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News 02/04/2544


INDIVIDUALISED THERAPY FOR MIGRAINE POSSIBLE AS THE TRIPTAN FAMILY EXPANDS
With the advent of the triptans, the approach to the treatment of migraine is changing.

SELF-TREATMENT OF ANDROGENETIC ALOPECIA
Not all hair loss can be treated successfully -- pharmacists can help patients identify which products offer valid treatments.

GEMFIBROZIL USE REDUCES CHD EVENTS IN MEN BY INCREASING HDL CHOLESTEROL
In men with a history of coronary heart disease and low levels of both LDL and HDL cholesterol, gemfibrozil use significantly reduces the risk of future CHD events by increasing HDL cholesterol levels, according to a report in The Journal of the American Medical Association for March 28.

FDA CONSIDERS RELABELING OF ACETAMINOPHEN
Liver failure due to a toxic dose of acetaminophen may be more common than previously thought, according to Dr. William Lee, a hepatologist and professor of internal medicine at the University of Texas Southwestern Medical Center at Dallas.


Individualised Therapy for Migraine Possible as the Triptan Family Expands

[Drug & Ther Perspect 17(2):4-10, 2001. © 2001 Adis International Limited]


Introduction

With the advent of the triptans, the approach to the treatment of migraine is changing. These migraine-specific medications are selective 5-HT1B/1D agonists which are believed to reverse the mechanisms of migraine, stopping pain and associated symptoms. The hydrophilic agent sumatriptan works peripherally, reducing vasodilation and neurogenic inflammation. The more recently introduced triptans (zolmitriptan, naratriptan, rizatriptan) may in addition interfere with central transmission. A number of new triptans (eletriptan, frovatriptan, almotriptan) are undergoing clinical development.
The available triptans can be distinguished by formulation - sumatriptan is the most versatile, available in several different dosage forms. With regard to clinical efficacy, headache response at 2 hours seems somewhat higher for sumatriptan, zolmitriptan and rizatriptan and lower for naratriptan (see Differential features table), although data from direct clinical comparisons are limited and naratriptan has a tendency towards less recurrence. Common adverse events, 'triptan sensations', are similar for oral sumatriptan, zolmitriptan and rizatriptan. There are significantly fewer adverse events for naratriptan.
Clinical use will yield familiarity with the various triptans, and it should be possible to match individual patient needs with the specific characteristics of the individual triptans to optimise therapeutic benefit.

Cause of Migraine Becoming Clearer

The exact pathophysiology of migraine remains unknown. However, events thought to contribute to migraine may include changes in dural vessel calibre, neurogenic inflammation and central trigeminal neuronal activation. These changes are believed to be reversed by agonists at certain serotonin (5-hydroxytriptamine, 5-HT) receptors.[1]
5-HT1B receptors, located on the meningeal vessels, constrict these vessels when activated by 5-HT1 agonists. 5-HT1D receptors are presynaptic inhibitory autoreceptors on trigeminal sensory neurons. Activation of these receptors turns off the neurogenic inflammation by inhibiting the release of neuropeptides such as calcitonin gene-related peptide.[1]
5-HT1D receptors are also located centrally in the trigeminal nucleus caudalis.[4] Activation of these receptors appears to interfere with central transmission of pain signals.[1]

Guidelines Assist in Efficacy Assessment

As alleviation of headache pain is a subjective parameter, measuring response to drug treatment in patients with migraine is not always straightforward. The International Headache Society (IHS) has published guidelines which can be used to assess the efficacy of medications for headache (see table 1).[5]

Sumatriptan: the Original Triptan

Sumatriptan, the first designer 5-HT1B/1D agonist, has now been available for almost 10 years. It is estimated to have been used in over 200 million migraine attacks by close to 10 million patients.[1]

Different Dosage Forms Provide Flexibility

Sumatriptan is available in several different dosage forms - an oral tablet, a subcutaneous injection, a nasal spray and a suppository (see Differential features table) - allowing the patient and physician to match the form of administration to the intensity and speed of onset of the pain as well as to the degree of disability produced.
The injection has a very fast onset of action and is packaged as a self-administration unit, which improves patient acceptance.[6] Sumatriptan injection provides very fast relief and high 1- and 2-hour efficacy. A disadvantage with sumatriptan, however, is the relatively high recurrence rate after use.[1]
Although not as rapidly acting as the injection, sumatriptan nasal spray provides a faster onset of effect than the tablets.[1] The spray comes in a single-use device. The patient sprays once into a single nostril without sniffing and discards the device.
A sumatriptan suppository is available in some European and Asian countries. Its efficacy is similar to that of the other dosage forms.[1]

