these factors may be present. The precipitous weight loss characteristic of advanced AIDS seems to be related to infection, with low serum albumin and normal or even raised basal metabolic rate in relation to lean body mass. Acute-phase responses may be attenuated in the disease, even when severe proteinenergy malnutrition is absent. There is some evidence of excess loss of lean body mass, again characteristic of cachexia rather than undemutrition. Conversely, gastrointestinal tract infections and tumours are common, and convincing evidence is given of malabsorption as a critically important aspect of this disease, with resulting undernutrition and metabolic compensation (reduced basal metabolic rate). There are many reasons why nutritional intake may be compromised in HIV infection. Oral and oesophageal candidosis causes pain; central nervous system mycobacterial infection leads to nausea; and drugs cause side-effects. Depression is common and worsens existing anorexia. Additionally, weight loss is probably aggravated by the raised metabolic rate
during infections. These issues were thrown into sharp focus when the AIDS Interest Group of the British Dietetic Association drew a large audience from diverse backgrounds for the first UK Conference on Nutrition and HIV in London last April. The meeting opened with a rapid-fire account of a San Francisco practice of almost as many AIDS patients as there are in the entire UK. Treat them early and treat them aggressively. Treat them with algorithms, with supplements, with glutamine, with purines, with pyrimidines; treat them enterally and parenterally! That is what the patients want, and it might help. Some do badly, some do better-maybe nutrition plays a part. Only in discussion did it emerge that there is no evidence that any of these approaches will alter the course of the disease. The assertion that malnutrition can be diagnosed from the patient’s voice over the telephone sparked some doubts among the participants, as did the insistence that low serum albumin is the best biochemical marker for malnutrition-low serum albumin usually indicates infection not malnutrition. Alongside all this, the humbler observations of real data by dietitians and psychologists seemed reassuringly solid, although results of controlled studies and representative sampling are not yet available. Many of the AIDS patients well enough to be approached for questioning depend on liquid feed supplements, yet still they fade away. Body weight lurches further downwards with each acute infection, towards death at about 12 kg (16%) below usual weight. The argument for nasogastric feeding to diminish weight loss during acute infection seems worth further exploration. However, starvation alone does not kill when loss of weight is only 16%. Home parenteral feeding seems to prolong life in terminal cases, especially with cryptosporidial infection. A study from Bloomsbury found this approach was well
tolerated and improved quality of life so that patients were better able to come to terms with their approaching death and to complete specific tasks. The biggest area of debate for further research is early HIV infection. At this stage there are no detectable biochemical abnormalities and there is no evidence yet that dietary modification will affect immune function or the course of the disease. Some vociferous HIV patients accused scientists of neglecting the study of potential diet treatments and of espousing an "ice cream and crisps" philosophy while research focuses on drugs. Of those patients who had sought dietetic advice, 93% had altered their diets towards the healthy-eating guidelines for the general
population. The interpretation-that this was inappropriate since blood cholesterol and heart disease do not matter-may have missed the point that HIV patients still want to think optimistically about the long-term and to have a sensible diet as seen by others. The conference certainly achieved its aim of setting people thinking. AIDS doctors need to get together with specialists in nutrition to design studies. Clear scientific assessment is required of the various nutritional options suggested for HIV patients. Until these are available, there is no sense at all in adopting untested treatments with vitamins, minerals, or
special diets. The general healthy-eating guidelines are as good as any starting point and usually lead to a more nutrient-dense diet. Maintaining or restoring weight and treating any micronutrient deficiencies after acute infection are the next goals. Methods to achieve weight gain need to be refined. Temporarily improving the quality of life and delaying death by enteral or parenteral feeding in terminal cases is reasonable if the patient wishes it, preferably with psychological guidance. 1. Raiten DJ. Nutrition and HIV infection. A review and evaluation of the extant knowledge of the relationship between nutrition and HIV infection. Bethesda: Life Sciences Research Office, Federation of American Societies for Experimental Biology, 1990.
