mother and child ensues. The extremities in advanced cases show epiphyseal enlargement and various degrees and types of curving. The arms are usually not as deformed as the legs. Bowlegs (genu varum) or
VITAMIN D DEFICIENCY
365
knock knees (genu valgum) are easily recognized. Deformities in the proximal end of the femur and in the region of the ankle may occur. Deformities of the spine, the pelvis and the legs result in a reduction in the height of the body or rachitic dwarfism. In the roentgenograms, the epiphyseal ends of the long bones appear frayed. Cupping is seen most readily at the distal ends of the ulna, radius, tibia and fibula but is absent at the distal end of the femur and the proximal end of the tibia. For the diagnosis of rickets roentgenograms of the wrist are therefore better than those of the knee. Demineralization, "greenstick" fractures and curving of the long bones may also be seen. The values for inorganic serum phosphorus may be below 3 or even 2 mg. per 100 cc. PROGNOSIS
The extent of the rachitic changes, as well as the. intensity of the treatment, determines the outcome. Progress of the healing can be observed most satisfactorily in a series of roentgenograms of the wrists. The characteristic sign of healing rickets is the line of primary calcification, which is seen as a transverse band running parallel to the distal margins of the metaphysis of the radius and ulna. This line of primary calcification becomes denser and broader as healing progresses, until it joins the metaphysis. Healing is noticeable also in the cortical parts of the shaft, where calcium salts are deposited in the osteoid tissue under the periosteum. Thus, in the roentgenogram the shaft appears to have a double contour, an appearance which is often mistaken for "periostitis." Within two or three weeks after intensive treatment, definite signs of healing can be seen in advanced cases of rickets. If the rachitic process is not rigorously treated in the advanced stage, permanent deformities of the skeleton may develop which are not reparable by the administration of vitamin D and may require orthopedic correction. Rickets in itself is not a fatal disease, but diseases such as tetany, pneumonia, tuberculosis, anemia and enteritis are more likely to cause death in children with protracted rickets than in normal children.
366
JOSEF WARKANY PROPHYLAXIS AND TREATMENT
Infantile rickets can and should be prevented under all circumstances. Sunlight, the natural prophylactic agent, is not readily available in the winter. Only during the summer can sunlight be considered adequate to prevent rickets. Since the amount of active ultraviolet light varies in sunlight according to place and season, it is impossible to prescribe definitely the time of exposure required for antirachitic prophylaxis. Tanning of large areas of the skin usually is assumed to be a sign of sufficient exposure. Adequate treatment by means of artificial light also prevents rickets. Mercury vapor and carbon arc lamps are frequently used. The lamp is placed at a distance of 3 feet from the body and exposure should not exceed two minutes at the beginning. Treatment is usually given every other day, the front and back of the body being exposed alternately. The eyes should be protected by dark glasses and the skin by oil or vaseline. If no untoward reactions occur, the exposures may be gradually extended to half an hour. This can be achieved in four to six weeks. Such a series of treatments will not only prevent rickets but will serve as a therapeutic measure in cases of active rickets. The chief obstacle to the general use of the lamps lies in their cost, which makes it impossible for most families to use this form of prophylaxis for their children. Treatment at clinics and in doctors' offices is often inconvenient and there is danger of cross infections. In any case, light treatment is more time-consuming than dietary treatment. Whenever light treatment is not feasible, peroral administration of vitamin D is required for the prevention and treatment of rickets. As has been pointed out, most foodstuffs used in the diet of infants are poor sources of vitamin D and supplements are required. Numerous antirachitic supplements are available at the present time, but cod liver oil is the most extensively used. One gram of standard cod liver oil contains at least 85 LU. of vitamin D. Since 800 LU. are usually considered a safe prophylactic dose for full-term infants, two teaspoonfuls of cod liver oil daily are recommended for this purpose. Four teaspoonfuls (1600 LU.) daily are required for
VITAMIN D DEFICIENCY
367
the cure of mild cases of rickets."" In addition to vitamin D, cod liver oil furnishes fat, vitamin A and iodine, all of which are valuable supplements to the diet of infants. Sometimes cod liver oil is not well tolerated by infants or it may be refused by older children because of its fishy taste. In such cases and in those which require higher doses of vitamin D, one must resort to other preparations. Premature infants may require 3000 LV. of vitamin D or more per day for prophylactic purposes. In the treatment of advanced cases of rickets, 5000 LV. should be given; and in the rare cases of vitamin D refractory rickets, 50,000 LV. or more may be required to achieve satisfactory results. It is obvious that such doses cannot be administered in the form of standard cod liver oil. Among the concentrated preparations for cases requiring more than 1600 LV. are cod liver oil concentrates (6000 LV. per gram), fish liver oils of high potency, such as percomorph oil (8500 LV. per gram), and preparations of irradiated ergosterol in vegetable oils or propylene glycol (10,000 I.V. per gram). The cod liver oil concentrates and the fish liver oils of high potency taste the same as cod liver oil, but in the small quantities required for the average case are not as obje~tionable. They are also excellent sources of vitamin A. The preparations of irradiated ergosterol (viosterol and drisdol) are free from the fishy taste. They do not contain vitamin A unless the label on the bottle states this specifically. For practical purposes, one may assume that 40 drops of the oily concentrated preparations correspond to 1 gm. The accompanying simplified table may be useful in daily practice, although it is not claimed to be absolutely accurate or complete. The doses recommended are somewhat larger than those required for cases for average severity. Since no harm results even from far larger doses, it appears wise to err on the side of giving more rather than less than is needed. The danger of producing toxic symptoms by the administration of vitamin D' preparations has been overestimated. By present ... These figures and the doses calculated from them are approximations. Although not strictly accurate, they will suffice for practical purposes. Space does not permit the enumeration of other preparations of different concentrations which are available.