Adverse Effects Not Usually Serious

There is a spectrum of adverse events with sumatriptan, now referred to as 'triptan sensations' as they are common to all of the drugs in this class (see Differential features table).[1] Although these events are generally not serious, drug withdrawal is recommended if the patient experiences a particularly intense sensation of tightness in the throat or chest because it may be caused by coronary vasoconstriction or anaphylaxis.[1,2]
Sumatriptan nasal spray has an additional adverse effect of an unpleasant bitter taste. The taste can be minimised and the absorption, efficacy and consistency of response maximised by having the patient spray upward and forward with the head in a neutral position without sniffing or swallowing.[1]

Potential for Vascular Events...

A major concern with the triptans has been their potential to cause vasoconstrictive effects. In fact, all of the triptans cause similar mild coronary artery contraction.[1] However, it is thought unlikely that the drugs would cause myocardial ischaemia at therapeutic plasma concentrations in healthy patients.
Even patients with cardiovascular risk factors, but without established cardiovascular disease, are not considered to be at increased risk.

...But Only in Those With Known Disease

Triptans are not recommended, however, for use in patients with known cardiovascular or cerebrovascular disease.[1]

Avoid Concurrent Use With Some Antidepressants...

Because of a risk of CNS toxicity, sumatriptan should not be used in patients receiving treatment with mono-amine oxidase inhibitors (MAOIs) or selective serotonin reuptake inhibitors (SSRIs).[1,2] Furthermore, if these drugs are discontinued, a suitable 'wash-out' period (e.g. 2 weeks) should elapse before sumatriptan can be used.

...and Ergotamine

Sumatriptan and ergotamine should not be use concurrently because of an increased risk of vasospasm.[2] If required, ergotamine could be used 6 hours after the last dose of sumatriptan or, conversely, sumatriptan could be administered 24 hours after the last dose of ergotamine.

Newer Triptans Offer Advantages

Zolmitriptan, naratriptan and rizatriptan have been launched after sumatriptan and each has some distinct clinical advantages. All of the newer triptans are more lipophilic and have higher oral bioavailability than sumatriptan.[1,7]

Zolmitriptan Rapidly Absorbed

The second triptan to be marketed, zolmitriptan, was developed with the goal of creating a centrally acting drug which is more lipophilic and more rapidly orally absorbed than sumatriptan.[1] In addition to the oral tablet, a fast melt preparation and a nasal spray are being developed.
The efficacy of zolmitriptan has been demonstrated in a number of randomised placebo-controlled double-blind trials in adults with moderate to severe attacks.[8] The drug is effective across a wide range of migraine subtypes.[8]
Because zolmitriptan is, in part, metabolised by monoamine oxidase type A, the dosage of zolmitriptan should be reduced in patients treated with MAOIs, such as moclobemide.[1,2]
Dosage reduction is also appropriate in patients receiving cimetidine, fluvoxamine or quinolones as these drugs inhibit the metabolism of the triptan.[2] As with sumatriptan, zolmitriptan should not be used concurrently with ergotamine.[2]
The most commonly reported adverse events in patients receiving zolmitriptan are the typical triptan sensations.[1]

Naratriptan: The 'Gentle Triptan'

Naratriptan has a relatively slow onset of action and appears to have a somewhat lower headache response at 2 hours than some other triptans. However, it is associated with the lowest headache recurrence rate of the currently available triptans (see Differential features table).[1] The low recurrence rate may be enhanced in those patients who use naratriptan early in a migraine attack, treat less severe attacks and obtain complete pain relief.[9]
The incidence of triptan sensations, and all adverse effects, with naratriptan is very low. In fact, in some cases the incidence of adverse events was lower with naratriptan than with placebo. Therefore, naratriptan has been referred to as 'the gentle triptan'. Furthermore, because naratriptan is metabolised by a variety of cytochrome P450 enzymes and not the MAO system, it is not associated with significant drug interactions.[1,2]

Rizatriptan Available as a 'Melt'

