1467
TABLE l-LATEX AGGLUTINATION AND CULTURE RESULTS
customers’ requirements. Since 96 % of people we surveyed wished to be called patients this view should be respected by all health-care providers. We would encourage those who want to care for patients in both the private and public sectors to treat them as such. Leicester General Hospital, Leicester LE5 4PW. UK
C. S. J. PROBERT T. BATTCOCK J. F. MAYBERRY
Horse chestnut seed extract SIR,—Professor Schonhofer (March 31,
p 788) describes Klinge company that sues authors who publish negative on horse chestnut seed extract (’Venostasin retard’), suggesting that the company uses litigation to restrict the freedom of science. This is not true. The author of the book in question stated that the efficacy of treatment with venostasin could not be replicated and that the risk-benefit ratio was unacceptable because of adverse drug reactions that have not been reported to the West German drug-regulatory authority or to the manufacturers. The author was not willing to withdraw this libel and recourse to the law was the only way for Klinge Pharma to protect itself against such unfounded
Pharma verdicts
as a
statements.
reduction in transcapillary filtration rate is a effect of venostasin retard, proved in a randomised, placebo-controlled crossover trial in volunteers and in patients.1 The reduction in and prevention of peripheral venous oedema are clinically relevant and reflect the therapeutic efficacy demonstrated in randomised, controlled trials.2-4 These trials have been reviewed by Hitzenberger. The independent scientific expert appointed by the court attested to the clinical efficacy of venostasin retard. Klinge Pharma regrets the need for litigation, but there was no other way. A
22%
pharmacological
Medical Department, Klinge Pharma Gmbh,
D-8000 Munich 80, West Germany
*5 patients not tested adequately upon admission tPattents were observed for diarrhoea during hospital stay. ‡Administration of antimicrobial agents during 2 months
preceding admission
collected upon admission. 218 patients were tested on admission and a further 5 were followed up. Further samples were taken after 2 and 4 weeks and extra samples were taken during any period of diarrhoea during the hospital stay. Stools were cultured, 2-18 h after collection, on selective medium. Colonies with characteristic morphology and staining gram-positive were confirmed as C difficile by membrane gas-chromatography.5 We used the ’Culturette’ rapid latex test (Marion Scientific) and followed the manufacturer’s guidelines carefully, the controls required being included. 84 C difficile latex agglutination positive samples, 29 culture positive samples (23 also positive on the latex test), and 17 negative samples in both tests were further studied by tissue cytotoxin assay.6 A cytopathic effect was confirmed by C sordellii antitoxin neutralisation. Samples, frozen at 40°C, were thawed and filtered just before assay, a procedure that does not result in loss of reactivity. 126 patients were admitted to the outbreak ward and 92 to the control ward. Upon admission 29% were positive by latex agglutination and 11 % by culture (table I). Diarrhoeal episodes were noted in 21 patients-14 were in the outbreak ward and 7 in the control ward; 11 were latex positive and 10 were culture positive (table i). Stool cultures of the diarrhoea patients revealed growth of no other intestinal bacterial or viral pathogen. 10 % of the 197 patients without diarrhoea were C difficile culture positive and 39% were latex agglutination positive. Both tests were positive in 5%. Of the 84 latex positive samples selected for further study 6 were positive in the cytotoxin assay (table II). The corresponding figure for culture-positive stools was 21%. The sensitivities of the latex test and culture were 100% but for specificity was only 23% and 77%, respectively, for an overall accuracy of 27% and 79%. Of the 218 patients 27% had had infections treated with an antimicrobial agent before admission or during the hospital stay. C difficile culture was positive or turned positive in 57% of the 59 antibiotic users