- Email: [email protected]
PERIORAL DERMATITIS
491 seen, we have successfully treated a cerebral infection caused by a Staph. aureus resistant to penicillin, chloramphenicol, and lincomycin.! One further patient with a history of anaphylaxis to penicillin was admitted with pneumococcal meningitis and was cured by 6 g cefotaxime per day. Other cephalosporins (cefacetrile4 cefuroximel) and the cephamycin cefoxitincan give sufficient CSF levels to treat meningitis caused by penicillin resistant strains. Experience with cefotaxime in treating cerebral infections in encouraging, but controlled clinical trials are necessary before the compound can be recommended as drug of choice in such cases.
FAMILIAL PSEUDOHYPERKALÆMIA
aureus was
Infection Laboratory, Centre for Internal Medicine, Johann Wolfgang Goethe University, 6000 Frankfurt am Main 70, West Germany
PRAMOD M. SHAH
PERIORAL DERMATITIS
SIR,-Your Jan. 12 editorial stresses the important role of potent topical corticosteroids in the induction and perpetuation of perioral dermatitis. Credit is rightly given to Wilkinson et al. for their long-term study of this interesting disorder. However, both their paper and your editorial largely discount other xtiological factors and blame the rise in incidence since the mid-1960s on increased prescribing of topical corticosteroids. During my dermatological training in London I was well aware of this widely held view. Since moving to North America I have come to feel that this is only part of the story, albeit a large part. In thirty months from July, 1977,I examined 57 cases of perioral dermatitis (54 female, 3 male). 44 had previously used at least one topical corticosteroid preparation, although 21 stated that the eruption had preceded the use of that preparation (here, as in the U.K., the dermatoses we see are largely steroid-resistant). In 3 patients I could not establish the history of corticosteroid use with certainty but in 10 cases (18-) the patient had not used corticosteroids either from a doctor or from another source. Since this was almost heresy I checked this by repeated ques-
tioning. Therefore I began to look for other possible causes. 4 of these patients were pregnant at the onset of the eruption and 10 were taking an oral contraceptive. These figures are similar to those of Wilkinson et al. and not significantly different from the expected although, perhaps because of my interest in skin problems during pregnancy, I feel that a more intensive study may show a hormonal relationship. The second possibility was that cream bases might be worsening this disorder, as suggested by Bendl.88 of my 10 cases who had not been using a topical corticosteroid had been using moisturisers. As noted by Wilkinson et al.,7 many of these women complain of dry facial skin. It is possible that the rise in incidence of this disorder since the mid-1960s is due not only to the increased use of topical corticosteroids but also to the change from the powdered "look" to today’s creamed "look". Re-education of these patients to avoid moisturisers might prevent the occasional steroid-unrelated recurrences. Division of Dermatology, Department of Medicine, University of British Columbia,
Vancouver, B.C., Canada V5Z 1L7
SIR,-Familial pseudohyperkalxmia has recently been It was the first report of this syndrome unrelated to leukxmia or thrombocythasmia. We have investigated a patient with a similar syndrome and found the same serum-potassium pattern in one of her two daughters. A 67-year-old woman was admitted in July, 1979, because of asthenia and depression. Physical examination was normal. Routine laboratory investigations at the time of admission revealed hyperkalmmia (6-2 mmol/1) and repeated plasma potassium determinations ranged from 5.6to 7.8mmol/1. The patient was taking no medication. Plasma sodium, chloride, and bicarbonate, urinary electrolytes, and creatinine clearance were normal. There was no acidosis (arterial blood pH 7-4) nor electrocardiographic changes suggestive of hyperkalxmia. Plasma renin activity, aldosterone, and cortisol and response to oral glucose load were normal. Pseudohyperkalaemia was finally suspected, and several assays on blood-samples centrifuged and separated immediately confirmed normal potassium (range 4-4—3 mmol/1 ; n=8). Plasma potassium determinations were then performed after prolonged in-vitro incubation of blood at 37, 22, and 9°C. The results in our patient and her two daughters and the mean values obtained for six normal volunteers are shown in the figure. A significant rise in plasma potassium without macroscopic hxm-olysis was observed in our patient and in one of her daughters (daughter 1) during blood incubation at 22 and 9°C, but not in the controls. Our patient had no htmolytic ansemia, nor pathological states reported to affect movements of sodium and potassium across the erythrocyte membrane. White blood cells and platelets counts were normal. Our results closely resemble those reported by Stewart et al.,confirming the existence of an inherited pseudohyperkalæmia syndrome. J.-C. LUCIANI T. LAVABRE-BERTRAND
reported.’
Service de Médecine
D,
Hôpital Saint-Charles, 34059-Montpellier France Laboratoire d’Explorations Biophysiques, Centre Gui de Chauliac, Montpellier
J. FOURCADE P. BARJON A. MIMRAN A. CALLIS
GW, Corrall RJM, Fyffe JA, Stockdill G, Strong JA. pseudohyperkalæmia. Lancet 1979; n: 175-77.
1. Stewart
Familial
J. ALASTAIR CARRUTHERS
4. Correa Lima MB, Carvalho Neto E, Gorinstein J, Casz I. A preliminary communication on the use of cephacetrile as monotherapy in the treatment of purulent meningitis. Drug Res 1974; 24: 1512-15. Norby R, Foord RD, Price JD. Pharmacokinetic and clinical studies on cefuroxime. Proc Roy Soc Med 1977; 70: suppl 91, 25-32. 6. Cherubin CE. Clinical experience with cefoxitin. 1st Mediterranean CongressofChemotherapy, 1978. 7. Wilkinson DS, Kirton V, Wilkinson JD. Perioral dermatitis: a 12 year review. Br J Dermatol 1979; 101: 245-57. 8. Bendl BJ. Perioral dermatitis: Etiology and treatment. Cutis 1976; 17: 903.