Rizatriptan is a very fast acting oral triptan, with a recurrence rate similar to that of oral sumatriptan. Like zolmitriptan, it was synthesised in the hope of creating a faster acting, more lipophilic, tablet and its efficacy has also been demonstrated in a number of large randomised trials.[10] The drug is available as both a tablet and an orally dissolving melt, which is placed on the tongue and dissolves rapidly. The melt is used for convenience where liquid is not available or when the patient wants to use the medication discretely. The melt is not absorbed from the tongue or mucous membranes but rather dissolves in, and is subsequently swallowed with, saliva for gastrointestinal absorption.[1]
Propranolol may increase the plasma concentration of rizatriptan, most probably because of a first-pass metabolic interaction since MAO type A plays a role in the metabolism of both drugs.[2,11] Therefore, rizatriptan should be administered at half the usual dose (i.e. 5mg) in patients receiving propranolol.[1,2] Rizatriptan should be avoided in patients receiving MAOIs and should not be administered concurrently with ergotamine.[1,2]

Can Future Triptans Offer More?

The development of triptans is still ongoing with more drugs in this class being synthesised and studied. Some of the features of the emerging triptans are outlined in table 2.
Eletriptan 80mg orally has very high efficacy and has consistently been significantly superior to sumatriptan 100, 50 and 25mg for headache response at 2 hours.[1] However, adverse events (classic triptan sensations) occur with a higher frequency at this dose compared with lower doses. Lower doses of eletriptan show efficacy similar to that of sumatriptan (see table 2). Recurrence rates are low.
Frovatriptan has a very long half-life compared with other triptans and has an onset of action and efficacy similar to those of naratriptan, although direct comparative efficacy data are lacking. The drug has recurrence rates which are among the lowest for any triptan.[1]
Almotriptan has the highest oral bioavailability of all the triptans. Headache response with almotriptan is similar to that with oral sumatriptan but the newer drug is associated with a lower rate of headache recurrence.[1]

Table 1. International Headache Society clinical end-points used to assess efficacy of medication in patients with migraine[5]

Parameter Definition
Headache response Reduction of migraine intensity from moderate or severe to none or mild at a point in time
Therapeutic gain Percentage of patients who respond to active drug therapy minus percentage of patients who respond to placebo (30% suggests good drug response, 40% excellent, 50% superb)
Pain-free state Decrease in migraine severity from moderate or severe to no pain at a given time after medication administrationa
Relief of associated symptoms Effect of medication on symptoms such as nausea, phono- and photophobia a
Time of pain relief Chance of obtaining headache relief over time. Calculated using a sliding scale or survivor curve
Time to headache relief Survival of the headache
Recurrence The return of moderate to severe headache within 24 hours of treatment following initial headache response at 2 hours
Complete or sustained pain-free response Patient is pain-free at 2 hours with no recurrence or use of rescue medications within 24 hours

(a) Preferably measured at 2 hours post-administration.


Table 2. Selected features of various triptans which are still undergoing development[1,12-15]

Feature Almotriptan Eletriptan Frovatriptan
Usual dose (mg) 12.5 40 2.5
Pharmacokinetic parameters
tmax (h) 1.4-3.8 1-2 2-4
t1/2 (h) 3.2-3.7 3.6-5.5 25
Lipophilicity ?
Bioavailability (%) 70-80 50 24-30
Efficacy
Headache response at 2h (%) 57-65 65 36-46
Therapeutic gain (%)a 15 41 13-19
Recurrence rate (%) 18 19-23 7-25

(a) Percentage of patients who respond to active drug therapy minus percentage of patients who respond to placebo.
Abbreviations and symbols: h = hours; tmax = time to achieve maximum plasma concentration; t1/2 = elimination half-life; = low; = high; ? = unknown.


