피나스테라이드: 프로페시아,핀페시아,프로스카,핀카등 전세계 피나스테리드계열 제네릭의약품 정보.
두타스테라이드: 아보다트, 제네릭아보다트 정보/ 미녹시딜정 : 먹는 미녹시딜 / 스피로놀락톤:알닥톤,스피로닥톤
미녹시딜 5%액 : 로게인,리게인, 잔드록스,마이녹실,스칼프메드등 minoxidil계열의 정보
기타의약품:시메티딘,로아큐탄,스티바A(트레티노인),다이안느, 드로겐정, 판토가
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전체[피나스테리드] [re] 시간이 없어서 그냥 원문만 옮겨 놓을께요
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>전 프샤복용한지 이제 막 한달이 되었습니다
>처음엔 머리기름도 줄고 빠지는 양도 거의 없더니 3주쯤 되니까 갑자기 우수수수 떨어지는겁니다
>너무 당황되고 솔직히 무섭습니다
>탈모는 상당부분 진행된 상태로 지내다가 마지막 희망을 갖고 프샤를 복용하고 있습니다
>새딩이 보편적인 현상인지,또 그 지속상태는 어느정도인지 알고 싶군요
>이대로 가다가는 전부 빠져버리겠습니다....
>새딩이 일어나면 약의 효과가 없는건지,나한테 안맞는건지도 궁급합니다
>저는 크게 피곤한건 모르겠고 조금 피로함은 느끼고 있어요.
>문제는 새딩입니다
>꼭 알려주세요!
minoxidil.com에서 퍼 왔습니다.
참고로 하세요...(성장기 탈모.. anagen effluvium과는 관계없을 것 같아서 옮겨오지 않았습니다.)
SHEDDING AND HAIR LOSS
With its cycle of repetitive planned obsolescence and rebirth, hair is a unique organ system. It’s of little wonder that with its complex and continuous recycling, there can be multiple clinical disorders based on cycling abnormalities. Although much is known about the organization and composition of the hairs themselves and of the follicles, we still have an incomplete and rudimentary understanding of relevant pathways and mechanisms that regulate follicular function. In this article, we are addressing only entities that cause hair loss or shedding, rather than problems of hypertrichosis or overgrowth of hair.
The first hair follicles on the scalp form at approximately the 9th week of gestation. On the average, the human scalp will have 100,000 follicles and no further follicular neogenesis occurs after birth. You are born with as many hair follicles as you are ever going to have. The same follicles that produced lunago (unpigmented ultra-fine) hair in the fetus and immediate postnatal life, eventually produce terminal hair. It is important to note that during one’s lifetime, the same follicles can intermittently produce vellus or terminal hair.
A knowledge of the hair cycle is essential to understanding hair problems. Hair growth on the human scalp is an asynchronous regeneration of the hair follicle in repeated cycles, referred to as a mosaic pattern of follicular growth. The growth stage is the anagen phase. The duration and rate of growth of the anagen phase normally varies at different body sites, in different individuals, and at various ages. Scalp hairs have a relatively long anagen phase typically ranging from 2 to 5 years, but has been documented to be as long as 10 years. The short-lived catagen period, usually 2 to 4 weeks in duration, is the transitional portion of the cycle. At this time, each terminal hair bulb moves from its location in the dermis to a more superficial location by means of shrinkage and remolding of that portion below the bulge region where the arrector pili muscle inserts. This muscle is not present on true vellus hair and allows terminal hairs to ‘stand on end’. Once a hair has made the transition to the telogen phase, its existing hair shaft will not grow any longer. The hair shaft during the telogen phase is no longer anchored securely in the dermis as it was in the anagen phase and can be easily dislodged with the gentle traction of brushing or shampooing or combing. Usually the shedding is unnoticed. Since the hair can accumulate in the shower drain or on soapy hands, patients can erroneously associate washing the hair with causing hair loss. The telogen hair has a club shaped proximal end within the hair follicle and retains the club shape when it is shed. The new hair produced from the subsequent anagen phase does not "push out" the hair from the previous cycle and may on occasion be found adjacent to the temporarily retained club hair within the follicular canal
Many of the causes of alopecia listed above are rare and are not frequently encountered in any practice. A good dermatology textbook will describe the entities. However, it is important to understand that there are many causes for hair loss.
Although it may sound contradictory, shedding and hair loss is not synonymous. First, we must define our terms. Shedding refers to hair shafts that easily or spontaneously fall out of the scalp. There are multiple causes of shedding. Shedding normally occurs at the end of the telogen phase, but, in pathological cases, can also occur during anagen. As a rule, shedding usually refers to a temporary event and suggests that the hair shaft will grow back again as thick as before, providing there is not an intervening pathological process.