but in only 8% of the 159 patients without antibiotic use. In the latex agglutination test the figures for antibiotic users and non-users were 54% and 35%, respectively. The finding of many false-positive C difficile latex tests among stool samples collected on geriatric wards has prompted us to reconsider our policy on antimicrobial treatment for C difficilerelated diseases. We used to give vancomycin or metronidazole to patients with diarrhoea who were latex agglutination positive, and patients were often isolated. We now use culture as a first-line test, because it is more specific than the latex test. Latex agglutination
first stool
sample was
admitted; 213
were
-
MICHAEL BECK
1. Bisler
H, Pfeiffer R, Klüken N, Pauschinger P. Wirkung von Roßkastaniensamenextrakt auf die transkapillare Filtration bei chronischer venoser Insuffizien. Dtsch Med Wochenschr 1986; 35: 1321. 2. Rudofsky G, Neiß A, Otto K, Seibel K. Ödemprotektive Wirkung und klinische Wirksamkeit von Roßkastaniensamenextrakt im Doppelblindversuch. Phlebol Proktol 1986; 15: 47. 3. Sterner M, Hillemanns HG. Untersuchung zur odemprotektiven Wirkung eines Venentherapeutikums. Munch Med Wochenschr 1986; 31: 551. 4 Marshall M, Dormandy JA. Oedema of long distant flights. Phlebology 1987; 2: 123. 5. Hitzenberger G. Die therapeutische Wirksamkeit des Roßkastaniensamenextraktes. Wien Med Wochenschr 1989; 17: 385.
False-positive Clostridium difficile latex agglutination tests SIR,-Clostridium difficile is responsible for pseudomembranous colitis and antibiotic-associated diarrhoea. C difficile-associated diseases are diagnosed by stool culture, by tissue culture for cytotoxin, and by a rapid latex agglutination test. All three tests have disadvantages. Culture detects all strains of C difficile, irrespective of toxin-producing capacity; the cytotoxin assay is widely accepted but is not standardised; and the latex test detects factors related to C difficile-associated diseases but not toxin A itself. 1,2 A combination of tests has been recommended3,.. but immediate decisions are usually made on the latex agglutination result. In April and May, 1988, there was an outbreak of diarrhoea on a geriatric ward in Turku City Hospital. We investigated all patients in the affected ward and in a control ward using routine culture techniques for all clinically important intestinal pathogens, including C difficile culture and latex-agglutination test. The wards did not differ with respect to the frequency of latex agglutinationpositive faecal samples (37% outbreak ward, 40% control ward) but C difficile cultures were positive at rates of 18% and 3%, respectively (p < 0-02). Most inpatients at the department of medicine, Turku City Hospital, are geriatric and long-stay. All patients admitted to the outbreak ward and a control ward from June to December, 1988, were investigated by C difficile culture and latex agglutination. The
or
during hospital stay
TABLE ll-CYTOTOXIN, LATEX, AND CULTURE RESULTS
1468
CLINICAL DETAILS BEFORE TREATMENT
be used only to confirm culture-positive cases. The highest frequency of C difficile culture positivity was in patients transferred from other hospitals (table I), suggesting that other hospitals are likely sources of C difficile for geriatric units.7 The high frequency of positive samples in non-diarrhoea patients indicates a common cross-reacting factor in the geriatric patients studied but we have not yet identified the agent responsible for false-positive results. One possibility is reactivity against other bacteria such as C sporogenes, Peptostreptococcus anaerobius, and Bacteroides asaccharolyticus.1,8,9 The latex agglutination test is still in wide clinical use despite recommendations that it should be used only where the prevalence of C difficile disease is high (eg, 10-20% 10). Where the prevalence is low the positive predictive value of the latex agglutination test is reduced (eg, to 17 % for a prevalence of 2%), and our finding of low specificity creates further problems for the routine use of this test. can
