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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