Differential features

Comparison of various features of selected triptans for the treatment of acute migraine[1-3]

Feature Naratriptan Rizatriptan† Sumatriptan Zolmitriptan
  Tablet Tablet and water (melt) Tablet SC injection Nasal spray Suppository† Tablet
Dosage information
Usual dose (mg)a 2.5 10b 50 6 20c 25 2.5
Time when repeat dose can be given (h) 4 2 2 1 2 NS 2
Maximum dose in 24h (mg) 5 30 (US)
20 (EU)		 200 (US)
300 (EU)		 12 40 50 10-15
Pharmacokinetic parameters
tmax (h) 2-3 1.3d 2.5 0.2 1
(range 0.08-4)		 - 2
t1/2 (h) 5-6.3 2-3 2     - 2.5-3
Lipophilicity      
Bioavailability (%) 63 (men)
74 (women)		 45 14 97 17 - 40-48
Efficacy
Headache response at 2h (%) 48 67-77 61 77e 64 68 62-65
Therapeutic gain (%)f 18 27-40 33 48 34 43 28-29
Recurrence rate (%)f 17-28 30-47 32 34-38 32-34 44 30
Consistency (mean % of attacks aborted over 1 year) 70 at 4h 80 at 2h 84 at 2
(100mg dose)		 70 at 1h 77 at 2h - 95 with 1-2 doses of 2.5-5mg
Tolerability
Common adverse effects Paraesthesia, heaviness, tightness in any part of the body (especially throat and chest)g , flushing, heat sensations, dizziness, feeling of weakness, fatigue, nausea and vomiting
Drug interactions:
   avoid concurrent
   use		 § Ergotamine, MAOIs Ergotamine, MAOIs, SSRIs Ergotamine
   dosage adjustment
   required		 § Propranolol - Cimetidine, fluvoxamine, MAOIs, quinolones
Acquisition costh
In the UK (£) 4.00 4.46 4.70 19.57 6.00 † 4.00
In the US ($) 16.74 11.93 16.00 48.61 20.81 † 14.17

† Rizatriptan is not available in Australia and France; sumatriptan suppositories are not available in Australia, Canada, France, Spain, the UK and the US.
a Oral dosage listed, unless otherwise specified.
b Also available in a 'melt' formulation, a wafer which dissolves rapidly when placed on the tongue and is then swallowed for gastrointestinal absorption.
c Use 1 spray in 1 nostril only.
d tmax for tablet is 1.3h; water (melt) has similar pharmacokinetic properties.
e Response at 1h.
f See table 1 for definition.
g Discontinue drug if sensation intense as it may be due to coronary vasoconstriction or anaphylaxis.
h For a single dose at the usual dosage.
Abbreviations and symbols: EU = European Union; h = hour(s); MAOIs= monoamine oxidase inhibitors; NS = not specified; SC = subcutaneous; SSRIs = selective serotonin (5-hydroxytriptamine, 5-HT) reuptake inhibitors; tmax = time to achieve maximum plasma concentration; t1/2 = elimination half-life; = low; = moderate; = high; § = there are currently no recognised drug interactions with naratriptan.


References

  1. Tepper SJ, Rapoport AM. The triptans: a summary. CNS Drugs 1999 Nov; 12 (5): 403-17
  2. British National Formulary. No. 39. London: The Pharmaceutical Press, 2000 Mar: 219-20, 596-7
  3. Drug Topics Red Book. Montvale (NJ): Medical Economics Company, 2000
  4. Edvinsson L, Goadsby PJ. Neuropeptides in headache. Eur J Neurol 1998; 5: 329-41
  5. International Headache Society Committee on Clinical Trials in Migraine. Guidelines for controlled trials of drugs in migraine. 1st ed. Cephalalgia 1991; 11: 1-12
  6. Gobel H, Baar H, Beikufner HD, et al. Practicability and acceptance of subcutaneous self-administration of the selective serotonin agonist sumatriptan. Headache 1998; 38: 267-9
  7. Tfelt-Hansen P, De Vries P, Saxena PR. Triptans in migraine: a comparative review of pharmacology, pharmacokinetics and efficacy. Drugs 2000 Dec; 60 (6): 1259-87
  8. Spencer CM, Gunasekara NS, Hills C. Zolmitriptan: a review of its use in migraine. Drugs 1999 Aug; 58 (2): 347-74
  9. Sheftell F, O'Quinn S, Watson C, et al. Low headache recurrence with naratriptan: clinical parameters related to recurrence. Headache 2000 Feb; 40 (2): 103-10
  10. Dooley M, Faulds D. Rizatriptan: a review of its efficacy in the management of migraine. Drugs 1999 Oct; 58 (4): 699-723
  11. New Ethicals Compendium. 7th edition. Auckland: Adis International Limited, 2000: 1110-2
  12. Goadsby PJ, Ferrari MD, Eletriptan Steering Committee. Eletriptan in acute migraine: a double-blind, placebo-controlled comparison to sumatriptan. Neurology 2000 Jan 11; 54 (1): 156-63
  13. Holm KJ, Spencer CM. Almotriptan. CNS Drugs 1999 Feb; 11 (2): 159-64
  14. Easthope S, Goa KL. Frovatriptan. CNS Drugs. In press
  15. Bardsley-Eliot A, Noble S. Eletriptan. CNS Drugs 1999 Oct; 12 (4): 325-33



