AboutPeter J. Panagotacos, <B>M.D.</B> Expertise I have 30 years experience in the field of medical and surgical Hair Restoration and am Board Certified
in Dermatology and Hair Restoration Surgery.
Experience I have 30 years experience in the field of medical and surgical Hair Restoration and am Board Certified
in Dermatology and Hair Restoration Surgery.
More information can be found at my website
www.hairdoc.com
Question Dr. Panagotacos: I am 31 years old and have had diffuse hair thinning/loss all over my scalp since September of 2005 and my scalp biopsy said I most likely have Androgenetic Alopecia or Telogen Effluvium.
My dermatologist believes it is Androgenetic Alopecia but I question that because no member of my family (parents or grandparents) has any baldness/thinning and in fact all have full heads of hair. I have had a lot of stress the past few months, my husband lost his job, marital problems, we are moving away from family but my dermatologist says "stress" wouldn't be a cause of my hair loss. I am using Minoxidil 2% twice a day and I have a sulfa allergy so instead of Spironolactone, he prescribed Propecia. In your experience has Propecia been effective for women? I am not planning on getting pregnant so this isn't a concern for me. Also, my DHEA was 94 (reference range 35-430) and my testosterone was 27 (reference range 14-76). Wouldn't these be higher if I had Androgenetic Alopecia? Or do blood tests not reveal if you have Hereditary hair loss? Also, in your opinion are my DHEA and Testosterone low normal and could that cause my hair loss? My ferritin is 61 and I think that's okay. Thanks for your input and for reviewing my information; I just appreciate any thoughts on this!! Hope you enjoy the upcoming weekend! Heather Rockwood
Answer An inherited pattern can sometimes be difficult to prove because there may be genes from each side which may add up to thinning in your case which may not be so obvious in either parent. The genes could be passed down through several generations of women without showing much baldness. You do not need excess androgens to have the thinning if you have the genes for thinning. From what you have written it would seem you may have a chronic telogen effluvium " stress" which can cause considerable thinning. Taking Propecia does help to some degree in women but a newer medication is dutasteride 0.5mg AVODART which lowers the DHT much more than Propecia. Your hormone levels are not abnormal but blocking the DHT can't hurt and may prevent the aging process of the hairs. Normal hormone levels cause thinning in women with the right genes. Your serum ferritin is probably high enough not to be a factor. Do you eat a lot of fish? If so you may want to get a serum mercury level done. Have you eliminated any medications which could cause hair loss such as antidepressants?
I'd suggest you use 5% Minoxidil once a day in the morning and get on Ortho Tri Cyclen and Spironolactone 50 to 100 mg daily and if you want add Avodart too. Shampoo daily with Neutragena's new Daily shampoo with Zinc Pyrithione or use Head and Shoulders.
Spironolactone is not contraindicated if you have a sulfa allergy. I will add something from a google search which you can do as well to confirm this.
You may well have chronic telogen effluvium which is making you thin but could also have inheritied balding making it worse.
l 20, No. 2 May 2003 SULFONAMIDE CROSS-REACTIONS EXPLAINED
A frequent question received by SDIS is “What drug can be used by a patient with a sulfa allergy�? The most common approach to this problem is avoidance of all sulfonamides. Analysis of the literature, however, indicates that cross-reaction among different classes of sulfonamide drugs is unlikely to occur; thus we may be withholding appropriate therapies from patients unnecessarily.
SULFONAMIDES DEFINED
Sulfonamides are compounds than contain sulfur in a SO2NH2 moiety directly attached to a benzene ring.1 Many medications contain sulfur but are not sulfonamides, e.g., amoxicillin, captopril, omeprazole, spironolactone, sulfates and sulfites.2 There is no risk of cross-reactivity between these substances and sulfonamides.2
Sulfonamides can be divided into two groups; the antibiotics (eg, sulfamethoxazole, sulfisoxazole, sulfacetamide) and the non-antibiotic sulfonamides (e.g., thiazides, furosemide, glyburide, sumatriptan, celecoxib). Certain chemical structures unique to the antibiotic group are implicated in the production of hypersensitivity reactions - an arylamine moiety at the N4 position and substitutions at the N1 position of the benzene ring.1
CROSS-REACTIVITY AMONG SULFONAMIDES
Cross-reactivity is the likelihood that a person who has had a hypersensitivity reaction to one drug will have the same reaction to a structurally similar drug. In theory, therefore, cross-reactivity would be expected to occur among different members of the antibiotic sulfonamides but not between different classes of sulfonamides.1,4 In fact, reports in the literature documenting the safe use of sulfonamide medications in patients with a previous history of allergy to a sulfonamide outnumber reports of adverse reactions to two or more sulfonamides.1
A possible explanation for reports of sulfonamide cross-sensitivity may be the tendency of certain patients to be more susceptible to hypersensitivity reactions. Patients allergic to one antimicrobial drug are reported to be 10 times more likely to react to another non-structurally related drug than patients without a history of allergy.7 Thus, reactions to more than one sulfonamide may actually represent multiple allergies rather than a specific allergy to sulfonamides.7
RISK FACTORS FOR HYPERSENSITIVITY REACTIONS
Patients with a history of previous reactions to other drugs, including non-sulfonamides, are at the highest risk of adverse reactions.1 Other risk factors include concurrent infection (appears to increase susceptibility to the effects of haptenation products)1, genetic predisposition (patients with the slow acetylator phenotype shunt more drug into the CYP oxidative pathway that forms the reactive metabolite) 8, and glutathione deficiency (glutathione plays an important role in detoxifying reactive metabolites) 9.
MANAGEMENT STRATEGIES
1. History of severe life-threatening reaction to a sulfonamide (e.g., Stevens Johnson syndrone, toxic epidermal necrolysis, hepatotoxicity, anaphylaxis) is an absolute contraindication to the use of sulfonamides.6
2. A mild to moderate reaction is not necessarily a contraindication to the use of another class of sulfonamide but when available, a non-sulfonamide alternative of equivalent efficacy and safety is the preferred option.6 (Table 2)
3. If there is not an appropriate alternative, the patient should be started on a low dose of the sulfonamide and closely monitored.7 Patient counselling should include a discussion of the risks and benefits of the therapy.6
4. For patients with a demonstrated allergy to a necessary drug, e.g., loop diuretics in congestive heart failure, co-trimoxazole for Pneumocystis carinii pneumonia, desensitization can be tried.1,6 Desensitization involves starting with a very small amount of the drug and gradually increasing to the therapeutic dose. Sucessful protocols for co-trimoxazole, furosemide and sulfasalazine have been reported.1,6
Table 2: Commonly used sulfonamides and non-sulfonamide alternatives 2,6
