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Vitamin alopecia

Domestic goats (Capra sp.) fed a zinc-deficient diet (15 mg Zn/kg) developed skin histopathology and alopecia (hair loss) after 177 days zinc-deficient diets lacking Vitamin A hastened the process, with signs evident between 46 and 68 days (Chhabra and Arora 1989). No signs were evident in goats fed Vitamin A-adequate diets containing 80 mg Zn/kg ration (Chhabra and Arora 1989). [Pg.679]

A chronically iU patient on long-term (home) parenteral nutrition develops metabolic acidosis, a grayish pallor, scaly dermatitis, and alopecia (hair loss). These symptoms subside upon addition of the B vitamin biotin to the alimentation fluid. [Pg.260]

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]

Biotin (vitamin B ) is widespread in foods and is also synthesized by intestinal bacteria. It is a coenzyme for the carboxylation of pyruvate, acetyl-coenzyme-A (CoA), propionyl CoA, and /1-methyl-crotonyl CoA and is involved in fatty acid formation and in energy release from carbohydrates. In humans deficiencies only occur in patients with an abnormal gut flora and manifests itself as exfoliative dermatitis and alopecia. [Pg.474]

IU/day by the oral route with routine blood work to monitor plasma levels. Toxicity due to excess vitamin A is not common but is potentially fatal. Acute toxicity presents as vertigo, diplopia, seizures, and exfoliative dermatitis. Chronic toxicity manifests very differently (i.e., dry skin, alopecia, amenorrhea, symptoms of liver fibrosis, etc.). It is imperative to monitor plasma vitamin A levels regularly, especially in the setting of the large doses required to treat ABL. [Pg.298]

Hair follicles also have calcitriol receptors and type 11 vitamin D-resistant rickets (Section 3.4.2), which is caused hy lack of calcitriol receptor function, is associated with total alopecia, suggesting that calcitriol has a role in their development. [Pg.97]

Type 11 vitamin D-resistant rickets is characterized by a lack of responsiveness of target tissues to calcitriol and is caused by a genetic defect in the calcitriol receptor. Affected children develop more or less normally until about 9 months of age, then develop severe rickets with alopecia and a wide variety of disorders, including immune system dysfunction. Three variants are known ... [Pg.101]

R. A. and Matthews, B.W., Type II restriction endonucleases structural, functional, and evolutionary relationships, Curr. Opin. Chem. Biol. 3, 578-583, 1999 Akar, A., Orkunoglu, F.E., Ozata, M., Sengul, A., and Gur, A.R., Lack of association between vitamin D receptor Fokl polymorphism and alopecia areata, Eur. J. Dermatol. 14, 156-158, 2004 Guy, M., Lowe, L.C., Bretherton-Watt, D. et al., Vitamin D receptor gene polymorphisms and breast cancer risk, Clin. Cancer Res. 10, 5472-5481, 2004 Claassen, M., Nouwen, J., Fang, Y. et al., Staphylococcus aureus nasal carriage is not associated with known polymorphism in the Vitamin D receptor gene, FEMS Immunol. Med. Microbiol. 43,173-176, 2005 Bolu,... [Pg.106]

Vitamin A Hypercarotenosis Increased intracranial pressure Headache Sleep disturbances Nausea, vomiting, diarrhea Chronic liver disease Dry skin, fissures, depigmentation, and pruritus Alopecia Bone tenderness Teratogenesis (renal and nervous system)... [Pg.3687]

An autosomal recessive disease known as hereditary vitamin D-resistant riekets, type II is caused by defects in the gene for the vitamin D receptor which renders it nonfunctional. Thus, this knockout of VDR function illustrates its importance. Patients with this disease have high circulating levels of 1,25-(OH)2D (unlike type 1 disease which is due to la-hydroxylase deficiency, discussed earlier), severe rickets, and alopecia. The alopecia may... [Pg.883]

In pigs, biotin deficiency causes foot lesions, alopecia (hair loss) and dry scaly skin. In growing pigs, both growth rate and food utilisation are adversely affected. In breeding sows, a deficiency of the vitamin can adversely influence reproductive performance. [Pg.96]

A water-soluble vitamin of the B group. It is an essential coenzyme for carboxylase reactions in man. Dietary deficiency is rare but when it occurs produces the symptoms of alopecia and dermatitis. [Pg.54]

The synthesis of inositol by the bacterial fiora of the mouse has been definitely established by Woolley (111). Cultures of the intestinal contents of the mouse in a synthetic medium, showed that the intestinal organisms were capable of synthesizing the vitamin. This phenomenon furnished adequate explanation to the observation (112) that deficient mice with alopecia exhibited spontaneous cures while subsisting on an inositol-free regime (113). The amount of the vitamin stored was found to be lower in the bodies of mice with alopecia as compared with that stored by mice showing spontaneous cures. Moreover, the bacterial flora of the former showed poor synthesis as compared with the latter, when such flora was grown in synthetic media. [Pg.30]


See other pages where Vitamin alopecia is mentioned: [Pg.599]    [Pg.235]    [Pg.36]    [Pg.2676]    [Pg.3645]    [Pg.2838]    [Pg.109]    [Pg.296]    [Pg.388]    [Pg.200]    [Pg.38]    [Pg.32]    [Pg.54]    [Pg.57]   
See also in sourсe #XX -- [ Pg.97 ]

See also in sourсe #XX -- [ Pg.97 ]

See also in sourсe #XX -- [ Pg.97 ]




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Alopecia

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