- Email: [email protected]
INTERFERON IN TREATMENT OF SUBACUTE SCLEROSING PANENCEPHALITIS
1059
hypothermia caused by pentobarbitone.4Barbiturates are widely used in the treatment of seizures and the patient had received phenobarbitone. Giving TRH to this patient may have antagonised the effect of the barbiturate, resulting in the epileptic attacks. TRH should be administered carefully to patients with epilepsy. Department of Psychiatry and Neurology, Kobe University School of Medicine,
KIYOSHI MAEDA KENJI TANIMOTO
Kobe 650, Japan
RAPID DESENSITISATION FOR DESFERRIOXAMINE ANAPHYLACTIC REACTION
SIR,-Desferrioxamine
mesylate
(’Desferal’)
given
by
infusion is an effective iron chelator.I Desferrioxamine (DF) is still the only agent available with the potential to prevent and treat the life-threatening complications or iron overload in susceptible individuals. Allergic reactions to DF are rare and difficult to manage. We report an effective desensitisation programme for a patient with a history of an anaphylactic reaction subcutaneous
to
DF.2
The patient, reportedis a 24-year-old Italian man with beta-thalassaemia major. He had had a splenectomy at age 3 because of hypersplenism and began receiving frequent transfusions at age 6. At that time, he also received intermittent intramuscular injections of DF. In 1964, at the age of 8, he had a severe local reaction described as marked swelling and erythema at the site of an i.m. injection of 500 mg DF. The iron chelation was stopped. His transfusion requirement continued and haemochromatosis developed. In 1976, desensitisation was once again attempted by weekly injection of increasing concentrations of DF intradermally. A severe local reaction occurred at a dose of 083 mg and the trial was discontinued. In 1977, desensitisation was again attempted; 30 min after receiving an intradermal injection of 166 mg DF he had an anaphylactic reaction characterised by generalised itching, back pain, tachycardia, wheezing, and cyanosis. He was treated with adrenaline, hydrocortisone, and diphenhydramine with complete resolution of the symptoms. After 1977, he continued to require transfusions of two units of packed red blood cells every 4-6 weeks. His symptoms of haemochromatosis have progressed with the development of congestive heart failure and pancreatic endocrine and exocrine insufficiency. In May, 1980, he was admitted to the New England Medical Center Hospital for the third attempt at desensitisation. Because of the risk of anaphylaxis pretreatment was started with prednisone 50 mg i.v. every 6 h and diphenhydramine 50 mg by mouth every 6 h from 18 h before desensitisation. Rapid desensitisation was accomplished by infusing increasing concentrations ofDF intravenously. The patient was admitted to the intensive care unit and desensitisation was started with a solution of 1/10 000 000 of the anticipated final infusion concentrations:
previously
Each bottle was infused
over
20-30 min.
During the infusion of
bottles 2 and 5 the patient had two reactions characterised by chest and back
pain, tachycardia, and mild shortness of breath
but
without wheezing. No hypotension occurred. The infusion
was
stopped and 50 mg i.v. diphenhydramine was given. The symptoms
resolved and the infusions were restarted and completed without further incident. At the conclusion of the rapid desensitisation phase, the patient was immediately started on a 24 h continuous s.c. infusion of 1500 mg DF (pump model no AS 3B, Autosyringe Inc. Hooksett, New Hampshire). Steroids were continued at the same dose for a further 24 h and then stopped. The s.c. infusion ofDF was then tapered as follows:
During the
18 h
infusion of DF the patient had a generalised
erythematous pruritic rash which resolved with 50 mg oral diphenhydramine. The patient was discharged home and has continued to receive 1500 mg DF daily by s.c. infusion. The infusion time has been reduced to 10 h per day with no untoward reactions. Intermittent mild erythematous reactions at the injection site have been treated with 1% hydrocortisone ointment. He is now excreting 85 mg urinary iron in 24 hours, on 1500 mg DF daily. The case represents the first successful rapid i.v. desensitisation in a patient with DF anaphylactic sensitivity. While the mechanism of anaphylactic sensitivity in this patient is not clear, we decided to follow the protocol usually recommended for penicillin-allergic individuals (i.e., rapid i.v. desensitisation3). The pathogenesis of symptoms related to DF sensitivity include several possibilities: the patient may have IgE antibody directed against DF itself; or the patient may have IgE antibody directed against microbial impurities related to the Streptococcus pilosis source ofDF; or direct release of histamine by mast cells and basophils may occur in the absence of reaginic antibody directed against DF or related products. In light of this last possibility, and since the mechanism of sensitivity to DF in this
patient was unknown, pretreatment with steroids and diphenhydramine was administered in a manner consistent with the published experience in patients with iodinated contrast dye 4 sensitivity and direct non-IgE mediated histamine release.4 This case highlights the utility of the rapid i.v. desensitisation approach in the treatment of marked sensitivity to a life-sustaining drug, where no other therapy is available. Divisions of Hematology-Oncology and Allergy, Department of Medicine, Tufts-New England Medical Center,
Boston, Massachusetts 02111, U.S.A.