Supported by Sigrid Juselius Foundation (P. H.). We thank Dr Jeri Hill for advice and Tarja Laine and Kerttu Saarinen for technical assistance. Department of Medical Microbiology, University of Turku, 20520 Turku, Finland, Department of Medicine, Turku City Hospital, and Department of Clinical Microbiology, Tampere University Central Hospital
PENTTI HUOVINEN ISMO RÄIHÅ RISTO VUENTO ERKKI EEROLA AAPO LEHTONEN
Lyerly DM, Krivan HC, Wilkins TD. Clostridium difficile: its disease and toxins. Clin Microbiol Rev 1988; 1: 1-18. 2. Lyerly DM, Wilkins TD. Commercial latex test for Clostridium difficile toxin A does not detect toxin A. J Clin Microbiol 1986; 23: 622-23. 3. Sherman ME, DeGirolami PC, Thome GM, Kimber J, Eichelberger K. Evaluation of a latex agglutination test for diagnosis of Clostridium difficile-associated colitis. Am J Clin Pathol 1988; 89: 228-33. 4. Baron EJ. Assessment of currently available laboratory tests for Clostridium difficile-associated diarrhea. Clin Microbiol Newslett 1989; 11: 118-20. 5. Eerola E, Lehtonen O-P. Optimal data processing procedure for automatic bacterial identification by gas-liquid chromatography of cellular fatty acids. J Clin Microbiol 1988; 26: 1745-53. 6. Willey SH, Bartlett JG. Cultures for Clostridium difficile in stools containing a cytotoxin neutralized by Clostridium sordellii antitoxin. J Clin Microbiol 1979; 10: 1.
880-84. 7. Editorial. Clostridium difficile—a neglected pathogen in chronic care facilities. Lancet 1986; ii: 790-91. 8. Miles BL, Siders JA, Allen SD. Evaluation of a commercial latex test for Clostridium difficile for reactivity with C difficile and cross-reaction with other bacteria. J Clin Microbiol 1988; 26: 2452-55. 9. Lyerly DM, Ball DW, Toth J, Wilkins TD. Characterization of cross-reactive proteins detected by Culturette brand rapid latex test for Clostridium difficile. J Clin Microbiol 1988; 26: 397-400. 10. Bennett RG, Laughon BE, Mundy LM, et al. Evaluation of latex agglutination test for Clostridium difficile m two nursing home outbreaks. J Clin Microbiol 1989; 27: 889-93.
Successful treatment of atopic dermatitis with
complexes of allergen and specific antibodies
SIR,—Atopic dermatitis seems, at least in some patients, to involve exacerbation or triggering of symptoms through an immune response to allergens, and increased levels of IgE antibodies to common allergens are usually found.1 Direct evidence for the involvement of aeroallergens remains tenuous, although patch tests with house dust mite allergens can induce lesions resembling those of atopic dermatitis.2 Dermatophagoides pteronyssinus allergens bind to specific IgE antibodies on the Langerhans cell in patients with atopic dermatitis,3suggesting that suppression of this specific response could be of therapeutic benefit in patients with atopic dermatitis who were hypersensitive to D pteronyssinus. Our an
experience in patients with bronchial asthma to whom we gave complexes of specific autologous antibodies and antigen to increase specific anti-idiotype antibodies showed that D pteronyssinus antibody levels fell asthma symptoms improved significantly’ (and unpublished). Encouraged by these results, we next looked at atopic dermatitis, and report here results in six patients inoculated intradermally with allergen-antibody complexes. The patients (table) met diagnostic criteria for atopic dermatitis.S They also had more than 20% of body surface affected, a history of exacerbation upon exposure to D pteronyssinus, and high serum
concentration of total and specific IgE antibodies. Antibodies to D pteronyssinus were isolated by immunoadsorption6 and used to prepare complexes with antigen in antibody excess; the solution contained 20 µg specific antibodies and 4 µg antigen per ml. The complex was administered once a week for 3 weeks, fortnightly for 8 weeks, and then once a month for 10 months. 25 and 50 µ1 was given in the first two injections, and 100 µ1 after that. The therapy was well tolerated; first signs of clinical improvement were observed after about 50 days. Skin lesions and pruritus disappeared in four patients over the year, and the patients voluntarily stopped taking their previous topical and/or systemic treatment.
