- Email: [email protected]
SERUM ANGIOTENSIN-CONVERTING ENZYME IN SARCOIDOSIS AND OTHER DISEASES
382
by
an
influenza A virus similar
50% (411 boys
of
to
A/USSR/92/77
the attack-
population of 821), and the seroconversion rate of a large sample of the school was 90%. Although the uncomplicated illness was usually of only mild to moderate severity, 29 boys (7% of those infected) became much more prostrated than the others, with prolonged or recurrent pyrexia and productive cough. They all had adventitious sounds in the lungs, and 4 had pleurisy. 7 of them were rate was
out
a
yngeal, or laryngeal receptors, the upper airway cannot neglected as a possible cause of night cough in a child.
be
Departments of Ear-Nose-Throat Surgery and Human Genetics, Genetics. Free University, Amsterdam 11, Netherlands
J. WIND
further
investigated, and in every case there was marked neuand signs of consolidation in the chest X-ray. 1 boy whose sputum Streptococcus pneumoniæ was isolated
trophilia
from had a white-cell count of 30 900/ul with 88% neutrophils. The incidence and severity of respiratory complications in this outbreak was much greater than in the five outbreaks due to H3N2 and B viruses which the school has experienced since 1970. The Infirmary, Christ’s Hospital, Horsham, West Sussex
T. W. HOSKINS
RUBELLA VACCINATION
SIR,—May an American comment on the question of British rubella-vaccination policy? I agree with Dr Goldwater and colleagues’ who argue that vaccination of prepubescent girls should be continued. Although the American policy may have had some success in reducing the incidence of rubella in children, rubella continues’to occur in adolescents and young adults. Moreover, recent reports suggest that 10-20% of American adolescents previously vaccinated as children lack antibody,2 and it may therefore be preferable to vaccinate later in life. The recent introduction of RA/27-3 strain rubella vaccine in the United States may improve the duration of immunity in vaccinated infants, but additional data.are needed. Goldwater et al. urge that vaccination of adult women on contraceptives should be encouraged, but they express concern about the lack of data on risks to the fetus associated with the RA/27-3 vaccine, licensed for eight years outside the U.S. I agree with the need for more data and that pregnant women should not be vaccinated. Some comfort, however, may be taken from the fact that at least twelve seronegative pregnant women have been vaccinated with RA/27-3 and examinations of the products of conception have failed to reveal virus.3,4 Infectious Diseases Division Virus Laboratory, and and Virus Laboratory, Joseph Stokes, Jr. Research Institute, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, U.S.A.
STANLEY A. PLOTKIN
NIGHT COUGH IN CHILDREN as a cause of night of because the in children improbability of the secrecough tions entering "the larynx and trachea, the site of cough receptors". However, the cough reflex threshold is very low in children. Furthermore, there are various other receptor sites, such as the ear canal wall and the nasal and pharyngeal mucous membranes. Ear, nose, and throat surgeons and general practitioners know well that most children referred for adenoidectomy (in my patients 70-80%) have a dry night cough which disappears after surgery. While we do not know whether this cough is caused by stimulation of the nasal, phar-
SiR,-Dr Phelan5 denies postnasal drip
1. Goldwater, P. N., Quiney, J. R., Banatvala, J, E Lancet, 1978, ii, 1298. 2. Balfour, H. H., Amren, D. P. Am. J. Dis. Child. 1978, 132, 573. 3. Furukawa, T., Miyata, T., Kondo, K., Kuno, K., Isomura, S., Takakochi, T. ibid. 1969, 118, 262. 4 Bernstein, D. I., Ogra, P L. Personal communication, 1973. 5. Phelan, P. D. Lancet, 1978, ii, 1309.
