- Email: [email protected]
Advertising acyclovir
288
reported, but some equally toxic organophosphate may have been responsible. Organosphosphorus chemical warfare agents inhibit acetylcholinesterase and do so rapidly. The rate of recovery is determined by the degree of poisoning and by what caused it, and enzyme activity can remain depressed for weeks. Inhibition of acetylcholinesterase would explain the symptoms reported by most of the patients in Mardin, and the rate of recovery. The fact that no traces of an organophosphate agent were found might be explained by the time delay between poisoning and blood collection. Bread had been singled out as the most likely source of the poisoning but we can find no evidence to support this claim. The bread sample we received may not have been representative or a toxic organophosphate originally present in the bread may have been inactivated. No detailed investigation in the camp was done and the source of the cholinesterase inhibiting agent remains unknown. These refugees had fled from chemical attacks on their homes in northern Iraq in August, 1988. They now claim to have been the victims of another mass-poisoning attempt. The evidence available does suggest something very sinister. It is unlikely that we are talking about a common commercially available chemical, so the chance of accidental poisoning is remote. Most of the victims have recovered, and the UN High Commission for Refugees now has access to Kurdish refugee camps in Turkey. If this poisoning was, as we strongly suspect, deliberate, it has serious implications for the international community. We thank Dr J. Henry and Dr B. Widdop (National Poison Unit, Guy’s Hospital); Dr A. Walker and Dr A. Taylor (St Luke’s Hospital, Guildford); and Dr T. Delves and Mr C. Fellows (Southampton University) for help and advice. Kurdish Scientific and Medical Association, London WC1
DLAWER ALA’ALDEEN JOHN FORAN
Poison Unit, New Cross Hospital, London
IVON HOUSE
Department of Chemical Old Medical School, University of Leeds, Leeds LS2 9JT, UK
ALASTAIR HAY
1.
study from the USA in 1988 reported less post-zoster pain in patients given a 10-day course of oral acyclovir, and this fmding has prompted further studies with longer courses; however, these have yet to be published. Only time will tell if acyclovir is indeed effective in reducing post-herpetic neuralgia and what the ideal dosage regimen should be. Wellcome has failed to point out the negative findings of the UK study and to state that the American study used a regimen not currently recommended. I believe this advertisement breaches clause 4.2 of the code ("information should accurately reflect current knowledge or responsible opinion"), and I am surprised that exaggerated and unfounded claims and potentially offensive and unnecessary photography should be associated with such an A
ethical company. Drug Information Centre, Derbyshire Royal Infirmary, Derby DE1 2QY, UK 1. Morton
P, Thomson AN. Oral acyclovir in the treatment of herpes zoster in general practice. N Z Med J 1989; 102: 93-95. 2. McKendrick MW, McGill JI, Wood MJ. Lack of effect of acyclovir on post-herpetic neuralgia. Br Med J 1989; 298: 431. 3. Huff JC, et al Therapy of herpes zoster with oral acyclovir. Am J Med 1988, 85 (suppl 2A): 84-89.
** This letter has been shown follows.-ED. L.
Independent June 2, 1989. R, Romer J. The
2. Thomas
use of small charcoal/alumina clean-up columns m the detection of tricothecene mycotoxins in foods and feeds. J Assoc Off Analyt Chem 1986; 69: 699-703.
Advertising acyclovir SIR,-Recent promotional literature on ’Zovirax’ (acyclovir; Wellcome) focuses on the role of this drug in treating herpes zoster. Some may be forgiven for mistaking this publicity for a special issue of Playgirlmagazine, with insets of naked bodies on the front cover and a hairy male torso in large format on page 3. What is the relevance of the naked bodies? I and my dermatological colleagues can detect no hint of vesicular eruption. These photographs do not "illustrate pictorially the message of the text" and thus contravene clause 7.6 of the ABPI (Association of the British Pharmaceutical Industry) Code of Practice. This advertisement also incorporates dubious claims, which may contravene the ABPI code. The publicity material claims that acyclovir had been shown to "reduce the suffering of post-herpetic neuralgia"-and that it is "now of proven value in post-herpetic neuralgia". The November, 1989, data sheet for this product does not refer to a reduction in the incidence or severity of post-herpetic neuralgia. I understand that an amendment has now been issued, the effect being merely to remove a negative statement about acyclovir and post-herpetic neuralgia rather than replacing it with a positive indication. Nevertheless, such claims seem premature. I know of only two controlled studies with the data sheet dosage of 800 mg five times a day for 7 days. One study in general practice from New Zealand on 83 patients reported some reduction in the prevalence of chronic pain and neurological symptoms,’ whilst a larger UK study, which enrolled 376 patients, detected no effect on incidence or severity of post-herpetic neuralgiaAll other studies have failed to show a significant benefit over placebo. This is hardly emphatic evidence in support of "proven value".
