931 be used for a comparison with pineal activity in post-mortem tissue from schizophrenic patients and patients with Huntington’s chorea. Department of Pharmaceutical Chemistry, University of Bradford, Bradford BD71DP
Department of Neurological Surgery and Neurology,
Addenbrookes Hospital, Cambridge Department of Pharmacology, Medical School, University of Cambridge
E. G. S. SPOKES E. D. BIRD
K. P. MINNEMAN
INFLAMMATORY BOWEL DISEASE
SIR,-Erythema nodosum developing before clinical presentation of inflammatory bowel disease in a patient with no previous gastrointestinal symptoms is rare. An 18-year-old woman has been treated for alopecia areata since 1970. Despite steroids, ultraviolet light, and other drugs, hair loss continued; all drugs were stopped in April, 1976. She presented in June, 1977, with tender, red nodules over both legs but no other symptoms. Chest X-ray, antistreptolysin-0 titre, throat swab; and tine test were negative. Erythema nodosum was diagnosed; oral prednisolone and tetracycline were prescribed. a dermatology ward 17 days later, she had and vomiting. Examination revealed pallor, alopecia totalis, mild fever, and florid erythema nodosum. On four occasions the patient passed a small amount of loose faeces with traces of blood. Sigmoidoscopy revealed acute patchy proctitis more suggestive of Crohn’s disease than ulcerative colitis, but rectal biopsy suggested ulcerative colitis. Barium enema demonstrated ulceration of caecum and ascending, descending, and pelvic colon with features of both Crohn’s and ulcerative colitis. Further direct questioning revealed no previous symptoms suggestive of inflammatory bowel disease. Inflammatory bowel disease was diagnosed and the patient was put on intramuscular corticotrophin, sulphasalazine, and codeine phosphate. Response was slow but after 25 days she was allowed to return home on corticotrophin. She was readmitted as an emergency 4 days later having had frequent bowel actions and abdominal pain. Examination showed resolving erythema nodosum but signs of generalised peritonitis. At laparotomy, faecal peritonitis with a perforation in the transverse colon was found, necessitating a total colectomy. Histological examination of the excised colon showed typical changes of acute ulcerative colitis and no evidence of Crohn’s disease. Erythema nodosum is seen in only about 2% of cases of ulcerative colitisl.2 and it is rarer still in Crohn’s disease.3 Erythema nodosum before the first attack of ulcerative colitis is even more uncommon. In Edwards and Trulove’s series2 of 624 cases of ulcerative colitis only 3 out of the 14 patients with erythema nodosum presented in this way. Tetracycline does alter bowel flora and cause diarrhoeabut it does not usually lead to rectal blood-loss, and, though it has been implicated as a cause of pseudomembranous colitis,4 the results of investigations do not incriminate the drug in the above case. Prednisolone given for the erythema nodosum failed to prevent the onset of inflammatory bowel disease. Successful treatment of the colitis by sulphasalazine, steroids, or surgery will be followed by resolution of the erythema nodosum,3.5 as happened in this patient. Thus where no cause is found for erythema nodosum by the usual screening tests it
On admission to
nausea
2. 3.
Gastroenterology Department, Broadgreen Hospital, Liverpool
even
B. D. LINAKER
J. A. SMITH
ERYTHEMA NODOSUM PRESENTING BEFORE
1.
may be useful to search for inflammatory bowel disease when the patient has no gastrointestinal symptoms.
Goligher, J. C., de Dombal, F. T., Watts, J. McK., Watkinson, Colitis; p.136. London, 1968.
G. Ulcerative
Edwards, F., Trulove, S. C. Gut, 1964, 5, 1. Jacobs, W. H. Gastroenterology, 1959, 37, 286. 4. Goodman, L. S., Gilman, A. The pharmacological Basis of Therapeutics; p. 1184. New York, 1975. 5. Samitz, M. H., Greenberg, M. S. Gastroenterology, 1951, 19, 478.
&bgr;-THROMBOGLOBULIN RELEASE FROM HUMAN PLATELETS AFTER IN VIVO ULTRASOUND IRRADIATION
SIR,-Our in-vitro studies have shown that therapeutic intensities of ultrasound set up hydrodynamic forces which damage platelets,I.2 releasing the contents of their secretory granules,1,3 inducing their aggregation4 and decreasing recalcification time.5 In vivo these forces induce platelet aggregation and thrombus formation within the intact vascular system of small mammals.6 The detection of platelet aggregates within the microcirculatory bed of the guinea pig pinna irradiated invivo with a commercial therapeutic device’ prompted this study of the effect of ultrasound on human platelets in vivo. Blood was drawn from 10 normal adult male volunteers, none of whom had taken drugs known to affect platelets during the previous 7 days. A 19G butterfly cannula was inserted into the median cubital vein so that the tip of the needle pointed upstream-i.e., towards the hand. 2-5 ml volumes of blood, collected in plastic tubes containing iced ethylenediaminetetra-acetate/theophylline to anticoagulate the blood and render the platelets functionally inert, were stored at 0-4C and centrifuged for 30 min at 4°C. j-thromboglobutin ((3-T.G.), a platelet-specific protein liberated with secretory granule components,8 was measured in the supernatant with a radioimmunoassay kit from the Radiochemical Centre, Amersham. MEAN
(±S.D.) PLASMA 13-T.G. (ng/ml) IN BLOOD IRRADIATED IN VIVO WITH ULTRASOUND
n=19 (three good samples volunteer).
