Philippe Van de Perre
National AIDS Control Programme
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American Journal of Obstetrics and Gynecology | 1995
Philippe Van de Perre
Human milk has been considered only recently as a source of transmission for the human immunodeficiency virus. The estimated postnatal transmission rate from mothers who acquired human immunodeficiency virus infection while lactating is 26% (95% confidence interval 13% to 39%) and may be in the range of 8% to 18% from mothers who were infected before becoming pregnant. Risk factors for postnatal transmission include maternal immune deficiency and the presence of human immunodeficiency virus-infected cells in milk. Some milk factors may be protective against postnatal transmission such as specific immunoglobulin A and immunoglobulin M and a molecule able to inhibit the binding of human immunodeficiency virus to CD4. In addition to its safety and its birth-spacing properties, breast-feeding provides immunologic protection and an ideal nutritional content to the infant. In a poor hygienic environment artificial feeding dramatically increases morbidity and mortality from diarrheal diseases and respiratory infections. Consequently, according to our current knowledge the World Health Organization and the United Nations Childrens Fund reasonably recommend continuing breast-feeding promotion in women living in settings where infectious diseases and malnutrition are the primary causes of infant deaths such as in many developing countries. In settings where infectious diseases and malnutrition are not the primary causes of infant deaths, such as in most of the settings in the developed world, the advisory group recommends against breast-feeding for mothers with proved human immunodeficiency virus-1 infection.
The Lancet | 1992
S.D.R Green; Nganga A; W.A.M. Cutting; Davies Ag; Philippe Lepage; Philippe Van de Perre; Msellati P; François Dabis; Patrick Matondo
Dr. Athale and colleagues from Lusaka (Aug 15 p434) have suggested that in countries of high HIV prevalence BCG (bacillus Calmette-Guerin) vaccination should be given only to children over 12 months of age because of the risk of disseminated BCG infection. By that age it should be clear which children are infected. In a prospective study in Zaire of children born to HIV positive and negative mothers (seroprevalence 3.8% vertical transmission rate 23%) all received BCG at birth. During follow-up of 2 years 9 of 21 HIV-infected children developed tuberculosis which was disseminated in only 1 and 7 had a family contact. None had BCG adenitis. All responded well to short- course chemotherapy (avoiding thiacetazone). In the 2 matched control groups uninfected by HIV 12 developed tuberculosis--4 born to 21 HIV- positive mothers and 8 born to 21 HIV-negative mothers. None of these had disseminated infection and 1 had BCG adenitis (mother seronegative). The HIV-infected and noninfected groups did not differ significantly. In the past 10 years we have had only 1 case of probable disseminated BCG infection in a child of 5 months. He was vaccinated at 3 months and developed suppurating axillary BCG adenitis. His weight curve was static and he had persistent fever. Radiography showed typical miliary lesions and he responded well to short-course therapy. His mother was seropositive for HIV and he had no family tuberculosis contacts. We agreed that many cases of tuberculosis in children infected with HIV simulate the adult form with cavitation and extensive pneumonias but only in children over 2 years old. We suggest that this finding is probably due to progression of the primary focus rather than reactivation or progression of BCG vaccination. Such children respond well to short-course therapy but tend to relapse and have persisting problems because of lung damage (bronchiectasis). HIV infection in infants has a bimodal presentation. The early presenters will have symptoms by 12 months but only a few late presenters will have them. We would not expect nursing staff at a busy clinic or vaccination center to have time to pick out these with mildly symptomatic HIV infection. Although there is some evidence that BCG at 3 months produces a larger induration more frequent scar formation and less lymphadenopathy than if it is given at birth we suggest that in African countries this is not the time to change the policy of giving BCG near birth. Attendance at vaccination clinics falls off strikingly after the measles vaccine at 9 months and therefore many healthy children would not receive BCG. However a good case could be made for chemoprophylaxis for children for HIV-positive mothers who have had active tuberculosis in the previous 2 years. (full text)
International Journal of Infectious Diseases | 1996
Jean Batungwanayo; Henri Taelman; J. Bogaerts; Jan Clerinx; A. Kagame; Armand Van Deun; Ingrid Morales; Joseph Van Den Eynde; Philippe Van de Perre
Abstract Objectives: To analyze and compare the clinical, diagnostic, and therapeutic features of tuberculosis (TB) in human immunodeficiency virus (HIV)-seropositive and seronegative patients. Methods: A 1-year retrospective review of medical records and charts of TB patients admitted to and followed-up at the Department of Internal Medicine of the Centre Hospitalier de Kigali (CHK), Kigali, Rwanda. Results: Tuberculosis was diagnosed in 510 patients. Complete data, including HIV serologic testing, were available for 377 patients (74%) of whom 227 were male and 150 female, aged 17–70 years (mean, 33 y). Human immunodeficiency virus antibodies were detected in 334 (88.6%) of the 377 evaluable patients. A definite diagnosis of TB was established in similar proportions of HIV-seropositive (66%) and HIV-seronegative (63%) patients. The HIV-infected patients differed from the patients without HIV infection in the following features: proportion of patients in the age group 20–39 years (80% vs. 58%; P=0.001), extrapulmonary manifestations (56% vs. 40%; P=0.045), lower/middle lobe infiltrates (18% vs. 6%; P=0.07), presence of cavities (15% vs. 34%; P=0.002), pleural disease (23 vs. 12%; P=0.08), tuberculin anergy (67% vs. 26%; P Conclusions: Active TB was strongly associated with HIV infection in urban Rwanda. The clinical and radiographic presentation of TB, described in HIV-seropostive patients hospitalized at teh CHK, is most frequently atypical and highly suggestive of advanced HIV disease.
JAMA | 1992
Susan Allen; Antoine Serufilira; J. Bogaerts; Philippe Van de Perre; Nsengumuremyi F; Christina P. Lindan; Michel Caraël; William Wolf; Thomas J. Coates; Stephen B. Hulley
JAMA | 1991
Susan Allen; Christina P. Lindan; Antoine Serufilira; Philippe Van de Perre; Amy Chen Rundle; Nsengumuremyi F; Michel Caraël; Joan Schwalbe; Stephen B. Hulley
Studies in Family Planning | 1991
Susan Allen; Christina P. Lindan; Antoine Serufilira; Philippe Van de Perre; Amy Chen Rundle; Nsengumuremyi F; Michel Caraël; Joan Schwalbe; Stephen B. Hulley
Studies in Family Planning | 1993
Susan Allen; Antoine Serufilira; J. Bogaerts; Philippe Van de Perre; Nsengumuremyi F; Christina P. Lindan; Michel Caraël; William Wolf; Thomas J. Coates; Stephen B. Hulley
Cahiers d'études et de recherches francophones / Santé | 1997
Xavier Anglaret; François Dabis; Jean Batungwanayo; Christian Perronne; Henri Taelman; Dominique Bonard; Fatoumata Sylla-Koko; Valériane Leroy; Philippe Van de Perre; Jean-Louis Vildé; Roger Salamon
Archive | 1992
D.G. Hitimana; Philippe Lepage; Philippe Van de Perre; Philippe Msellati; B. Mukamabano; Etienne Karita; François Dabis
Cahiers d'études et de recherches francophones / Santé | 1994
François Dabis; Philippe Lepage; Philippe Msellati; Philippe Van de Perre; Nsengumuremyi F; D.G. Hitimana; Joël Ladner; Valériane Leroy