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disease whose incidence is as low as 1 in lo6 peop1e.I However, they provide little information about age, time of onset, and associated diseases. Our patient was unresponsive to drug therapy and showed little improvement to dietary measures; this is in line with others’ findings. Of course, the crucial point is to make the differential diagnosis between primary and secondary LPL deficiency. Among the secondary forms of hypertriglyceridaemia in chylomicronaemic patients the most common is non-insulin dependent diabetes mellitus (NIDDM) .’ NIDDM patients who carry dysfunctional LPL alleles are at risk of severe lipaemia, and the physiological defects in NIDDM may be additive or synergistic with heterozygous LPL deficiency.’ Wienbicki and Reynolds’ patients probably were at least 30-35 years old and had a frank NIDDM. Our patient, by contrast, was very young (1 6 years) when she showed insulinresistant diabetes mellitus, which cannot be regarded as clear type 2. On the other hand, it is unlikely that she had maturity-onset diabetes of the young (MODY), which is an apparent specific subgroup of NIDDM. In Europeans, MODY seems to be rare, and statistically most patients will have IDDM that can be easily controlled by small insulin doses. Finally, diabetes developed in our case 2 years after chylomicronaemia appeared, suggesting a determinant role of the high triglyceride concentrations in the development of insulin resistance and diabetes. As can easily be understood, if there is a gene defect leading to a deficiency of LPL, drugs such as fibrates associated with omega-3 fatty acids and nicotinic acid cannot improve the function of LPL. In addition, the use of lipidlowering drugs, such as fibric acid derivatives, in patients with primary LPL or apo C-I1 deficiency, is controversial.’ Omega-3 fatty acids are effective in hypertriglyceridaemia, and in primary chylomicronaemia due to familial hypertriglyceridaemia, but not in LPL deficiency.’ Our patients have tried such oral therapy for a long time without much or sustained lowering of plasma triglycerides. We disagree that the “moderate atherosclerotic risk in this disorder is more likely to be related to diabetes mellitus or insulin resistance than hyperchylomicronaemia itself”. Premature atherosclerosis can occur in patients with familial chylomicronaemia as a result of mutations in LPL gene.5 In addition, the presence of typically very low plasma highdensity lipoprotein-cholesterol concentrations is another relevant atherosclerotic risk factor. We used the surgical approach in our patient as a last resort and, in fact, triglycerides and plasma glucose returned to normal values without any drug treatment and with the patient on an unrestricted diet. Another goal achieved was the rapid disappearance of the cutaneous, diffuse skin eruptions, which were a relevant aesthetic problem for this young patient.

*G Gasbarrini, G Mingrone, A V Greco, M Castagneto ‘Universita Cattolica del Sacro Cuore. and Centro Shock C N R FacoitB di Medicina e Chirurgia “AgostinoGemeili”.Italy 1

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Tattershall RB.Mild familial diabetes with dominant inheritance. Q J Med 1974;70: 339-57. Chait A, Brunzell JD. Chylomicronaemia syndrome. A d v Intern M e d 1991;37: 249-73. Wilson DA, Hata A, Kwong LK,et al. Mutations in exon 3 of the lipoprotein lipase gene segregation in a family with hyperuiglyceridemia, pancreatitis, and non-insulin-dependent diabetes.J Clin Invest 1993;92: 203-1 1. Richter WO,Jacob BG, Ritter MM, Schwandt P. Treatment of primary chylomicronaemia due to familial hypertriglyceridemia by w-3 fatty acids. Metabolism 1992;41: 1100-05. Benlian P, De Gennes JL, Foubert L, Zhang H, Gagne E, Hayden M. Premature atherosclerosis in patients with familial chylomicronaernia caused by mutations in the lipoprotein lipase gene. NEnglJ M e d 1996; 335: 848-54.