SERUM ANGIOTENSIN-CONVERTING ENZYME IN SARCOIDOSIS AND OTHER DISEASES
gratified that the report of Dr Studdy and colleagues! angiotensin-converting enzyme (SACE) activity in sarcoidosis and other granulomatous disorders, using our method,2 confirms our observations and the effect of steroid therapy on SACE levels in 116 patients with sarcoidosis.3-’ We found that an increased SACE (59% of 46 recently diagnosed, untreated patients) is diagnostically useflil6 and that steroids lowered SACE in 15 of 16 patients.’ However, SACE remained above normal in a third of cases during the first year of therapy and in half of patients with progressive disease after four years of therapy.’ The correlation of SACE activity with the stage of disease was not statistically significant, although pulmonary infiltration tended to be associated with higher SACE SIR,-We
are
on serum
levels.’ Steroids had no influence on the ACE assay in vitro.8 SACE levels less than 2 standard deviations from the normal mean were seldom found.6 SACE values greater than 70 nmol/ min/ml were present in 20% (22/116) of all patients but in 30% (14/46) of newly diagnosed, ’untreated patients;6 SACE activity above 70 nmol/min/ml tended to occur in patients with sufficient disease activity to require steroid therapy.’ Activity tended to diminish with increasing duration of disease, particularly after two years.’ We have suggested that serial measurements of SACE may be useful in the clinical management of sarcoidosis, including assessment of the degree of activity, the need for steroid therapy, therapeutic result, and the
prognosis.’ Contrary
to the statement of Studdy et al. our work indithat sarcoidosis lymph-node ACE is less stable than normal,s and there is no enrichment of serum ACE, but rather it is the tissue ACE that is increased in the lung.9 Our observation of a statistically significant association between raised serum lysozyme values and SACE in sarcoidosis’O does not necessarily mean that SACE is a biochemical marker for increased macrophage activity, as stated by Studdy et al. Rather, this association suggests to us that the same cell in increased numbers is probably involved in both enzyme changes without regard to its general state of activation, since lysozyme secretion in mononuclear phagocytes does not vary with their state of activation," macrophage ACE did not increase in response to endotoxin activation in culture, 12 and ACE synthesis was specifically induced by glucocorticosteroids,8 in the absence of general activation. Whatever the pathogenesis of sarcoidosis and the increased ACE associated with it," it is clear that abundant ACE is localised in sarcoidosis epithelioid and giant cells,’’* and that mononuclear phagocytes, which
cates
1. Studdy, P., Bird, R., Geraint James, D., Sherlock, S. Lancet, 1978, ii, 133. 2. Friedland, J., Silverstein, E. Am. J. clin. Path. 1976, 66, 416. 3. Silverstein, E., Friedland, J., Lyons, H., Kitt, M. Clin. Res. 1975, 23, 352A. 4. Silverstein, E., Friedland, J., Lyons, H. A., Gourin, A. Ann. N. Y. Acad. Sci.
1976, 278, 498. 5. Silverstein, E., Friedland, J., Lyons, H. A., Gounn, A. Proc. natn. Acad. Sci. U.S.A. 1976, 73, 2137. 6. Silverstein, E., Friedland, J., Kitt, M., Lyons, H. A. Israel J. med. Sci. 1977, 7. 8. 9. 10. 11. 12. 13. 14.
13, 995. Silverstein, E., Friedland, J., Lyons, H. A. ibid. 1977, 13, 1001. Friedland, J., Setton, C., Silverstein, E. Science, 1977, 197, 64.
Cushman, D., Cheung, H. S. Biochem. biophys. Acta, 1971, 250, 261. Silverstein, E., Friedland, J., Ackerman, T. Am. J. clin. Path. 1977, 68, 219. Gordon, S., Todd, J., Cohn, Z. A. J. exp. Med. 1974, 139, 1228. Silverstein, E., Friedland, J., Setton, C. Israel J. med. Sci. 1978, 14, 314. Silverstein, E. Med. Hypoth. 1976, 2, 75. Silverstein, E., Fnedland, J., Kim, D. S., Pertschuk, L. P. Paper read at 8th international conference on Sarcoidosis (Cardiff, September, 1978).
383
normallv have a paucity of ACE and a characteristic, abundant lv sozyme secretion," are nevertheless capable of being induced to increase ACE synthesis markedly.’, 11 BB’e have recently observed normal mean levels of SACE activity in the following disorders (values in nmol/min/ml +S.D, and proportion with increased values): monocytic leukaemia. 23.2±4.0 (0/2); Paget’s disease of bone, 31.2±5.8 (0/6); silicosis, 33.1 (0/1); giant lymph-node hyperplasia, 27.6 (0/1): scleroderma, 35.0±13.0(1/11); angioimmunoblastic lymphadenopathy, 25.2±3.0 (0/2). We thank Dr F. Shai and Dr M. Guttadauria for Paget’s disease and scleroderma blood-samples and C. Setton for SACE assays.