Details of the other two patients follow.
Patient 1 (30, F, atopic dermatitis for 7 years). Three or four times a year she had had acute exacerbations and house dust, milk, and virus infections were triggering factors. Acute skin infections due to Staphylococcus aureus were observed and she also had allergic rhinitis. When we first saw her as an outpatient she had widespread pruritus and erythema accompanied by follicular eczema and lichenified lesions with scarring and scratch marks. She was using emollients, topical steroids, oxatomide, and methylprednisolone. The pruritus gradually disappeared over the first month of therapy. The erythema and follicular lesions persisted for 3 weeks, with a mild recrudescence during the second month. By the third month the eczema had disappeared. After a few weeks of treatment the patient no longer took oral steroids, and ceterizine was her only other medication. Over the next 10 months tiny sporadic follicular lesions reappeared over the wrists and fingers and an exacerbation of dermatitis was observed during an upper-respiratory-tract viral infection. Symptoms of allergic rhititis had almost disappeared by the fourth month of treatment. Patient 2 (33, F, atopic dermatitis since the age of 5). A partial regression had been observed between the ages of 12 to 22 years but after that severe widespread lesions recurred. House dust, grass pollens, and cereals were triggering factors. She also had asthma upon exposure to house dust and mild intermittent rhinitis. When we saw her she had generalised pruritus and burning pain on face, neck, and arms. The skin was red and oedematous over the entire body surface and lichenification was seen. She was using emollients, antihistamines, and corticosteroids. After 1 month of complex
inoculation both pruritus and skin tenderness had been almost eliminated. Steroids were then withdrawn. Short-term urticarial flushes persisted for 10 weeks and then disappeared. Her only medication then was ceterizine. A 3-week recurrence of dermatitis coincided with unusually high house-dust exposure and humid weather. Occasional bouts of urticaria, without dermatitis were noted thereafter. Residual atopic dermatitis was minor and only
TABLE l-LATEX AGGLUTINATION AND CULTURE RESULTS
customers’ requirements. Since 96 % of people we surveyed wished to be called patients this view should be respected by all health-care providers. We would encourage those who want to care for patients in both the private and public sectors to treat them as such. Leicester General Hospital, Leicester LE5 4PW. UK
C. S. J. PROBERT T. BATTCOCK J. F. MAYBERRY
Horse chestnut seed extract SIR,—Professor Schonhofer (March 31,
p 788) describes Klinge company that sues authors who publish negative on horse chestnut seed extract (’Venostasin retard’), suggesting that the company uses litigation to restrict the freedom of science. This is not true. The author of the book in question stated that the efficacy of treatment with venostasin could not be replicated and that the risk-benefit ratio was unacceptable because of adverse drug reactions that have not been reported to the West German drug-regulatory authority or to the manufacturers. The author was not willing to withdraw this libel and recourse to the law was the only way for Klinge Pharma to protect itself against such unfounded
Pharma verdicts
as a
statements.
