1
1125 LATE RELAPSE OF TESTICULAR GERM-CELL TUMOURS AFTER RADIOTHERAPY SIR,-A patient who relapsed 5 years after chemotherapy for testicular teratoma is described by Dr Chan and others (Oct 5, p 773). A relapse 6 years after radiotherapy is reported here. In October, 1977, a 24-year-old man presented to another centre with painless left testicular enlargement. Inguinal orchidectomy was performed, and the histology was that of a malignant teratoma intermediate (MTI) with infiltration of the epididymis. 2 weeks after surgery his serum a-fetoprotein (AFP) was raised (37 g/1); sequential assays were not performed. There was no clinical evidence of metastases, and chest X-ray was normal. A lymphogram demonstrated an enlarged node with a 2 cm diameter filling defect in the left para-aortic region. He was treated with megavoltage irradiation to the para-aortic and bilateral iliac nodes by an inverted -Y technique (40 Gy, 20 fractions, 4 weeks). At the end of treatment his serum-AFP had fallen to less than 1 g/1. On regular follow-up he remained well with a normal AFP. He moved into this area in 1982. In September, 1983, a routine AFP was found to be 1250 U/ml, and 1 month later had risen to 1500 U/ml. chorionic gonadotropin was normal. A computerised tomographic scan of thorax and abdomen demonstrated two nodes, 2 cm and 3 cm in diameter, in the left para-aortic sulcus. Treatment was started with bleomycin, etoposide, and cisplatin and, after four cycles, AFP had fallen to 43 U/ml, with partial regression of the para-aortic nodes. In March, 1984, the residual masses were completely excised, and histology revealed differentiated teratoma with small foci of malignant teratoma. He has subsequently remained well and disease free with a normal plasma AFP. This report emphasises further the risk of late relapse following therapy for non-seminomatous germ-cell testicular tumours (NSGCT). I CT scanning is of value for demonstrating the exact extent and bulk of metastatic disease both before and after therapy2 but was not available at the time of completion of radiotherapy, so it is not clear whether residual disease was present at that time. Residual masses after therapy should be excised where possible3 and follow-up should be continued with tumour marker estimations beyond 5 years after therapy for NSGCT. Department of Clinical Oncology, Western General Hospital, Edinburgh EH4 2XU R. E. TAYLOR 1. Geier LJ, Volk SA, Weldon D, Redmond J. Late relapse in testicular cancer after chemotherapy. Lancet 1983; i: 1049 2. Husband JE, Gnmer DP. Staging testicular tumours: the role of CT scanning. J Roy Soc Med 1985; 78 (suppl 6): 25-31 3: Tait D, Peckham MJ, Hendry WF, Goldstraw P. Post-chemotherapy surgery in advanced non-seminomatous germ-cell testicular tumours: the significance of histology with particular reference to differentiated (mature) teratoma. Br J Cancer 1984; 50: 601-09. SIR,-It is increasingly accepted, particularly in the United States, that after treatment of patients with metastatic germ-cell tumour with chemotherapy, there is a plateau in the disease-free survival curve which begins 18-24 months after completion of treatment. This is only true if the patient is in complete remission. The demonstration that patients with residual mature teratoma left after chemotherapy have a 50% incidence of disease progression within five years1 suggests that it is inappropriate to consider two years disease-free as an end point for treatment studies in this disease. Our experience supports this conclusion.2,3 In a series of 349 patients, followed up for more than five years, 1 of these was known to have had a mass palpable for four years before diagnosis of relapse and had mature teratoma on histology. In a second series of 120 patients referred for chemotherapy to one of us (R. T. D. 0.) since 1978, there have been 16 patients who have relapsed after radiotherapy. Of these, 2 (1 a seminoma, 1 a malignant teratoma intermediate) had relapsed at ten and five years, respectively. Since none of these cases had their primary management in the era of modern computerised tomographic scanning scans, it is difficult to be sure that they ever achieved complete remission. Nevertheless, these observations emphasise the importance of surgery after chemotherapy to remove residual disease masses. Department of Medical Oncology, London Hospital Medical College, London E1 2AD R. T. D. OLIVER 1. Loehrer PJ, Williams SD, Clark SA, et al. Teratoma following chemotherapy for non- seminomatous germ cell tumour (NSGCT): a clinicopathologic correlation. Proc Am Soc Clin Oncol 1983; 2: 139. 