5
Plasma-potassium of patient
and her daughters and mean of controls in relation to standing-time and temperature before centrifugation. values
(±SEM)
FAMILIAL PSEUDOHYPERKALÆMIA
aureus was
Infection Laboratory, Centre for Internal Medicine, Johann Wolfgang Goethe University, 6000 Frankfurt am Main 70, West Germany
PRAMOD M. SHAH
PERIORAL DERMATITIS
SIR,-Your Jan. 12 editorial stresses the important role of potent topical corticosteroids in the induction and perpetuation of perioral dermatitis. Credit is rightly given to Wilkinson et al. for their long-term study of this interesting disorder. However, both their paper and your editorial largely discount other xtiological factors and blame the rise in incidence since the mid-1960s on increased prescribing of topical corticosteroids. During my dermatological training in London I was well aware of this widely held view. Since moving to North America I have come to feel that this is only part of the story, albeit a large part. In thirty months from July, 1977,I examined 57 cases of perioral dermatitis (54 female, 3 male). 44 had previously used at least one topical corticosteroid preparation, although 21 stated that the eruption had preceded the use of that preparation (here, as in the U.K., the dermatoses we see are largely steroid-resistant). In 3 patients I could not establish the history of corticosteroid use with certainty but in 10 cases (18-) the patient had not used corticosteroids either from a doctor or from another source. Since this was almost heresy I checked this by repeated ques-
tioning. Therefore I began to look for other possible causes. 4 of these patients were pregnant at the onset of the eruption and 10 were taking an oral contraceptive. These figures are similar to those of Wilkinson et al. and not significantly different from the expected although, perhaps because of my interest in skin problems during pregnancy, I feel that a more intensive study may show a hormonal relationship. The second possibility was that cream bases might be worsening this disorder, as suggested by Bendl.88 of my 10 cases who had not been using a topical corticosteroid had been using moisturisers. As noted by Wilkinson et al.,7 many of these women complain of dry facial skin. It is possible that the rise in incidence of this disorder since the mid-1960s is due not only to the increased use of topical corticosteroids but also to the change from the powdered "look" to today’s creamed "look". Re-education of these patients to avoid moisturisers might prevent the occasional steroid-unrelated recurrences. Division of Dermatology, Department of Medicine, University of British Columbia,
Vancouver, B.C., Canada V5Z 1L7
SIR,-Familial pseudohyperkalxmia has recently been It was the first report of this syndrome unrelated to leukxmia or thrombocythasmia. We have investigated a patient with a similar syndrome and found the same serum-potassium pattern in one of her two daughters. A 67-year-old woman was admitted in July, 1979, because of asthenia and depression. Physical examination was normal. Routine laboratory investigations at the time of admission revealed hyperkalmmia (6-2 mmol/1) and repeated plasma potassium determinations ranged from 5.6to 7.8mmol/1. The patient was taking no medication. Plasma sodium, chloride, and bicarbonate, urinary electrolytes, and creatinine clearance were normal. There was no acidosis (arterial blood pH 7-4) nor electrocardiographic changes suggestive of hyperkalxmia. Plasma renin activity, aldosterone, and cortisol and response to oral glucose load were normal. Pseudohyperkalaemia was finally suspected, and several assays on blood-samples centrifuged and separated immediately confirmed normal potassium (range 4-4—3 mmol/1 ; n=8). Plasma potassium determinations were then performed after prolonged in-vitro incubation of blood at 37, 22, and 9°C. The results in our patient and her two daughters and the mean values obtained for six normal volunteers are shown in the figure. A significant rise in plasma potassium without macroscopic hxm-olysis was observed in our patient and in one of her daughters (daughter 1) during blood incubation at 22 and 9°C, but not in the controls. Our patient had no htmolytic ansemia, nor pathological states reported to affect movements of sodium and potassium across the erythrocyte membrane. White blood cells and platelets counts were normal. Our results closely resemble those reported by Stewart et al.,confirming the existence of an inherited pseudohyperkalæmia syndrome. J.-C. LUCIANI T. LAVABRE-BERTRAND
reported.’
Service de Médecine
D,
Hôpital Saint-Charles, 34059-Montpellier France Laboratoire d’Explorations Biophysiques, Centre Gui de Chauliac, Montpellier
J. FOURCADE P. BARJON A. MIMRAN A. CALLIS
GW, Corrall RJM, Fyffe JA, Stockdill G, Strong JA. pseudohyperkalæmia. Lancet 1979; n: 175-77.
1. Stewart
Familial
J. ALASTAIR CARRUTHERS
4. Correa Lima MB, Carvalho Neto E, Gorinstein J, Casz I. A preliminary communication on the use of cephacetrile as monotherapy in the treatment of purulent meningitis. Drug Res 1974; 24: 1512-15. Norby R, Foord RD, Price JD. Pharmacokinetic and clinical studies on cefuroxime. Proc Roy Soc Med 1977; 70: suppl 91, 25-32. 6. Cherubin CE. Clinical experience with cefoxitin. 1st Mediterranean CongressofChemotherapy, 1978. 7. Wilkinson DS, Kirton V, Wilkinson JD. Perioral dermatitis: a 12 year review. Br J Dermatol 1979; 101: 245-57. 8. Bendl BJ. Perioral dermatitis: Etiology and treatment. Cutis 1976; 17: 903.
5
Plasma-potassium of patient
and her daughters and mean of controls in relation to standing-time and temperature before centrifugation. values
(±SEM)