In distinction, hair loss can refer to either the temporary or permanent loss of hair or a loss not in the number of hair shafts, but in the volume and texture of the hair shaft. For example, permanent hair loss can be caused by a scarring alopecia, such as occurs in third degree burns or radiation to the scalp. Typical of a loss in the volume of hair, but not in the number of follicles, would be the miniaturization of the follicle due to male pattern baldness (MPB).
A complete medical history can almost always determine the cause of alopecia. If necessary, there are alternative ways for determining aberrations of scalp hair cycling. The first is the ‘hair pull’. This simple technique involves gentle traction from the base to the terminal ends of a group of 25 to 50 hairs. Normally, only a few hairs are dislodged on six to eight such hair pulls. Shedding of two to three hairs per pull is pathologic. If there is increased shedding, the proximal ends should be evaluated to determine if there is an intact hair shaft and bulb, which would indicate either an effluvium (Latin for "a flowing out") or hair breakage.
A biopsy of the scalp may or may not be helpful with the diagnosis of a particular hair disorder. The information it delivers about cycling aberrations is merely confirmatory to that obtained by other simpler, less expensive means, and the diagnosis of hair shaft abnormalities cannot be made by a scalp biopsy. The real value of a scalp biopsy is in the insight it can offer into mechanisms of alopecia.
Since this article is being written primarily for the information of patients affected by pattern baldness, we’ll limit the subject of shedding and hair loss due to physiologic processes, medications, telogen effluvium, anagen effluvium and male pattern baldness.
PHYSIOLOGIC SHEDDING
Since it would be normal to have 10 to 15% of all the hairs on the scalp in the telogen phase, we can expect that 50-100 of those hairs are at the end of the phase and will readily shed. The anagen phase is in proportion to the size of the follicle and can vary from months to years. Vellus hairs have an anagen period of a few months. However, regardless of the length of the growing period or of the size of the hair follicle, the length of the telogen phase remains fairly stable, i.e. approximately 100 days. As a consequence, the anagen/telogen ratio in an area affected by male pattern baldness is higher than in areas unaffected or less affected by male pattern baldness (MPB), so in any given time period, there will be more shedding of hair from the areas affected by MPB than there will be in the remainder of the scalp.
At the end of the telogen phase, the follicle will re-enlarge and re-organize and begin producing a new hair shaft. To date, we do not have any medications that can be used safely to shorten the telogen phase.
SHEDDING DUE TO CHEMICAL AGENTS
Minoxidil
For the same reasons that minoxidil promotes hair growth, it can also cause shedding. Despite many years of research and use, the exact physiologic mechanisms whereby minoxidil stimulates hair growth is not known. The stimulatory effect of minoxidil on the hair follicle can cause hair that is in the telogen phase to shed before the end of the normal 100-day telogen period.
The effect of minoxidil on the hair follicles is dose dependent. The initial shedding was rarely reported during use of topical 2% minoxidil. With 5% topical minoxidil, it was usually not noticeable, but was infrequently reported. With the use of currently available minoxidil concentrations of 12.5%, the initial shedding is commonly reported. The shedding can be noted within weeks of initial use of topical minoxidil.
Since shedding due to the use of topical minoxidil only effects hair that is in the telogen phase, the increased shedding should not last longer than 100 days and should only effect those areas of the scalp where the topical minoxidil is being applied.
Finasteride(이게 프로스카/프로페샤 인건 알고 계시죠?)
There have been multiple reports of excessive shedding several months after finasteride therapy. Typically, there is a good response to finasteride to prevent or reverse MPB. Then, around the 11th to 16th week, there can be sudden shedding, sometimes on a massive scale. The entire phenomenon fits the description of a telogen effluvium. It is a common observation that post-partum women often suffer the same temporary hair loss. In the case of finasteride use, the telogen effluvium appears to be a reaction to the sudden change in the systemic levels of the sex hormone, DHT. Often the cause of a telogen effluvium are obscure, but has been related to high fevers, stress, trauma, medications, etc.
The shedding is generally diffuse (global) and can affect areas of the scalp not usually affected by MPB. So, it would be common to note shedding from the sides and back of the head in addition to the crown, vertex and frontal areas. The shedding tends to be fairly symmetrical, but will be more noticeable in the areas affected by MPB, because there is a higher ratio of hairs in the telogen phase than in the other areas of the scalp.
