CLINICS FOR HEAD-AND-NECK CANCER PATIENTS

CLINICS FOR HEAD-AND-NECK CANCER PATIENTS

350 MEDICINE AND THE MARKET SIR,-I cannot let Dr Owen’s Point of View (July 7, p 30) pass without comment. While American medicine is in an interesti...

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350 MEDICINE AND THE MARKET

SIR,-I cannot let Dr Owen’s Point of View (July 7, p 30) pass without comment. While American medicine is in an interesting state of change and the effect on a doctor’s freedom is hard to predict, I well remember this freedom during my years in the British NHS. During my surgical house job the waiting list for a cholecystectomy was two years and in my six months more people on the waiting-list for inguinal hernia repair died than had their operation. Later, when I was a registrar in a purpose-built cardiothoracic centre, cardiologists, cardiac surgeons, and anaesthetists fretted under a maximum of 400 open-heart cases per year imposed by bureaucratic diktat, while the waiting lists for valve replacement stretched to 18 months and for coronary surgery to 8 months-some freedom. I do not know where Owen obtained his figures for life expectancy in the United States but the death rate for people 25-64 years of age declined an average of less than 1% per year from 1950 to 1970, but fell by 2-3% per year during the 1970s.1 The bulk of this improvement was the result of a 28% fall in cardiac death rates. The over-65 figures are similar. In the UK heart disease death-rates are static. Owen himself was once in a position to influence preventive measures but I do not recall any effective measures to reduce cigarette consumption or to encourage seat-belt legislation during that period, policies which would have avoided much morbidity and early mortality. Certainly, epidemiology has a low place in American priorities and the popular notion that good health is something that comes out of a bottle prevails, but is this not also true in the UK? Cardiology Associates of Florence, PA, Pee Dee Medical Park Suite 204, 506 East Cheves Street, Florence, South Carolina 29501, USA

declines, impairment of zinc-dependent senses of taste and smelli may be expected to reduce further the desire for food. These considerations led us to the idea that zinc supplementation might be of value in anorexia nervosa.1,2 Dietary zinc deficiency may be quite common in the UK. A 1981 diet to be about survey reported the zinc intake from an averageThe 10-55 mg daily, with risk of less for vegetarians. US National status

PETER MARX

1. Kleinman

States

JC, Fingerhut LA, Feldman JJ. Trends in mortality. In: Health United (DHHS Pub 81-1232). Washington, DC: US Government Printing Office,

1981:

23, 139.

CASE OF ANOREXIA NERVOSA RESPONDING TO ZINC SULPHATE

SIR,-A 13-year-old girl presented weighing 37 kg, miserable and tearful. Her mother had noticed progressive loss of weight and increasing depression. Within a month the patient lost another 31/2 kg and she was referred to a consultant adolescent psychiatrist who confirmed anorexia nervosa. Two months later, despite counselling, her weight had fallen to 31 - 5 kg. Zinc deficiency was tentatively diagnosed when it was noted that the patient could not taste a 0 - 107o solution ofZnS04.7H2O in distilled water, whereas we and members of our families could taste it easily, with strong aversion in some instances. Hypogeusia is a common early symptom of zinc deficiency.1 A zinc solution containing 15 mg Zn (provided by 66 mg ZnS04.7H20) in distilled water was then given orally three times per day with meals. When the patient was next seen, 2 weeks later, her appetite and demeanour had obviously improved. This was the first consultation during which she had not wept. Supplementation was continued at the higher level of 50 mg Zn three times daily in the form of ’Zincomed’ zinc sulphate capsules. After 4 months, her weight had increased by 13 kg to 44 -5 kg, her appetite and demeanour were normal, and she could taste the O. 1% zinc sulphate solution. Zinc supplementation was discontinued, but after 10 months she showed signs of recurrence: her weight had fallen by 2 kg to 42-55 kg, she appeared somewhat depressed again, and responded only weakly to the "taste test". Zinc supplementation with zincomed was reintroduced at the previous dose level. Within 2 months her weight returned to 44 - 5 kg, she was cheerful again, and the taste test was strongly positive. There is a scientific rationale for the use of zinc in anorexia nervosa. We do not doubt that the reduced food intake initially results from social factors. However, starvation (in common with other stresses) paradoxically increases urinary zinc excretion,22 thereby exacerbating the effect of reduced dietary intake. As zinc

Academy normal

of Sciences recommends 15 mg, 20 mg, and 25 mg for pregnant women, and lactating mothers,

adults,

respectively.4 Department of Chemistry, University of Reading, Reading RG6 2AD

D. BRYCE-SMITH

Health Centre,

Wayside Green, Woodcote, Reading 1.

