Biotin alopecia

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. 

When a normal diet is followed, biotin dehciency is rare. Clinical symptoms of dehciency are alopecia and cntaneons abnormalities snch as seborrhoeic dermatitis (especially in patients affected by phenylketonnria), periorihcial erythema, and fnngal infection. The main sonrces of biotin are liver, kidney, egg yolk, some vegetables snch as soybeans, nnts, spinach, mnshrooms, and lentils. In green plants and frnits, biotin occnrs in water-extractable forms, whereas in yeast and animal prodncts, it is a hrmly bonnd complex [417]. The variability on the amonnts of biotin in foods is due to both natural variation, bnt also to methodological problems. 

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. 

Acquired biotin deficiency is extremely rare but may occur in special conditions such as long-term parenteral nutrition without biotin supplementation, short bowel syndrome and after excessive intake of raw egg white, which contains the potent bio-tin-binding protein avidin. The main symptoms are alopecia and skin abnormalities which resolve after administration of biotin [2, 30]. 

Deficiency can be due to two known genetic disorders of biotin metabolism or be induced by excess intake of avidin, which binds biotin and thus leads to poor absorption. Symptoms are alopecia, eczema around nose and mouth, conjunctivitis, hyperaesthesia, paraesthesia, depression, and muscle pain 29 The recommended daily allowance is 30 to 35 fig.112... 

If the child with profound biotinidase deficiency is symptomatic, then the biochemical abnormalities and seizures resolve rapidly after biotin treatment. This is usually followed by improvement of the cutaneous abnormalities. Hair growth returns over a period of weeks to months in the children with alopecia. Optic atrophy and hearing loss are usually resistant to therapy, especially if several months have elapsed between the time of diagnosis and the initiation of treatment. Some treated children have rapidly regained lost developmental milestones, whereas others have continued to show deficits. 

Biotin deficiency and the functional deficiency associated with lack of holo-carboxylase synthetase (Section 11.2.2.1), or biotinidase (Section 11.2.3.1), causes alopecia (hair loss) and a scaly erythematous dermatitis, especially around the body orifices. The dermatitis is similar to that seen in zinc and essential fatty acid deficiency and is commonly associated with Candida albicans infection. Histology of the skin shows an absence of sebaceous glands and atrophy of the hair follicles. The dermatitis is because of impaired metabolism of polyunsaturated fatty acids as a result of low activity of acetyl CoA carboxylase (Section 11.2.1.1). In biotin-deficient experimental animals, provision of supplements of long-chain 6 polyunsaturated fatty acids prevents the development of skin lesions (Mock et al., 1988a, 1988b Mock, 1991). 

Biotin deficiency in animals results in alopecia, a. scaly dermatitis, anorexia, and eventually death. Some of the biochemical changes occurring in rats consuming a biotin-deficient diet containing raw egg white are illustrated in Figure 9.33. The animals consumed the diet for up to 30 days. The activities of three biotin-requiring enzymes were determined in the livers of rats killed at the indicated times. The en iymes measured were acetyl-CoA carboxylase ( , propionyl-Co A carboxylase (O), and pyruvate carboxylase (A). 

The metabolic action of biotin is mediated through biotin-dependent enzymes that actively synthesize purines. It is a stable monocarboxylic acid, soluble in water and alcohol, and acts as a coenzyme as well as a growth factor, even in very small quantities. Biotin deficiencies cause scaly dermatitis, hyperkeratosis and alopecia. Topical application of biotin reduces the secretion of sebum. 

Biotinidase deficiency A failure of biotin recycling results in an organic aciduria, developmental delay, seizures, alopecia, hypotonia and hearing loss... 

Biotin Al F 30 [xg M 30 [xg Liver Egg yolk Conjunctivitis central nervous system abnormalities glossitis alopecia dry, scaly dermatitis... 

Terroine (1954) has examined the effect of ascorbic acid on biotin deficiency in rats. She used lower levels than in her later experiments on thiamine and riboflavin deficiencies. She found that 0.1-0.5% ascorbic acid only slightly improved growth and appetite but considerably reduced the incidence of signs of biotin deficiency. Thus, in 92 days, all the deficient animals had developed alopecia, but only 30% of those receiving ascorbic acid. Similarly, 90% of the deficient group had spectacle eyes, but none... 

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. 

Recently, a biotin plus zinc deficiency after surgery (pancreatico duode-nectomy) was reported in a 16-year old patient. She was diagnosed as biotin-deficient because of dermatological clinical signs (alopecia, skin scales). The authors recommend an early diagnosis to prevent sequel of biotin deficiency with an adequate supplementation of biotin and zinc as treatment (Yazbeck et al. 2010). 

Arslan, M., Vurucu, S., Balamtekin, N., Unay, B., Akin, R., Kurt, I., and Ozcan, O., 2009. The effects of biotin supplementation on serum and liver tissue biotinidase enzyme activity and alopecia in rats which were administrated to valproic acid. Brain cfe Development. 31 405 10. 

Holocarboxylase synthetase deficiency [3, 4] is the classic infantile form of multiple carboxylase deficiency. Untreated it is uniformly fatal, while early diagnosis and treatment with biotin usually lead to the disappearance of all of the manifestations of the disease. Life-threatening illness is associated with massive ketosis and metabolic acidosis. A bright red cutaneous eruption may cover the body, and there is alopecia totalis. Immune function, both T and B cell, may be defective. 

Human biotin deficiency is extremely rare. Deficiency symptoms include anorexia, nausea, vomiting, glossitis, pallor, mental depression, dry scaly dermatitis and, after long-lasting, severe biotin deficiency, hair loss (alopecia). Biotin is extremely important in animal production. Spontaneous biotin deficiency has led to heavy losses in certain livestock species. Consequently, biotin is added to feed mixes for poultry, pigs and fish in order to ensure optimal growth, healthy skin and bones and efficient reproduction. 

Nielsen and Black (41) have reported that rats given sulfasuxidine in a so-called synthetic diet, with supplements of thiamine, riboflavin, pyridoxin, and pantothenic acid and with or without additional supplements of biotin and an L. casei factor concentrate, developed a symmetrical alopecia. Inositol supplementation prevented the onset of this condition and animals receiving it grew better and had a more tidy appearance. No reports confirmatory of these ob.servations have as yet appeared. 

---