hypertensive patients was 57-7 mm Hg, which was less than 15 mm Hg per hour. By comparison, the abrupt rise in blood pressure in the case reported by Schillaci and colleagues was more than 40 mm Hg/h systolic and more than 20 mm Hg/h diastolic in the morning, and these values were higher than expected. The patient had 99% stenosis of the ipsilateral common carotid bifurcation and had a history of transient ischaemic attacks, indicating that his brain circulation had been continuously ischaemic. Abrupt rise in blood pressure following the onset of stroke has been reported.’ Such findings suggest another pathophysiological sequence in the case reported by Schillaci et al: that the extreme rise in blood pressure might result from brain ischaemia and a subsequent severe subclinical ischaemic attack, rather than a causal trigger of the onset of stroke. *Yasushi Osaki, Kozo Matsubayashi, Tomoko Wada, Yoshinori Doi
Kiyohito Okumiya,
Department of Medicine and Geriatrics, Kochi Medical School, Nankoku 783, Japan
HAV
IgM Ab, anti-HCV Ab, HDV Ag,
spontaneously resolved after 2 weeks. Polyarthralgia and myalgia resolved 4 weeks later with onset of jaundice. 4 months later, liver enzymes had returned to normal but the only modification of the HBV serological profile was disappearance of HBe Ag together with appearance of anti-HBe Ab. The patient was then lost to follow-up. Despite absence of definitive serological proof, the clinical and biological presentation of our patient strongly suggests that the PPGSS she had was related to hepatitis B infection. The alternative hypothesis is a reactivation during chronic hepatitis B. In either case, this observation shows that any patient with PPGSS should be serologically tested for hepatitis B virus infection. Indeed, such a diagnosis has far more consequences for patients and their close relatives than infection with one of the other four viruses previously reported to cause PPGSS. *F
Guibal, P Buffet, F Mouly, P Morel, M Rybojad
Service de
1 Schillaci G, Verdecchia P, Benemio G, et al. Blood pressure rise and ischemic stroke. Lancet 1995; 346: 1366-67. 2 Kuwajima I, Mitani K, Miyao M, et al. Cardiac implications of the morning surge in blood pressure in elderly hypertensive patients: relation to arising time. Am J Hypertens 1995; 8: 29-33. 3 Britton M, Carlsson A, de Faire U. Blood pressure course in patients with acute stroke and matched controls. Stroke 1986; 17: 861-64.
75010 Paris, France
Bagot M, Revuz J. Papular-purpuric "gloves and socks" syndrome: primary infection with parvovirus B19? J Am Acad Dermatol 1991; 25:
2
Perez-Ferriols A,
341.
Martinez-Aparicio A, Aliaga-Boniche A. Papularand socks" syndrome caused by measles virus. J Am Acad Dermatol 1994; 30: 291-92. Harms M, Feldmann R, Saurat JH. J Am Acad Dermatol 1994; 30: 292. Carrascosa JM, Bielsa I, Ribera M, Ferrandiz C. Papular-purpuric gloves-and-socks syndrome related to cytomegalovirus infection. Dermatology 1995; 191: 269-70. Harms M, Feldmann R, Saurat JH. Papular-purpuric "gloves and socks" syndrome. J Am Acad Dermatol 1990; 23: 850-54. purpuric "gloves
4
SIR-Papular-purpuric gloves and socks syndrome (PPGSS) an eruption of pruritic erythema and oedema followed by purpuric papules localised on the distal parts of the limbs. PPGSS has been associated with parvovirus B19 infection, measles, coxsackie B6 infection, and cytomegalovirus (CMV) infection.1-4 Yet in many cases no cause can be found.’ We report PPGSS with hepatitis B (HBV) infection. A 22-year-old woman had burning erythema and oedema in her hands and feet with fever for 1 week. She had typical PPGSS (figure) and a temperature of 37-9°C, diffuse myalgia, inflammatory polyarthralgia, and mild tenderness over her liver. Laboratory examinations showed leucopenia (39X 109/L) with mild neutropenia (2 14X 109/L) and a
Dermotologie, Hôpital Saint-Louis,
1
3
Papular-purpuric gloves and socks syndrome with hepatitis B infection
and anti-HDV Ab
absent. PPGSS
were
5
is
pronounced increase of the liver enzymes: aspartate aminotransferase 1150 IU/L; alanine aminotransferase 492 IU/L ; alkaline phosphatase 325 IU/L. Antibodies for HIV-1 and HIV-2, enterovirus, and coxsackie virus were absent. Serological testing for toxoplasmosis, parvovirus B 19, CMV, and Epstein-Barr virus were negative, and rubella showed previous immunisation. Serological testing for HBV showed HBs Ag, anti-HBc IgM Ab, and HBe Ab. HBV viral DNA was detected in the blood. Anti-HBs Ab, anti-HBe, anti-
Upper limb disease in breast
women
treated for
cancer
for his fair and of what remains a fear for many women treated for breast cancer-and for what, for too many, is still a reality. I strongly endorse his call for surgeons to consult and discuss with clinical oncologists preoperatively on the management of the axilla. I would also agree that a clinically involved axilla should be cleared. However, I am surprised that Sainsbury’s commentary does not encourage his surgical colleagues to address the question of whether axillary dissection is always necessary. In an era of breast screening should we not question the role and extent of such dissections in impalpable or welldifferentiated tumours, while agreeing that there is no place for radical dissections in noninvasive disease? For example, when managing a patient with impalpable disease that may be well differentiated or noninvasive-and to reduce the numbers of surgical procedures and avoid the very common neurological and wound problems of axillary surgery-is there no place for a formal level-one dissection (a true
SiR-Sainsbury is to be congratulated comprehensive resume (Dec 2, p 1444)1
sample)? It might
also be useful if our surgical colleagues could the labels they apply to their procedures. So often agree clearance is short hand for dissection, which may cover anything from the first to all three levels. How can a clinical oncologist determine the appropriate role for radiotherapy when the surgical procedure is so poorly defined? on
Alan
Rodger
William Buckland Radiotherapy Centre, Alfred Hospital, Victoria 3181, Australia
1
Figure : Rash
on
forearm
on
admission
Sainsbury R. Upper limb disease in Lancet 1995; 346: 1444.
women
treated for breast
cancer.
473