2. Blandy JP, Oliver RTD, Hope-Stone HF. A British approach to the management of patients with testicular tumours. In: Donohue J, ed. Testis tumours. Baltimore: Williams and Williams, 1983: 207-23. 3. Oliver RTD. Testicular germ cell tumours: a model for a new approach to treatment of adult solid tumours. Postgrad Med J 1985; 61: 123-31. 4. Oliver RTD, Blandy JP, Hendry WF, et al. Evaluation of radiotherapy and/or surgico- pathological staging after chemotherapy in the management of metastatic germ cell tumours. Br J Urol 1983; 55: 764. PROLONGED EXPIRATORY APNOEA AND HYPOXAEMIA SIR,-Professor Milner and Dr Fagan (Oct 12, p 835) interpret our results (Sept 14, p 571) as indicating that prolonged expiratory apnoea (PEA) is more likely to result from a primary active expiration (AE) than from primary alveolar instability with atelectasis. We have an open mind on this possibility but would emphasise that AE will only empty the lungs of oxygen if performed against an open airway. Against a closed or partly closed glottis AE can be a highly effective way of supporting respiration in conditions predisposing to alveolar collapse, as with the grunting in respiratory distress syndrome (RDS). We showed, by microlaryngoscopy in 3 cases, that the upper airway was closed during AE and in one case demonstrated grunting whenever the child was awake. Thus we still regard alveolar collapse as a major component, if not the primary problem, in this form of apnoea. The clinical and physiological relevance of our observations may be emphasised by answering Milner and Fagan’s comments and by providing data not included in our paper. Although our fig 3 does not show large inspiratory pressures at the termination of one apnoeic episode, inspiratory recovery pressures in others ranged from 42 to 70 cm H20 (eg, 50 cm H20 in our fig 2). We are investigating lung mechanics in the periods preceding apnoeic episodes. The most important clue to alveolar collapse comes from the severity and rapidity of the falls in arterial oxygenation (eg, Pa02 from 95 to 23 mm Hg in 14 s). The hypoxaemia was more rapid and severe than expected from the model outlined in our table n for apnoea at residual volume. Moreover, active expiration was accompanied by upper airway closure, a technique usually adopted to improve lung volume, The mechanism of alveolar collapse proposed by Talbert and Southall2 would provide a more satisfactory explanation for these major changes in Pa02. Although chest fluoroscopy confirmed a high diaphragm, the recovery in absolute volume shown in fig 3 is small. However, we contend that the distribution of gas within the lung is the critical determinant of arterial oxygenation. We suggest that reflex closure of the upper airway, redistribution of lung gas from alveoli into airways (ie, an increase in dead space/tidal volume ratio), or a prior lower functional residual capacity (FRC) may explain this. The accompanying figure shows that all five infants tested had low levels of phosphatidylcholine with values similar to those reported post mortem in hyaline membrane disease. 3 In 24 cases the proportion of phosphatidylcholine was 60 - 8±2 - 4% (SE), values similar to those shown in our figure. This evidence, together with the increased levels of phosphatidylcholine after continuous positive airways pressure, cannot alone specify a primary or secondary role for surfactant but do suggest that the immediate effect of apnoea is likely to be atelectasis. We disagree with Milner and Fagan’s comments on RDS, where cyanotic episodes are frequent, especially where upper airway closure is prevented by a nasotracheal airway. The mechanisms whereby PEA might explain these episodes have been fully covered in our Sept 14 paper and elsewhere.l,2 With regard to apnoea of prematurity, a common sequel to RDS in preterm infants, we feel that the available evidence supports an innappropriate sensory feedback from the lungs rather than failure of the central control