Self-Treatment of Androgenetic Alopecia

W. Steven Pray, Ph.D., R.Ph., Professor of Nonprescription Products and Devices,, School of Pharmacy, Southwestern Oklahoma State University, Weatherford, OK

[U.S. Pharmacist 26(2) 2001. © 2001 Jobson Publishing Corp.]


Introduction

Hair loss is an immensely frustrating condition for many men and women. In men, a full head of hair is commonly thought to connote youth, health, ability and energy; therefore, loss of hair causes men to be judged as old, ill, worn-out and less capable. In women, hair is often seen as a vital component of beauty. Thus, thinning hair can be devastating for a female's sense of self-worth, causing many to feel less attractive.
Also, because female baldness is much less common than male baldness, women may feel that there is no one with whom to discuss the problem.

The Life Cycle of Hair

Hair growth is a dynamic processes in which certain hairs are actively growing (anagen phase), others are resting, and still others are actively shedding (exogen phase).1 Eventually, each hair must be shed to prepare the way for a new anagen phase. It is important to note, however, that the cycle of a particular hair is independent of those surrounding it.2 Therefore, loss of a specific hair is normally imperceptible due to the great number of anagen hairs in the immediate vicinity.

Reasons for Hair Loss

Hairs may be actively shed, or lost through normal activities such as combing, brushing and shampooing. However, hair loss may also be an adverse effect of medical therapy, such as medications (e.g., certain antineoplastics) or radiation. It may be due to conditions that scar the scalp, such as tinea capitis or burns, or repeated trauma, as occurs in the psychological condition of repetitive hair pulling, known as trichotillomania. Should the pharmacist suspect that one of these is the cause of hair loss, the patient must be referred. Hair loss may also be due to hairstyles that subject hair to prolonged traction, such as cornrows or ponytails. In this case, the patient might be simply counseled to choose another hairstyle. The only other type of hair loss that is potentially self-treatable is the familial type -- androgenetic alopecia.

Androgenetic Alopecia

Androgenetic alopecia is described in this month's patient leaflet. It is thought to be inherited from either parent, and is due to the effects of androgens on hair follicles. The pharmacist may first suggest that the patient with androgenetic alopecia attempt regrowth with nonprescription minoxidil. If results are unsatisfactory, the patient may be referred to the physician for prescription finasteride (Propecia).

Minoxidil

Minoxidil is available in two concentrations. The 2% solution is available as Rogaine For Men, Rogaine For Women, and generically. The 5% solution is only available as Rogaine Extra Strength for Men.
Minoxidil should only be used by patients aged 18 and older.3 It is indicated for vertex hair loss in men and thinning on the top of the head in women. Frontal hair loss in men is not an approved indication for minoxidil as its efficacy for this has not been demonstrated. Women should not use the 5% solution since, for them, it is no better than the 2% solution and it may cause the growth of facial hair. Women who are pregnant or breastfeeding should seek the advice of a physician before using the 2% solution; use of the 5% solution during this time is contraindicated because of possible harm to the fetus/infant.
Patients might be cautioned against over-optimistic expectations with minoxidil. Patients cannot expect to regrow all of their hair. After four months of using 2% minoxidil, 26% of men reported moderate to dense hair regrowth and 33% experienced minimal regrowth. In female users, the 2% solution caused moderate hair regrowth in 19%, and minimal regrowth in 40%. The 5% solution is more effective than the 2% solution for male users.
Results with minoxidil will not be sudden or dramatic because hair only grows 0.5-1 inch each month. The patient may need to apply the 2% solution for four months before growth is noted; men may note results with the 5% solution after only two months. If a male does not notice results in 12 months with the 2% solution or four months with the 5% solution, he should discontinue use. The female should only use 2% minoxidil for eight months with no results before ceasing use.
Patients often wonder if they can stop using minoxidil when their maximal regrowth is achieved. If they stop use, they will gradually lose hair that was regrown over a period of several months. In addition, the bald spot may be larger than it was before the use of minoxidil. This is due to the natural progression of hair loss over time. For example, a male patient with androgenetic alopecia who is not using minoxidil would experience a progressive loss of vertex hair from the years 2001-2010. However, if he began using Rogaine in 2001 and ceased using it in 2009 would look the same in 2010 as if he had never used minoxidil at all.