were not
obtained from
one arm
of
one
The first 1 ml of blood was discarded, while the transducer face of a ’Sonacel Multiphon’ (Rank Stanley Cox) ultrasonic therapy device was acoustically coupled to the skin overlying the vein just upstream of the needle tip. The transducer was not activated while the first 2.5 ml control sample was collected, A further 1 ml of blood was discarded while the transducer’s power was increased from zero to the maximum tolerated by the volunteer (this level was kept low by the proximity of bony tissue). A frequency of 0.75 MHz was used. A second 2.5 ml sample (test) was then collected. The ultrasonic generator was switched off and a further 1 ml of blood discarded before a second control 2.5 ml sample was collected. Both arms of each volunteer were sampled in this way. Exposure was for 15-35 s (the time taken to collect the 2.5 ml test sample.) A single blood cell remained in the region of maximum intensity for about 1 s, assuming venous blood flows at 0.2
ml/s. 1. Williams, A. R, J. acoust. Soc. Am. 1974, 56, 1640. 2. Williams, A. R., Sykes, S. M., O’Brien, W. D. Ultrasound Med. Biol. 1976,
2, 311. 3. Williams, A. R., Chater, B. V., Allen, K. A., Sherwood, M. R., Sanderson, J. H. Unpublished. 4. Chater, B. V., Williams, A. R. Thrombo. Hœmostas. (in the press). 5. Williams, A. R., O’Brien, W. D., Coller, B. S. Ultrasound Med. Biol. 1976,
2, 113. 6. Williams, A. R. ibid. (in the press). 7. Zarod, A. P., Williams, A. R. Lancet, 1977, i, 1266. 8. Ludlam, C. A., Moore, S., Bolton, A. E., Pepper, D. S., Cash, bosis Res. 1975, 6, 543.
J. D.
Throm-
Department of Neurological Surgery and Neurology,
Addenbrookes Hospital, Cambridge Department of Pharmacology, Medical School, University of Cambridge
E. G. S. SPOKES E. D. BIRD
K. P. MINNEMAN
INFLAMMATORY BOWEL DISEASE
SIR,-Erythema nodosum developing before clinical presentation of inflammatory bowel disease in a patient with no previous gastrointestinal symptoms is rare. An 18-year-old woman has been treated for alopecia areata since 1970. Despite steroids, ultraviolet light, and other drugs, hair loss continued; all drugs were stopped in April, 1976. She presented in June, 1977, with tender, red nodules over both legs but no other symptoms. Chest X-ray, antistreptolysin-0 titre, throat swab; and tine test were negative. Erythema nodosum was diagnosed; oral prednisolone and tetracycline were prescribed. a dermatology ward 17 days later, she had and vomiting. Examination revealed pallor, alopecia totalis, mild fever, and florid erythema nodosum. On four occasions the patient passed a small amount of loose faeces with traces of blood. Sigmoidoscopy revealed acute patchy proctitis more suggestive of Crohn’s disease than ulcerative colitis, but rectal biopsy suggested ulcerative colitis. Barium enema demonstrated ulceration of caecum and ascending, descending, and pelvic colon with features of both Crohn’s and ulcerative colitis. Further direct questioning revealed no previous symptoms suggestive of inflammatory bowel disease. Inflammatory bowel disease was diagnosed and the patient was put on intramuscular corticotrophin, sulphasalazine, and codeine phosphate. Response was slow but after 25 days she was allowed to return home on corticotrophin. She was readmitted as an emergency 4 days later having had frequent bowel actions and abdominal pain. Examination showed resolving erythema nodosum but signs of generalised peritonitis. At laparotomy, faecal peritonitis with a perforation in the transverse colon was found, necessitating a total colectomy. Histological examination of the excised colon showed typical changes of acute ulcerative colitis and no evidence of Crohn’s disease. Erythema nodosum is seen in only about 2% of cases of ulcerative colitisl.2 and it is rarer still in Crohn’s disease.3 Erythema nodosum before the first attack of ulcerative colitis is even more uncommon. In Edwards and Trulove’s series2 of 624 cases of ulcerative colitis only 3 out of the 14 patients with erythema nodosum presented in this way. Tetracycline does alter bowel flora and cause diarrhoeabut it does not usually lead to rectal blood-loss, and, though it has been implicated as a cause of pseudomembranous colitis,4 the results of investigations do not incriminate the drug in the above case. Prednisolone given for the erythema nodosum failed to prevent the onset of inflammatory bowel disease. Successful treatment of the colitis by sulphasalazine, steroids, or surgery will be followed by resolution of the erythema nodosum,3.5 as happened in this patient. Thus where no cause is found for erythema nodosum by the usual screening tests it
On admission to
nausea
2. 3.