KENNETH B. MILLER LANNY J. ROSENWASSER JO-ANNE M. BESSETTE DENNIS J. BEER ROSS E. ROCKLIN
INTERFERON IN TREATMENT OF SUBACUTE SCLEROSING PANENCEPHALITIS
SIR,-Subacute sclerosing panencephalitis (SSPE) is
a
rare,
progressive and fatal inflammatory disease of the central nervous system associated with persistent measles virus inflection.5 Normally, the clinical course is divided into three stages-subtle intellectual deterioration, followed by neurological signs, and ultimately a vegetative state. There is, however, great variation in the duration of the disease and remissions may occur. 80% of patients die within two years of onset and 10% die from fulminant encephalitis within three months.6 In a further 10% of cases the disease lasts from five to ten years and apparent recovery has been reported? ,’8 SSPE is diagnosed on a combination of characteristic clinical, electrophysiological, pathological, immunological, and virological findings. 3. Van Arsdel PP Jr. Adverse drug reactions. In: Middleton E Jr, Need CE, Ellis
EF, eds. C. V. Mosby, 1978: 1155-56. 4. Zweiman B, Mishkin MM, Hildreth HA. An approach to the performance of contrast studies in contrast material reactive persons. Ann Intern Med 1975; 83: 150. 5. ter Meulen V, Katz M. Slow virus infections of the central nervous system Heidelberg.
Allergy, principles and practice. St Louis:
Prange AJ, Breese GR, Cott JM, Martin BM, Cooper BR, Wilson IC, Plotnikoff NP. Thyrotropin releasing hormone: Antagonism of pentobarbital in rodents. Life Sci 1974; 14:
447-55.
Propper RD, Cooper B, Rufo RR, Neinhuis AW, Anderson WF, Bunn HF, Rosenthal A, and Nathan DG Continuous subcutaneous administration of desferrioxamine in patients with iron overload. N Engl J Med 1979; 297: 418-23. Authanosiou A, Shepp MA, Nechles TF. Anaphylactic reaction to desferrioxamine. Lancet 1977; ii: 616.
Springer Verlag,
1977
6. Gilden DH, Rorke LB, Tanaka R. Acute SSPE Arch Neurol 1975; 32: 644-46. 7. Cobb WA, Hughes JAM Non-fatal subacute sclerosing leucoencephalitis. JNeurol
Neurosurg Psychiat 1968; 31: 115-23 8. Risk WS, Haddad FS, Chemali R. Substantial spontaneous long-term improvement in subacute sclerosing panencephalitis. Arch Neurol 1978; 35: 494-502.