Vol348 * November 30, 1996

Making real sense of MRSA SIR-In a commentary, Patterson (Sept 28, p 836)’ makes several useful points about controlling methicillin-resistant Staphylococcus uureus (MRSA) in hospitals. We agree with Patterson’s assessment of the importance of MRSA infections, which may be both difficult and expensive to treat. MRSA isolates are certainly no less pathogenic than methicillin-sensitive strains, and have sometimes been associated with a significantly higher mortality.’ Furthermore, the community has certainly become an important reservoir for MRSA in which transmission occurs and from which strains may be reintroduced into the hospital environment. However, we wish to express our concern that “standard precautions”’ may be inadequate for acute-care patients, especially in the many UK health care facilities where hand-washing facilities are inadequate or inaccessible, leading to poor compliance with hand-washing-the single most important infection control measure. Under these circumstances the isolation or cohort nursing of patients with MRSA colonisation can be central to reducing nosocomial spread, both in outbreak and non-outbreak situations, if only by providing a reminder to health care workers to wash their hands. We are therefore concerned about the message that this commentary may send to those who question the considerable efforts to detect and isolate patients with MRSA in high risk areas. Our interpretation of both UK guidelines for controlling epidemic MRSA‘ and North American guidelines for isolation precautions in hospitals’ is that patients with colonisation or infection by these organisms should be isolated in a single room or cohort nursed. Clearly the resources available to us for controlling MRSA are limited, and we agree with Patterson that control strategies must be determined at a local level and modified according to individual clinical situations. Our final concern is about surveillance cultures, which “are not recommended as a routine measure”. Without undertaking at least some microbiological screening we would be unable to determine the baseline endemic rate of MRSA colonisation or to estimate the rate of nosocomial acquisition. We would therefore be unable to rapidly detect an outbreak needing further investigation and intervention. Neither would we be able to monitor or appraise our infection control measures. Controlling MRSA can be a time-consuming and sometimes thankless task but we are not yet persuaded that efforts should be relaxed. *Paul R Chadwick, Bryan Marshall, Maeve G L Keaney, Cynthia Shorrock, Pamela Rowland Department of Microbiology. Hope Hospltal. Salford M6 8HD, UK

1 Patterson JE.Making real sense of MRSA. Lancet 1996; 348: 836-37. 2 Cunney RJ, McNamara EB, AlAnsari N, Smyrh EG. Community and hospital acquired Stuphylococcuc uureus septicaemia: 1 15 cases from a Dublin teaching hospital.J Infect 1996;33: 11-1 3. 2 Hospital Infection Control Practices Advisory Committee. Centers for Disease Control and Prevention. Guideline for isolation precautions in hospitals. A m J Infect Control 1996;24: 24-52. 4 Working party of the Hospital Infection Society and British Society for Antimicrobial Chemotherapy. Revised guidelines for the control of epidemic methicillin-resistant Staphylococcus uureus. J Hosp Infect 1990; 16: 351-77.

SIR-Patterson‘ outlines what may be an appropriate response to the problem of MRSA control in the USA. This approach is influenced by a prevalence of MRSA in US hospitals of 29% in 1991.’ The suggestion that acute-care patients colonised or infected by MRSA usually do not require isolation unless the patient is uncooperative, has poor personal hygiene, has an MRSA wound infection that cannot be controlled, or has MRSA pneumonia, is not helpful to 1525

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infection control teams in the UK. This is not a logical approach if, as is accepted in the commentary, stringent control measures are required if an outbreak of MRSA is occurring. Many hospitals in the U K d o not have such a high prevalence rate as that in the USA, and their infection control teams are putting a great deal of their resources and time into MRSA control to prevent a major outbreak. It is our experience that MRSA will spread on acute care wards unless patients colonised or infected with MRSA are isolated and a major outbreak will occur especially if dealing with epidemic strains. At a time when many infection control teams are striving to convince managers that the effort and expense of MRSA controls is worthwhile it is a cause of great concern that an approach applicable to hospitals with very high prevalence rates will be quoted inappropriately as a reasonable strategy for most U K hospitals. Simon F Hill Public Health Laboratory, Poole Hospital, Poole BH15 2JB. U K 1 Evans Patterson J. Making real sense of MRSA. Lancet 1996; 348: 836. 2 Panlilo AL, Culver DH, Gaynes RP,et al. Methicillin resistant Staphylococcus aureus in US hospitals, 1975-1991. Infect Contr Hosp Epidemiol 1992; 13: 582.

SIR-htterSOn’ raises a n important issue in questioning control measures for MRSA infections. Certainly MRSA in chronic care settings is endemic without causing great problems and a more relaxed approach is justified in these institutions. Unfortunately advising such an attitude in acute care settings is impractical. We do not disagree that MRSA strains in some settings can be diverse, but this is not the usual situation. In the U K there are three predominant strains of MRSA (designated EMRSA 3, 15 and 16).2 In our and other U K institutions over 90% of MRSAs are EMRSA 15 or 16. Whether infections due to these strains are sporadic or part of an outbreak becomes a matter of semantics. I n any event it is rarely possible to identify sporadic cases and, therefore, to have a different approach for sporadic cases is not realistic. Furthermore, even if strains were distinct, there would be a delay of a few days before information on molecular or phage typing would be available, and infection control practices would have to be implemented before this information was available. T o avoid cross infection, control procedures have to be implemented as if these strains were epidemic. If strains are distinct, one can never exclude the possibility that a patient may be harbouring a strain which, although distinguishable from known epidemic strains, nevertheless has epidemic potential. For the above reasons we endorse the recommendations of the Hospital Infection Society’ and the World Health Organization‘ as well as the US consensus view.’ Patients identified as being carriers of MRSA or those with MRSA infections should be isolated in single rooms. * A P Fraise, R Wise City Hospital NHS Trust, Birmingham 818 7QH. UK

