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ABSENCE OF HBsAg AND ANTI-HBs IN SPINAL FLUID
1514 whereas 1 such case occurred among 145 individuals transfused with blood lacking anti-HB.. Yet these figures are
inadequate to support such a far-reaching assumption grounds. Even 5 events of hepatitis B in the
statistical
on
exposed to anti-HBs would not fulfil the requirement for significance (p> 008), which would however be met if the original figures are multiplied by 4 (p < 003). In general, clinical or subclinical disease is presumably more directly related to infectivity than serological phenomena. Yet the close association of HBs-antigen to disease certainly reflects a higher risk of infectivity of HBs-antiNevertheless, to reject gen compared with anti-HBs. anti-HBs as a marker for disease transmission is difficult to accept. One crucial question to be answered is: what is the time sequence between recovery, clinical or biochemical, and the disappearance of the infectious agent from circulating blood ? Although there is good reason to believe that infectivity is limited in time after uncomplicated hepatitis, there is no ’evidence that the appearance of anti-HBs coincides with loss of infectivity. We therefore believe that screening blood-donors for anti-HB, will reduce the risk of transmitting hepatitis to some extent. This is especially true when repeat donors are involved. Once an.ti-HBs carriers are removed from the donor pool, only freshly acquired anti-HBs in acceptably small numbers will be detected, indicating recent infection and possibly high risk of infectivity. group
German Red Cross Blood Bank, Oberer Eselsberg 10, 7900 Ulm, Germany.
ABSENCE OF
HANS SEIFERT ANDREAS GANZONI.
by both C.E.P. and R.I.A., the third was positive by R.I.A. only. The HBsAg specificity of this specimen was confirmed by neutralisation with human anti-HBs antibody. The two samples positive by c.E.P. were also found to contain blood as assessed by the labstix test. The spinal fluid which was positive by R.I.A. only was negative for occult blood by this procedure. This latter specimen was obtained from a patient with fulminant hepatitis. Specimens from 5 other cases of fulminant hepatitis were found to be negative. Anti-HBs was not found in any of the spinal fluids examined. Occasional weak HBsAg positivity can signify either increased permeability of the blood-brain barrier or minute of undetected blood contamination. Piazza et al. also failed to detect HBsAg in spinal fluid of 9 patients in coma with fulminant hepatitis. These data suggest that HBsAg does not usually cross the blood-brain barrier in pathological conditions associated with H.B.V. infection. It is therefore unlikely that the C.N.s. dysfunctions occasionally observed in association with hepatitis result from a direct effect of H.B.v. The absence of either HBsAg or anti-HBs in spinal fluid argues against the possibility that H.B.v. plays a role in the aetiology of degenerative diseases of the C.N.S. Laboratory of Hygiene and
amounts
Clinique des Maladies Infectieuses, Lyons, France; Virus Laboratory, New York Blood Center, New York City; and Division of Gastroenterology, Department of Medicine, New York Hospital-Cornell Medical Center, New York City.
HBsAg AND ANTI-HBs IN SPINAL REACTION TO PHENOXYBENZAMINE
FLUID
SIR,-Although predominantly affecting the liver, viral hepatitis has been considered to be a generalised disease.1 Central-nervous-system (c.N.s.) dysfunctions with electroencephalographic changes, as well as a few cases of Guillain-Barre syndrome,3 have been reported in association with acute hepatitis. It is not clear, however, whether hepatitis virus A or B was involved, since most of these reports predate the discovery of HBsAg, a specific serological marker for hepatitis-B virus (H.B.v.). H.B.V. is associated with a high frequency of chronic carrier-type infections. Such chronic carrier states involving common viruses are now suspected to be responsible for some inflammatory degenerative diseases of the c.N.s. of unknown aetiology. Subacute sclerosing panencephalitis, for example, is likely to result from a persistent measles infection.4 To investigate the possibility of the role of
H.B.v. in chronic c..s. syndromes we looked for the presence of HBsAg and its antibody (anti-HBs) in spinal fluid of patients with HBs antigenaemia. 20 spinal fluids were obtained from 19 HBsAg-positive patients with various clinical syndromes including viral hepatitis with meningitis-like symptoms (5), polyarteritis nodosa (2), fulminant hepatitis (6), and cirrhosis with encephalopathy (6). Spinal fluids were examined by routine cytological, bacteriological, and biochemical techniques and were also tested for the presence of occult blood withLabstix’ paper (Ames). Tests for HBsAg were carried out by C.E.P. and by radioimmunoassay (’ Ausria ’ I) after 1 : 2 dilution with normal human serum. Anti-HBs was tested by passive haemagglutination. 3 out of 20 spinal fluids were positive for HBsAg; 2 were positive some acute or
Conrad, M. E., Schwartz, F. D., Young, A. A. Am. J. Med. 1964, 37, 789. 2. Stokes, J. F., Owen, J. R., Holmes, E. G. Br. med. J. 1945, ii, 642. 3. Plough, I. C., Ayerle, R. S. New Engl. J. Med. 1953, 249, 61. 4. Connolly, J. H. J. clin. Path. 1972, 25, suppl. 6, p. 73. 1.
