Hair Loss Treatment at the Proctor Clinic. We treat hair loss.
Cleve Clin J Med. 2009;76:361
Diffuse hair loss: its triggers and management.
Harrison S, Bergfeld W.
TRIGGERS OF DIFFUSE TELOGEN HAIR LOSS
Triggers of telogen effluvium are numerous
Physiologic stress such as surgical trauma high fever chronic systemic illness and hemorrhage11 are well known to cause telogen effluvium 2 to 3 months after the insult. Telogen hair shedding can be experienced 2 to 4 months after childbirth (telogen gravidarum)
The relationship between emotional stress and hair loss is difficult to ascertain, and hair loss itself is stressful to the patient. Historically, acute reversible hair loss occurring with great stress has been reported. However, the relationship between chronic diffuse hair loss and psychological stress is controversial. Evidence for this association appears to be weak, as everyday stresses are likely not enough to trigger hair loss.
Both hypothyroidism and hyperthyroidism can cause diffuse telogen hair loss that is usually reversible once the euthyroid state is restored. Chronic systemic disorders such as systemic amyloidosis, hepatic failure, chronic renal failure, inflammatory bowel disease, and lymphoproliferative disorders2 can cause telogen hair shedding. Telogen hair loss has also been reported in autoimmune diseases such as systemic lupus erythematosus and dermatomyositis, as well as in chronic infections such as human immunodeficiency virus type 19 and secondary syphilis.11 Inflammatory disorders such as psoriasis, seborrheic dermatitis, and allergic contact dermatitis can all cause diffuse telogen hair loss.
Nutritional causes of diffuse telogen hair loss are zinc deficiency and iron deficiency. Severe protein, fatty acid and caloric restriction with chronic starvation and crash dieting can also induce diffuse telogen hair loss. Malabsorption syndromes and pancreatic disease can precipitate telogen hair shedding. Essential fatty acid deficiency can also be associated with diffuse telogen hair shedding usually 2 to 4 months after inadequate intake. Vitamin D is an essential vitamin in cell growth, and vitamin D deficiency may be associated with diffuse hair loss. Biotin deficiency can result in alopecia, but this is a very rare cause of hair loss.
Cell Stress Chaperones. 2008 Spring;13(1):31-8. Epub 2008 Feb 5.
Prevention of chemotherapy-induced alopecia in rodent models.
Alopecia (hair loss) is experienced by thousands of cancer patients every year. Substantial-to-severe alopecia is induced by anthracyclines (e.g., adriamycin), taxanes (e.g., taxol), alkylating compounds (e.g., cyclophosphamide), and the topisomerase inhibitor etoposide, agents that are widely used in the treatment of leukemias and breast, lung, ovarian, and bladder cancers. Currently, no treatment appears to be generally effective in reliably preventing this secondary effect of chemotherapy. We observed in experiments using different rodent models that localized administration of heat or subcutaneous/intradermal injection of geldanamycin or 17-(allylamino)-17-demethoxygeldanamycin induced a stress protein response in hair follicles and effectively prevented alopecia from adriamycin, cyclophosphamide, taxol, and etoposide. Model tumor therapy experiments support the presumption that such localized hair-saving treatment does not negatively affect chemotherapy efficacy..
Alopecia (hair loss) is arguably the most feared side effect of cancer chemotherapy (Dorr 1998; Munstedt et al. 1997). Despite substantial efforts, no reliable and generally effective preventative treatment has become available (Hesketh et al. 2004; Wang et al. 2006). Scalp tourniquets and cooling devices have been utilized for decades to restrict blood flow to the scalp during chemotherapy treatment. Although such treatments were found to be successful in reducing alopecia in connection with certain chemotherapy regimens, they were difficult to standardize and not generally useful over the wide range of pharmacological regimens used in the clinic. Although more recent studies utilizing improved hypothermia devices reported increased reliability, certain antineoplastic drug combinations, notably combinations comprising a taxane could not be protected against (Katsimbri et al. 2000; Christodoulou et al. 2002). Among the many pharmacological approaches for alopecia prevention that were investigated, vitamin D3 appeared to be the most promising protective compound because it was effective against several different antineoplastic agents in preclinical experiments (e.g., Jimenez et al. 1995; Schilli et al. 1998). However, a clinical trial was ultimately unsuccessful (Hidalgo et al. 1999; Wang et al. 2006).All cells possess protective mechanisms that increase their resistance to various adverse conditions. Perhaps best known is the ubiquitous stress protein (Hsp) response that involves the enhanced expression of classical stress proteins such as Hsp90, Hsp70, and Hsp25, and of certain other proteins such as P-glycoprotein, in response to physical or chemical stresses (Parsell and Lindquist 1993; Vilaboa et al. 2000). Elevated levels of Hsps are known to result in increased stress tolerance (Li and Werb 1982; Liu et al. 1992; Lavoie et al. 1993).
The spectrum of toxicants an activated stress protein response can mitigate against is broad. As shown by previous studies, elevated levels of the cohort of Hsps or of individual Hsps are also protective against cytotoxicity from many antineoplastic agents used in the clinic. Table 1 summarizes selected studies relating to the reduction or prevention of toxicity from adriamycin, cyclophosphamide, taxol, and etoposide. Because the stress protein response is an intracellular protective mechanism, it should be possible to locally activate a stress protein response in noncancerous tissues without affecting the cytotoxic effects of an antineoplastic agent in cancerous tissues. We hypothesized that localized activation of a stress protein response in the hair follicles of a patient’s scalp (and eyebrows) would prevent chemotherapy-induced hair loss and that this protective effect could be achieved without reduction of tumor therapy efficacy. ..snip...