Department of Medicine,
E. SILVERSTEIN
S U.N Y. Downstate Medical Center, Brooklyn, N.Y. 11203, U.S.A.
J. FRIEDLAND
NEUROSYPHILIS YESTERDAY AND TODAY
SIR,-Questions such as "Does adequate antisyphilitic therapy prevent neurosyphilis?", discussed by Dr Luxon and her colleagues in their interesting article entitled Neurosyphilis Today (Jan. 13, p. 90) were hotly debated earlier this century and are still unanswered. In the early 1900s many hoped, like Fournier,’ that adequate early treatment of syphilis would prevent general paralysis of the insane (G.P.I.) but statistics soon showed that a proportion of patients who were well treated by the standards of the day (i.e., with mercury) still proceeded to studies even showed that treatment shortened the G.P.I.; interval between syphilis and onset of G.p.l.,2 and a few observers in the 1920s regarded "metalues" as a consequence of "modern" treatment of syphilis.3.4 Most, however, felt that it was the inadequacy of treatment for early syphilis that might be damaging. The difficulty then, as now, was to determine what was adequate treatment in this context. It was hoped in the early days of neoarsphenamine treatment that this drug would prove a better prophylactic against neurosyphilis than mercury. However, when in 1937 I studied 863 male G.P.I. patients treated in Bonhoffer’s clinic at the Charite, Berlin, between 1925 and 1935, 1 found56 that several patients had already received what was then regarded as appropriate arsenical treatment for their syphilis. Your contributors’ finding, among their much more recent patients, that most "had not received adequate antisyphilitic therapy", also applied to the G.P.I. patients of the Charite, Berlin both between 1910 and 1924 in the mercury era2 and between 1925 and 1935 (neoarsphenamine5,6). However, in both eras cases of neurosyphilis presented despite appropriate antisyphilitic therapy; and this has been confirmed for penicillin-treated patients also.7.8 Yoder8 in 1975 asked for further investigation of the adequacy of penicillin-G treatment as recommended today. Perhaps today’s "adequate" antisyphilitic therapy may, in certain cases at least, again some
prove madequate tomorrow. L C H Alcoholism O.P. St Pancras Hospital, London NW1
(Teaching)
Centre
M. M. GLATT
SIR,- The series of cases of neurosyphilis reported on by D; Luxon and her colleagues did not include an acute meningo ascular case. A recent case prompts us to emphasise this pres entation. A
22-year-old North-African
man was
admitted
15. Friedland, J,
to
hospita
Setton, C., Silverstein, E. Biochem. biophys. Res. Comm 1978, 83, 843. 1. Fournier, J.C. Zbl Nervenheilk. 1906, 29, 617. 2. Jossman. P. Mon. Psychiat.1932/33, 84, 245.
3. Gartner. Z Hyg 1921, 92, 341. Wilm anns, KKlin Wschr. 1925, 1097, 1145. 5. Glatt, M.,M M.D thesis,Universityof Berlin, 1937. Glatt, M., M. Confneurol 1938, 1, 257.
4.