Systemic lupus erythematosus in pregnancy
Although a large proportion of patients with systemic lupus erythematosus (SLE) are women of reproductive age, a clear picture of the effects of pregnancy on the disease (and vice versa) was slow to emerge. The initial small retrospective studies of this interaction yielded conflicting results. Confounding factors were the lack of agreed criteria for the diagnosis of exacerbation and the potential confusion between certain features of normal pregnancy and lupus flare. Over the past decade a degree of consensus seems to have been achieved. If possible, pregnancy should be deferred until the disease is either in remission or has been controlled medically. In a patient with active lupus, pregnancy seems to run a more troubled
with therapy Immunosuppressive prednisone or azathioprine should not be reduced or discontinued merely because of the pregnancy; this may make the lupus very much worse. Although immunosuppressive drugs might harm the fetus many researchers feel that the baby would be at greater danger from uncontrolled maternal disease.’The view that pregnancy per se carries an increased risk of exacerbation has not been supported by comparative studies of non-pregnant control patients. Exacerbations that do occur in pregnancy are often characterised by skin and joint manifestations, which may be controlled with additional prednisone. Termination of pregnancy is not effective in bringing about remission of disease.’ Before the introduction of effective drug therapy maternal deaths were not uncommon, especially after delivery. More recently recognition of milder forms of the disease and improvements in medical management have resulted in low rates of associated maternal mortality. Nevertheless, anxiety about lifethreatening postpartum exacerbation remains and prophylactic steroid cover during the puerperium is often recommended. Wong and colleagues8 arbitrarily augmented the pre-existing dose of prednisone from the thirtieth week of gestation until 4 weeks after delivery and there were no postpartum exacerbations. A randomised trial will be required to establish the value of this approach. Fetal outcome is undoubtedly less favourable in SLE patients than in healthy women. Although there is no evidence of an increase in congenital anomalies, increased frequencies of miscarriage, stillbirth,
growth retardation, and preterm delivery are recognised. There are probably several underlying mechanisms. For example, renal disease and hypertension from any cause may compromise the uteroplacental circulation and SLE is no exception. Hayslett1 noted that the fetal survival rate was 88% in patients with quiescent lupus nephritis but only 64% in those with active disease. Antiphospholipid antibodies were originally detected in patients with SLE. Their presence (especially in high titre) undoubtedly carries an increased risk of pregnancy failure although their exact mechanism of action is uncertain. Suppression of these antibodies with high doses of prednisone improved the fetal outcome in women with a history of recurrent pregnancy loss.9 Enthusiasm for this approach has been tempered by the realisation that not all women with antibodies will lose the fetus, that suppression of antibodies does not always improve fetal outcome, and that there are substantial risks of iatrogenic disease.10 In women without a bad obstetric history, attempts to suppress antiphospholipid antibodies are probably not justified. The reported frequency of fetal loss in SLE pregnancies is highly variable and may depend upon the precise distribution of risk factors (active disease, renal impairment, antiphospholipid antibodies)
within each study population. Overall, about 70-80 % of these pregnancies will result in a livebirth. In view of the potential for obstetric complications these women should be monitored intensively for signs of fetal compromise. Maternal low-dose aspirin therapy in these high-risk cases has yet to be fully evaluated. A small proportion of the newborn infants get a neonatal lupus syndrome," the most serious component being congenital heart block. This complication occurs almost exclusively in the offspring of women with anti-Ro antibodies. The reported incidence of such heart block is 1 in 60 for all SLE pregnancies and 1 in 20 if the mother has the antibody.12 Some of these children will require a permanent pacemaker. Both recurrent pregnancy failure and the delivery of a baby with congenital heart block may predate the diagnosis of connective tissue disease in the mother by several years. After delivery, breastfeeding is generally thought to be safe if the mother is receiving only aspirin or low-dose steroids but is best avoided if other immunosuppressive agents are being taken. There is no evidence that pregnancy alters the long-term survival prospects of a woman with SLE. 1.
Hayslett JP. Effect of pregnancy in patients with SLE. Am J Kidney Dis 1982; 2: 223-28. MW, Meehan RT, Syrop CH, Strottman MP, Goplerud CP.
Pregnancy in patients with systemic lupus erythematosus. Am J Obstet Gynecol 1983; 145: 1025-40. 3. Fine LG, Barnett EV, Danovitch GM, et al. Systemic lupus erythematosus in pregnancy. Ann Intern Med 1981; 94: 667-77. 4. Mintz G, Niz J, Gutierrez G, Garcia-Alonso A, Karchmer S. Prospective study of pregnancy in systemic lupus erythematosus: results of a multidisciplinary approach. J Rheumatol 1986; 13: 732-39. 5. Lockshin MD, Reinitz E, Druzin ML, Murrman M, Estes D. Lupus pregnancy case-control prospective study demonstrating absence of lupus exacerbation during or after pregnancy. Am J Med 1984; 77: 893-98. 6. Meehan RT, Dorsey JK. Pregnancy among patients with systemic lupus
erythematosus receiving immunosuppressive therapy. J Rheumatol 1987; 14: 252-58. 7. Donaldson LB, De Alvarez RR. Further observations on lupus erythematosus associated with pregnancy. Am J Obstet Gynecol 1962; 83: 1461-73.
Wong KL, Chan FY, Lee CP. Outcome of pregnancy in patients with systemic lupus erythematosus: a prospective study. Arch Intern Med
1991; 151: 269-73. 9. Lubbe WF, Butler WS, Palmer SJ, Liggins GC. Fetal survival after prednisone suppression of maternal lupus-anticoagulant. Lancet 1983; i: 1361-63. 10. Lockshin MD, Druzin ML, Qamar T. Prednisone does not prevent recurrent fetal death in women with antiphospholipid antibody. Am J Obstet Gynecol 1989; 160: 439-43. 11. Editorial. Neonatal lupus syndrome. Lancet 1987; ii: 489-90. 12. Ramsey-Goldman R, Hom D, Deng J, et al. Anti-SS-A antibodies and fetal outcome in maternal systemic lupus erythematosus. Arthritis Rheum 1986; 29: 1269-73.
in child abuse
Cycles of violence
Although physical punishment is often used by parents to enforce compliance in young children,1,2 abuse of children by adults or the infliction of physical injury on a child more severe than that which is culturally acceptable is uncommon. In the USA,