Aggett PJ, Harries JT. Current status of zinc in health and disease states. Arch Dis Child 1979; 54: 909-17. EJ. Trace elements Academic Press, 1977.

2 Underwood 3 4.

R. I. D. SIMPSON

in human and animal nutrition, 4th ed. London

Ministry of Agriculture, Fisheries and Food. Survey of copper and zinc in food (Food Surveillance Paper no 5). London: HM Stationery Office, 1981. Recommended dietary allowances, 8th ed. Washington, DC: National Academy of Sciences,

1974.

CLINICS FOR HEAD-AND-NECK CANCER PATIENTS

SiR,-Dr Sutton (June 9,

p 1300) seems to think that if a tumour it will be metastatic disease suitable only for palliation. Far from it. In head-and-neck cancer, for example, a local recurrence after radiotherapy is often cured by "salvage" surgery, and metastatic recurrence in the regional lymph nodes is curable by radical neck dissection.’ The early detection ofa tumour recurrence can be difficult and, for nodal metastases, may be crucial for longterm survival. Moreover, the incidence of second primary tumours is about 15% in patients with head-and-neck cancer,most of which are metachronous. For these reasons, we believe that an informed and alert long-term follow-up on all head-and-neck cancer patients is essential. If the follow-up and review of patients is properly done, then efficacy of local treatment policies will be known, and formal treatment protocols for specified tumours can be laid down. This reduces the need for a "combined tumour clinic" to decide on treatment, but does not remove the need to retain the combined conference, where difficult or unusual cases are presented and discussed. Whatever the method for deciding "best treatment", the consultants from the different specialties must agree on the responsibility for the supervision of management and follow-up of any particular patient. Of course the patients must also know who the consultant is that is primarily concerned with their management, otherwise they may feel lost. A combined cancer clinic does have the advantage of bringing interested parties together so that arrangements concerning treatment can be finalised at a single meeting and the maintenance of a local tumour registry is made more simple. We have been striving for years to establish good combined cancer clinics and follow-up facilities. We find statements such as Sutton’s too general to be constructive or helpful. recurs

Department of Otolaryngology, Green Lane Hospital, Auckland 3, New Zealand

R. P. MORTON

Clinical Oncology Unit, Auckland Hospital

C. S. BENJAMIN

1. 2.

Conley J. Radical neck dissection. Laryngoscope 1974; 84: 1344-52 Hordijk GJ, de Jong JMA. Synchronous and metachronous tumours in head and neck cancer. J Laryngol Otol 1983; 97: 619-21.

patients with

SIR,-We were sorry to see that Dr Sutton has had unfortunate experiences in running combined clinics and that he recommends that such clinics be disbanded. What he has to say may apply to many forms of cancer, but what he recommends would be very dangerous in head-and-neck cancer. He argues that joint clinics between surgeons and radiotherapists should be disbanded because

351 the treatment for most tumours is now known. However, most of us patients rather than tumours, and fine judgment and much experience are often needed to know what is best for a specific patient. Sutton states that there is no value in follow-up of a patient who has been treated by radiotherapy, since the only place for further treatment is that of metastases. This is certainly not true for head-and-neck cancer: the place of follow-up clinics for patients with this disease is to detect primary and/or lymph node metastases, the treatment of which results in the salvage of a further 30% of patients. It would be very dangerous to abandon such clinics, because patients are often unaware of a tumour recurrence, especially one in lymph-nodes.

TABLE 11-DISTRIBUTION OF LEAD

University Department of Oto-rhino-laryngology, Royal Liverpool Hospital, Liverpool L69 3BX Institute of Laryngology and Otology,

P. M. STELL D. F. N. HARRISON

London WC1X 8EE

DOES THE CHOROID PLEXUS REALLY PROTECT THE BRAIN FROM LEAD?

SIR,-The choroid plexus produces CSF and regulates its composition by two-way transport of ionic substances. It also3

