POSTPARTUM COLLAPSE DUE TO ACUTE DILATED CARDIOMYOPATHY

1500 content

from

"tannin"

covers

less

hazardous

distilled

liquors. However,

very different groups of chemicals-the tannins and the condensed tannins. Hydrolysable hydrolysable tannins can be degraded to form compounds such as ellagic acid, which inhibit carcinogenesis in the oesophagus and elsewhere,s5 while the condensed variety are more likely to potentiate cancer. The evidence accumulated by Morton6 is very persuasive, especially that relating to the consumption of tea. Tea contains condensed tannins. If Sagar and Ellwood are using the birds as a test for tannins, perhaps they should do a positive control experiment and tempt their alcoholic birds with tea, without milk (which would bind the tannins) but with lemon juice and sugar, if they wish. As stressed by Dr Rose (May 16, p 1143), the aetiology of oesophageal cancer is multifactoral. A reasonable working hypothesis is that oesophageal cancer is initiated worldwide by the only potent oesophageal carcinogens known, the nitrosamines, but. the levels of exposure seem too low to account for the high incidence of the disease, so additional factors are essential if cancer is to develop. The controversy goes on. It is not vitamin deficiency but tannins (Oterdoom, Mar 28, p 745): it is not nutrition but alcohol and tobacco (Sagar and Ellwood, Feb 28, p 508). But are not risk factors likely to be additive? Alcoholic beverages, tobacco, tannins, two

scalding liquids, deficient diets, food contaminated by fungi, silica fibres, or sour pomegranate seeds, all contribute to the potentiation: their relative importance depends on geographical location. Every known risk factor carries its own weight and must be taken into account.’ The combination of onslaughts damages the initiated latent cancer cell, which might otherwise have remained dormant, until it can no longer keep up the repair of genetic and phenotypic damage. Control mechanisms break down, and the differentiated, well-behaved oesophageal cell becomes an autonomous, aggressive, malignant intruder. MRC Toxicology Unit, Medical Research Council Laboratories, Carshalton, Surrey SM5 4EF

VALDA M. CRADDOCK

1. O’Donovan MB, Novellie L. Kaffircorn malting and brewing studies XV: the fusel oils of Kaffir beers. J Sci Fd Agric 1966; 17: 362-65. 2. Tuyns AJ, Pequignot G, Abbatucci JS. Esophageal cancer and alcohol consumption: importance of type of beverage. Int J Cancer 1979; 23: 443-47. 3. Leake CD, Silverman M. The chemistry of alcoholic beverages. In: Kissim B, Begleiter H, eds. The biology of alcoholism: Vol I. Biochemistry. New York: Plenum Press, 1971: 575-612. 4. Khani SC, Zaphiropoulos PG, Fujita VS, Porter TD, Koop DR, Coon MJ. cDNA and derived amino acid sequence of ethanol-inducible rabbit liver cytochrome P-450 isozyme 3a (P-450ALC). Proc Natl Acad Sci USA 1978; 84: 638-42.

S, Shivapurkar N, Superezynski M, Stoner GD. Inhibition of methylbenzylnitrosamine-induced esophageal tumors in rats by ellagic acid. Proc

5. Mandal

Am Assoc Can Res 1986; abstr 489. 6. Morton JF. Further associations of plant tannins and human cancer. Quart J Crude Drug Res 1972; 12: 1829-41. 7. Tuyns AJ, Riboli E, Doornbos G, Pequignot G. Diet and esophageal cancer in Calvados (France). Nutr Cancer 1987; 9: 81-92.

