The Treatment of Rheumatoid Arthritis With Large Doses of Vitamin D

Abrams, Nathan R.; Bauer, Walter

doi:10.1001/jama.1938.02790440026006

Cited by 17 publications

(3 citation statements)

References 15 publications

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“…In the 1940s, massive doses of vitamin D (200,000–300,000 IU/day) were considered an effective treatment strategy for chronic illnesses as diverse as tuberculosis and rheumatoid arthritis. Because hypercalcemia was observed in some patients thus treated, individual doctors discontinued the massive doses and the symptoms of VDT disappeared after a few months ( 4 , 12 ). However, those clinical observations alerted physicians to the possibility of VDT, and the practice of administering massive doses of vitamin D was later discontinued nationally.…”

Section: Defining Vdt and How Often It Occursmentioning

confidence: 99%

Vitamin D Toxicity–A Clinical Perspective

Marcinowska-Suchowierska

et al. 2018

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Confusion, apathy, recurrent vomiting, abdominal pain, polyuria, polydipsia, and dehydration are the most often noted clinical symptoms of vitamin D toxicity (VDT; also called vitamin D intoxication or hypervitaminosis D). VDT and its clinical manifestation, severe hypercalcemia, are related to excessive long-term intake of vitamin D, malfunctions of the vitamin D metabolic pathway, or the existence of coincident disease that produces the active vitamin D metabolite locally. Although VDT is rare, the health effects can be serious if it is not promptly identified. Many forms of exogenous (iatrogenic) and endogenous VDT exist. Exogenous VDT is usually caused by the inadvertent or improper intake of extremely high doses of pharmacological preparations of vitamin D and is associated with hypercalcemia. Serum 25-hydroxyvitamin D [25(OH)D] concentrations higher than 150 ng/ml (375 nmol/l) are the hallmark of VDT due to vitamin D overdosing. Endogenous VDT may develop from excessive production of an active vitamin D metabolite – 1,25(OH)2D in granulomatous disorders and in some lymphomas or from the reduced degradation of that metabolite in idiopathic infantile hypercalcemia. Endogenous VDT may also develop from an excessive production of 25(OH)D and 1,25(OH)2D in congenital disorders, such as Williams–Beuren syndrome. Laboratory testing during routine clinical examinations may reveal asymptomatic hypercalcemia caused by the intake of vitamin D even in doses recommended for the general population and considered safe. That phenomenon, called hypersensitivity to vitamin D, reflects dysregulated vitamin D metabolism. Researchers have proposed many processes to explain VDT. Those processes include elevated activity of 1α-hydroxylase or inhibited activity of 24-hydroxylase, both leading to increased concentration of 1,25(OH)D; increased number of vitamin D receptors; and saturation of the capacity of vitamin D binding protein. Increased public awareness of vitamin D–related health benefits might increase the risk of VDT due to self-administration of vitamin D in doses higher then recommended for age and body weight or even higher than the established upper limit intake values. Consequently, the incidence of hypercalcemia due to hypervitaminosis D might increase.

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Section: Defining Vdt and How Often It Occursmentioning

confidence: 99%

Vitamin D Toxicity–A Clinical Perspective

Marcinowska-Suchowierska

et al. 2018

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“…Foods to which a patient may be sensitive should be avoided. Various vitamin deficiencies have been suggested to be of aetiologic significance, but treatment with massive doses of the deficient vitamin has not been attended with any success (Abrams and Bauer, 1938). Occasional blood transfusions in acute cases with a low haemoglobin content are often valuable, as in the active phases of this disease the administration of iron seems to have little effect in raising the haemoglobin content.…”

Section: Hospitals Dublinmentioning

confidence: 99%

Treatment of Rheumatoid Arthritis in Children

Roden¹

1942

BMJ

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“…As for gout, we know Jittle morsil than did our ancestors, and the, probjems stillre ng solution are disappointingly many. Furthermore, in the study of all forms of arthtitis and rheumatism the importance of aller-gy (Aschoff, 1938) must not be forgotten, while dietary factors and avitamincsis must not be lost sight of (Abrams and Bauer, 1938).' It is obvious from these consid0ratioris that no one factor is going to prove responsible for Xthe.-various forms of chronic rheumatic diseases, anr,' if we-turn our attention in any pa'rticular dire'ction il mustCbe clearly understood that the factor under discussion is only contributory to the formation of the total picture, and is in no sense to be regarded as the sole or even the major causal agency.…”

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confidence: 99%

Psychological Factor in Rheumatism

Gordon¹

1939

BMJ

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Chronic rheumatic diseases comprise a complex group of conditions-which are very common, very disabling, and by no means easy to treat. A great deal has been written about them, but there is no unanimity yet as to their interrelationship, their pathology, or their treatment. Roughly these diseases may be divided into four main groups-rheumatoid arthritis, osteo-arthritis, fibrositis, and, standing rather apart, gout.It is generally held that in the rheumatoid group the most important pathogenic factor is infection, probably by one o-r other strain of streptococcus. In the osteoarthritic group degenerative and arteriosclerotic factors are most significant; in fibrositis infection is considered to play an important part in the younger victims, and metabolic and degenerative changes in the older subjects; while in gout there is almost certainly a hereditary factor which governs, the metabolic changes that characterize the attack.In the rheumatoid group we have a condition that many would call "true rheumatoid," in which, while infection is almost certainly of great importance, nevertheless it is difficult to determine its exact source. A few years ago great play was made with the shibboleth of focal infection, yet in a recent communication Cecil and Angevine (1938) (Aschoff, 1938) must not be forgotten, while dietary factors and avitamincsis must not be lost sight of (Abrams and Bauer, 1938).' It is obvious from these consid0ratioris that no one factor is going to prove responsible for Xthe.-various forms of chronic rheumatic diseases, anr,' if we-turn our attention in any pa'rticular dire'ction il mustCbe clearly understood that the factor under discussion is only contributory to the formation of the total picture, and is in no sense to be regarded as the sole or even the major causal agency. The subject of this paper, then, is how far the result iof emotional disturbance may contribute to the picture of ichronic rheumatic.disease. In dealing with the effects of emotional disturbance on the function of the body it is ,necessary to divide the effects into two groups.The first of these consists of those changes produced through abnormal action of the autonomic system on the 'circulatory and secretory organs and on the tone of plain 'muscles. Wittkower (1935)

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The Treatment of Rheumatoid Arthritis With Large Doses of Vitamin D

Cited by 17 publications

References 15 publications

Vitamin D Toxicity–A Clinical Perspective

Vitamin D Toxicity–A Clinical Perspective

Treatment of Rheumatoid Arthritis in Children

Psychological Factor in Rheumatism

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