Finasteride (Propecia)

Finasteride's mechanism of action is tied to testosterone.4 Testosterone is metabolized by type II 5 alpha-reductase to DHT in the inner root sheath of the hair follicle. DHT is thought to be responsible for male-pattern baldness. Finasteride may competitively inhibit the action of type II 5 alpha-reductase to reduce levels of DHT in the hair follicle. The dose in men is 1 mg orally once daily, without regard to meals. It is contraindicated in females. The drug was given a Pregnancy Category rating of X by the Food and Drug Administration; in pregnant females it may cause feminization of a male fetus to the extent of producing abnormalities of the male genitalia.5
Hair loss may be inherited, or it may be due to hairstyles, medical therapy, or conditions that scar the scalp.

How to Identify Genetic Hair Loss

Hair loss can be inherited from either parent, so you should look at other family members of the same sex to help confirm your hair loss as genetic in origin. For instance, if you are male, look at your father, grandfathers, brothers and sons. Male first cousins may also provide clues. If you are female, look at your mother, grandmothers, sisters, female first cousins, and daughters.
Although hair loss is an extremely common genetic condition, a patient with no apparent family history may still have androgenetic alopecia. Other clues to look at are the quantity of hair loss, the locations from which hair has been lost, and the time span over which the hair was lost. True androgenetic alopecia should have caused a gradual thinning of hair over several years' duration, and the pattern of hair loss for men should be receding of the front hair-line in either a uniform or "U" shape. Men may also notice a bald spot beginning at the back center of the scalp, known as the "vertex" of the head. Women with androgenetic alopecia experience a general thinning of hair along the top of the head, usually starting at the midline, with a slowly enlarging area of loss. For help in recognizing this type of hair loss, consult your pharmacist.

When to See a Physician

If the hair loss is sudden, or if large amounts of hair are lost at one time, this may be an indication of a serious condition that should be checked by a physician. A physician should also be seen if the hair loss involves patches of the scalp. Hair loss can also be caused by pregnancy, use of some prescription medications, too little iron, too much vitamin A, low thyroid activity, discontinuing the use of birth control tablets, chemotherapy, and some diseases that scar the scalp. None of these would be self-treatable and a physician should be seen.

Over-the-Counter and Prescription Products

If your hair loss is self-treatable, your pharmacist can point out a nonprescription product known as minoxidil, which may be helpful when used as directed on the labeling. Should minoxidil not work, you physician can prescribe a product known as Propecia. Neither of the products should be seen as a cure for hair loss. Nevertheless, they are the only two products that are proven safe and effective for hair loss.

Internet Resources

The Internet contains many web sites that promote unproven hair growth products. Many of the sites seem to present scientific explanations for why their products work, but virtually all should be avoided. For a good explanation of the sites and why their claims cannot be true, visit the web site www.hairquackery.com

References

  1. Paus R. Principles of hair cycle control. J Dermatol. 1998;25(12): 793-802.
  2. Sperling LC, Mezebish DS. Hair diseases. Med Clin North Am. 1998;82(5):1155-1169.
  3. Pharmacia & Upjohn Consumer Healthcare. Rogaine For Men, Rogaine For Women, Rogaine Extra Strength For Men package inserts. Kalamazoo, MI, 1996-1997.
  4. McLellan KJ, Markham A. Finasteride. Drugs. 1999;57(1):111-126.
  5. Walsh P. Physicians' Desk Reference. 54th ed. Montvale NJ: Medical Economics; 2000:1874-1876.

What Time of Day Should the Patient Apply Minoxidil Solution?

Minoxidil should be allowed to dry on the scalp for at least four hours to allow full effectiveness.1 The patient should apply 1 mL in the morning after the shower/bath, but should refrain from placing a hat, scarf, or other headgear on the head. A 1 mL reapplication about 12 hours later is necessary, but the patient should apply minoxidil at least four hours before bedtime, since normal movements of the head would cause freshly applied minoxidil to be rubbed off on the pillow. Suggested times for those with daytime shift jobs might be 7:00 am and 7:00 pm. The patient should also avoid swimming after application or allowing the scalp to get wet from rain.

