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BACKGROUND: Both the global incidence and the prevalence of sexually transmitted infections (STIs) continue to increase, affecting hundreds of millions of individuals, particularly in low-to middle-income countries. Although a definitive diagnosis is desirable to inform STI treatment, syndromic management is the most widely used strategy in resource-limited settings. With the development of point-of-care (POC) tests, it is important to discuss how laboratories will need to adapt to new training and supervisory roles in support of testing, which will largely be performed by peripheral clinical staff. OBJECTIVES: To discuss potential applications of STI POC tests, how they could improve existing STI control strategies and the role of clinical and reference laboratories in support of initiatives to improve STI management and control activities. SOURCES: Narrative literature review and expert opinion. CONTENT: The paper outlines the current status of the STI epidemic worldwide and discusses the problems associated with current approaches to control these infections, particularly in low-resource settings. The roles of clinical and reference laboratories will need to change to provide support for POC and near-patient STI testing as these technologies are introduced into clinical as well as laboratory settings. IMPLICATIONS: Laboratories will be expected to play a leading role in the introduction and implementation of POC and near-patient STI testing. They will be required to facilitate training and provide technical and supervisory support to clinical staff on the use of these technologies to augment existing STI management and surveillance programmes. In order to provide quality service, they will need to develop, introduce and maintain sustainable local quality control and external quality assurance systems. Evidence from implementation research for introduction and scale up of STI POC tests in different STI epidemic and laboratory infrastructure settings is required.

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Experimental and clinical data implicate inadequate erythropoietin production as an important reason that infants acquire this anemia and suggest that recombinant human erythropoietin (r-HuEPO) might be used to treat or prevent it. We therefore randomly assigned 20 small premature infants (birth weight less than or equal to 1250 gm) who were highly likely to require erythrocyte transfusions for anemia of prematurity to receive 6 weeks of treatment with either intravenously administered r-HuEPO (at a dose of 100 units/kg twice each week) or a placebo. Hematologic measurements, transfusion requirements, and growth were followed during therapy and for 6 months thereafter. Treated (EPO) and control babies did not differ with respect to weight, hematocrit, overall mean absolute reticulocyte count, calculated erythrocyte mass, or rate of growth. However, reticulocyte counts increased earlier in patients given r-HuEPO. Six of ten babies in the EPO group, and 8 of 10 assigned to the control group, received at least one erythrocyte transfusion during treatment. For all infants the amount of blood sampled for laboratory tests was strongly predictive of the volume of packed erythrocytes transfused (r = 0.890; p = 0.0001). Of nine infants who had less than 20 ml packed erythrocytes removed for laboratory tests, none of four given r-HuEPO received a transfusion, whereas three of five infants assigned to the placebo group received one. No toxic effects were attributable to r-HuEPO, and no significant changes in leukocyte or platelet counts occurred during treatment. Reticulocyte counts were correlated with simultaneous platelet counts and were inversely related to absolute neutrophil counts in both study groups. We conclude that r-HuEPO administration is safe and feasible at the dose studied. Additional controlled trials utilizing higher doses of r-HuEPO and larger numbers of patients are justified.

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A cohort of 129 infants with birth weights less than or equal to 1250 gm was followed for more than 4 1/2 years (mean +/- SD: 60 +/- 10 months) to determine the independent effects of two medical risk factors--intracranial hemorrhage and severe chronic lung disease--and a parenting risk factor (abuse or neglect) on neurodevelopmental outcome. In infants without any intracranial hemorrhage or parenting risk factors, severe chronic lung disease was not related to neurologic or cognitive outcome. Infants with increasing grades of intracranial hemorrhage had increasing rates of neurologic and cognitive abnormalities. However, the factor associated with the highest incidence of later abnormality was the parenting risk factor. We conclude that infants with medical risk factors may have additional social risk factors, and that both of these influences must be considered in an examination of the long-term sequelae of neonatal complications.

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Sixty of 63 newborn infants weighing less than 1,250 gm, admitted consecutively to the Intensive Care Nursery during a 15-month period, were prospectively investigated for the incidence of intraventricular hemorrhage by early computerized tomography or by autopsy. Nineteen of the 60 infants had evidence of IVH. The incidence of IVH was correlated with the presence of possible neonatal, obstetrical, asphyxial, or therapeutic risk factors. There was a significant difference in only one of the risk factors: birth outside the perinatal center. Fifteen of 27 outborn infants (56%) developed IVH, whereas only four of 33 inborn infants (12%) developed IVH (P less than 0.001). There were no statistically significant differences in maternal obstetrical risk factors, infant risk factors, or indices of birth asphyxia in the inborn compared with the outborn infants. However, perinatal therapeutic risk factors differed between the two groups. Outborn infants were less likely to have received betamethasone (P less than 0.001), were less likely to have their arterial blood gases monitored and stabilized during the first 20 minutes after birth (P less than 0.001), and were given more bicarbonate (P less than 0.001) and more boluses of fluid intravenously (P less than 0.02). The risk of IVH in very low birth-weight infants may be significantly decreased by therapeutic factors at birth. Maternal transport to a perinatal center and intensive neonatal resuscitation may contribute to decreasing the incidence of intraventricular hemorrhage.

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We examined the influence of fetal sex on the occurrence of respiratory distress syndrome in premature infants after maternal treatment with betamethasone. Among treated infants of 1,251 to 1,750 gm birth weight, the incidence of RDS was 40.9% in 22 males and 7.1% (P = 0.03) in 14 females. Cord serum levels of betamethasone were similar for infants of both sexes, and there was no sex difference in suppression of serum cortisol, dehydroepiandrosterone sulfate, and growth hormone after treatment. These findings suggest that prenatal corticosteroid therapy is less effective in male infants than in female infants. This effect is not due to a difference in transfer or metabolism of betamethasone, nor is it reflected in the responsiveness of the fetal hypothalamic-pituitary-adrenal axis to synthetic glucocorticoid.

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The outcome of 114 infants of birth weight 750 to 1,750 gm who received prenatal betamethasone therapy was compared retrospectively to that of 138 infants delivered to untreated women. The incidence of respiratory distress syndrome in all treated infants was 37.7% compared with 50.7% (P = 0.05) in untreated infants. There was no apparent benefit of therapy among infants delivering less than 48 hours after the first dose and among infants less than 750 gm birth weight. Among infants delivering two to ten days after therapy, RDS 25.0 vs 50.7%) and mortality (8.9 vs 22.5%) were significantly reduced. Among surviving infants with RDS, fewer infants in the two to ten-day treated group required oxygen at FIO2 greater than 0.5 for more than 24 hours. Our findings confirm previous reports that prenatal glucocorticoid treatment reduces the incidence of RDS and mortality in premature infants. In addition, they indicate that therapy is more effective when delivery is delayed at least two days, that very small premature infants do not benefit from treatment, and that RDS may be less severe after prenatal exposure to betamethasone.

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