SIR,-Both Dr Oterdoom and Dr Rose draw attention to our study1 which reported no effect of riboflavin, retinol, and zinc

supplements on the prevalence of chronic oesophagitis in a high-incidence area for oesophagitis in China. However, subsequent analysis of the data by logistic regression has revealed a lower prevalence of chronic oesophagitis associated with improvements in blood retinol concentrations. This happened because in the reanalysis we considered changes in blood retinol concentrations

on an individual basis and related these to the of chronic oesophagitis, whereas previously absence presence only group comparisons had been made. Improvement in nutritional status occurred in both test and placebo groups and this was particularly evident in respect of fat-soluble vitamin status.’ We now find that plasma retinol concentrations increased by more than 20 % in 71 % of the test group and in 45 % of the placebo group. This large placebo effect may explain why the effect of the vitamin treatment was obscured in the initial analysis. We agree with Rose that our first report did not exclude all possible involvement of vitamins in the aetiology of oesophageal cancer. 13 months of vitamin treatment cannot be relied on to counter a life-time’s exposure to putative environmental carcinogens although we did anticipate that it would modify the lesion, if the lesion was specifically due to deficiencies in retinol, or

zinc. We now believe, however, that the vitamin insufficient to normalise nutritional status. The increase in plasma retinol in the placebo group may have been partly due to seasonal factors (the final sample was taken two months later in the year than the initial one) and partly to the changing social conditions affecting rural Chinese communities in this highincidence area; both the variety and amount of foods available are improving. Unlike Oterdoom, we believe that "the old hobbyhorse vitamins in the aetiology of oesophageal cancer" is not yet dead. Experimental support for the tannin hypothesis seems weak to us but epidemiological studies to test this idea need to be done.

riboflavin,

or

treatment was

Clinical

Investigation Unit, Dudley Road Hospital, Birmingham B18 7QH

D. I. THURNHAM

International Agency for Research on Cancer, Lyon, France

NUBIA MUNOZ

Institute of Epidemiology and Biometry, German Cancer Research Centre, Heidelberg, West Germany

J. WAHRENDORF

Institute Regina Elena,

Rome, Italy

M. CRESPI

1. Munoz N, Warendorf

J, Lu JB, et al. No effect of riboflavin, retinol and zinc prevalence of precancerous lesions on the oesophagus. Lancet 1985; ii: 111-14.

on

POSTPARTUM COLLAPSE DUE TO ACUTE DILATED CARDIOMYOPATHY

SIR,-A 21-year-old woman in her first pregnancy had normal weeks, after which she was consistently hypotensive (100/50 mm Hg) with tachycardia (100/min, regular). These findings did not seem to warrant investigation and she remained symptom-free until 38 weeks when she noticed mild shortness of breath on exertion. Physical examination at the blood pressure until 28

antenatal clinic revealed no other abnormalities. In labour an epidural catheter was placed for analgesia but the first doseofO 5% bupivacaine caused profound hypotension. The initial diagnosis, complete spinal anaesthesia, was rejected because of her immediate spontaneous recovery. The labour and delivery were otherwise uneventful. 14 h after delivery, she collapsed (blood pressure unrecordable, central pulses faint, 160/min). She was cyanosed and breathing was rapid and shallow. After resuscitation she denied chest pain but felt severely short of breath. Tachycardia and cyanosis were the only physical signs. A chest X-ray suggested cardiomegaly; the ECG revealed sinus tachycardia; central venous pressure was raised; arterial blood gases showed hypoxia with a ventilation-perfusion mismatch; electrolytes were normal; cardiac enzymes were later reported as greatly increased. The provisional diagnosis was pulmonary embolism and the patient was given oxygen and anticoagulation (pretreatment coagulation studies normal). Over the next 24 h she felt better. A chest X-ray revealed some right midzone shadowing but was otherwise unchanged, as was the ECG. 72 h post partum, she began to feel more short of breath, and the tachycardia worsened. Physical examination revealed some dullness at the lung bases and cardiomegaly had increased. With diagnosis of recurrent pulmonary embolism she was transferred to a cardiothoracic unit. Echocardiography revealed gross dilatation and decreased amplitude of movement of the left ventricle, tricuspid valve incompetence, and cardiac failure. Left-ventricular ejection fraction was 5 % of normal. Dilated cardiomyopathy was diagnosed and the patient was started on diuretics and inotropic support. Full heparinisation, bed rest, and fluid restriction were advised. Within 36 h she felt less dyspnoeic, but the tachycardia persisted. Cardiac catheterisation confirmed left-ventricular dilatation with a poor ejection fraction. Histological examination of myocardial biopsy samples revealed non-specific changes of cardiomyopathy. The patient has now had a cardiac transplant because of worsening cardiac function and failure of medical treatment. Her immediate postoperative course has been satisfactory.