reduction in transcapillary filtration rate is a effect of venostasin retard, proved in a randomised, placebo-controlled crossover trial in volunteers and in patients.1 The reduction in and prevention of peripheral venous oedema are clinically relevant and reflect the therapeutic efficacy demonstrated in randomised, controlled trials.2-4 These trials have been reviewed by Hitzenberger. The independent scientific expert appointed by the court attested to the clinical efficacy of venostasin retard. Klinge Pharma regrets the need for litigation, but there was no other way. A
22%
pharmacological
Medical Department, Klinge Pharma Gmbh,
D-8000 Munich 80, West Germany
*5 patients not tested adequately upon admission tPattents were observed for diarrhoea during hospital stay. ‡Administration of antimicrobial agents during 2 months
preceding admission
collected upon admission. 218 patients were tested on admission and a further 5 were followed up. Further samples were taken after 2 and 4 weeks and extra samples were taken during any period of diarrhoea during the hospital stay. Stools were cultured, 2-18 h after collection, on selective medium. Colonies with characteristic morphology and staining gram-positive were confirmed as C difficile by membrane gas-chromatography.5 We used the ’Culturette’ rapid latex test (Marion Scientific) and followed the manufacturer’s guidelines carefully, the controls required being included. 84 C difficile latex agglutination positive samples, 29 culture positive samples (23 also positive on the latex test), and 17 negative samples in both tests were further studied by tissue cytotoxin assay.6 A cytopathic effect was confirmed by C sordellii antitoxin neutralisation. Samples, frozen at 40°C, were thawed and filtered just before assay, a procedure that does not result in loss of reactivity. 126 patients were admitted to the outbreak ward and 92 to the control ward. Upon admission 29% were positive by latex agglutination and 11 % by culture (table I). Diarrhoeal episodes were noted in 21 patients-14 were in the outbreak ward and 7 in the control ward; 11 were latex positive and 10 were culture positive (table i). Stool cultures of the diarrhoea patients revealed growth of no other intestinal bacterial or viral pathogen. 10 % of the 197 patients without diarrhoea were C difficile culture positive and 39% were latex agglutination positive. Both tests were positive in 5%. Of the 84 latex positive samples selected for further study 6 were positive in the cytotoxin assay (table II). The corresponding figure for culture-positive stools was 21%. The sensitivities of the latex test and culture were 100% but for specificity was only 23% and 77%, respectively, for an overall accuracy of 27% and 79%. Of the 218 patients 27% had had infections treated with an antimicrobial agent before admission or during the hospital stay. C difficile culture was positive or turned positive in 57% of the 59 antibiotic users but in only 8% of the 159 patients without antibiotic use. In the latex agglutination test the figures for antibiotic users and non-users were 54% and 35%, respectively. The finding of many false-positive C difficile latex tests among stool samples collected on geriatric wards has prompted us to reconsider our policy on antimicrobial treatment for C difficilerelated diseases. We used to give vancomycin or metronidazole to patients with diarrhoea who were latex agglutination positive, and patients were often isolated. We now use culture as a first-line test, because it is more specific than the latex test. Latex agglutination
first stool
sample was
admitted; 213
were
-
MICHAEL BECK
1. Bisler
H, Pfeiffer R, Klüken N, Pauschinger P. Wirkung von Roßkastaniensamenextrakt auf die transkapillare Filtration bei chronischer venoser Insuffizien. Dtsch Med Wochenschr 1986; 35: 1321. 2. Rudofsky G, Neiß A, Otto K, Seibel K. Ödemprotektive Wirkung und klinische Wirksamkeit von Roßkastaniensamenextrakt im Doppelblindversuch. Phlebol Proktol 1986; 15: 47. 3. Sterner M, Hillemanns HG. Untersuchung zur odemprotektiven Wirkung eines Venentherapeutikums. Munch Med Wochenschr 1986; 31: 551. 4 Marshall M, Dormandy JA. Oedema of long distant flights. Phlebology 1987; 2: 123. 5. Hitzenberger G. Die therapeutische Wirksamkeit des Roßkastaniensamenextraktes. Wien Med Wochenschr 1989; 17: 385.