Patterson JF. Making real sense of MRSA. Lancer 1996; 348: 836-37. PHLS. Epidemic methicillin resistant Staphylococcus aureus. Comnlrrtr Dis Rep 1996; 6: 197. 3 Combined Working Party of the Hospital Infection Society and British Society of Antimicrobial Chemotherapy. J Hasp Infect 1990; 16: 351-77. 4 Ayliffe GAJ. Recommendations for the control of methicillin resistant Staphylococcus aureus. Geneva: World Health Organization, 1996. 5 Mulligan ME, Murray-Leisure KA, Ribner BS, et al. Methicillin resistant Staphylocuccs aureus: a consensus review of the microbiology, pathogenesis, and epidemiology with implications for prevention and management. A m J M e d 1993; 94: 313-28.

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Serum total homocysteine concentration and risk of stroke SIR-In our nested case-control study,’ based on the British Regional Heart Study cohort, men with pre-existing coronary heart disease (CHD) were unintentionally excluded from control selection in 15 of the 17 study towns. This deficit of men with evidence of pre-existing C H D disease in the control group (5% zu 21% expected) has inflated the overall case-control difference in serum homocysteine (tHcy) concentrations. However, the association between tHcy and risk of stroke persists in analyses restricted to cases and controls who were without evidence of C H D at screening. In the original paper, we reported that levels of tHcy (geometric mean, 95% CI) were significantly higher in cases (n=107) than in controls (118): 13.7 (12.7-14.8) versus 11.9 (1 1.3-12.6) pmol/L; p=0.004. The odds ratio for stroke was significantly increased in the fourth quarter of homocysteine relative to the first, odds ratio 2.8 (95% CI 1.3-5.9), with odds ratios of 1.3 and 1.9 in the second and third quarters, respectively. In a n analysis restricted to men without evidence of C H D at baseline (67 cases and 112 controls), levels of tHcy were also significantly higher in cases than controls: 13.1 (12.1-14.2) versus 11.8 (11.2-12.4) pmol/L; p=0.04. T h e odds ratio for stroke was also significantly increased in the fourth quarter of homocysteine relative to the first, odds ratio 2.5 (1.1-6.1), with odds ratios of 1.6 and 1.4 in the second and third quarters, respectively. * I J Perry, on behalf of all authors of original report Department of Primary Care and Population Science, Royal Free Hospital School of Medicine. London NW3 2PF. UK

1 Perry IJ, Refsum H, Morris RW, Ebrahim SB, Ueland PM, Shaper AG. Prospective study of serum total homocysteine concentration and risk of stroke in middle-aged British men. Laircet 1995; 346: 1395-98.

Paediatric HIV infection SIR-Scarlatti’s comment (Sept 28, p 866)’ that “children rarely develop Kaposi’s sarcoma and other HIV-associated tumours” has prompted us to share some preliminary observations. T h e AIDS epidemic is of recent onset in South Africa, and the first symptomatic children were recognised from about 1989 at the King Edward VIII Hospital in Durban, which is one of the largest such facilities in southern Africa, and the only tertiary referral and teaching centre in KwaZulu Natal, serving a paediatric population of about 3-4 million (89% of whom are Black). T h e current antenatal HIV prevalence in black mothers at this institution is 21-24%, and on the basis of a vertical transmission rate of about 34%’ we estimate that about 8% of black infants in KwaZulu Natal are HIV infected. This province is the epicentre of the evolving HIV epidemic in South Africa. Records at our oncology clinic for the past 15 years’ show the rapid impact of HIV/AIDS on the overall pattern of childhood cancer. T h e harbinger of this change was a patient with acute promyelocytic leukaemia diagnosed in 1990. Up to July, 1996, we have diagnosed 14 patients with HIVassociated malignant diseases-12 of these in the past 15 months. Patients with solid tumours and brain tumours have not been included. T h e diagnoses were: Kaposi sarcoma (4); acute leukaemia (2); Burkitt lymphoma (2); T-cell lymphoma (2); mucosa-associated lymphoid tissue (MALT) lymphoma (3) (all with parotid involvement); and an undifferentiated abdominal tumour (1). The most striking

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Vol348 November 30, 1996