sequesters the toxic metals, mercury,’ leadand arsenic. Friedheim et al3 have shown that the lateral choroid plexus (LCP) contains lead concentrations of the order of tens of parts per million, and the burden increases with age. We obtained LCPs from 5 patients, 3 of whom died from motor neurone disease. The other 2 had a history of alcohol abuse but died from other causes. The specimens were lyophilised and analysed for lead by means of stable isotope dilution (table i). The concentrations were 100-fold and 10-fold greater in the LCP than in the cortical grey matter and renal cortex, respectively. The latter is known to be the site of active transport of lead from the glomerular ultrafiltrate back to plasma.’Cadmium concentrations in the LCP were also elevated, but they merely reflect the higher zinc content of this region (120-140 fg/g). Thus, unlike other toxic metals, cadmium does not accumulate in the LCP. Our findings support the conclusions of O’Tuama et al2 and Friedheim et al3 that one of the roles of the choroid plexus is to protect the brain from lead. However, we have found5 a wide range of lead concentrations in plasma and CSF. For blood lead levels less than 20 fg/dl, average CSF lead is 40% of plasma lead (table n), and the fraction rises to 80-90% in patients with plumbism. These figures do not reflect the existence of an effective barrier to the entry of lead into the CSF, and in fact, they approximate to the concentration of ultrafilterable lead in dogs’ plasma,4indicating that lead in CSF results solely from passive diffusion. We analysed plasma and CSF from an 11-year-old child to confirm a diagnosis of plumbism based upon neurological symptoms and a blood lead determination by a commercial laboratory. Her blood lead was normal, 6’ 3 g/dl, and her plasma and CSF leads were indistinguishable from those of adults (table n). Thus, we refute the argument that the CSF lead levels observed in adults chronically exposed to lead are abnormally elevated through reduced efficiency of the choroid plexus to protect the brain. There is no clinical evidence of great sensitivity of the CNS to lead in CSF. A 64-year-old man with a CSF lead level 25 times higher than normal did not have CNS dysfunction,and a 34-year-old man with lead poisoning from a retained bullet had unimpaired CNS

(g/dt) IN BLOOD, PLASMA,

AND CEREBROSPINAL FLUID

treat

I

i

i

function even though he had suffered a severe motor neuropathy and his CSF lead level was 65 times higher than normal.7 Our observations lead us to question whether the accumulation of lead in the LCP is related to the regulation of CSF lead and thus the exposure of the brain to lead. The significant fact, however, is that the LCP accumulates lead. Excessively high concentrations of lead in plasma damage the proximal tubules of the kidney with resulting Fanconi syndrome. The capacity of the LCP to harbour lead cannot be infinite. At some point its normal function will be impaired. What the sequelae will be is not clear, but it seems to us that the encephalopathy of lead poisoning may result from failure of the LCP to regulate the composition of CSF. The propensity of encephalopathy to occur in young children may well reflect differences between the immature and the fully developed choroid

plexus. University of Texas at Dallas, Richardson, Texas 75080, USA

W. I. MANTON

Methodist Hospital, Houston, Texas

J. B.

Scottish Rite Hospital, Dallas, Texas

J. D. COOK

KIRKPATRICK

M, Ullberg S. Accumulation and retention of mercury in the mouse. I. An autoradiographic study after a single intravenous injection of mercuric chloride.

1. Berlin

Arch Environ Health 1963, 6: 589-601 LA, Kim CS, Gatzy JT, Krigman

2. O’Tuama

3. 4. 5. 6. 7.

MR, Musak P The distribution of

guinea pig brain and neural barrier tissues in control and leadpoisoned animals. Toxicol Appl Pharm 1976, 36: 1-9 Friedheim E, Corvi C, Graziano J, Donelli T, Breslin D. Choroid plexus as protective sink for heavy metals? Lancet 1983; i. 981-82 Vander AJ, Taylor DL, Kalitis K, Mouw DR, Victery W. Renal handling of lead in dogs. clearance studies Am J Physiol 1977, 233: F523-38. Manton WI, Cook JD. High accuracy (stable isotope dilution) measurements of lead in serum and cerebrospinal fluid Br J Ind Med (in press) Manton WI, Malloy CR Distribution of lead in body fluids after ingestion of soft solder. Br J Ind Med 1983, 40: 51-57. Linden MA, Manton WI, Stewart RM, Thal ER, Felt H Lead poisoning from retained bullets. Pathogenesis, diagnosis and management. Ann Surg 1982, 195: 305-13. inorganic lead

in

TRIMETHADIONE (TROXIDONE) DISSOLVES PANCREATIC STONES

SIR,-Sahel and Sarles have described seven patients with chronic calcific pancreatitis whose pancreatic stones had been partly dissolved by administration of a citrate preparation. Our invitro experiments show that the weak organic acid dimethadione induces a concentration-dependent increase in solubility of calcium carbonate (CaC03), the main constituent of pancreatic stones, and has almost the same potency in this respect as tartaric and citric acids.2 We describe here the use of oral trimethadione (3,5, 5-trimethyl-2,4-oxazolidinedione), the precursor of dimethadione, to dissolve pancreatic stones, first in a canine model3,4 and then in

patients.

TABLE I-DISTRIBUTION OF LEAD AND CADMIUM IN LATERAL CHOROID PLEXUS AND OTHER TISSUES I

I

I

1a=alcohol abuse MND=motor neurone disease LCP=lateral choroid plexus. CCx=cerebral cortex RCx=renal cortex. * CSF lead at necropsy 0 025 f’g/dl ’t’Mean±SD of up to 8 specimens taken bilaterally from frontal, motor, sensory, and occipital cortices.