1060 A variety of treatments have been tried, all without proven effect. Claims of benefit have been made, notably for transfer factor but we have found transfer factor therapy to be useless in SSPE, a conclusion reached by others.9 We recently treated three children with interferon-two boys aged 6 and 7 and a girl of 13. All three cases had typical SSPE with the characteristic clinical course and EEG findings, high serum and CSF titres of antimeasles antibodies, increased IgG in the CSF, and conspicuous CSF oligoclonal bands on electrophoresis. Both boys were at the end of the second stage; the girl was still in the first stage, but neurological signs were developing. All three children had had a thymectomy and the girl had also had three 2 litre plasma
exchanges.10 Human leucocyte interferon (IFN a type P-IF-A) was purchased from a Danish laboratory. The interferon had been produced by in vitro induction in human buffy coat leucocytes using Sendai virus. The activity of the semi-purified product was 3 x 106 IU/ml, assayed by plaque reduction of vesicular stomatitis virus in human amniotic cells. The first boy was given 25 daily intramuscular injections of 1 ml. The second boy had 90 similar intramuscular injections and the girl was given 20 daily doses. No clinical improvement was detected. The first boy deteriorated rapidly and died after the last injection. There were no changes in EEGs, in serum or CSF titres of antimeasles antibodies, or in CSF IgG or oligoclonal bands. The titres of antimeasles antibodies increased in the second boy after therapy. The girl was given an additional 12 x 106 IU of interferon intrathecally over 3 days. This led to a sterile meningitis (7000 leucocytes/1 CSF) accompanied by fever, but no clinical benefit. Mild rises in temperature were associated with the intramuscular injections in all the children and usually occurred 3-4 h after the injections. No other side effects were noted. In coded samples of CSF from these patients, from other patients with SSPE, and from patients with multiple sclerosis, no interferon activity was detected except in one specimen of CSF containing 10 IU/ml from the child who had had 90 injections of interferon. These results suggest that partly purified human leucocyte interferon is of no value in SSPE. Department of Neurology, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF
SIR,-There are two reasons for supposing that human chorionic gonadotrophin (HCG) localisation in testicular teratomas might be of prognostic significance. Firstly, the serum level of HCG is an established marker of the course of the disease in patients with testicular germ cell tumours.1 Secondly, HCG has been localised in the syncytial element of cytotrophoblast and trophoblast a syncytiotrophoblast forming villi, component of some teratomas which are associated with a high mortality.3 However, trophoblast is found in less than 5% ofteratomas.3 The major and only other site of HCG production is isolated syncytia,2which have been reported in haematoxylin and eosin stained sections in 40% of teratomas and were found to have no significant effect on the outcome of the disease.3Heyderman,2using an immunoperoxidase technique, isolated syncytia containing HCG in 54% of teratomas, and she suggested that their presence adversely affected prognosis. Summary of
the conference Arch Neurol
1975, 32: 489-93. 10. Sell KW, Ahmed A, Bailey DW. Attempts to remove an inhibitor of cellular immunity found in plasma and spinal fluid in patients with SSPE. Arch Neurol 1975; 32: 502-03.
Norgaard-Pedersen B. Clinical use of AFP and HCG in testicular tumours of germ-cell origin. Lancet 1978, ii: 1042. 2. Heyderman E. Multiple tissue markers in human malignant testicular tumours. Scand J Immunol 1978; 8: suppl 8, 119-26 3. Pugh RCB, Cameron, KM. Teratoma. In: Pugh RCB ed. Pathology of the testis. 1.
Oxford: Blackwell, 1976; 199-244.
While there was considerable variation in the amount of tissue sampled from each tumour, no significant difference was found in the incidence of (3-HCG positive neoplasms according to the number of blocks examined (1-5). All patients who succumbed to their disease died within 4 years, and the survivors, all free of tumour, have been followed-up from 3 to 18 years (average 9-6 years). Of the 58 patients with tumours containing HCG positive cells 36 (62%) are alive compared with 22 out of 31 (71%) without this feature; this difference is not significant. Nor could a quantitative relationship be demonstrated between HCG positive cells and survival, contrary to a previous suggestion made by one of
(61%).
US.5 It therefore appears that the identification of HCG positive cells has no place in a prognostic classification of MTI (PI) neoplasms. This supports the view that increase serum HCG predicts the course of the disease by reflecting tumour bulk, rather than indicating an inherent difference in the degree of malignancy conferred by HCG production. Prof. K. Bagshawe kindly supplied the anti-human (3-HCG antibody, and the 1st International reference preparation of chorionic gonotrophin, 0-subunit human (batch 75/551) was given by the World Health Organisation.
CONSTANCE PARKINSO Department of Histopathology, Institute of Urology, St Paul’s Hospital, London WC2 9AE