with hemiplegia of rapid onset and brachiofacial distribution. His history was not contributory except for acute enteritis a week before admission. He had no history of syphilis. The patient was febrile. No meningeal signs were observed. There was a motor and sensory deficit. Cardiac auscultation was benign. Funduscopy was normal. A computerised tomographic scan on the first day was normal. C.S.F. examination revealed a normal glucose, mild lymphocytosis, slightly increased protein; the c.s.F. was negative by direct examination and acid-fast test and on culture, and blood cultures were also negative. 2 days after the patient’s admission a positive blood test for syphilis was recorded. Antisyphilitic therapy was stated and the patient
rapidly improved. Meningovascular syphilis
may thus present as a "stroke", and we believe that an emergency test for syphilis should be done in all cases of acute-onset cerebrovascular disease, especially in young patients. Department of Internal Medicine, St Pierre University Hospital,
G. DECAUX M. SZYPER
B-1000 Brussels, Belgium
LEUCOCYTE-COUNTS AND SURVIVAL IN UNRESECTABLE LUNG CANCER
SIR,-Dr Check and colleagues’ in their series-of 51 patients, found a high correlation between the leucocyte-count assessment of the patient, and subin sequent survival-time, patients with unresectable lung cancer. I have analysed tuberculin reactivity as a predictor of survival-time in similar patients2 and took the opportunity to attempt to validate Check’s findings. After exclusion of patients with operable disease and those with oat-cell tumours, to ensure comparability with Check’s series, 59 sets of patient records were available for study. Leucocyte-counts had been done at the time of initial diagnosis (Technicon ’Hemalog 8’ automated cell counter). The mean-
performed
at
the initial
SURVIVAL OF PATIENTS WITH UNRESECTABLE LUNG CANCER
RELATIVE TO LEUCOCYTE-COUNT
rz=0.009; not significant. in patients surviving less than four months The table, constructed identically to Check’s table n, shows survival-times of patients whose leucocytecounts were greater or less than 9900/µ1. There is no association between white-cell count and survival-time on this basis, nor is there any obvious correlation when the results of individual leucocyte-counts are plotted graphically against survival-time in days. Unfortunately, only 16 patients had had full differential counts; of these, 7 patients with a neutrophilia survived less than four months, and 5 for more than four months (one for nearly two years). 2 patients with a marked eosinophilia (> 15%) survived only seventeen and thirty-two days. There was no statistically significant difference in mean haemoglobin level or mean erythrocyte-sedimentation rate between patients surviving for more than four months and those surviving for less. These findings do not support those of Check et al;nonethe-
leucocyte-count was
9900/µ1.
6.
7. Dattner, B Am J. Syph. Gonorrh. vener. Dis. 1949, 33, 571. 8. Yo der, F W.
J Am med. Ass.1975, 232, 270
1. Check, I. J., DeMeester, T., Vardiman, 1317. 2. Snell, N J. C. Thorax (in the press).
J., Hunter, R. L Lancet, 1978,
ii,
by
an
influenza A virus similar
50% (411 boys
of
to
A/USSR/92/77
the attack-
population of 821), and the seroconversion rate of a large sample of the school was 90%. Although the uncomplicated illness was usually of only mild to moderate severity, 29 boys (7% of those infected) became much more prostrated than the others, with prolonged or recurrent pyrexia and productive cough. They all had adventitious sounds in the lungs, and 4 had pleurisy. 7 of them were rate was
out
a
yngeal, or laryngeal receptors, the upper airway cannot neglected as a possible cause of night cough in a child.
be
Departments of Ear-Nose-Throat Surgery and Human Genetics, Genetics. Free University, Amsterdam 11, Netherlands
J. WIND
further
investigated, and in every case there was marked neuand signs of consolidation in the chest X-ray. 1 boy whose sputum Streptococcus pneumoniæ was isolated
trophilia
from had a white-cell count of 30 900/ul with 88% neutrophils. The incidence and severity of respiratory complications in this outbreak was much greater than in the five outbreaks due to H3N2 and B viruses which the school has experienced since 1970. The Infirmary, Christ’s Hospital, Horsham, West Sussex
T. W. HOSKINS
RUBELLA VACCINATION
SIR,—May an American comment on the question of British rubella-vaccination policy? I agree with Dr Goldwater and colleagues’ who argue that vaccination of prepubescent girls should be continued. Although the American policy may have had some success in reducing the incidence of rubella in children, rubella continues’to occur in adolescents and young adults. Moreover, recent reports suggest that 10-20% of American adolescents previously vaccinated as children lack antibody,2 and it may therefore be preferable to vaccinate later in life. The recent introduction of RA/27-3 strain rubella vaccine in the United States may improve the duration of immunity in vaccinated infants, but additional data.are needed. Goldwater et al. urge that vaccination of adult women on contraceptives should be encouraged, but they express concern about the lack of data on risks to the fetus associated with the RA/27-3 vaccine, licensed for eight years outside the U.S. I agree with the need for more data and that pregnant women should not be vaccinated. Some comfort, however, may be taken from the fact that at least twelve seronegative pregnant women have been vaccinated with RA/27-3 and examinations of the products of conception have failed to reveal virus.3,4 Infectious Diseases Division Virus Laboratory, and and Virus Laboratory, Joseph Stokes, Jr. Research Institute, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, U.S.A.