C. TREPO J. F. BOLOT D. ROBERT M. SEPETJIAN A. M. PRINCE.
SiR,—Iwish to report a reaction to the a-blocking agent,
phenoxybenzamine, that is not well documented in the literature. This drug was given by intravenous infusion to treat a hypertensive crisis caused by a phaeochromocytoma. A 70-year-old man, who had a phasochromocytoma resected in 1962, lately had a recurrence of symptoms. Investigations confirmed that he had another phaeochromocytoma. During a severe hypertensive crisis (260/170 mm. Hg) he was given an intravenous infusion of 500 mg. phenoxybenzamine in 300 ml. of 5 % dextrose over three hours. Within half an hour of starting x-blockade, he suddenly lost consciousness, sweated profusely, and developed piloerection with intense vasoconstriction of the skin. He had a sinus tachycardia (160 per minute) and his bloodpressure was unrecordable. Phenoxybenzamine infusion was stopped and a small intravenous dose of practolol (12-5 mg) administered. The tachycardia settled immediately and he became normotensive within five minutes. The other signs of &bgr;-stimulation also resolved quickly, but he did not regain consciousness for a further six hours. The following day he had completely recovered.
The dose of phenoxybenzamine used in this hypertensive crisis is that recommended by the manufacturers in the pamphlet in the drug package. In fact the rate of infusion was considerably slower than advised, and by the time the patient collapsed he had received 80 mg. phenoxybenzamine. It now transpires that this information only accompanies older stock, and was based on work by Allen.6 Current recommendations of the dose are 0-5-10 mg. per
kg.7
The cause of this patient’s shock was intense &bgr;-stimulation in the face of complete
inadequate to support such a far-reaching assumption grounds. Even 5 events of hepatitis B in the
statistical
on
exposed to anti-HBs would not fulfil the requirement for significance (p> 008), which would however be met if the original figures are multiplied by 4 (p < 003). In general, clinical or subclinical disease is presumably more directly related to infectivity than serological phenomena. Yet the close association of HBs-antigen to disease certainly reflects a higher risk of infectivity of HBs-antiNevertheless, to reject gen compared with anti-HBs. anti-HBs as a marker for disease transmission is difficult to accept. One crucial question to be answered is: what is the time sequence between recovery, clinical or biochemical, and the disappearance of the infectious agent from circulating blood ? Although there is good reason to believe that infectivity is limited in time after uncomplicated hepatitis, there is no ’evidence that the appearance of anti-HBs coincides with loss of infectivity. We therefore believe that screening blood-donors for anti-HB, will reduce the risk of transmitting hepatitis to some extent. This is especially true when repeat donors are involved. Once an.ti-HBs carriers are removed from the donor pool, only freshly acquired anti-HBs in acceptably small numbers will be detected, indicating recent infection and possibly high risk of infectivity. group
German Red Cross Blood Bank, Oberer Eselsberg 10, 7900 Ulm, Germany.
ABSENCE OF
HANS SEIFERT ANDREAS GANZONI.
by both C.E.P. and R.I.A., the third was positive by R.I.A. only. The HBsAg specificity of this specimen was confirmed by neutralisation with human anti-HBs antibody. The two samples positive by c.E.P. were also found to contain blood as assessed by the labstix test. The spinal fluid which was positive by R.I.A. only was negative for occult blood by this procedure. This latter specimen was obtained from a patient with fulminant hepatitis. Specimens from 5 other cases of fulminant hepatitis were found to be negative. Anti-HBs was not found in any of the spinal fluids examined. Occasional weak HBsAg positivity can signify either increased permeability of the blood-brain barrier or minute of undetected blood contamination. Piazza et al. also failed to detect HBsAg in spinal fluid of 9 patients in coma with fulminant hepatitis. These data suggest that HBsAg does not usually cross the blood-brain barrier in pathological conditions associated with H.B.V. infection. It is therefore unlikely that the C.N.s. dysfunctions occasionally observed in association with hepatitis result from a direct effect of H.B.v. The absence of either HBsAg or anti-HBs in spinal fluid argues against the possibility that H.B.v. plays a role in the aetiology of degenerative diseases of the C.N.S. Laboratory of Hygiene and
amounts
Clinique des Maladies Infectieuses, Lyons, France; Virus Laboratory, New York Blood Center, New York City; and Division of Gastroenterology, Department of Medicine, New York Hospital-Cornell Medical Center, New York City.