False-positive Clostridium difficile latex agglutination tests SIR,-Clostridium difficile is responsible for pseudomembranous colitis and antibiotic-associated diarrhoea. C difficile-associated diseases are diagnosed by stool culture, by tissue culture for cytotoxin, and by a rapid latex agglutination test. All three tests have disadvantages. Culture detects all strains of C difficile, irrespective of toxin-producing capacity; the cytotoxin assay is widely accepted but is not standardised; and the latex test detects factors related to C difficile-associated diseases but not toxin A itself. 1,2 A combination of tests has been recommended3,.. but immediate decisions are usually made on the latex agglutination result. In April and May, 1988, there was an outbreak of diarrhoea on a geriatric ward in Turku City Hospital. We investigated all patients in the affected ward and in a control ward using routine culture techniques for all clinically important intestinal pathogens, including C difficile culture and latex-agglutination test. The wards did not differ with respect to the frequency of latex agglutinationpositive faecal samples (37% outbreak ward, 40% control ward) but C difficile cultures were positive at rates of 18% and 3%, respectively (p < 0-02). Most inpatients at the department of medicine, Turku City Hospital, are geriatric and long-stay. All patients admitted to the outbreak ward and a control ward from June to December, 1988, were investigated by C difficile culture and latex agglutination. The
or
during hospital stay
TABLE ll-CYTOTOXIN, LATEX, AND CULTURE RESULTS
1468
CLINICAL DETAILS BEFORE TREATMENT
be used only to confirm culture-positive cases. The highest frequency of C difficile culture positivity was in patients transferred from other hospitals (table I), suggesting that other hospitals are likely sources of C difficile for geriatric units.7 The high frequency of positive samples in non-diarrhoea patients indicates a common cross-reacting factor in the geriatric patients studied but we have not yet identified the agent responsible for false-positive results. One possibility is reactivity against other bacteria such as C sporogenes, Peptostreptococcus anaerobius, and Bacteroides asaccharolyticus.1,8,9 The latex agglutination test is still in wide clinical use despite recommendations that it should be used only where the prevalence of C difficile disease is high (eg, 10-20% 10). Where the prevalence is low the positive predictive value of the latex agglutination test is reduced (eg, to 17 % for a prevalence of 2%), and our finding of low specificity creates further problems for the routine use of this test. can
Supported by Sigrid Juselius Foundation (P. H.). We thank Dr Jeri Hill for advice and Tarja Laine and Kerttu Saarinen for technical assistance. Department of Medical Microbiology, University of Turku, 20520 Turku, Finland, Department of Medicine, Turku City Hospital, and Department of Clinical Microbiology, Tampere University Central Hospital
PENTTI HUOVINEN ISMO RÄIHÅ RISTO VUENTO ERKKI EEROLA AAPO LEHTONEN
Lyerly DM, Krivan HC, Wilkins TD. Clostridium difficile: its disease and toxins. Clin Microbiol Rev 1988; 1: 1-18. 2. Lyerly DM, Wilkins TD. Commercial latex test for Clostridium difficile toxin A does not detect toxin A. J Clin Microbiol 1986; 23: 622-23. 3. Sherman ME, DeGirolami PC, Thome GM, Kimber J, Eichelberger K. Evaluation of a latex agglutination test for diagnosis of Clostridium difficile-associated colitis. Am J Clin Pathol 1988; 89: 228-33. 4. Baron EJ. Assessment of currently available laboratory tests for Clostridium difficile-associated diarrhea. Clin Microbiol Newslett 1989; 11: 118-20. 5. Eerola E, Lehtonen O-P. Optimal data processing procedure for automatic bacterial identification by gas-liquid chromatography of cellular fatty acids. J Clin Microbiol 1988; 26: 1745-53. 6. Willey SH, Bartlett JG. Cultures for Clostridium difficile in stools containing a cytotoxin neutralized by Clostridium sordellii antitoxin. J Clin Microbiol 1979; 10: 1.
880-84. 7. Editorial. Clostridium difficile—a neglected pathogen in chronic care facilities. Lancet 1986; ii: 790-91. 8. Miles BL, Siders JA, Allen SD. Evaluation of a commercial latex test for Clostridium difficile for reactivity with C difficile and cross-reaction with other bacteria. J Clin Microbiol 1988; 26: 2452-55. 9. Lyerly DM, Ball DW, Toth J, Wilkins TD. Characterization of cross-reactive proteins detected by Culturette brand rapid latex test for Clostridium difficile. J Clin Microbiol 1988; 26: 397-400. 10. Bennett RG, Laughon BE, Mundy LM, et al. Evaluation of latex agglutination test for Clostridium difficile m two nursing home outbreaks. J Clin Microbiol 1989; 27: 889-93.