STANLEY A. PLOTKIN
NIGHT COUGH IN CHILDREN as a cause of night of because the in children improbability of the secrecough tions entering "the larynx and trachea, the site of cough receptors". However, the cough reflex threshold is very low in children. Furthermore, there are various other receptor sites, such as the ear canal wall and the nasal and pharyngeal mucous membranes. Ear, nose, and throat surgeons and general practitioners know well that most children referred for adenoidectomy (in my patients 70-80%) have a dry night cough which disappears after surgery. While we do not know whether this cough is caused by stimulation of the nasal, phar-
SiR,-Dr Phelan5 denies postnasal drip
1. Goldwater, P. N., Quiney, J. R., Banatvala, J, E Lancet, 1978, ii, 1298. 2. Balfour, H. H., Amren, D. P. Am. J. Dis. Child. 1978, 132, 573. 3. Furukawa, T., Miyata, T., Kondo, K., Kuno, K., Isomura, S., Takakochi, T. ibid. 1969, 118, 262. 4 Bernstein, D. I., Ogra, P L. Personal communication, 1973. 5. Phelan, P. D. Lancet, 1978, ii, 1309.
SERUM ANGIOTENSIN-CONVERTING ENZYME IN SARCOIDOSIS AND OTHER DISEASES
gratified that the report of Dr Studdy and colleagues! angiotensin-converting enzyme (SACE) activity in sarcoidosis and other granulomatous disorders, using our method,2 confirms our observations and the effect of steroid therapy on SACE levels in 116 patients with sarcoidosis.3-’ We found that an increased SACE (59% of 46 recently diagnosed, untreated patients) is diagnostically useflil6 and that steroids lowered SACE in 15 of 16 patients.’ However, SACE remained above normal in a third of cases during the first year of therapy and in half of patients with progressive disease after four years of therapy.’ The correlation of SACE activity with the stage of disease was not statistically significant, although pulmonary infiltration tended to be associated with higher SACE SIR,-We
are
on serum
levels.’ Steroids had no influence on the ACE assay in vitro.8 SACE levels less than 2 standard deviations from the normal mean were seldom found.6 SACE values greater than 70 nmol/ min/ml were present in 20% (22/116) of all patients but in 30% (14/46) of newly diagnosed, ’untreated patients;6 SACE activity above 70 nmol/min/ml tended to occur in patients with sufficient disease activity to require steroid therapy.’ Activity tended to diminish with increasing duration of disease, particularly after two years.’ We have suggested that serial measurements of SACE may be useful in the clinical management of sarcoidosis, including assessment of the degree of activity, the need for steroid therapy, therapeutic result, and the
prognosis.’ Contrary
to the statement of Studdy et al. our work indithat sarcoidosis lymph-node ACE is less stable than normal,s and there is no enrichment of serum ACE, but rather it is the tissue ACE that is increased in the lung.9 Our observation of a statistically significant association between raised serum lysozyme values and SACE in sarcoidosis’O does not necessarily mean that SACE is a biochemical marker for increased macrophage activity, as stated by Studdy et al. Rather, this association suggests to us that the same cell in increased numbers is probably involved in both enzyme changes without regard to its general state of activation, since lysozyme secretion in mononuclear phagocytes does not vary with their state of activation," macrophage ACE did not increase in response to endotoxin activation in culture, 12 and ACE synthesis was specifically induced by glucocorticosteroids,8 in the absence of general activation. Whatever the pathogenesis of sarcoidosis and the increased ACE associated with it," it is clear that abundant ACE is localised in sarcoidosis epithelioid and giant cells,’’* and that mononuclear phagocytes, which
cates
1. Studdy, P., Bird, R., Geraint James, D., Sherlock, S. Lancet, 1978, ii, 133. 2. Friedland, J., Silverstein, E. Am. J. clin. Path. 1976, 66, 416. 3. Silverstein, E., Friedland, J., Lyons, H., Kitt, M. Clin. Res. 1975, 23, 352A. 4. Silverstein, E., Friedland, J., Lyons, H. A., Gourin, A. Ann. N. Y. Acad. Sci.
