Mahalialee4
New Member
http://www.centralpractice.4mg.com/hair_loss.htm
here is a brief excerpt:
" Nonscarring Alopecia. Most often, alopecia is nonscarring, with male- and female-pattern baldness accounting for most cases. Male-pattern baldness (androgenetic alopecia) is symmetric, usually beginning in the frontoparietal scalp. Its development is related to age, genetic predisposition, and the presence of androgenic hormones. The inheritance is probably dominant, with incomplete penetrance. The process is permanent, with pigmented scalp hairs replaced by fine, unpigmented vellus hairs.
The presence of male-pattern hair loss in a female patient should provoke concern about androgen excess, manifested by hirsutism in mild cases and virilization in more serious cases. Polycystic ovary disease and hyperprolactinemia are common causes of mild androgen excess and hirsutism. Frank virilization occurs with androgen-producing ovarian and adrenal tumors. Dihydrotestosterone inhibits the growth of scalp hair while it stimulates the growth of facial hair and promotes a male pattern of pubic hair growth. Laboratory investigation reveals increased levels of free testosterone, sulfated dehydroepiandrosterone (DHEA), or both.
The mechanisms of female-pattern baldness are similar to those of male-pattern baldness, but female-pattern baldness is more diffuse; usually, the central and frontal areas are affected, without complete baldness. Age, family tendency, and androgenic hormones are important factors. Postpartum alopecia resolves within 18 months, but about half of women feel they have less hair after childbirth than they did before pregnancy.
Nonscarring alopecia often is associated with systemic disease, a metabolic abnormality, or the use of certain medications. Alopecia areata, a condition of unknown cause in which hair is rapidly lost, usually in circular patterns, is probably the second most common form of nonscarring alopecia. Alopecia totalis is the loss of all scalp hair, and in alopecia universalis, facial and body hair are lost as well. The course of alopecia areata is unpredictable. Some persons have one episode, in which the development of one or several bald spots is followed by spontaneous regrowth. In others, new areas of baldness may develop, and they become totally bald. Onset before puberty is associated with a poorer prognosis. Most investigators believe that an autoimmune mechanism is involved and that an association with other autoimmune diseases exists.
Alopecia may follow infectious diseases that produce a high, persistent fever, such as typhoid or pneumonia. Secondary syphilis, superficial folliculitis, and tinea capitis also may produce nonscarring alopecia. Commonly used medications that can cause alopecia include b-blockers, tricyclic antidepressants, anticonvulsants, warfarin anticoagulants, allopurinol, antithyroid drugs, quinine, verapamil, indomethacin, sulfasalazine, haloperidol, and vitamin A in excessive doses. Antineoplastic agents such as 5-fluorouracil, paclitaxel, cyclophosphamide, and methotrexate predictably produce hair loss. Oral contraceptives, hyperandrogenism, and pregnancy are known to interfere with the relation between resting and growing hairs and cause hair loss.
Diffuse hair thinning may occur in thyroid disease and iron deficiency. Less commonly, hypopituitarism and parathyroid disease produce hair loss. Alopecia is a manifestation of connective tissue diseases, notably systemic lupus erythematosus and dermatomyositis. Occasionally, hair loss is self-induced, a condition known as trichotillomania. Such patients may not be aware that they are plucking hairs, and the condition may indicate significant psychiatric disturbance.
Hair Breakage. Hair loss must be differentiated from hair breakage, which results from physical or chemical stress to the shaft. The term proximal trichorrhexis is sometimes used to describe hair breakage within the first centimeter from the scalp, whereas breakage beyond this point is called distal trichorrhexis. Hair straightening can cause proximal trichorrhexis. Patients often recognize distal breakage as split ends; such breakage may be accelerated by exposure to sunshine or swimming in chlorinated pools." hope this helps someone. bonjour
here is a brief excerpt:
" Nonscarring Alopecia. Most often, alopecia is nonscarring, with male- and female-pattern baldness accounting for most cases. Male-pattern baldness (androgenetic alopecia) is symmetric, usually beginning in the frontoparietal scalp. Its development is related to age, genetic predisposition, and the presence of androgenic hormones. The inheritance is probably dominant, with incomplete penetrance. The process is permanent, with pigmented scalp hairs replaced by fine, unpigmented vellus hairs.
The presence of male-pattern hair loss in a female patient should provoke concern about androgen excess, manifested by hirsutism in mild cases and virilization in more serious cases. Polycystic ovary disease and hyperprolactinemia are common causes of mild androgen excess and hirsutism. Frank virilization occurs with androgen-producing ovarian and adrenal tumors. Dihydrotestosterone inhibits the growth of scalp hair while it stimulates the growth of facial hair and promotes a male pattern of pubic hair growth. Laboratory investigation reveals increased levels of free testosterone, sulfated dehydroepiandrosterone (DHEA), or both.
The mechanisms of female-pattern baldness are similar to those of male-pattern baldness, but female-pattern baldness is more diffuse; usually, the central and frontal areas are affected, without complete baldness. Age, family tendency, and androgenic hormones are important factors. Postpartum alopecia resolves within 18 months, but about half of women feel they have less hair after childbirth than they did before pregnancy.
Nonscarring alopecia often is associated with systemic disease, a metabolic abnormality, or the use of certain medications. Alopecia areata, a condition of unknown cause in which hair is rapidly lost, usually in circular patterns, is probably the second most common form of nonscarring alopecia. Alopecia totalis is the loss of all scalp hair, and in alopecia universalis, facial and body hair are lost as well. The course of alopecia areata is unpredictable. Some persons have one episode, in which the development of one or several bald spots is followed by spontaneous regrowth. In others, new areas of baldness may develop, and they become totally bald. Onset before puberty is associated with a poorer prognosis. Most investigators believe that an autoimmune mechanism is involved and that an association with other autoimmune diseases exists.
Alopecia may follow infectious diseases that produce a high, persistent fever, such as typhoid or pneumonia. Secondary syphilis, superficial folliculitis, and tinea capitis also may produce nonscarring alopecia. Commonly used medications that can cause alopecia include b-blockers, tricyclic antidepressants, anticonvulsants, warfarin anticoagulants, allopurinol, antithyroid drugs, quinine, verapamil, indomethacin, sulfasalazine, haloperidol, and vitamin A in excessive doses. Antineoplastic agents such as 5-fluorouracil, paclitaxel, cyclophosphamide, and methotrexate predictably produce hair loss. Oral contraceptives, hyperandrogenism, and pregnancy are known to interfere with the relation between resting and growing hairs and cause hair loss.
Diffuse hair thinning may occur in thyroid disease and iron deficiency. Less commonly, hypopituitarism and parathyroid disease produce hair loss. Alopecia is a manifestation of connective tissue diseases, notably systemic lupus erythematosus and dermatomyositis. Occasionally, hair loss is self-induced, a condition known as trichotillomania. Such patients may not be aware that they are plucking hairs, and the condition may indicate significant psychiatric disturbance.
Hair Breakage. Hair loss must be differentiated from hair breakage, which results from physical or chemical stress to the shaft. The term proximal trichorrhexis is sometimes used to describe hair breakage within the first centimeter from the scalp, whereas breakage beyond this point is called distal trichorrhexis. Hair straightening can cause proximal trichorrhexis. Patients often recognize distal breakage as split ends; such breakage may be accelerated by exposure to sunshine or swimming in chlorinated pools." hope this helps someone. bonjour