Peripartum cardiomyopathy (PPCM)1-3 develops in about 1 in 4000 pregnancies, and high-risk factors are colour (black), age (over

1501

30), and obstetric history (twin pregnancies and multigravidae). Our patient was white, under 30, and in her first pregnancy. The usual signs and symptoms are dyspnoea, chest pain, haemoptysis, cardiomegaly, tachycardia or tachyarrhythmia, heart murmurs, or features of thromboembolic disease.2 80% of cases become symptomatic within 3 months of delivery. The differential diagnoses are left-ventricular failure and pre-existing subclinical heart disease exacerbated by pregnancy. The diagnosis of PPCM is suggested by the history and physical signs, and is confirmed by echocardiography, angiography, and myocardial biopsy; ECG changes are non-specific. Rigorous adherence to the definition of PPCMl should exclude most cases of pre-existing non-pregnancyrelated cardiomyopathy. Optimum management depends upon early diagnosis and prompt treatment of heart failure. In our patient PPCM was not diagnosed until she was very ill. The early clues to her impending illness were subtle (hypotension and mild dyspnoea in late pregnancy), but the clinical features of her acute illness were typical. PPCM should be borne in mind in any antenatal or puerperal patient with signs or symptoms of cardiovascular illness where the clinical picture does not fit the more common diseases encountered. Such patients deserve full and early

investigation. Maternity Unit, Watford General Hospital, Watford, Hertfordshire WD1

1. Veille

J. H. PHIPPS J. RASHID D. R. GRIFFIN

8HB

J. Peripartum cardiomyopathy:

a

review.

Am J Obstet Gynecol 1984;

148:

805-15. 2. Julian DG, Szekely P. Peripartum cardiomyopathy. Prog Cardiovasc Dis 1985; 27: 223-40. 3. Homans DC. Peripartum cardiomyopathy. N Engl J Med 1985; 312: 1432-37.

ECHOCARDIOGRAPHIC EVIDENCE OF ALTERED CARDIAC DIASTOLIC FUNCTION IN ANKYLOSING SPONDYLITIS

SIR,-Professor Brewerton and colleagues (May 2, p 995) report early, left-ventricular, diastolic abnormalities in 16 of 30 patients with ankylosing spondylitis (AS). Our experience is similar.1 Because of the probable excess risk of fatal outcome from cardiovascular causes in patients with As,z,3 we studied cardiac function in 20 patients with AS and in 25 normal controls to determine if there is evidence of cardiac dysfunction before any clinical signs of cardiac disease.1 Standard, 12-lead resting electrocardiograms (ECG) were recorded before cross-sectional Doppler echocardiography; intracardiac flow velocities were estimated by pulsed echocardiography. Atrial, ventricular, and aortic dimensions were similar in patients and controls. However, left and right ventricular diastolic functions were altered in the patients: peak velocity of early inflow was significantly decreased, and peak velocity with atrial systole was increased, resulting in a decreased ratio between these two variables (table). The patients also had a decreased diastolic filling time. Systolic function, as judged by ejection peak velocity and ejection time, were similar in the two groups. Thus we have observed alterations of diastolic function, primarily impaired ventricular relaxation, in both ventricles. Based on Brewerton and colleagues’ findings increased fibrous .tissue in VENTRICULAR DIASTOLIC FUNCTION (MEAN AND SD)

*Analysis of coverage, including heart tEv = peak velocity of early inflow. tAv = peak velocity with atrial systole.

rate as

independent variable.