HBsAg AND ANTI-HBs IN SPINAL REACTION TO PHENOXYBENZAMINE
FLUID
SIR,-Although predominantly affecting the liver, viral hepatitis has been considered to be a generalised disease.1 Central-nervous-system (c.N.s.) dysfunctions with electroencephalographic changes, as well as a few cases of Guillain-Barre syndrome,3 have been reported in association with acute hepatitis. It is not clear, however, whether hepatitis virus A or B was involved, since most of these reports predate the discovery of HBsAg, a specific serological marker for hepatitis-B virus (H.B.v.). H.B.V. is associated with a high frequency of chronic carrier-type infections. Such chronic carrier states involving common viruses are now suspected to be responsible for some inflammatory degenerative diseases of the c.N.s. of unknown aetiology. Subacute sclerosing panencephalitis, for example, is likely to result from a persistent measles infection.4 To investigate the possibility of the role of
H.B.v. in chronic c..s. syndromes we looked for the presence of HBsAg and its antibody (anti-HBs) in spinal fluid of patients with HBs antigenaemia. 20 spinal fluids were obtained from 19 HBsAg-positive patients with various clinical syndromes including viral hepatitis with meningitis-like symptoms (5), polyarteritis nodosa (2), fulminant hepatitis (6), and cirrhosis with encephalopathy (6). Spinal fluids were examined by routine cytological, bacteriological, and biochemical techniques and were also tested for the presence of occult blood withLabstix’ paper (Ames). Tests for HBsAg were carried out by C.E.P. and by radioimmunoassay (’ Ausria ’ I) after 1 : 2 dilution with normal human serum. Anti-HBs was tested by passive haemagglutination. 3 out of 20 spinal fluids were positive for HBsAg; 2 were positive some acute or
Conrad, M. E., Schwartz, F. D., Young, A. A. Am. J. Med. 1964, 37, 789. 2. Stokes, J. F., Owen, J. R., Holmes, E. G. Br. med. J. 1945, ii, 642. 3. Plough, I. C., Ayerle, R. S. New Engl. J. Med. 1953, 249, 61. 4. Connolly, J. H. J. clin. Path. 1972, 25, suppl. 6, p. 73. 1.
C. TREPO J. F. BOLOT D. ROBERT M. SEPETJIAN A. M. PRINCE.
SiR,—Iwish to report a reaction to the a-blocking agent,
phenoxybenzamine, that is not well documented in the literature. This drug was given by intravenous infusion to treat a hypertensive crisis caused by a phaeochromocytoma. A 70-year-old man, who had a phasochromocytoma resected in 1962, lately had a recurrence of symptoms. Investigations confirmed that he had another phaeochromocytoma. During a severe hypertensive crisis (260/170 mm. Hg) he was given an intravenous infusion of 500 mg. phenoxybenzamine in 300 ml. of 5 % dextrose over three hours. Within half an hour of starting x-blockade, he suddenly lost consciousness, sweated profusely, and developed piloerection with intense vasoconstriction of the skin. He had a sinus tachycardia (160 per minute) and his bloodpressure was unrecordable. Phenoxybenzamine infusion was stopped and a small intravenous dose of practolol (12-5 mg) administered. The tachycardia settled immediately and he became normotensive within five minutes. The other signs of &bgr;-stimulation also resolved quickly, but he did not regain consciousness for a further six hours. The following day he had completely recovered.
The dose of phenoxybenzamine used in this hypertensive crisis is that recommended by the manufacturers in the pamphlet in the drug package. In fact the rate of infusion was considerably slower than advised, and by the time the patient collapsed he had received 80 mg. phenoxybenzamine. It now transpires that this information only accompanies older stock, and was based on work by Allen.6 Current recommendations of the dose are 0-5-10 mg. per
kg.7
The cause of this patient’s shock was intense &bgr;-stimulation in the face of complete