1976, 278, 498. 5. Silverstein, E., Friedland, J., Lyons, H. A., Gounn, A. Proc. natn. Acad. Sci. U.S.A. 1976, 73, 2137. 6. Silverstein, E., Friedland, J., Kitt, M., Lyons, H. A. Israel J. med. Sci. 1977, 7. 8. 9. 10. 11. 12. 13. 14.
13, 995. Silverstein, E., Friedland, J., Lyons, H. A. ibid. 1977, 13, 1001. Friedland, J., Setton, C., Silverstein, E. Science, 1977, 197, 64.
Cushman, D., Cheung, H. S. Biochem. biophys. Acta, 1971, 250, 261. Silverstein, E., Friedland, J., Ackerman, T. Am. J. clin. Path. 1977, 68, 219. Gordon, S., Todd, J., Cohn, Z. A. J. exp. Med. 1974, 139, 1228. Silverstein, E., Friedland, J., Setton, C. Israel J. med. Sci. 1978, 14, 314. Silverstein, E. Med. Hypoth. 1976, 2, 75. Silverstein, E., Fnedland, J., Kim, D. S., Pertschuk, L. P. Paper read at 8th international conference on Sarcoidosis (Cardiff, September, 1978).
383
normallv have a paucity of ACE and a characteristic, abundant lv sozyme secretion," are nevertheless capable of being induced to increase ACE synthesis markedly.’, 11 BB’e have recently observed normal mean levels of SACE activity in the following disorders (values in nmol/min/ml +S.D, and proportion with increased values): monocytic leukaemia. 23.2±4.0 (0/2); Paget’s disease of bone, 31.2±5.8 (0/6); silicosis, 33.1 (0/1); giant lymph-node hyperplasia, 27.6 (0/1): scleroderma, 35.0±13.0(1/11); angioimmunoblastic lymphadenopathy, 25.2±3.0 (0/2). We thank Dr F. Shai and Dr M. Guttadauria for Paget’s disease and scleroderma blood-samples and C. Setton for SACE assays.
Department of Medicine,
E. SILVERSTEIN
S U.N Y. Downstate Medical Center, Brooklyn, N.Y. 11203, U.S.A.
J. FRIEDLAND
NEUROSYPHILIS YESTERDAY AND TODAY
SIR,-Questions such as "Does adequate antisyphilitic therapy prevent neurosyphilis?", discussed by Dr Luxon and her colleagues in their interesting article entitled Neurosyphilis Today (Jan. 13, p. 90) were hotly debated earlier this century and are still unanswered. In the early 1900s many hoped, like Fournier,’ that adequate early treatment of syphilis would prevent general paralysis of the insane (G.P.I.) but statistics soon showed that a proportion of patients who were well treated by the standards of the day (i.e., with mercury) still proceeded to studies even showed that treatment shortened the G.P.I.; interval between syphilis and onset of G.p.l.,2 and a few observers in the 1920s regarded "metalues" as a consequence of "modern" treatment of syphilis.3.4 Most, however, felt that it was the inadequacy of treatment for early syphilis that might be damaging. The difficulty then, as now, was to determine what was adequate treatment in this context. It was hoped in the early days of neoarsphenamine treatment that this drug would prove a better prophylactic against neurosyphilis than mercury. However, when in 1937 I studied 863 male G.P.I. patients treated in Bonhoffer’s clinic at the Charite, Berlin, between 1925 and 1935, 1 found56 that several patients had already received what was then regarded as appropriate arsenical treatment for their syphilis. Your contributors’ finding, among their much more recent patients, that most "had not received adequate antisyphilitic therapy", also applied to the G.P.I. patients of the Charite, Berlin both between 1910 and 1924 in the mercury era2 and between 1925 and 1935 (neoarsphenamine5,6). However, in both eras cases of neurosyphilis presented despite appropriate antisyphilitic therapy; and this has been confirmed for penicillin-treated patients also.7.8 Yoder8 in 1975 asked for further investigation of the adequacy of penicillin-G treatment as recommended today. Perhaps today’s "adequate" antisyphilitic therapy may, in certain cases at least, again some
prove madequate tomorrow. L C H Alcoholism O.P. St Pancras Hospital, London NW1
(Teaching)
Centre
M. M. GLATT
SIR,- The series of cases of neurosyphilis reported on by D; Luxon and her colleagues did not include an acute meningo ascular case. A recent case prompts us to emphasise this pres entation. A
22-year-old North-African
man was
admitted
15. Friedland, J,
to
hospita
Setton, C., Silverstein, E. Biochem. biophys. Res. Comm 1978, 83, 843. 1. Fournier, J.C. Zbl Nervenheilk. 1906, 29, 617. 2. Jossman. P. Mon. Psychiat.1932/33, 84, 245.