the myocardium of AS patients may explain the impaired ventricular relaxation. We have also observed that AS patients have minor abnormalities of the QRS complex of the ECG that could also be a consequence of a diffuse increase of interstitial connective tissue. 9 AS patients had slight prolongation of the QRS complex, defined as greater than 100 ms, compared with 4 controls (p = 0-06). 2 of our AS patients were found to have ventricular ectopy, and 1 had left bundle-branch block. Our results confirm and extend the observations of Brewerton et al by demonstrating that, among AS patients, minor ECG abnormalities are common and systolic function is normal, but left and right ventricular diastolic function is altered. Department of Medicine, Cleveland Metropolitan General Hospital, Cleveland, Ohio 44109, USA

MUHAMMAD A. KHAN

JING PING SUN ROBERT C. BALHER

JP, Khan MA, Bahler RC. Impairment of cardiac diastolic function in patients with ankylosing spondylitis, as evaluated by Doppler echocardiography. Br J Rheumatol 1987; 26 (suppl 1): 71 (abstr). 2. Khan MA, Khan MK, Kushner I. Survival among patients with ankylosing spondylitis- a life-table analysis. J Rheumatol 1981; 8: 86-90. 3. Radford EP, Doll R, Smith PE. Mortality among patients with ankylosing spondylitis not given X-ray therapy. N Engl J Med 1977; 297: 572-76. 1. Sun

RECURRENCE OF LOIN PAIN/HAEMATURIA SYNDROME AFTER RENAL AUTOTRANSPLANTATION

SiR,—The loin pain/haematuria syndrome is a rare condition, predominantly affecting young women, in which recurrent and often severe pain and tenderness is associated with frank or microscopic haematuria.1 In many cases renal biopsy reveals granular deposition of C3 in arteriolar walls, and angiography in several (but not all) cases reveals abnormalities in the intrarenal vasculature.2 Patients may show accelerated reactions to specific intradermal recall antigens.3 The pain may be so disabling that opioid dependency is a hazard.3,4 Splanchnic nerve blockade or renal denervation can afford temporary relief of pain, suggesting that reinnervation occurs over several months.4,S In an attempt to disconnect the kidney permanently from its autonomic nervous supply, renal autotransplantation has been done, with encouraging results in selected patients with severe pain. We describe a patient whose pain recurred 12 months after renal autotransplantation. A 45-year-old woman presented in1982 with right loin pain which increased in severity over the next 3 years. She often had intense pain every day, sometimes accompanied by vomiting and dysuria. Infrequent mild episodes of left-sided loin pain caused her no distress. Urine cultures were repeatedly sterile but microscopy demonstrated many deformed red blood cells, which suggests a renal origin.6 Radioisotope studies and excretion urography done while she was in pain showed no features of obstructive uropathy, and renal angiography revealed normal vasculature in both kidneys. Plasma biochemistry, complement levels, and a urological examination were normal and she had no features of a psychiatric disorder. Renal biopsy revealed a mild mesangioproliferative glomerulonephritis and widespread arteriolar deposition of C3. An intradermal injection of streptokinase/streptodornase produced a type III hypersensitivity reaction. A diagnosis of loin pain/ haematuria syndrome was made. A phenol sympathectomy, splanchnic nerve blockade, and a trial of high-dose prednisolone had no effect on her pain which was to eventually only controlled with parenteral opioids. In an relieve these incapacitating symptoms, her right kidney was autotransplanted and the operation was followed by dramatic relief of pain. 11weeks after surgery the left loin pain became severe but there was no evidence of urinary tract infection or obstruction. Radioisotope studies demonstrated normal function in the left kidney and in the transplanted right kidney. Left-sided autotransplantation was done because of the intensity of the pain. 12 months after the first operation she developed recurrent, severe, right iliac fossa pain, like that previously experienced in the loin, and investigation failed to identify a cause. Treatment with dipyridamole was unsuccessful in controlling the pain and the

attempt