PETER O. BEHAN
HCG LOCALISATION OF NO PROGNOSTIC VALUE IN TESTICULAR TERATOMA
9. Lennette EH. Cellular immunity and SSPE.
To establish the incidence and prognostic value of HCGcontaining syncytia, early stage teratomas of the same grade were selected. All intermediate malignant teratomas confined to the testis (MTI pathological stage PI) from the Testicular Tumour Panel3 files were re-examined. From 89 neoplasms adjacent sections were for P-HCG using an stained with haematoxylin and eosin indirect immunoperoxidase technique.and HCG positive cells were present in 58 tumours (65%), and were associated with undifferentiated tisue or yolk-sac elements in 54
JOHN R. W. MASTERS ANU KRISHNASWAMY DAVID N. BUTCHER
FAILURE OF ANTILYMPHOCYTIC GLOBULIN IN ACUTE ULCERATIVE COLITIS
SIR,-Sometimes a patient with severe acute ulcerative colitis does not respond to medical treatment and colectomy is needed. There is evidence that cytotoxic lymphocytes may be involved in the pathogenesis of ulcerative colitis, and it has been suggested that antilymphocytic globulin (ALG) might be useful in this disease. 2,3 We have done a small trial of ALG to see if the remission rate of acute ulcerative colitis, in patients receiving corticosteroids, was improved by adding ALG. The study was approved by the hospital’s ethical committee, and patients gave their informed consent. None had evidence of allergy to equine ALG on skin testing. The patients had all had a severe acute attack of ulcerative colitis requiring treatment in hospital. Patients aged less than 18 years, pregnant women, those with a history of allergy to horse serum, and patients who had been taking azathioprine during the previous 8 weeks were not studied. Equine anti-human-lymphocyte globulin was supplied by HoechstBehringwerke. Neville AM. Shorter immunoperoxidase technique for the demonstration of carcinoembryonic antigen and other cell products J Clin Pathol
4. Heyderman E,
1977, 30: 138-40. C, Beilby JOW. Testicular germ-cell tumours- should current classification be revised? Invest Cell Pathol 1980; 3: 135-40. German-Lluch JR, Begent RHJ, Bagshawe, KD. Tumour-marker levels and prognosis in malignant teratoma of the testis. Br J Cancer 1980; 42: 850-855
5. Parkinson 6.
BJ, Alpert E. Inflammatory bowel disease: Study of cell mediated cytotoxicity for isolated human colonic epithelial cells. Gut 1980; 21: 353-59. 2. Oberling F, Hiebel G. Intravenous ALS in the treatment of severe rectocolitis N Eng. J Med 1971; 285: 409-10. 3. Marmont A, Giordano D, Santini G, Damasio E, Carella M, Bacigalupo A The treatment of autoimmune blood diseases with antilymphocyte globulin Postgrad Med J1976; 52: suppl 5: 139-46. 1. Kemler
hypothermia caused by pentobarbitone.4Barbiturates are widely used in the treatment of seizures and the patient had received phenobarbitone. Giving TRH to this patient may have antagonised the effect of the barbiturate, resulting in the epileptic attacks. TRH should be administered carefully to patients with epilepsy. Department of Psychiatry and Neurology, Kobe University School of Medicine,
KIYOSHI MAEDA KENJI TANIMOTO
Kobe 650, Japan
RAPID DESENSITISATION FOR DESFERRIOXAMINE ANAPHYLACTIC REACTION
SIR,-Desferrioxamine
mesylate
(’Desferal’)
given
by
infusion is an effective iron chelator.I Desferrioxamine (DF) is still the only agent available with the potential to prevent and treat the life-threatening complications or iron overload in susceptible individuals. Allergic reactions to DF are rare and difficult to manage. We report an effective desensitisation programme for a patient with a history of an anaphylactic reaction subcutaneous
to
DF.2
The patient, reportedis a 24-year-old Italian man with beta-thalassaemia major. He had had a splenectomy at age 3 because of hypersplenism and began receiving frequent transfusions at age 6. At that time, he also received intermittent intramuscular injections of DF. In 1964, at the age of 8, he had a severe local reaction described as marked swelling and erythema at the site of an i.m. injection of 500 mg DF. The iron chelation was stopped. His transfusion requirement continued and haemochromatosis developed. In 1976, desensitisation was once again attempted by weekly injection of increasing concentrations of DF intradermally. A severe local reaction occurred at a dose of 083 mg and the trial was discontinued. In 1977, desensitisation was again attempted; 30 min after receiving an intradermal injection of 166 mg DF he had an anaphylactic reaction characterised by generalised itching, back pain, tachycardia, wheezing, and cyanosis. He was treated with adrenaline, hydrocortisone, and diphenhydramine with complete resolution of the symptoms. After 1977, he continued to require transfusions of two units of packed red blood cells every 4-6 weeks. His symptoms of haemochromatosis have progressed with the development of congestive heart failure and pancreatic endocrine and exocrine insufficiency. In May, 1980, he was admitted to the New England Medical Center Hospital for the third attempt at desensitisation. Because of the risk of anaphylaxis pretreatment was started with prednisone 50 mg i.v. every 6 h and diphenhydramine 50 mg by mouth every 6 h from 18 h before desensitisation. Rapid desensitisation was accomplished by infusing increasing concentrations ofDF intravenously. The patient was admitted to the intensive care unit and desensitisation was started with a solution of 1/10 000 000 of the anticipated final infusion concentrations:
previously
Each bottle was infused
over
20-30 min.