to
the manufacturers, whose
reply
SIR,-Wellcome has had a product licence for several years for the of ’Zovirax’ (acyclovir) in herpes zoster infections. Recently, following submission of new data1,2 to the Medicines Control Agency confirming that zovirax reduced the incidence of postherpetic neuralgia when given in the treatment of shingles, a product licence variation was granted. The Licensing Authority
use
allowed omission of the
Pathology,
DAVID ANDERTON
statement
"whilst
a
beneficial effect of
shown, studies have not yet demonstrated an effect on post herpetic neuralgia" from the data sheet. Our promotion seeks to bring that change to the attention of doctors and pharmacists. Promotional statements should be considered in their entirety and not taken out of context. We disagree with Mr Anderton’s assessment of the data. Although the UK study3 did not reveal a beneficial effect on post-herpetic neuralgia, that does not necessarily mean that the drug is ineffective.
treatment on acute
pain has
been
Later studies in New Zealand and the US have recorded
significant reductions in the incidence of post-herpetic neuralgia during the first 3 months after treatment with zovirax. Although the differences were no longer significant at 6 months of follow-up chronic pain occurred in very few of the treated patients at that time. The possibility of the longer treatment period (as in the US trial) being important in reducing the incidence of post-herpetic neuralgia has been considered, but it is not thought to be a likely explanation, because the New Zealand study, although smaller, clearly demonstrated an effect after 7 days. These studies show that oral acyclovir 800 mg five times daily for 7 or 10 days confers significant clinical benefit in the acute disease and in the longer term complications of post-herpetic neuralgia in immunocompetent adults with herpes zoster. Treatment is more effective when it starts within 48 hours of rash onset or when the symptoms on presentation are more severe. In promotional material, taste is a matter of opinion, and we do not share your correspondent’s views about the pictures. The material is clearly in good taste and recognises the professional standing of those to whom it is addressed. Medical and Consumer Scientific Services Division, Wellcome Foundation Ltd, Crewe, Cheshire CW1 1 UB, UK
E. B. WILLIAMS
P, Thomson AN. Oral acyclovir in the treatment of herpes zoster in general practice. N Z Med J 1989; 102: 93-95. 2. Huff JC, Bean B, Balfour HH, et al. Therapy of herpes zoster with oral acyclovir. Am J Med 1988; 85 (suppl 2A): 84-89. 3. Wood MJ, Organ PH, McKendrick MW, Care CD, McGill JI, Webb EM. Efficacy of oral acyclovir treatment on acute herpes zoster. Am J Med 1988; 85 (suppl 2A) 1. Morton
79-83
reported, but some equally toxic organophosphate may have been responsible. Organosphosphorus chemical warfare agents inhibit acetylcholinesterase and do so rapidly. The rate of recovery is determined by the degree of poisoning and by what caused it, and enzyme activity can remain depressed for weeks. Inhibition of acetylcholinesterase would explain the symptoms reported by most of the patients in Mardin, and the rate of recovery. The fact that no traces of an organophosphate agent were found might be explained by the time delay between poisoning and blood collection. Bread had been singled out as the most likely source of the poisoning but we can find no evidence to support this claim. The bread sample we received may not have been representative or a toxic organophosphate originally present in the bread may have been inactivated. No detailed investigation in the camp was done and the source of the cholinesterase inhibiting agent remains unknown. These refugees had fled from chemical attacks on their homes in northern Iraq in August, 1988. They now claim to have been the victims of another mass-poisoning attempt. The evidence available does suggest something very sinister. It is unlikely that we are talking about a common commercially available chemical, so the chance of accidental poisoning is remote. Most of the victims have recovered, and the UN High Commission for Refugees now has access to Kurdish refugee camps in Turkey. If this poisoning was, as we strongly suspect, deliberate, it has serious implications for the international community. We thank Dr J. Henry and Dr B. Widdop (National Poison Unit, Guy’s Hospital); Dr A. Walker and Dr A. Taylor (St Luke’s Hospital, Guildford); and Dr T. Delves and Mr C. Fellows (Southampton University) for help and advice. Kurdish Scientific and Medical Association, London WC1
DLAWER ALA’ALDEEN JOHN FORAN
Poison Unit, New Cross Hospital, London
IVON HOUSE
Department of Chemical Old Medical School, University of Leeds, Leeds LS2 9JT, UK
ALASTAIR HAY
1.
study from the USA in 1988 reported less post-zoster pain in patients given a 10-day course of oral acyclovir, and this fmding has prompted further studies with longer courses; however, these have yet to be published. Only time will tell if acyclovir is indeed effective in reducing post-herpetic neuralgia and what the ideal dosage regimen should be. Wellcome has failed to point out the negative findings of the UK study and to state that the American study used a regimen not currently recommended. I believe this advertisement breaches clause 4.2 of the code ("information should accurately reflect current knowledge or responsible opinion"), and I am surprised that exaggerated and unfounded claims and potentially offensive and unnecessary photography should be associated with such an A
ethical company. Drug Information Centre, Derbyshire Royal Infirmary, Derby DE1 2QY, UK 1. Morton
P, Thomson AN. Oral acyclovir in the treatment of herpes zoster in general practice. N Z Med J 1989; 102: 93-95. 2. McKendrick MW, McGill JI, Wood MJ. Lack of effect of acyclovir on post-herpetic neuralgia. Br Med J 1989; 298: 431. 3. Huff JC, et al Therapy of herpes zoster with oral acyclovir. Am J Med 1988, 85 (suppl 2A): 84-89.