368
]OSEF W ARKANY
TABULATION DAILY DOSES OF VITAMIN D
PREPARATIONS
Cod Liver Oil Percomorph Concentrates Oil
I.U.
Cod Liver Oil
Prophylaxis in Full-Term Infants
1000
2-3 teaspoonfuls
7 drops
Pr¥.~Ylaxis i;' Premature Infants, WlflS, etc.
3000
15 drops
12 drop,
5000
............. .............
21 drops
Cure of Rickets
35 drops
25 drops
20 drops
5 drops
Viosterol 4 drops
methods of irradiation, the toxic by-products formerly contained in irradiated ergosterol have been avoided. However, vitamin D in a highly concentrated form should be considered a drug rather than a food, and should be administered only under the supervision of a physician. For prophylactic purposes, children whose treatment could not be continuously supervised have been given enormous single doses of vitamin D without adverse effects. Children with severe rickets, whose parents cannot be trusted to give the vitamin, may be treated successfully in an out-patient clinic. By giving the patients 2 teaspoonfuls of a vitamin D concentrate once a week, complete healing of advanced rickets may be attained within two months. In juvenile, adult and senile rickets, large doses of the vitamin D concentrates (10,000 I.V. daily or more) should be given for therapeutic purposes. , An ample supply of vitamin D is available in this country at the present time. In addition, recognition of the necessity for antirachitic prophylaxis has been spread abroad among all classes of the population. Cod liver oil is considered an essential part of a child's diet. However, if it becomes scarce and the concentrates become expensive, rickets may no longer be a rare disease. There is a certain danger, too, in the fact that many young mothers have never seen a case of severe rickets and may not be sufficiently impressed with the necessity for antirachitic prophylaxis. Young mothers should be reminded constantly that sunshine or vitamin D is absolutely necessary for the health of their children.
VITAMIN D DEFICIENCY
369
BIBLIOGRAPHY
1. Hess, A. F.: Rickets Including Osteomalacia and Tetany. Philadelphia, Lea 8t Febiger, 1929.
2. Eliot, M. and Park, E. A.: Rickets. Brennemann's Practice of Pediatrics, Vol. 1, Chapter 36. Hagerstown, Md., W. F. Prior Co., Inc.
