1408
patient’s knowledge of the diagnosis and its implications, or from cytotoxic (or other unpleasant) treatment, or from the patient being under continuous medical care. The essential questions-how do emotional damage and psychosocial distress induce such striking changes in endocrine function and how might these changes affect outcome-are beyond the scope of our pilot study. E.
Departments of Endocrinology and Haematology, Centre of Internal Medicine, Johann Wolfgang Goethe University, D-6000 Frankfurt am Main, West Germany
JUNGMANN
J. BINDER U. JESTÄDT P. S. MITROU P.-H. ALTHOFF K. SCHÖFFLING
1. Mitrou PS, Hechler P, Kippstein T, Lautenschlager G, Burkhardt KL, Jungmann E. Chemotherapy with adriamycin, bleomycm, vincristine, etoposide and prednisone + radiotherapy in Hodgkin’s disease. 5th European Congress of Clinical Oncology (London, Sept 2-7, 1989). 2. Gold PW, Loriaux DL, Roy A, et al. Responses to corricotropin-releasing hormone in the hypercortisolism of depression and Cushing’s disease. N Engl J Med 1986; 314: 1329-35. 3. von Bardeleben U, Wiedemann K, Holsboer F. Altered brain-pituitary-adrenocortical activity in major depression. In: Casanueva FF, Dieguez C, eds. Recent advances in basic and clinical neuroendocrinology. Excerpta Med Int Congr Ser 1989; no 864: 357-67. 4. Jungmann E, Remer P, Luderer E, et al. Postoperative evaluation of adrenocortical function by a corticotropin-releasing factor test in patients with large pituitary adenomas. In: Landolt AM, Heitz PU, Zapf J, et al, eds. Advances in pituitary adenoma research. Oxford: Pergamon, 1988: 431-32. 5. Kleinberg DL. Prolactin and breast cancer. N Engl J Med 1987; 316: 269-71.
Psychological correlates of hormone receptor status in breast cancer SIR,-Dr Razavi and his colleagues (April 21, p 931) report greater psychological distress in patients with receptor-negative breast cancers than in those with receptor-positive tumours, and suggest that these findings may account for the association between psychosocial variables and survival in this disease. Unfortunately there is a potential source of bias in Razavi and colleagues’ data which may affect the validity of their conclusions. The initial psychological evaluation was undertaken during "the first days of radiation therapy" and at a mean of more than 3 months after diagnosis. Razavi et al report that 10 (56%) of 18 patients with receptor-negative tumours received chemotherapy whereas 30 (40%) of 75 with receptor-positive tumours did so. Even though this difference was not significant such imbalances could have sufficient influence on psychological distress, as measured by a self-report scale (SCL90-R), to invalidate the reported fmdings.At least 20% of the 90 items in this scale are directly concerned with somatic symptoms such as nausea and upset stomach, feeling weak, low energy, and poor appetite. Higher scores recorded for such items in the receptor-negative group may simply reflect the toxicity due to chemotherapy, Patients undergoing adjuvant chemotherapy emotional symptoms such as tearfulness and hopelessness than those who do not.2 The possibility that receptor status may determine the putative relation between psychosocial variables and disease outcome in breast cancer is, however, of interest. We have reportedthe findings of a case-control study of the frequency of stressful life experiences in 50 patients with a first recurrence of breast cancer and in 50 controls who remained in remission. The patients and controls were matched on a pair-wise basis for the main physical and pathological factors known to be of prognostic importance in breast cancer, including axillary lymph-node status and histological grade of tumour. Oestrogen receptor (ER) status was not used for matching since some pairs had first presented before such measurement was routinely,available. The main findings were that women whose breast cancer had relapsed were significantly more likely to have had severe adverse life events or continuing difficulties than were their matched controls. Further group-wise analysis of the data from this study has now been undertaken to assess the possible influence of ER status on the relation between severe life events and relapse. When all patients were considered, 26 women who relapsed had a severe life event also have
