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Acrodynia

Goldberger and Lillie in 1926 found that rats fed certain nutritionally deficient diets developed dermatitis acrodynia, a skin disorder characterized by edema and lesions of the ears, paws, nose, and tail. Szent-Gyorgyi later found that a factor he had isolated prevented these skin lesions in the rat. He proposed the name vitamin Bg for his factor. Pyridoxine, a form of this vitamin found in plants (and the form of Bg sold commercially), was isolated in 1938 by three research groups working independendy. Pyridoxal and pyridoxamine, the forms that predominate in animals, were... [Pg.597]

The last of the B vitamins to be identified in the water-soluble vitamin complex from milk was pyridoxine, vitamin B6 (Birch and Gyorgy, 1936). This was needed to prevent a type of dermatitis in rats which was different from pellagra or acrodynia and could be accompanied by convulsions. Much of the early work on the mode of action of this vitamin came from experiments on microbial metabolism (Chapter 6). [Pg.29]

If a pregnant woman is affected by mercury poisoning, the consequences may affect the child. As a result, the child may suffer from profound mental deficiency, atrophy of cerebral cortex, commisure and cerebellum neuron destruction. Acrodynia is a syndrome that affects children exposed to organic and inorganic mercury compounds. Symptoms include itchy, measles-like rash followed by desquamation of palm and foot skin, essential tachycardia, generalized swellings, hypertension and salivation (Harada, 1995). [Pg.341]

On significant inhalation of metallic mercury vapors, some people (primarily children) exhibit a syndrome known as acrodynia, or pink disease. Symptoms include severe leg cramps, irritability, erythema, and subsequent peeling of the hands, nose, and soles of the feet. ... [Pg.437]

Prior to the 1990s mercury compounds were routinely added to interior and exterior paint to prevent bacterial and fungal growth. The practice of adding mercury to paint was halted after the adverse effects of inhaled mercury were seen in a 4-year-old boy. The child s unventilated bedroom was painted with mercury-containing interior latex paint. The boy was diagnosed with acrodynia a rare disease caused by mercury exposure and characterized by flushed cheeks, pink, scaling palms and... [Pg.99]

Deficiency of this coenzyme can lead to many manifestations. Clinical signs include retarded growth, acrodynia, alopecia, skeletal changes and anemia, while changes in neurotransmitters, such as dopamine, serotonin, norepinephrine (noradrenaline), tryptamine, tyramine, histamine, y-aminobutyric acid, and taurine, affect the brain function and can lead to seizures and convulsions. An overdose of vitamin Bg leads to neuronal damage and sensory and motor effects [417],... [Pg.636]

Mercury Elemental mercury Respiratory tract Soft tissues, especially kidney, CNS CNS tremor, behavioral (erethism) gingivostomatitis peripheral neuropathy acrodynia pneumonitis (high-dose) Inhibits enzymes alters membranes Elemental Hg converted to Hg2+. Urine (major) feces (minor)... [Pg.1228]

A deficiency of the vitamin can result in lymphopenia, convulsions, dermatitis, irritability, and nervous disorders in humans. A defidency in monkeys may cause arteriosclerosis, while in rats, acrodynia. Research indicates that all animals require vitamin Bg, Bacteria in intestines generate some of this vitamin, but relatively little is available to humans in this form. Endogenous sources are available to plants, fungi, and some bacteria. [Pg.1701]

In vitamin Be-deflcient experimental animals, there are skin lesions (e.g., acrodynia in the rat) and fissures or ulceration at the corners of the mouth and over the tongue, as well as a number of endocrine abnormalities defects in the metabolism of tryptophan (Section 9.5.4), methionine (Section 9.5.5), and other amino acids hypochromic microcytic anemia (the first step of heme biosynthesis is pyridoxal phosphate dependent) changes in leukocyte count and activity a tendency to epileptiform convulsions and peripheral nervous system damage resulting in ataxia and sensory neuropathy. There is also impairment of immune responses, as a result of reduced activity of serine hydroxymethyltransferase and hence reduced availability of one-carbon substituted folate for nucleic acid synthesis (Section 10.3.3). It has been suggested... [Pg.246]

In vitamin Bg-deficient experimented emimals, there are skin lesions (e.g., acrodynia in the rat) emd fissures or ulceradon at the corners of the mouth emd over the tongue, as well as a number of endocrine abnormalides defects in the metabolism of tryptophan (Secdon 9.5.4), methionine (Section... [Pg.246]

Erythroderma Desquamativum and Acrodynia. Studies on erythroderma desquamativum at different stages in several nursing infants were carried out in 1953 by some authors (B13, S2, S3). [Pg.106]

Peressini (P4) followed xanthurenic acid excretion in two children with acrodynia loaded with L-tryptophan. Xanthurenuria was influenced by administration of both deoxypyridoxine and pyridoxine which, respectively, increased and normalized the levels. [Pg.106]

Acrodynia, or Pink disease, discussed above, was common among infants in the UK and USA until the late 1940s when it became evident that the condition was caused by exposure to calomel in teething powders and in antihelmintic preparations. An allergic reaction towards mercury with variable susceptibihty is considered to be involved in the pathogenesis of Pink disease because the syndrome develops in only a small proportion of all exposed (less than 1%) [65]. Furthermore, only infants and small children are affected. [Pg.817]

This profile contains a discussion of acrodynia under Relevance to Public Health (Section 2.5). [Pg.51]

Acrodynia is an idiosyncratic hypersensitivity response from exposure to mercury and is characterized by certain cardiovascular, dermal, and neurological effects, among others. In the section on health effects by route of exposure, the relevant symptoms are discussed under the appropriate headings without reference to the syndrome. This occurs, in part, because there is some overlap between symptoms characteristic of acrodynia and those seen in persons who are not hypersensitive and, in part, because not every report of a study in which the symptoms were observed states whether the authors considered the affected person to have suffered from acrodynia. [Pg.51]

Foulds D, Copeland K, Franks R. 1987. Mercury poisoning and acrodynia. Am J Dis Children 141 124-125. [Pg.606]

Tunnessen WW, McMahon KJ, Baser M. 1987. Acrodynia Exposure to mercury from fluorescent light bulbs. Pediatrics 79 786-789. [Pg.651]


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