3. Gartner. Z Hyg 1921, 92, 341. Wilm anns, KKlin Wschr. 1925, 1097, 1145. 5. Glatt, M.,M M.D thesis,Universityof Berlin, 1937. Glatt, M., M. Confneurol 1938, 1, 257.
4.
with hemiplegia of rapid onset and brachiofacial distribution. His history was not contributory except for acute enteritis a week before admission. He had no history of syphilis. The patient was febrile. No meningeal signs were observed. There was a motor and sensory deficit. Cardiac auscultation was benign. Funduscopy was normal. A computerised tomographic scan on the first day was normal. C.S.F. examination revealed a normal glucose, mild lymphocytosis, slightly increased protein; the c.s.F. was negative by direct examination and acid-fast test and on culture, and blood cultures were also negative. 2 days after the patient’s admission a positive blood test for syphilis was recorded. Antisyphilitic therapy was stated and the patient
rapidly improved. Meningovascular syphilis
may thus present as a "stroke", and we believe that an emergency test for syphilis should be done in all cases of acute-onset cerebrovascular disease, especially in young patients. Department of Internal Medicine, St Pierre University Hospital,
G. DECAUX M. SZYPER
B-1000 Brussels, Belgium
LEUCOCYTE-COUNTS AND SURVIVAL IN UNRESECTABLE LUNG CANCER
SIR,-Dr Check and colleagues’ in their series-of 51 patients, found a high correlation between the leucocyte-count assessment of the patient, and subin sequent survival-time, patients with unresectable lung cancer. I have analysed tuberculin reactivity as a predictor of survival-time in similar patients2 and took the opportunity to attempt to validate Check’s findings. After exclusion of patients with operable disease and those with oat-cell tumours, to ensure comparability with Check’s series, 59 sets of patient records were available for study. Leucocyte-counts had been done at the time of initial diagnosis (Technicon ’Hemalog 8’ automated cell counter). The mean-
performed
at
the initial
SURVIVAL OF PATIENTS WITH UNRESECTABLE LUNG CANCER
RELATIVE TO LEUCOCYTE-COUNT
rz=0.009; not significant. in patients surviving less than four months The table, constructed identically to Check’s table n, shows survival-times of patients whose leucocytecounts were greater or less than 9900/µ1. There is no association between white-cell count and survival-time on this basis, nor is there any obvious correlation when the results of individual leucocyte-counts are plotted graphically against survival-time in days. Unfortunately, only 16 patients had had full differential counts; of these, 7 patients with a neutrophilia survived less than four months, and 5 for more than four months (one for nearly two years). 2 patients with a marked eosinophilia (> 15%) survived only seventeen and thirty-two days. There was no statistically significant difference in mean haemoglobin level or mean erythrocyte-sedimentation rate between patients surviving for more than four months and those surviving for less. These findings do not support those of Check et al;nonethe-
leucocyte-count was
9900/µ1.
6.
7. Dattner, B Am J. Syph. Gonorrh. vener. Dis. 1949, 33, 571. 8. Yo der, F W.
J Am med. Ass.1975, 232, 270
1. Check, I. J., DeMeester, T., Vardiman, 1317. 2. Snell, N J. C. Thorax (in the press).
J., Hunter, R. L Lancet, 1978,
ii,