The duration of a telogen effluvium is variable, but rarely lasts more than a few months and there is invariably complete restitution unless another pathologic process also occurs.
As a rule, treatment is not necessary because the hair will grow back. For most patients, there is no evidence of residual loss of hair within a year. However, there have been cases of patients taking finasteride and reporting repeated bouts of excessive shedding. In this situation, it would be advisable to discontinue use of finasteride in favor of alternative anti-androgens.
TELOGEN EFFLUVIUM(휴지기 탈모)
This is a common type of temporary hair loss and may occur at any age. The phenomenon represents a precipitous shift of a percentage of anagen hairs to telogen, typically 3 to 4 months after an inciting event. The reaction can be to a variety of physical or emotional stresses:
In a significant number of patients, no obvious cause is found for the telogen effluvium. Telogen effluvium is always potentially completely reversible and does not lead to total scalp loss. Rarely does more than 50% of the hair become involved in a telogen effluvium. For more details on telogen effluvium, please refer to the article found in the Journal Articles on this website.
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Telogen Effluvium (Including Postnatal, Postfebrile, Postpartum,
and Heparinoid Alopecia)
Unit 2-35: TOXIC AND PHYSIOLOGIC ALOPECIA Vol. 1 Section 2: DISEASES OF HAIR
The separation of this form of diffuse hair loss as a distinct pathogenetic disorder has only been accomplished in this century. Appreciation of this condition has been dependent on the establishment of methods for qualitative and quantitative evaluation of statistically significant numbers of hairs from an individual scalp; manual epilation and low-power microscopic examination of approximately 100 hairs as introduced by Van Scott and co-workers1 has proved to be reasonably atraumatic and effective diagnostically and prognostically, particularly in telogen and anagen alopecias.
INCIDENCE
Telogen alopecia (along with male-pattern baldness) surely represents the most common type of alopecia. Postnatal and postpartum alopecias affect virtually all children and probably the majority of parturient women, although the latter may be so minimally affected as to escape clinical notice. Prevalence of postfebrile alopecia is not known, although "epidemics" have been noted, for example, during the 1918 flu epidemic.2 Telogen effluvium also follows discontinuation of oral contraceptives, which is analogous to the well-recognized postpartum shedding. Because this form of hair loss represents in effect an acceleration of a normal and disease states will tend to overlap considerably.
CLINICAL MANIFESTATIONS, CAUSE, AND PROGNOOSIS
The characteristic feature of telogen alopecia is a latent period of several weeks between the inciting event and clinical hair loss. The data of Schiff and Kern3 concerning onset of hair loss following delivery can be represented graphically to follow a reasonable facsimile of a bell-shaped curve, with about one half of 98 cases beginning at 11 to 13 weeks. This agrees well with the often-stipulated 3-month interval (the normal average duration of retention of telogen hair in the scalp), but variation from 4 to 16 weeks should be expected. Onset within a few days of pregnancy, however, suggests the possibility of a concomitant or antecedent process compounding the event.
Complaints of clinical alopecia will vary with the sensitivity of the affected woman to the process and her concern with cosmetic appearance. This may be particularly frustration to the examining physician, because true increase in rate of loss of telogen hairs may be exceedingly difficult to detect. It must be remembered that about 50 hairs are lost from the average scalp per day. If this rate is increased to 150 per day, for example, and the scalp contains 100,000 or more hairs, the amount of hair lost over an entire week will be only about 1%. If these hairs are lost from follicles distributed randomly over the scalp, clinical detection of alopecia may be impossible; yet the patient is losing hair at three times the normal rate and may be justifiably concerned. This is true of all type of telogen alopecia.
The loss of hair is sometimes partially patterned rather than randomly diffuse and tends to follow the frontal distribution typical of male baldness. This is particularly true of the normal postnatal shedding observed in virtually all infants.4 This little-studied and apparently universal phenomenon of infant development is better known to mothers than physicians. Justification for this medical lack of interest presumably is based on the temporary nature of the process and complete restitution of normal scalp hair by the end of the first year of life.
All these processes may be regarded as physiologic and consequent to premature induction of the normal hair cycle termination without apparent pathologic implication. In addition, exogenous administration or accidental ingestion of anticoagulants (heparin, heparinoids, coumarin), gold compounds, and propranolol, causes telogen effluvium. The effect is believed to be related to dose - not duration of therapy.5
Although usually secondary to therapeutic administration, accidental poisoning with warfarin can result in the same process. The clinical features are identical with the other cases of telogen alopecia, that is, a diffuse hair loss with clinical severity dependent on a rate of loss, percentage of hairs converted to telogen, and extent of passive removal by manipulations such as excessive brushing.