The young rat is a commonly employed model of human hair regrowth in studies of chemotherapy-induced alopecia (Hussein et al. 1990). For many antineoplastic agents that cause significant alopecia in patients, dose regimens were identified that resulted in essentially complete loss of body hair in this model. In most of our experiments, heat was used to induce a stress protein response.
We obtained independent evidence that the protective effects were due to an activated stress protein response from experiments in which we injected animals s.c. with the benzoquinone ansamycin antibiotic geldanamycin (GA) 24 h before etoposide chemotherapy. Because benzoquinone ansamycins are selective inhibitors of Hsp90 function (Whitesell et al. 1994; Pratt and Toft 1997), and Hsp90 is a key repressor of heat shock factor 1, which mediates enhanced Hsp expression (Ali et al. 1998; Zou et al. 1998); these compounds can be considered to be the most specific activators of a stress protein response available at present. Dose-dependent, localized prevention of hair loss was observed (Fig. 1d).Next, we tested whether the same protective mechanism could also mitigate or suppress the alopecic effects of anthracyclines, alkylating agents, and taxanes. Groups of (typically four) animals were subjected to heat treatment to the nape of the neck or were not heat-treated. After a delay of 7 h, the groups were administered alopecia-causing doses of cyclophosphamide or a combination of cyclophosphamide and adriamycin. Because no alopecia-causing, sublethal i.p. dose of taxol could be identified, amounts sufficient to cause local hair loss were injected s.c. in the region that had previously been subjected to heat treatment. Results summarized in Table 2 indicated that hair in heat-treated areas was effectively protected against the latter antineoplastic agents. No protection was observed in unheated, drug-exposed animals. Subcutaneous injection of GA also prevented hair loss caused by cyclophosphamide and taxol (data not shown). Following standard practice in the field, we had observed and recorded protective effects at the time animals had lost most of their body hair, which occurred about 1 week after exposure to chemotherapeutic agents. Anticipating a potential future use of the same preventative method in human patients, we investigated whether the observed protective effects were long-lasting. We followed-up heat-preconditioned, chemotherapeutic drug-treated (etoposide, cyclophosphamide, or cyclophosphamide/adriamycin) animals for longer periods, in some cases, until they had acquired a new fur coat about 3 weeks after chemotherapy. We observed that a majority of animals, and in some groups, all animals exposed to 48–48.5°C heat for 20 min retained their patches of protected hair. However, at lower heat doses, animals tended to gradually lose their patches.
Finally, we carried out model cancer chemotherapy experiments to demonstrate that induced alopecia could be prevented without sacrificing chemotherapy efficacy. Targeted delivery of heat to skin areas in which alopecia induction is to be inhibited will preclude the induction of a stress protein response in tumors not located in the heated areas. However, although the stress protein response is an intracellular protective response, the possibility needed to be considered that heat exposure of skin and embedded structures could induce signals that could affect chemotherapy of a tumor located elsewhere. To address this question, 8-day-old rats randomly assigned to 4 groups (n=45, each) received an i.p. injection of MIA C51 rat chloroleukemic cells. One group was subjected to topical heat treatment (48°C/20 min) 6 h later and administered a single dose (35.5 ìg/g) of cyclophosphamide 24 h after heat treatment. Control groups received either only a heat treatment or cyclophosphamide, or remained untreated. Animals were killed 30 days later, and the presence of leukemia was determined from an analysis of bone marrow aspirates (>30% nonerythroid blasts). Results revealed that localized heat treatment did not significantly reduce the antineoplastic effect of cyclophosphamide (Fig. 2c; see p values included in the graph). This finding was confirmed in a second, similarly powered experiment.In summary, our data indicate that localized activation of a stress protein response is an effective new method for preventing chemotherapy-induced hair loss in animal models. As was hoped based on the known broad protective effects of an activated stress protein response, the method appears to afford protection against a diverse range of antineoplastic agents and combinations. Chemotherapy protocols utilized in the clinic not only differ in the drug or drug combination used but also in the number of drug doses administered per treatment cycle, the interval between doses and the duration of drug administration (i.e., injection or infusion). A preliminary experiment suggested that a one-time activation of a stress protein response protects the hair follicles of young rats from the toxic effects of a 5-day regimen of daily etoposide. If this result translates to humans, the present heat preconditioning method for preventing chemotherapy-induced alopecia should be compatible with or capable of adaptation to many of the chemotherapy protocols in clinical use.Although heat preconditioning was utilized primarily to induce a protective response, several experiments were conducted in which a similar response was obtained following s.c. or i.d. administration of GA or 17AAG, respectively. Effective methods of liposomal delivery of compounds deep into the hair follicles were developed in recent years (Li and Hoffman 1995; Hoffman 2006; Jung et al. 2006). It appears, therefore, feasible to develop a preventative therapy that is based on the activation of a stress protein response in the scalp either by administration of an appropriate heat dose or by delivery of an effective dose of an inducer such as GA or 17AAG by means of a liposomal vehicle.
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