Successful treatment of atopic dermatitis with
complexes of allergen and specific antibodies
SIR,—Atopic dermatitis seems, at least in some patients, to involve exacerbation or triggering of symptoms through an immune response to allergens, and increased levels of IgE antibodies to common allergens are usually found.1 Direct evidence for the involvement of aeroallergens remains tenuous, although patch tests with house dust mite allergens can induce lesions resembling those of atopic dermatitis.2 Dermatophagoides pteronyssinus allergens bind to specific IgE antibodies on the Langerhans cell in patients with atopic dermatitis,3suggesting that suppression of this specific response could be of therapeutic benefit in patients with atopic dermatitis who were hypersensitive to D pteronyssinus. Our an
experience in patients with bronchial asthma to whom we gave complexes of specific autologous antibodies and antigen to increase specific anti-idiotype antibodies showed that D pteronyssinus antibody levels fell asthma symptoms improved significantly’ (and unpublished). Encouraged by these results, we next looked at atopic dermatitis, and report here results in six patients inoculated intradermally with allergen-antibody complexes. The patients (table) met diagnostic criteria for atopic dermatitis.S They also had more than 20% of body surface affected, a history of exacerbation upon exposure to D pteronyssinus, and high serum
concentration of total and specific IgE antibodies. Antibodies to D pteronyssinus were isolated by immunoadsorption6 and used to prepare complexes with antigen in antibody excess; the solution contained 20 µg specific antibodies and 4 µg antigen per ml. The complex was administered once a week for 3 weeks, fortnightly for 8 weeks, and then once a month for 10 months. 25 and 50 µ1 was given in the first two injections, and 100 µ1 after that. The therapy was well tolerated; first signs of clinical improvement were observed after about 50 days. Skin lesions and pruritus disappeared in four patients over the year, and the patients voluntarily stopped taking their previous topical and/or systemic treatment.
Details of the other two patients follow.
Patient 1 (30, F, atopic dermatitis for 7 years). Three or four times a year she had had acute exacerbations and house dust, milk, and virus infections were triggering factors. Acute skin infections due to Staphylococcus aureus were observed and she also had allergic rhinitis. When we first saw her as an outpatient she had widespread pruritus and erythema accompanied by follicular eczema and lichenified lesions with scarring and scratch marks. She was using emollients, topical steroids, oxatomide, and methylprednisolone. The pruritus gradually disappeared over the first month of therapy. The erythema and follicular lesions persisted for 3 weeks, with a mild recrudescence during the second month. By the third month the eczema had disappeared. After a few weeks of treatment the patient no longer took oral steroids, and ceterizine was her only other medication. Over the next 10 months tiny sporadic follicular lesions reappeared over the wrists and fingers and an exacerbation of dermatitis was observed during an upper-respiratory-tract viral infection. Symptoms of allergic rhititis had almost disappeared by the fourth month of treatment. Patient 2 (33, F, atopic dermatitis since the age of 5). A partial regression had been observed between the ages of 12 to 22 years but after that severe widespread lesions recurred. House dust, grass pollens, and cereals were triggering factors. She also had asthma upon exposure to house dust and mild intermittent rhinitis. When we saw her she had generalised pruritus and burning pain on face, neck, and arms. The skin was red and oedematous over the entire body surface and lichenification was seen. She was using emollients, antihistamines, and corticosteroids. After 1 month of complex
inoculation both pruritus and skin tenderness had been almost eliminated. Steroids were then withdrawn. Short-term urticarial flushes persisted for 10 weeks and then disappeared. Her only medication then was ceterizine. A 3-week recurrence of dermatitis coincided with unusually high house-dust exposure and humid weather. Occasional bouts of urticaria, without dermatitis were noted thereafter. Residual atopic dermatitis was minor and only