VITAMIN D DEFICIENCY"" (RICKETS) JOSEF WARKANY, M.D.t
RICKETS is a systemic disease brought about by' certain faulty living conditions which frequently accompany the "higher forills" of civilization. For its development two factors must concur: insufficient exposure to ultraviolet rays and an inadequate intake of vitamin D. Wherever living habits lead to the coexistence of these two factors, rickets appears in an endemic form in infants. If one of these etiologic factors is excluded, the disease does not develop. As soon as this fact was recognized and artificial sources of ultraviolet rays and the various forms of vitamin D became available, rickets in an endemic form disappeared in all civilized countries. The war and its consequences, such as disruption of lines of communication and of industrial production, make rickets once more a very real menace to children all over the world. Unless definite steps are taken to prevent it, the disease will again become prevalent. ETIOLOGY
Rickets may be considered a climatic disorder occurring chiefly in the temperate zones. There, especially during the winter, the amount of sunshine available is rather small, and infants born during the fall and early winter are not sufficiently protected by natural irradiation. In cold weather they are kept indoors the greater part of the time and during their short outings are so heavily dressed that they are only .. From The Children's Hospital Research Foundation and the Department of Pediatrics, College of Medicine, University of Cincinnati. t Assistant Professor of Pediatrics, University of Cincinnati College of Medicine; Attending Pediatrician in the Pediatric Division and Attending Physician in the Contagious Division of the Pediatric Service, Cincinnati General Hospital (Cincinnati, Ohio'). 361
362
JOSEF W ARKANY
slightly exposed to sunlight. Moreover, in cities dust, smoke, and the shadows cast by the buildings reduce the antirachitic potency of the sunlight and skyshine by filtering out the effective ultraviolet rays (wavelengths of 230 to 313 mp.). Ultraviolet rays are required for the conversion of provitamin D, which is always present in the infant's skin, into active vitamin D. If this endogenous vitamin D cannot be procured, an exogenous source must be made available in order that rickets may be prevented. The foodstuffs usually given to infants contain little vitamin D. Breast milk is a poor source of the vitamin. This may seem surprising, since we know that breast-fed children develop rickets less often than the artificially fed. Other protective factors not entirely known to us must operate to the benefit of the breast-fed child. Certainly breast feeding in itself cannot be considered a prophylactic measure, and the breast-fed child requires supplements of vitamin D. The same is true of the artificially fed child. Cow's milk, sugar, cereals and vegetables are not good sources of vitamin D. Butter and eggs, though richer in the antirachitic factor, cannot be considered protective in the amounts given to infants. It is imperative, therefore, to add -a more concentrated form of vitamin D to the diet of infants. This is to be found in the fish liver oils and their substitutes. Without such supplements an infant's diet should always be considered inadequate in vitamin D. Several predisposing factors play a role in the etiology of rickets. Rapid growth is one that deserves special mention. It is often thought that vitamin deficiencies occur chiefly in undernournished persons. So far as rickets is concerned, this is not true, as vitamin D is needed particularly by the rapidly growing organism, and infants who are otherwise in a good state of health and nutrition may develop marked signs of rickets. The predisposition of premature children is partly due to their rapid growth. In such children, however, the lack of mineralization of the skeleton, which normally progresses rapidly in the last few weeks of intra-uterine life, may also be an important rachitogenic factor. Vitamin D deficiency manifests itself in different ways at different ages, although
VITAMIN D DEFICIENCY
363
the rachitic process is basically the same in the different age groups. It has been suggested, therefore, that the terms "juvenile," "adult" and "senile rickets" replace the older terms "late rickets," "osteomalacia" and "hunger or war osteopathy." Since older persons are rarely completely deprived of ultraviolet light and dietary vitamin D, the late forms of rickets are seldom seen. In certain regions of China or India, however, endemic foci of rickets beyond infancy do exist. A deficiency of vitamin D manifests itself particularly during puberty, pregnancy and lactation. The late forms of rickets respond well to treatment with vitamin D. Negro children have a definite tendency to develop rickets. Whether this is due to the pigmentation of their skin or to the conditions under which they live has not yet been determined. A few rare conditions of disturbed mineral metabolism occur in which osseous changes simulating those of vitamin D deficiency appear. Vitamin D refractory rickets is due to a chronic hypophosphatemia of unknown etiology. In a number of cases, healing has been achieved with very large doses of vitamin D. Renal rickets is caused by an abnormal mineral metabolism due to insufficiency' of the kidneys. Vitamin D is of no avail in renal rickets. DIAGNOSIS
In the diagnosis of rickets, recognition of the early signs is of the greatest importance. Since they are often inconspicuous and may occur in otherwise healthy children, they may escape even the trained observer. Craniotabes, an important early symptom of rickets, should be looked for particularly in premature infants. A parchmentlike softness in the squama of the occiput or, less often, in the parietal bones indicates clearly the onset of the rachitic process. Healing of rickets leads to a rapid hardening of these spots. Softness of the borders of the large fontanelle and a delay in the decrease of its size may also become noticeable in early rickets. Moderately enlarged costochondral junctions may be palpable. Slight thickening of the wrists and ankles is suggestive of early rickets, but in this stage the swellings are usually covered by fat and therefore are not visible. Gen-