Self-Treatment of Hair Loss

The first step in self-treating hair loss is determining whether your hair loss is the type that can be treated safely without visiting a physician for an examination. The only self-treatable hair loss is the genetic type, which usually begins around the time of puberty due to androgens. This is known medically as androgenetic alopecia.



Gemfibrozil Use Reduces CHD Events in Men by Increasing HDL Cholesterol

WESTPORT, CT (Reuters Health) Mar 27 - In men with a history of coronary heart disease and low levels of both LDL and HDL cholesterol, gemfibrozil use significantly reduces the risk of future CHD events by increasing HDL cholesterol levels, according to a report in The Journal of the American Medical Association for March 28.

"This is an extended analysis of a report that was published in 1999 in the New England Journal of Medicine, where we report a 22% reduction in CHD events with gemfibrozil compared with placebo," Dr. Sander J. Robins from Boston University School of Medicine told Reuters Health.

"In this extended analysis we demonstrate that it was only the increase in HDL cholesterol that could statistically predict a reduction in CHD events. This is the first lipid trial that shows that using a lipid drug which only increases HDL cholesterol will produce benefit without decreasing low-density lipoprotein cholesterol," he added.

Dr. Robins and colleagues from the Veterans Affairs High-Density Lipoprotein Intervention Trial (VA-HIT) studied 2531 men with a history of CHD who had low levels of HDL cholesterol as well as low levels of LDL cholesterol. The subjects were randomized to receive 1200 mg of gemfibrozil a day or placebo.

Multivariate analysis revealed that during 18 months of followup, there was an 11% reduction in CHD events for every 5 mg/dL increase in HDL cholesterol among the patients taking gemfibrozil, compared with controls.

Only the increase in HDL cholesterol was a significant predictor of lower risk. Triglyceride levels and LDL cholesterol levels at baseline or during the study period were not predictive of CHD events, the researchers note.

"However, the increase in HDL cholesterol with gemfibrozil could not account for most of the benefit of the drug. There was a lot left unexplained, which could not be attributed to any change in lipid values," Dr. Robins said.

Data from other studies indicate that this class of drugs reduces inflammatory markers, including C-reactive protein, he explained. "I think that that a reduction in C-reactive protein is playing a role in the benefit derived from gemfibrozil."

"Practicing physicians should use gemfibrozil for people with low LDL and HDL cholesterol who have a history of CHD, Dr. Robins concluded. "Gemfibrozil does work in these high-risk patients, and there is no evidence at this time that a statin gives an equivalent benefit."

JAMA 2001;285:1585-1591.


FDA Considers Relabeling of Acetaminophen

WESTPORT, CT (Reuters Health) Mar 28 - Liver failure due to a toxic dose of acetaminophen may be more common than previously thought, according to Dr. William Lee, a hepatologist and professor of internal medicine at the University of Texas Southwestern Medical Center at Dallas.

"People have no fear of acetaminophen and are consuming too much. They accidentally poison themselves by either taking too many pills in too short a time, or by taking several different preparations, all of which contain acetaminophen," Dr. Lee told Reuters Health. The total combined acetaminophen dose from all medications should not exceed 2 grams daily, he said.

In a previously reported study, Dr. Lee and colleagues followed 295 patients who had had liver failure. Acetaminophen overdose was the most commonly identified cause of hepatic failure, affecting 60 patients, or 20% of the total patient base.

These findings and data from the United Kingdom have prompted the US Food and Drug Administration to begin investigating whether more explicit warnings are needed on medications containing acetaminophen. The agency is reviewing its adverse drug event reporting system to determine what the data are showing regarding acetaminophen, according to FDA spokesperson Susan Cruzan.

"If we determine that there's a problem that can be corrected with labeling or education, then we'll decide whether those steps are necessary," she told Reuters Health.

According to McNeil Consumer Healthcare, the manufacturers of Tylenol, hepatic failure can only occur with substantial overdoses. "These new data do not suggest that acetaminophen is anything but a good OTC analgesic," vice president Dr. Anthony Temple told Reuters Health. "However, people need to take it as directed, and use it as directed. If the recommended dose is exceeded, a doctor or a poison control center needs to be consulted."


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