more
whereas 12 of those in remission did so (p = 0-007). Among the 57 patients with ER-positive tumours, 14 of the 26 who relapsed and 3 of the 31 who remained in remission had had a severe life event (p = 0-0004). Among the 15 patients with ER-negative tumours, 2 of the 8 who relapsed and 3 of the 7 who remained in remission had had a severe life event (p=0-6). These findings are clearly preliminary but support the hypothesis that the effect of psychosocial variables on outcome is mediated via a hormonal mechanism. AMANDA J. RAMIREZ MICHAEL A. RICHARDS WALTER GREGORY THOMAS K. J. CRAIG
ICRF Clinical Oncology Unit and Division of Psychiatry, United Medical and Dental Schools, Guy’s Hospital, London SE1 9RT, UK
1. Altman DG. Comparability of randomised groups. Statistician 1985; 34: 125-36. 2. Ramirez AJ. Psychological strategies in patient care. In: Fentiman IS, ed. Detection and treatment of early breast cancer. London: Martin Dunitz, 1990: 140-53. 3. Ramirez AJ, Craig TKJ, Watson JP, Fentiman IS, North WRS, Rubens RD. Stress and relapse of breast cancer. Br Med J 1989; 298: 291-93.
Phosphate and rickets SIR,-Dr Holland and his colleagues (March 24,
p 697) relate babies to prenatal phosphate deficiency. Their demonstration that hypercalciuria is associated with phosphate deficiency fits in with data in older children and adults with hypercalciuria.’ However, I have reservations about their method of assessing renal tubular phosphate handling. They calculated the percentage tubular reabsorption of phosphate (% TRP) and found a difference between those babies with radiological rickets subsequently and those without. Unfortunately this index is influenced by the filtered load of phosphate (and thus plasma phosphate), which may vary in immature babies. The % TRP cannot therefore be regarded as the most sensitive index of renal tubular phosphate handling. Similarly the TmP/GFR formula of Brodehl,2referred to by Holland et al in the discussion, can vary directly with plasma phosphate, so it is not surprising that they found a high correlation betwen TmP/GFR and plasma phosphate. The theoretical phosphate threshold TmP04/GFR proposed by Bijvoet3 remains the most sensitive index since it is independent of plasma phosphate and glomerular filtration. Recalculation of the TmP04/GFR from Holland et al’s data could be easily done and might influence the interpretation of the results, though the same differences could still be seen. In their final paragraph Holland et al state that "low plasma phosphate concentration and reduced tubular reabsorption of phosphate identified babies with impaired bone mineralisation". Surely they mean increased tubular reabsorption of phosphate?
rickets in
very-low-birthweight
Institute of Child Health, Royal Liverpool Children’s Liverpool L12 2AP, UK
Hospital,
N.J. SHAW
1. Editorial. Idiopathic hypercalciuria: new thoughts on the phosphate connection. Lancet 1987; i: 1412-13. 2. Brodehl J, Krause A, Hoyer P. Assessment of maximal tubular phosphate reabsorption: comparison of direct measurement with the nomogram of Bijvoet. Paediatr Nephrol 1988; 2: 183-89. 3. Bijvoet OLM. Indices for the measurement of the renal handling of phosphate. In: Massry SG, Fleisch H, eds. Renal handling of phosphate. New York: Plenum, 1980: 1-37.
*** This letter has been shown whose reply follows.-ED. L.
to
Dr Holland and his
colleagues,
SIR,-Dr Shaw is right to point out that the last paragraph of our paper should have referred to reduced renal tubular reabsorption of calcium (not phosphate) which identified babies with impaired bone mineralisation. The renal tubular phosphate handling was similar in the babies in whom rickets later developed and those in whom it did not, in that all (except one baby who had severe asphyxia) conserved phosphate with a tubular reabsorption of over 95% when plasma phosphate fell