364
JOSEF WARKANY
eral irritability, marked perspiration of the skin of the head, . and flaccidity of the muscles are often present. The inorganic serum phosphorus may fall below 3.5 mg. per 100 cc. The roentgenogram is the best means by which an early diagnosis , can be made. The wrist reveals cupping and fraying of the distal end of the ulna at an early stage. Neither pa~n nor impairment of locomotion betray the onset of rickets. Advanced cases of rickets are easily recognized. The infant's head appears square and the frontal and parietal bones become prominent. Sometimes these prominences are separated from each other by grooves, which correspond to the sutures of the flat bones. The large fontanelle remains widely open even after the child is eighteen months old. Dentition is delayed and disorderly. The teeth are irregular in shape and position and there are defects in the enamel. The rachitic rosary becomes visible. Harrison's groove, a furrow that runs from the ensiform process around the lower aperture of the thorax, becomes visible along the attachments of the diaphragm. The normal curve of the ribs is interrupted in the region of the costochondral junction, and their cartilaginous portions and the sternum may protrude to form a "pigeon breast" or be depressed to form a funnel-shaped thorax. Deformities of the spine, such as kyphosis and scoliosis, may develop at this stage. They are serious symptoms since they generally persist after the rachitic process has been checked. The flaccid abdominal muscles yield to the intra-abdominal pressure and a "pot belly" develops. The rachitic pelvis is small, and its entrance is further narrowed by a forward projection of the promontory. The lower parts of the sacrum and the coccyx appear to be bent forward in the sagittal plane, thus narrowing the pelvic exit. In the female these changes, if they become permanent, add to the hazards of childbirth, since the disproportion between the size of the child and the narrowed pelvis may result in obstruction. In such cases unless an operation is performed, the death of mother and child ensues. The extremities in advanced cases show epiphyseal enlargement and various degrees and types of curving. The arms are usually not as deformed as the legs. Bowlegs (genu varum) or
VITAMIN D DEFICIENCY
365
knock knees (genu valgum) are easily recognized. Deformities in the proximal end of the femur and in the region of the ankle may occur. Deformities of the spine, the pelvis and the legs result in a reduction in the height of the body or rachitic dwarfism. In the roentgenograms, the epiphyseal ends of the long bones appear frayed. Cupping is seen most readily at the distal ends of the ulna, radius, tibia and fibula but is absent at the distal end of the femur and the proximal end of the tibia. For the diagnosis of rickets roentgenograms of the wrist are therefore better than those of the knee. Demineralization, "greenstick" fractures and curving of the long bones may also be seen. The values for inorganic serum phosphorus may be below 3 or even 2 mg. per 100 cc. PROGNOSIS
The extent of the rachitic changes, as well as the. intensity of the treatment, determines the outcome. Progress of the healing can be observed most satisfactorily in a series of roentgenograms of the wrists. The characteristic sign of healing rickets is the line of primary calcification, which is seen as a transverse band running parallel to the distal margins of the metaphysis of the radius and ulna. This line of primary calcification becomes denser and broader as healing progresses, until it joins the metaphysis. Healing is noticeable also in the cortical parts of the shaft, where calcium salts are deposited in the osteoid tissue under the periosteum. Thus, in the roentgenogram the shaft appears to have a double contour, an appearance which is often mistaken for "periostitis." Within two or three weeks after intensive treatment, definite signs of healing can be seen in advanced cases of rickets. If the rachitic process is not rigorously treated in the advanced stage, permanent deformities of the skeleton may develop which are not reparable by the administration of vitamin D and may require orthopedic correction. Rickets in itself is not a fatal disease, but diseases such as tetany, pneumonia, tuberculosis, anemia and enteritis are more likely to cause death in children with protracted rickets than in normal children.
366
JOSEF WARKANY PROPHYLAXIS AND TREATMENT
Infantile rickets can and should be prevented under all circumstances. Sunlight, the natural prophylactic agent, is not readily available in the winter. Only during the summer can sunlight be considered adequate to prevent rickets. Since the amount of active ultraviolet light varies in sunlight according to place and season, it is impossible to prescribe definitely the time of exposure required for antirachitic prophylaxis. Tanning of large areas of the skin usually is assumed to be a sign of sufficient exposure. Adequate treatment by means of artificial light also prevents rickets. Mercury vapor and carbon arc lamps are frequently used. The lamp is placed at a distance of 3 feet from the body and exposure should not exceed two minutes at the beginning. Treatment is usually given every other day, the front and back of the body being exposed alternately. The eyes should be protected by dark glasses and the skin by oil or vaseline. If no untoward