Lifetime Costs of Vertically Transmitted HIV/AIDS
November 1, 1997
Lifetime Costs of Vertically Transmitted HIV/AIDS
ABSTRACT & COMMENTARY
Synopsis: The estimated lifetime costs of caring for a child with vertically acquired HIV/AIDS was estimated to be $493,936 from 1987 to 1995.
Source: Havens PL, et al. Lifetime cost of care for children with human immunodeficiency virus infection. Pediatr Infect Dis J 1997;16:607-610.
Havens and associates estimated the cost of caring for a child with vertically acquired HIV/AIDS in Wisconsin, a state with a low prevalence of HIV among pregnant women. The records of 29 children with perinatally acquired HIV infection were reviewed. Out patient and hospital charges were tallied for each child. These included charges for inpatient hospitalization, emergency room and outpatient clinic visits, as well as pharmacy, radiology, and laboratory testing costs. Physician fees and costs of nursing and social work involvement were not included. The median survival time of these children was 10 years, which is comparable to a median survival time of 113 months reported from a much larger series of patients.1 Havens et al assumed that hospital-based charges accounted for 83% of the total charges. The authors estimate that the lifetime medical costs of a child with vertically transmitted HIV/AIDS in their area is $493,936 (estimate ranged between $172,490 and $609,649). This is considerably higher than other reported cost estimates. It is possible to reduce the rate of perinatal transmission of HIV from an infected mother to her infant from 25.5% to 8.3% by means of prenatal identification and zidovudine therapy of the infected pregnant woman.2 Havens et al believe that, based upon their estimate of the cost of treating an infected child, programs to detect and treat infected mothers would be cost-effective.
COMMENT BY WARREN ANDIMAN, MD
It has become customary among the great health bureaucracies of the world to subject many public health interventions and treatments to cost-benefit analysis. For example, public health economists in the past have tried to decide whether the consumer was getting a good deal from immunization programs against common childhood pathogens. We spend millions of dollars each year successfully preventing paralytic polio and congenital rubellasevere diseases that are relatively exceptional outcomes of very common infections. Only those whose memories recede far enough into the past to recall the dreadful lives lived inside iron lungs or inside the deaf and blind bodies of children with congenital rubella understand fully the exceptional value associated with the viral vaccines of childhood.
AIDS is an expensive disease. As the work of Havens et al attests, it costs about a half million dollars to provide most of the medical care required during the median 10-year life of an HIV-infected child. Of course, the extraordinary dollars-and-cents cost of this disease says nothing about the emotional and physical toll that the disease exacts from the infected children and their families, not the least of whom are the uninfected siblings who bear witness to (and ultimately survive) the sicknesses, sadness, and deaths of their parents, brothers, and sisters.
It is now possible, using the findings from AIDS Clinical Trials Group protocol 076, to reduce by at least two-thirds the risk of vertical transmission of HIV. What’s required is universal counseling and testing of all pregnant women at risk for HIV so that those who are found to be infected can be treated with azidothymidine (AZT) during pregnancy and delivery. Havens et al estimate that even in a low-incidence state like Wisconsin, such a policy would have an extremely beneficial economic effect. Think of the emotional benefit that would accrue to the mother and the physical benefit that would accrue to the child each time an episode of vertical transmission is prevented by a bit of counseling, an HIV antibody test, and about a thousand dollars worth of AZT. Now, that’s real bang for your bucks. (Dr. Andiman is Professor of Pediatrics and Director of the Pediatric HIV Service, Yale University School of Medicine.)
References
1. Bernhardt HX, et al. Natural history of human immunodeficiency virus disease in perinatally infected children. Pediatrics 1996;97:710-716.
2. Centers for Disease Control and Prevention. Recommendations of the US Public Health Service Task Force on the use of zidovudine to reduce perinatal transmission of human immunodeficiency virus. MMWR Morb Mortal Wkly Rep 1994;43(RR12:1-10).