Telogen alopecia from medication causes diffuse hair loss or predominantly frontal shedding. The hair may not be shed until 3 months after starting the causative medication.
Some instances of alopecia cannot be related to specific physiologic or toxic events. Many observers have noted severe diffuse alopecia occurring in apparently temporal relation to severe antecedent emotional trauma.
The duration of telogen alopecia is somewhat variable, but complete restitution invariably occurs unless another pathologic process supervenes. In one series of subjects with postpartum alopecia, 56 or 98 patients returned to normal in 5 or 6 months. Apparently a few cases may persist for 1 or more years, but this is a distinct exception. It is difficult to assess reports of post-infectious alopecias persisting for years. In the usual case, assurance of complete return to normal with 1 year is entirely warranted.
The relationship of postpartum alopecia to recurrent pregnancies is of prognostic (and possibly pathogenetic) interest. Schiff and Kern stated that a new pregnancy established in the early postpartum period (prior to second menses) was not followed by alopecia.
ETIOLOGY AND PATHOGENESIS
Postpartum hair loss represents an apparent delay during the third trimester in the normal rate of anagen-telogen conversion. Those hairs that would have normally converted during this period apparently do so only after release from the hormonal alterations of pregnancy, resulting in a temporary increase in the number converted to telogen hairs during the postpartum period. This interpretation is based on the observation by Lynfield7 of an increased percentage of anagen hairs before delivery and a significant decrease (or increase in telogen) after delivery. The precise hormonal mechanism is unknown, although Lynfield cites the know influence of estrogen on prolonging the anagen stage.
The mechanism of postfebrile alopecia is unknown. Although clinical impressions would suggest that a major elevation of temperature is necessary there is no good quantitative evidence to support this supposition. Similarly, the induction of telogen alopecia by heparin and related compounds occurs by an unknown mechanism. The ability to produce telogen alopecia by purposeful prescription of known agents that in proper doses do not cause serious systemic toxicity provides unique opportunity for studies of pathogenesis. The interesting observation of an inconstant perivascular collagenous degeneration similar to that notes in alopecia areata8 and certain cicatricial alopecias9 requires additional investigation for appropriate interpretation.
DIAGNOSIS
The diagnosis of telogen alopecia, although reasonably evident from history in most cases, can be directly confirmed by identification of all shed hairs as morphologically normal telogen hairs by observation of a greatly increased number of telogen hairs (decreased anagen - telogen ratio) in the scalp, as reflected in a sample of epilated hairs. It must be emphasized, however, that even an anagen-telogen count must be interpreted with caution. A count late in the course of anagen alopecia when most growing hairs have already been lost would reveal a high proportion of telogen hairs by epilation: both experience and constant referral to the person are mandatory.
DIFFERENTIAL DIAGNOSIS
Diffuse nonpatterned alopecia will not normally be confused with any of the patchy or cicatricizing processes. In telogen effluvium the scalp skin is entirely normal, as are the hair shafts. Differentiation from (acute) anagen alopecia is generally not difficult. When all anagen hairs are severely damaged, 90% or more of the scalp hairs may be lost in a short time. Telogen alopecia by contrast rarely results in loss of more than 50% of scalp hair. Even this gross loss may be remarkably unspectacular clinically, particularly if the remaining hair is long and tends to mask the thinning. Observations of the hair roots will reveal characteristic differences in anagen or telogen alopecias. Hairs damaged in anagen will show specific morphologic dysplastic alterations. Hairs lost in telogen alopecia are morphologically normal resting hairs.
The situation may be more confusing when an agent responsible for anagen alopecia is delivered slowly rather than rapidly, as for example chronic ingestion of small amounts of a toxin. Similarly, smaller doses of a cancer chemotherapeutic agent may result in entirely reversible matrix inhibition or only a small percentage of visibly affected hairs. The magnitude of hair loss in such instances may be more similar to that in telogen alopecia than to gross loss of acute toxic anagen alopecia. Careful observation of spontaneously and manually epilated hairs should detect characteristic constrictions, breaks, or atrophic hairs in the latter instances.
Telogen alopecia resulting in male-pattern hair loss can be readily overlooked in the male; in the female it is less likely ignored. The etiology of male-pattern baldness in women is often obscure, but search for causes of underlying telogen alopecia is appropriate.
TREATMENT
There is no effective treatment for telogen alopecia. Careful explanation of cause and favorable prognosis, together with instructions to preserve as many telogen hairs in the scalp as possible by avoidance of manipulation until new growth has progressed, should be routine.
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