reactions occur, the exposures may be gradually extended to half an hour. This can be achieved in four to six weeks. Such a series of treatments will not only prevent rickets but will serve as a therapeutic measure in cases of active rickets. The chief obstacle to the general use of the lamps lies in their cost, which makes it impossible for most families to use this form of prophylaxis for their children. Treatment at clinics and in doctors' offices is often inconvenient and there is danger of cross infections. In any case, light treatment is more time-consuming than dietary treatment. Whenever light treatment is not feasible, peroral administration of vitamin D is required for the prevention and treatment of rickets. As has been pointed out, most foodstuffs used in the diet of infants are poor sources of vitamin D and supplements are required. Numerous antirachitic supplements are available at the present time, but cod liver oil is the most extensively used. One gram of standard cod liver oil contains at least 85 LU. of vitamin D. Since 800 LU. are usually considered a safe prophylactic dose for full-term infants, two teaspoonfuls of cod liver oil daily are recommended for this purpose. Four teaspoonfuls (1600 LU.) daily are required for
VITAMIN D DEFICIENCY
367
the cure of mild cases of rickets."" In addition to vitamin D, cod liver oil furnishes fat, vitamin A and iodine, all of which are valuable supplements to the diet of infants. Sometimes cod liver oil is not well tolerated by infants or it may be refused by older children because of its fishy taste. In such cases and in those which require higher doses of vitamin D, one must resort to other preparations. Premature infants may require 3000 LV. of vitamin D or more per day for prophylactic purposes. In the treatment of advanced cases of rickets, 5000 LV. should be given; and in the rare cases of vitamin D refractory rickets, 50,000 LV. or more may be required to achieve satisfactory results. It is obvious that such doses cannot be administered in the form of standard cod liver oil. Among the concentrated preparations for cases requiring more than 1600 LV. are cod liver oil concentrates (6000 LV. per gram), fish liver oils of high potency, such as percomorph oil (8500 LV. per gram), and preparations of irradiated ergosterol in vegetable oils or propylene glycol (10,000 I.V. per gram). The cod liver oil concentrates and the fish liver oils of high potency taste the same as cod liver oil, but in the small quantities required for the average case are not as obje~tionable. They are also excellent sources of vitamin A. The preparations of irradiated ergosterol (viosterol and drisdol) are free from the fishy taste. They do not contain vitamin A unless the label on the bottle states this specifically. For practical purposes, one may assume that 40 drops of the oily concentrated preparations correspond to 1 gm. The accompanying simplified table may be useful in daily practice, although it is not claimed to be absolutely accurate or complete. The doses recommended are somewhat larger than those required for cases for average severity. Since no harm results even from far larger doses, it appears wise to err on the side of giving more rather than less than is needed. The danger of producing toxic symptoms by the administration of vitamin D' preparations has been overestimated. By present ... These figures and the doses calculated from them are approximations. Although not strictly accurate, they will suffice for practical purposes. Space does not permit the enumeration of other preparations of different concentrations which are available.
368
]OSEF W ARKANY
TABULATION DAILY DOSES OF VITAMIN D
PREPARATIONS
Cod Liver Oil Percomorph Concentrates Oil
I.U.
Cod Liver Oil
Prophylaxis in Full-Term Infants
1000
2-3 teaspoonfuls
7 drops
Pr¥.~Ylaxis i;' Premature Infants, WlflS, etc.
3000
15 drops
12 drop,
5000
............. .............
21 drops
Cure of Rickets
35 drops
25 drops
20 drops
5 drops
Viosterol 4 drops
methods of irradiation, the toxic by-products formerly contained in irradiated ergosterol have been avoided. However, vitamin D in a highly concentrated form should be considered a drug rather than a food, and should be administered only under the supervision of a physician. For prophylactic purposes, children whose treatment could not be continuously supervised have been given enormous single doses of vitamin D without adverse effects. Children with severe rickets, whose parents cannot be trusted to give the vitamin, may be treated successfully in an out-patient clinic. By giving the patients 2 teaspoonfuls of a vitamin D concentrate once a week, complete healing of advanced rickets may be attained within two months. In juvenile, adult and senile rickets, large doses of the vitamin D concentrates (10,000 I.V. daily or more) should be given for therapeutic purposes. , An ample supply of vitamin D is available in this country at the present time. In addition, recognition of the necessity for antirachitic prophylaxis has been spread abroad among all classes of the population. Cod liver oil is considered an essential part of a child's diet. However, if it becomes scarce and the concentrates become expensive, rickets may no longer be a rare disease. There is a certain danger, too, in the fact that many young mothers have never seen a case of severe rickets and may not be sufficiently impressed with the necessity for antirachitic prophylaxis. Young mothers should be reminded constantly that sunshine or vitamin D is absolutely necessary for the health of their children.
VITAMIN D DEFICIENCY
369
BIBLIOGRAPHY
1. Hess, A. F.: Rickets Including Osteomalacia and Tetany. Philadelphia, Lea 8t Febiger, 1929.
2. Eliot, M. and Park, E. A.: Rickets. Brennemann's Practice of Pediatrics, Vol. 1, Chapter 36. Hagerstown, Md., W. F. Prior Co., Inc.