** This letter has been shown follows.-ED. L.
Independent June 2, 1989. R, Romer J. The
2. Thomas
use of small charcoal/alumina clean-up columns m the detection of tricothecene mycotoxins in foods and feeds. J Assoc Off Analyt Chem 1986; 69: 699-703.
Advertising acyclovir SIR,-Recent promotional literature on ’Zovirax’ (acyclovir; Wellcome) focuses on the role of this drug in treating herpes zoster. Some may be forgiven for mistaking this publicity for a special issue of Playgirlmagazine, with insets of naked bodies on the front cover and a hairy male torso in large format on page 3. What is the relevance of the naked bodies? I and my dermatological colleagues can detect no hint of vesicular eruption. These photographs do not "illustrate pictorially the message of the text" and thus contravene clause 7.6 of the ABPI (Association of the British Pharmaceutical Industry) Code of Practice. This advertisement also incorporates dubious claims, which may contravene the ABPI code. The publicity material claims that acyclovir had been shown to "reduce the suffering of post-herpetic neuralgia"-and that it is "now of proven value in post-herpetic neuralgia". The November, 1989, data sheet for this product does not refer to a reduction in the incidence or severity of post-herpetic neuralgia. I understand that an amendment has now been issued, the effect being merely to remove a negative statement about acyclovir and post-herpetic neuralgia rather than replacing it with a positive indication. Nevertheless, such claims seem premature. I know of only two controlled studies with the data sheet dosage of 800 mg five times a day for 7 days. One study in general practice from New Zealand on 83 patients reported some reduction in the prevalence of chronic pain and neurological symptoms,’ whilst a larger UK study, which enrolled 376 patients, detected no effect on incidence or severity of post-herpetic neuralgiaAll other studies have failed to show a significant benefit over placebo. This is hardly emphatic evidence in support of "proven value".
to
the manufacturers, whose
reply
SIR,-Wellcome has had a product licence for several years for the of ’Zovirax’ (acyclovir) in herpes zoster infections. Recently, following submission of new data1,2 to the Medicines Control Agency confirming that zovirax reduced the incidence of postherpetic neuralgia when given in the treatment of shingles, a product licence variation was granted. The Licensing Authority
use
allowed omission of the
Pathology,
DAVID ANDERTON
statement
"whilst
a
beneficial effect of
shown, studies have not yet demonstrated an effect on post herpetic neuralgia" from the data sheet. Our promotion seeks to bring that change to the attention of doctors and pharmacists. Promotional statements should be considered in their entirety and not taken out of context. We disagree with Mr Anderton’s assessment of the data. Although the UK study3 did not reveal a beneficial effect on post-herpetic neuralgia, that does not necessarily mean that the drug is ineffective.
treatment on acute
pain has
been
Later studies in New Zealand and the US have recorded
significant reductions in the incidence of post-herpetic neuralgia during the first 3 months after treatment with zovirax. Although the differences were no longer significant at 6 months of follow-up chronic pain occurred in very few of the treated patients at that time. The possibility of the longer treatment period (as in the US trial) being important in reducing the incidence of post-herpetic neuralgia has been considered, but it is not thought to be a likely explanation, because the New Zealand study, although smaller, clearly demonstrated an effect after 7 days. These studies show that oral acyclovir 800 mg five times daily for 7 or 10 days confers significant clinical benefit in the acute disease and in the longer term complications of post-herpetic neuralgia in immunocompetent adults with herpes zoster. Treatment is more effective when it starts within 48 hours of rash onset or when the symptoms on presentation are more severe. In promotional material, taste is a matter of opinion, and we do not share your correspondent’s views about the pictures. The material is clearly in good taste and recognises the professional standing of those to whom it is addressed. Medical and Consumer Scientific Services Division, Wellcome Foundation Ltd, Crewe, Cheshire CW1 1 UB, UK
E. B. WILLIAMS
P, Thomson AN. Oral acyclovir in the treatment of herpes zoster in general practice. N Z Med J 1989; 102: 93-95. 2. Huff JC, Bean B, Balfour HH, et al. Therapy of herpes zoster with oral acyclovir. Am J Med 1988; 85 (suppl 2A): 84-89. 3. Wood MJ, Organ PH, McKendrick MW, Care CD, McGill JI, Webb EM. Efficacy of oral acyclovir treatment on acute herpes zoster. Am J Med 1988; 85 (suppl 2A) 1. Morton
79-83