Identifying Vesicoureteral Reflux in Newborns
ABSTRACT & COMMENTARY
Synopsis: This paper describes a multicenter study that sought to identify the incidence of vesicoureteral reflux in newborns at higher risk of this abnormality by virtue of a family history. The authors seek to determine if the early institution of a long-term antimicrobial prophylaxis can prevent renal scarring and its sequelae.
Source: Scott JES, et al. Screening of newborn babies for familial ureteric reflux. Lancet 1997;350:396-400.
Over a three-year period, 20,891 women delivering infants at three hospitals in Great Britain completed a questionnaire regarding a family history of vesicoureteral reflux (VUR) in them, a previous baby, or another relative. Approximately 1% had a history in which VUR was either confirmed or presumed. Their infants underwent renal ultrasonography and contrast cystography anywhere from two days to more than 13 months after birth (median, 27 and 32 days, respectively). Thirty-eight infants had VUR (20%). In 27 of these (71%), the affected relative was either the mother or an older sibling. The risk of reflux was 22.5% if the mother or a sibling was the index case and 12% if the index case was another relative. As expected, ultrasonography was not helpful in diagnosing reflux. Infants with VUR also had DMSA cortical scintigraphy at three months, and one was abnormal, suggesting scarring or dysplasia. An attempt was also made to randomize infants with VUR to receive either long-term trimethoprim-sulfa prophylaxis or placebo. The number consenting to this phase of the study was restrictively small. Scott and colleagues conclude that pregnant women should be questioned regarding a family history of VUR, and, if such a history is documented, their newborns should be screened with cystography.
COMMENT BY THOMAS KENNEDY, MD, FAAP
This study nicely confirms what one may have surmised; infants born to families with a documented or suspected history of VUR will have a presumably higher incidence of this abnormality. I say presumably higher because the true incidence of reflux in the newborn population at large is not precisely known, and, for ethical reasons, it should not be. A compilation of data from many sources suggests the incidence is about 1.5%, thus making the 20% incidence in the current study much increased. However, we know the incidence of VUR is markedly increased in siblings with an incidence of 20-50%.
I feel uncomfortable with what the investigators did in this study, much the same way I feel about the recommendation to investigate the brothers and sisters of a child found to have reflux following a UTI. Scott et al performed radio contrast cystograms, a reasonably safe, but nevertheless invasive, test with finite radiation exposure on 186 infants, some of whom had a family history where the diagnosis of VUR was merely assumed. Although it is true that 20% showed reflux, 80% did not. Thus, the large majority of infants who underwent two expensive imaging studies had normal results. For those who were identified, it is not clear what, if any, clinical significance the VUR may have and what therapeutic measures should be considered. The proposal for a randomized, antimicrobial trial underscores this uncertainty, and I was relieved that Scott et al did not propose surgical reimplantation as a possible option.
Many of the answers regarding the natural history of VUR, its relation to renal scarring and long-term sequelae, with and without the presence of symptomatic infection, or asymptomatic bacteriuria remain frustratingly unclear. Current wisdom holds that an infant’s kidney is most susceptible to scarring caused by infection, and that parenchymal infection is more likely in the presence of reflux. Furthermore, additional scarring, progressive scarring, or both seems to occur largely independent of surgical correction of the reflux or prevention of future infections. Therefore, the challenge of UTIs in infancy to the pediatrician is clear. At a time when the diagnosis of UTI is most difficult because the signs and symptoms are so vague and nonspecific and the acquisition of urine so problematic, a prompt diagnosis and treatment is critical. The most important weapon a pediatrician can carry is a high index of suspicion for UTI when confronting a clinically ill or febrile infant. If the risks of VUR and UTI are understood by pediatricians and parents of infants with a family history (especially in the mother or a sibling), appropriate measures to identify and treat a first UTI can be taken, and invasive imaging can be avoided.
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