During the infusion of
bottles 2 and 5 the patient had two reactions characterised by chest and back
pain, tachycardia, and mild shortness of breath
but
without wheezing. No hypotension occurred. The infusion
was
stopped and 50 mg i.v. diphenhydramine was given. The symptoms
resolved and the infusions were restarted and completed without further incident. At the conclusion of the rapid desensitisation phase, the patient was immediately started on a 24 h continuous s.c. infusion of 1500 mg DF (pump model no AS 3B, Autosyringe Inc. Hooksett, New Hampshire). Steroids were continued at the same dose for a further 24 h and then stopped. The s.c. infusion ofDF was then tapered as follows:
During the
18 h
infusion of DF the patient had a generalised
erythematous pruritic rash which resolved with 50 mg oral diphenhydramine. The patient was discharged home and has continued to receive 1500 mg DF daily by s.c. infusion. The infusion time has been reduced to 10 h per day with no untoward reactions. Intermittent mild erythematous reactions at the injection site have been treated with 1% hydrocortisone ointment. He is now excreting 85 mg urinary iron in 24 hours, on 1500 mg DF daily. The case represents the first successful rapid i.v. desensitisation in a patient with DF anaphylactic sensitivity. While the mechanism of anaphylactic sensitivity in this patient is not clear, we decided to follow the protocol usually recommended for penicillin-allergic individuals (i.e., rapid i.v. desensitisation3). The pathogenesis of symptoms related to DF sensitivity include several possibilities: the patient may have IgE antibody directed against DF itself; or the patient may have IgE antibody directed against microbial impurities related to the Streptococcus pilosis source ofDF; or direct release of histamine by mast cells and basophils may occur in the absence of reaginic antibody directed against DF or related products. In light of this last possibility, and since the mechanism of sensitivity to DF in this
patient was unknown, pretreatment with steroids and diphenhydramine was administered in a manner consistent with the published experience in patients with iodinated contrast dye 4 sensitivity and direct non-IgE mediated histamine release.4 This case highlights the utility of the rapid i.v. desensitisation approach in the treatment of marked sensitivity to a life-sustaining drug, where no other therapy is available. Divisions of Hematology-Oncology and Allergy, Department of Medicine, Tufts-New England Medical Center,
Boston, Massachusetts 02111, U.S.A.
KENNETH B. MILLER LANNY J. ROSENWASSER JO-ANNE M. BESSETTE DENNIS J. BEER ROSS E. ROCKLIN
INTERFERON IN TREATMENT OF SUBACUTE SCLEROSING PANENCEPHALITIS
SIR,-Subacute sclerosing panencephalitis (SSPE) is
a
rare,
progressive and fatal inflammatory disease of the central nervous system associated with persistent measles virus inflection.5 Normally, the clinical course is divided into three stages-subtle intellectual deterioration, followed by neurological signs, and ultimately a vegetative state. There is, however, great variation in the duration of the disease and remissions may occur. 80% of patients die within two years of onset and 10% die from fulminant encephalitis within three months.6 In a further 10% of cases the disease lasts from five to ten years and apparent recovery has been reported? ,’8 SSPE is diagnosed on a combination of characteristic clinical, electrophysiological, pathological, immunological, and virological findings. 3. Van Arsdel PP Jr. Adverse drug reactions. In: Middleton E Jr, Need CE, Ellis
EF, eds. C. V. Mosby, 1978: 1155-56. 4. Zweiman B, Mishkin MM, Hildreth HA. An approach to the performance of contrast studies in contrast material reactive persons. Ann Intern Med 1975; 83: 150. 5. ter Meulen V, Katz M. Slow virus infections of the central nervous system Heidelberg.
Allergy, principles and practice. St Louis:
Prange AJ, Breese GR, Cott JM, Martin BM, Cooper BR, Wilson IC, Plotnikoff NP. Thyrotropin releasing hormone: Antagonism of pentobarbital in rodents. Life Sci 1974; 14:
447-55.