LATE RELAPSE OF TESTICULAR GERM-CELL TUMOURS AFTER RADIOTHERAPY

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1125

LATE RELAPSE OF TESTICULAR GERM-CELLTUMOURS AFTER RADIOTHERAPY

SIR,-A patient who relapsed 5 years after chemotherapy fortesticular teratoma is described by Dr Chan and others (Oct 5,p 773). A relapse 6 years after radiotherapy is reported here.In October, 1977, a 24-year-old man presented to another centre

with painless left testicular enlargement. Inguinal orchidectomywas performed, and the histology was that of a malignant teratomaintermediate (MTI) with infiltration of the epididymis. 2 weeksafter surgery his serum a-fetoprotein (AFP) was raised (37 g/1);sequential assays were not performed. There was no clinicalevidence of metastases, and chest X-ray was normal. A lymphogramdemonstrated an enlarged node with a 2 cm diameter filling defect inthe left para-aortic region.He was treated with megavoltage irradiation to the para-aortic and

bilateral iliac nodes by an inverted -Y technique (40 Gy, 20fractions, 4 weeks). At the end of treatment his serum-AFP hadfallen to less than 1 g/1.On regular follow-up he remained well with a normal AFP. He

moved into this area in 1982. In September, 1983, a routine AFPwas found to be 1250 U/ml, and 1 month later had risen to 1500U/ml. chorionic gonadotropin was normal. A computerisedtomographic scan of thorax and abdomen demonstrated two nodes,2 cm and 3 cm in diameter, in the left para-aortic sulcus. Treatmentwas started with bleomycin, etoposide, and cisplatin and, after fourcycles, AFP had fallen to 43 U/ml, with partial regression of thepara-aortic nodes. In March, 1984, the residual masses were

completely excised, and histology revealed differentiated teratomawith small foci of malignant teratoma. He has subsequentlyremained well and disease free with a normal plasma AFP.This report emphasises further the risk of late relapse following

therapy for non-seminomatous germ-cell testicular tumours

(NSGCT). I CT scanning is of value for demonstrating the exactextent and bulk of metastatic disease both before and after therapy2but was not available at the time of completion of radiotherapy, so itis not clear whether residual disease was present at that time.Residual masses after therapy should be excised where possible3 andfollow-up should be continued with tumour marker estimationsbeyond 5 years after therapy for NSGCT.

Department of Clinical Oncology,Western General Hospital,Edinburgh EH4 2XU R. E. TAYLOR

1. Geier LJ, Volk SA, Weldon D, Redmond J. Late relapse in testicular cancer afterchemotherapy. Lancet 1983; i: 1049

2. Husband JE, Gnmer DP. Staging testicular tumours: the role of CT scanning. J RoySoc Med 1985; 78 (suppl 6): 25-31

3: Tait D, Peckham MJ, Hendry WF, Goldstraw P. Post-chemotherapy surgery inadvanced non-seminomatous germ-cell testicular tumours: the significance ofhistology with particular reference to differentiated (mature) teratoma. Br J Cancer1984; 50: 601-09.

SIR,-It is increasingly accepted, particularly in the United

States, that after treatment of patients with metastatic germ-celltumour with chemotherapy, there is a plateau in the disease-freesurvival curve which begins 18-24 months after completion oftreatment. This is only true if the patient is in complete remission.The demonstration that patients with residual mature teratoma

left after chemotherapy have a 50% incidence of disease progressionwithin five years1 suggests that it is inappropriate to consider twoyears disease-free as an end point for treatment studies in thisdisease. Our experience supports this conclusion.2,3 In a series of349 patients, followed up for more than five years, 1 of these wasknown to have had a mass palpable for four years before diagnosis ofrelapse and had mature teratoma on histology. In a second series of120 patients referred for chemotherapy to one of us (R. T. D. 0.)since 1978, there have been 16 patients who have relapsed afterradiotherapy. Of these, 2 (1 a seminoma, 1 a malignant teratomaintermediate) had relapsed at ten and five years, respectively.Since none of these cases had their primary management in the era

of modern computerised tomographic scanning scans, it is difficultto be sure that they ever achieved complete remission. Nevertheless,

these observations emphasise the importance of surgery after

chemotherapy to remove residual disease masses.