Gastroenterology Department, Broadgreen Hospital, Liverpool
even
B. D. LINAKER
J. A. SMITH
ERYTHEMA NODOSUM PRESENTING BEFORE
1.
may be useful to search for inflammatory bowel disease when the patient has no gastrointestinal symptoms.
Goligher, J. C., de Dombal, F. T., Watts, J. McK., Watkinson, Colitis; p.136. London, 1968.
G. Ulcerative
Edwards, F., Trulove, S. C. Gut, 1964, 5, 1. Jacobs, W. H. Gastroenterology, 1959, 37, 286. 4. Goodman, L. S., Gilman, A. The pharmacological Basis of Therapeutics; p. 1184. New York, 1975. 5. Samitz, M. H., Greenberg, M. S. Gastroenterology, 1951, 19, 478.
&bgr;-THROMBOGLOBULIN RELEASE FROM HUMAN PLATELETS AFTER IN VIVO ULTRASOUND IRRADIATION
SIR,-Our in-vitro studies have shown that therapeutic intensities of ultrasound set up hydrodynamic forces which damage platelets,I.2 releasing the contents of their secretory granules,1,3 inducing their aggregation4 and decreasing recalcification time.5 In vivo these forces induce platelet aggregation and thrombus formation within the intact vascular system of small mammals.6 The detection of platelet aggregates within the microcirculatory bed of the guinea pig pinna irradiated invivo with a commercial therapeutic device’ prompted this study of the effect of ultrasound on human platelets in vivo. Blood was drawn from 10 normal adult male volunteers, none of whom had taken drugs known to affect platelets during the previous 7 days. A 19G butterfly cannula was inserted into the median cubital vein so that the tip of the needle pointed upstream-i.e., towards the hand. 2-5 ml volumes of blood, collected in plastic tubes containing iced ethylenediaminetetra-acetate/theophylline to anticoagulate the blood and render the platelets functionally inert, were stored at 0-4C and centrifuged for 30 min at 4°C. j-thromboglobutin ((3-T.G.), a platelet-specific protein liberated with secretory granule components,8 was measured in the supernatant with a radioimmunoassay kit from the Radiochemical Centre, Amersham. MEAN
(±S.D.) PLASMA 13-T.G. (ng/ml) IN BLOOD IRRADIATED IN VIVO WITH ULTRASOUND
n=19 (three good samples volunteer).
were not
obtained from
one arm
of
one
The first 1 ml of blood was discarded, while the transducer face of a ’Sonacel Multiphon’ (Rank Stanley Cox) ultrasonic therapy device was acoustically coupled to the skin overlying the vein just upstream of the needle tip. The transducer was not activated while the first 2.5 ml control sample was collected, A further 1 ml of blood was discarded while the transducer’s power was increased from zero to the maximum tolerated by the volunteer (this level was kept low by the proximity of bony tissue). A frequency of 0.75 MHz was used. A second 2.5 ml sample (test) was then collected. The ultrasonic generator was switched off and a further 1 ml of blood discarded before a second control 2.5 ml sample was collected. Both arms of each volunteer were sampled in this way. Exposure was for 15-35 s (the time taken to collect the 2.5 ml test sample.) A single blood cell remained in the region of maximum intensity for about 1 s, assuming venous blood flows at 0.2
ml/s. 1. Williams, A. R, J. acoust. Soc. Am. 1974, 56, 1640. 2. Williams, A. R., Sykes, S. M., O’Brien, W. D. Ultrasound Med. Biol. 1976,
2, 311. 3. Williams, A. R., Chater, B. V., Allen, K. A., Sherwood, M. R., Sanderson, J. H. Unpublished. 4. Chater, B. V., Williams, A. R. Thrombo. Hœmostas. (in the press). 5. Williams, A. R., O’Brien, W. D., Coller, B. S. Ultrasound Med. Biol. 1976,
2, 113. 6. Williams, A. R. ibid. (in the press). 7. Zarod, A. P., Williams, A. R. Lancet, 1977, i, 1266. 8. Ludlam, C. A., Moore, S., Bolton, A. E., Pepper, D. S., Cash, bosis Res. 1975, 6, 543.
J. D.
Throm-