Propper RD, Cooper B, Rufo RR, Neinhuis AW, Anderson WF, Bunn HF, Rosenthal A, and Nathan DG Continuous subcutaneous administration of desferrioxamine in patients with iron overload. N Engl J Med 1979; 297: 418-23. Authanosiou A, Shepp MA, Nechles TF. Anaphylactic reaction to desferrioxamine. Lancet 1977; ii: 616.
Springer Verlag,
1977
6. Gilden DH, Rorke LB, Tanaka R. Acute SSPE Arch Neurol 1975; 32: 644-46. 7. Cobb WA, Hughes JAM Non-fatal subacute sclerosing leucoencephalitis. JNeurol
Neurosurg Psychiat 1968; 31: 115-23 8. Risk WS, Haddad FS, Chemali R. Substantial spontaneous long-term improvement in subacute sclerosing panencephalitis. Arch Neurol 1978; 35: 494-502.
1060 A variety of treatments have been tried, all without proven effect. Claims of benefit have been made, notably for transfer factor but we have found transfer factor therapy to be useless in SSPE, a conclusion reached by others.9 We recently treated three children with interferon-two boys aged 6 and 7 and a girl of 13. All three cases had typical SSPE with the characteristic clinical course and EEG findings, high serum and CSF titres of antimeasles antibodies, increased IgG in the CSF, and conspicuous CSF oligoclonal bands on electrophoresis. Both boys were at the end of the second stage; the girl was still in the first stage, but neurological signs were developing. All three children had had a thymectomy and the girl had also had three 2 litre plasma
exchanges.10 Human leucocyte interferon (IFN a type P-IF-A) was purchased from a Danish laboratory. The interferon had been produced by in vitro induction in human buffy coat leucocytes using Sendai virus. The activity of the semi-purified product was 3 x 106 IU/ml, assayed by plaque reduction of vesicular stomatitis virus in human amniotic cells. The first boy was given 25 daily intramuscular injections of 1 ml. The second boy had 90 similar intramuscular injections and the girl was given 20 daily doses. No clinical improvement was detected. The first boy deteriorated rapidly and died after the last injection. There were no changes in EEGs, in serum or CSF titres of antimeasles antibodies, or in CSF IgG or oligoclonal bands. The titres of antimeasles antibodies increased in the second boy after therapy. The girl was given an additional 12 x 106 IU of interferon intrathecally over 3 days. This led to a sterile meningitis (7000 leucocytes/1 CSF) accompanied by fever, but no clinical benefit. Mild rises in temperature were associated with the intramuscular injections in all the children and usually occurred 3-4 h after the injections. No other side effects were noted. In coded samples of CSF from these patients, from other patients with SSPE, and from patients with multiple sclerosis, no interferon activity was detected except in one specimen of CSF containing 10 IU/ml from the child who had had 90 injections of interferon. These results suggest that partly purified human leucocyte interferon is of no value in SSPE. Department of Neurology, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF
SIR,-There are two reasons for supposing that human chorionic gonadotrophin (HCG) localisation in testicular teratomas might be of prognostic significance. Firstly, the serum level of HCG is an established marker of the course of the disease in patients with testicular germ cell tumours.1 Secondly, HCG has been localised in the syncytial element of cytotrophoblast and trophoblast a syncytiotrophoblast forming villi, component of some teratomas which are associated with a high mortality.3 However, trophoblast is found in less than 5% ofteratomas.3 The major and only other site of HCG production is isolated syncytia,2which have been reported in haematoxylin and eosin stained sections in 40% of teratomas and were found to have no significant effect on the outcome of the disease.3Heyderman,2using an immunoperoxidase technique, isolated syncytia containing HCG in 54% of teratomas, and she suggested that their presence adversely affected prognosis. Summary of
the conference Arch Neurol
1975, 32: 489-93. 10. Sell KW, Ahmed A, Bailey DW. Attempts to remove an inhibitor of cellular immunity found in plasma and spinal fluid in patients with SSPE. Arch Neurol 1975; 32: 502-03.