Department of Medical Oncology,London Hospital Medical College,London E1 2AD R. T. D. OLIVER

1. Loehrer PJ, Williams SD, Clark SA, et al. Teratoma following chemotherapy for non-seminomatous germ cell tumour (NSGCT): a clinicopathologic correlation. ProcAm Soc Clin Oncol 1983; 2: 139.

2. Blandy JP, Oliver RTD, Hope-Stone HF. A British approach to the management ofpatients with testicular tumours. In: Donohue J, ed. Testis tumours. Baltimore:Williams and Williams, 1983: 207-23.

3. Oliver RTD. Testicular germ cell tumours: a model for a new approach to treatment ofadult solid tumours. Postgrad Med J 1985; 61: 123-31.

4. Oliver RTD, Blandy JP, Hendry WF, et al. Evaluation of radiotherapy and/or surgico-pathological staging after chemotherapy in the management of metastatic germ celltumours. Br J Urol 1983; 55: 764.

PROLONGED EXPIRATORY APNOEA ANDHYPOXAEMIA

SIR,-Professor Milner and Dr Fagan (Oct 12, p 835) interpretour results (Sept 14, p 571) as indicating that prolonged expiratoryapnoea (PEA) is more likely to result from a primary activeexpiration (AE) than from primary alveolar instability withatelectasis. We have an open mind on this possibility but wouldemphasise that AE will only empty the lungs of oxygen if performedagainst an open airway. Against a closed or partly closed glottis AEcan be a highly effective way of supporting respiration in conditionspredisposing to alveolar collapse, as with the grunting in respiratorydistress syndrome (RDS). We showed, by microlaryngoscopy in 3cases, that the upper airway was closed during AE and in one casedemonstrated grunting whenever the child was awake. Thus we stillregard alveolar collapse as a major component, if not the primaryproblem, in this form of apnoea. The clinical and physiologicalrelevance of our observations may be emphasised by answeringMilner and Fagan’s comments and by providing data not includedin our paper.Although our fig 3 does not show large inspiratory pressures at the

termination of one apnoeic episode, inspiratory recovery pressuresin others ranged from 42 to 70 cm H20 (eg, 50 cm H20 in our fig 2).We are investigating lung mechanics in the periods precedingapnoeic episodes.The most important clue to alveolar collapse comes from the

severity and rapidity of the falls in arterial oxygenation (eg, Pa02from 95 to 23 mm Hg in 14 s). The hypoxaemia was more rapid andsevere than expected from the model outlined in our table n forapnoea at residual volume. Moreover, active expiration wasaccompanied by upper airway closure, a technique usually adoptedto improve lung volume, The mechanism of alveolar collapseproposed by Talbert and Southall2 would provide a more

satisfactory explanation for these major changes in Pa02. Althoughchest fluoroscopy confirmed a high diaphragm, the recovery inabsolute volume shown in fig 3 is small. However, we contend thatthe distribution of gas within the lung is the critical determinant ofarterial oxygenation. We suggest that reflex closure of the upperairway, redistribution of lung gas from alveoli into airways (ie, anincrease in dead space/tidal volume ratio), or a prior lowerfunctional residual capacity (FRC) may explain this.The accompanying figure shows that all five infants tested had

low levels of phosphatidylcholine with values similar to thosereported post mortem in hyaline membrane disease. 3 In 24 cases theproportion of phosphatidylcholine was 60 - 8±2 - 4% (SE), valuessimilar to those shown in our figure. This evidence, together withthe increased levels of phosphatidylcholine after continuous

positive airways pressure, cannot alone specify a primary orsecondary role for surfactant but do suggest that the immediateeffect of apnoea is likely to be atelectasis.We disagree with Milner and Fagan’s comments on RDS, where

cyanotic episodes are frequent, especially where upper airwayclosure is prevented by a nasotracheal airway. The mechanismswhereby PEA might explain these episodes have been fully coveredin our Sept 14 paper and elsewhere.l,2 With regard to apnoea ofprematurity, a common sequel to RDS in preterm infants, we feelthat the available evidence supports an innappropriate sensoryfeedback from the lungs rather than failure of the central control