Norgaard-Pedersen B. Clinical use of AFP and HCG in testicular tumours of germ-cell origin. Lancet 1978, ii: 1042. 2. Heyderman E. Multiple tissue markers in human malignant testicular tumours. Scand J Immunol 1978; 8: suppl 8, 119-26 3. Pugh RCB, Cameron, KM. Teratoma. In: Pugh RCB ed. Pathology of the testis. 1.
Oxford: Blackwell, 1976; 199-244.
While there was considerable variation in the amount of tissue sampled from each tumour, no significant difference was found in the incidence of (3-HCG positive neoplasms according to the number of blocks examined (1-5). All patients who succumbed to their disease died within 4 years, and the survivors, all free of tumour, have been followed-up from 3 to 18 years (average 9-6 years). Of the 58 patients with tumours containing HCG positive cells 36 (62%) are alive compared with 22 out of 31 (71%) without this feature; this difference is not significant. Nor could a quantitative relationship be demonstrated between HCG positive cells and survival, contrary to a previous suggestion made by one of
(61%).
US.5 It therefore appears that the identification of HCG positive cells has no place in a prognostic classification of MTI (PI) neoplasms. This supports the view that increase serum HCG predicts the course of the disease by reflecting tumour bulk, rather than indicating an inherent difference in the degree of malignancy conferred by HCG production. Prof. K. Bagshawe kindly supplied the anti-human (3-HCG antibody, and the 1st International reference preparation of chorionic gonotrophin, 0-subunit human (batch 75/551) was given by the World Health Organisation.
CONSTANCE PARKINSO Department of Histopathology, Institute of Urology, St Paul’s Hospital, London WC2 9AE
PETER O. BEHAN
HCG LOCALISATION OF NO PROGNOSTIC VALUE IN TESTICULAR TERATOMA
9. Lennette EH. Cellular immunity and SSPE.
To establish the incidence and prognostic value of HCGcontaining syncytia, early stage teratomas of the same grade were selected. All intermediate malignant teratomas confined to the testis (MTI pathological stage PI) from the Testicular Tumour Panel3 files were re-examined. From 89 neoplasms adjacent sections were for P-HCG using an stained with haematoxylin and eosin indirect immunoperoxidase technique.and HCG positive cells were present in 58 tumours (65%), and were associated with undifferentiated tisue or yolk-sac elements in 54
JOHN R. W. MASTERS ANU KRISHNASWAMY DAVID N. BUTCHER
FAILURE OF ANTILYMPHOCYTIC GLOBULIN IN ACUTE ULCERATIVE COLITIS
SIR,-Sometimes a patient with severe acute ulcerative colitis does not respond to medical treatment and colectomy is needed. There is evidence that cytotoxic lymphocytes may be involved in the pathogenesis of ulcerative colitis, and it has been suggested that antilymphocytic globulin (ALG) might be useful in this disease. 2,3 We have done a small trial of ALG to see if the remission rate of acute ulcerative colitis, in patients receiving corticosteroids, was improved by adding ALG. The study was approved by the hospital’s ethical committee, and patients gave their informed consent. None had evidence of allergy to equine ALG on skin testing. The patients had all had a severe acute attack of ulcerative colitis requiring treatment in hospital. Patients aged less than 18 years, pregnant women, those with a history of allergy to horse serum, and patients who had been taking azathioprine during the previous 8 weeks were not studied. Equine anti-human-lymphocyte globulin was supplied by HoechstBehringwerke. Neville AM. Shorter immunoperoxidase technique for the demonstration of carcinoembryonic antigen and other cell products J Clin Pathol
4. Heyderman E,
1977, 30: 138-40. C, Beilby JOW. Testicular germ-cell tumours- should current classification be revised? Invest Cell Pathol 1980; 3: 135-40. German-Lluch JR, Begent RHJ, Bagshawe, KD. Tumour-marker levels and prognosis in malignant teratoma of the testis. Br J Cancer 1980; 42: 850-855
5. Parkinson 6.
BJ, Alpert E. Inflammatory bowel disease: Study of cell mediated cytotoxicity for isolated human colonic epithelial cells. Gut 1980; 21: 353-59. 2. Oberling F, Hiebel G. Intravenous ALS in the treatment of severe rectocolitis N Eng. J Med 1971; 285: 409-10. 3. Marmont A, Giordano D, Santini G, Damasio E, Carella M, Bacigalupo A The treatment of autoimmune blood diseases with antilymphocyte globulin Postgrad Med J1976; 52: suppl 5: 139-46. 1. Kemler