Laser photocoagulation alters the pattern of staining for neurotrophin-4, GFAP, and CD68 in human retina.

AIMS: To investigate the staining pattern of neurotrophin-3 (NT3), neurotrophin-4 (NT4), and brain derived neurotrophic factor (BDNF) as well as glial fibrillary acid protein (GFAP) and CD68 in lasered human retina. METHODS: Retinal laser photocoagulation was performed on four patients (two males, two females) with choroidal malignant melanoma 1-6 days before enucleation. Three other enucleated eyes with malignant melanoma and three normal cadaveric donor eyes were used as controls. Immunohistochemistry was performed to investigate the pattern of staining of NT3, NT4, BDNF, GFAP, and CD68 in 7 mm sections of fixed specimens. RESULTS: Expression of NT4 was detected in the inner and outer nuclear layers of all the retinal sections examined but no NT3 and BDNF staining was seen. NT4 staining was found to be less intense in lasered and melanoma controls compared to normal cadaveric donor retinas. There was an upregulation of GFAP expression in both lasered and control eyes with melanoma in comparison with normal controls. CD68 staining was only observed in retinal pigment epithelium and choroid of lasered eyes. CONCLUSION: NT4 is expressed in inner and outer nuclear layers of normal human retina and its expression is downregulated following laser photocoagulation. This occurs in parallel with an increased expression of GFAP suggesting that reactive changes in Muller cells may be responsible for reduced NT4 staining. Expression of CD68 at the site of laser injury is consistent with a wound healing process as a response to local damage.

Enteral human IgG for prevention of necrotising enterocolitis: a placebo-controlled, randomised trial.

BACKGROUND: Neonatal necrotising enterocolitis is a serious, commonly fatal disease in premature neonates. Although feeding with expressed breast milk and other good nursery practices are partly protective, preventive measures are needed. Treating neonates enterally with a mixture of human IgA and IgG, prepared from donated blood, has been claimed to protect against necrotising enterocolitis. However, no IgA preparation is available in Australia. Our aim, therefore, was to identify whether or not enteral IgG could prevent the disorder. METHODS: We did a multicentre, double-blind, placebo- controlled trial. We randomly assigned 768 infants to receive human IgG 1200 mg/kg daily, and 761 to receive placebo, for up to 28 days. Treatment began at the same time as enteral feeding. The primary outcome measure was the proportion of infants who developed definite necrotising enterocolitis during the trial, and any deaths that resulted from the disorder in the treatment and placebo groups. Analysis was on an intention-to-treat basis. FINDINGS: 43 infants developed definite necrotising enterocolitis in the IgG group, ten of whom died. In the placebo group, 41 infants contracted the disorder and six died (p=0.47). 25 infants on IgG and 36 on placebo had suspect necrotising enterocolitis (p=0.14). INTERPRETATION: Supplementation of enteral feeds with human IgG does not reduce necrotising enterocolitis.

Late-onset infections of infants in neonatal units.

OBJECTIVE: To examine regional variations in the incidence of late-onset neonatal infections in Australian and New Zealand neonatal units. METHODOLOGY: A longitudinal, prospective surveillance study of systemic sepsis (septicaemia or meningitis) in 11 neonatal units: 10 in the Australian States of the Northern Territory, New South Wales, Queensland, Victoria and Western Australia, and 1 in Christchurch, New Zealand. The results are reported of late-onset neonatal infection (defined as sepsis after 48 h) for the second year of prospective surveillance, data being collected from 1 October 1992 to 30 September 1993. RESULTS: Data were available on 24535 live births in Australia, representing approximately 10% of all live births in the country. There were 320 episodes of sepsis in Australian units affecting 294 babies. One hundred of these episodes (31%) were early-onset; 3.0% of babies admitted to six tertiary care neonatal units attached to maternity hospitals developed late sepsis, and this rate did not differ between units. The proportion of babies infected was inversely related to birthweight: 22.6% of babies under 1OOOg, but 0.6% over 2000g. Coagulase negative staphylococci were the commonest cause of late-onset sepsis. There were 26 episodes of S. aureus septicaemia, of which only one was due to MRSA. Meningitis occurred in 13 babies (5.9%) with late-onset sepsis. The mortality from late-onset sepsis was 7.7%. CONCLUSIONS: Coagulase-negative staphylococci are the commonest cause of late-onset sepsis of babies in neonatal units. There were no major regional differences in the incidence of, or the organisms causing, late sepsis.

Humeroradioulnar synostosis in a patient with lambdoid synostosis.

We report on a patient with humeroradioulnar synostosis and lambdoid synostosis. The case differs from three previously described cases in minor details, but the upper limb abnormalities are strikingly similar.

Naproxen induced pseudoporphyria in juvenile chronic arthritis.

We report 6 cases of porphyria-like skin reactions in children taking naproxen for juvenile chronic arthritis. The lesions mimicked either erythropoietic protoporphyria or porphyria cutanea tarda, with both forms occurring in 2 patients. Biochemical studies excluded abnormal porphyrin metabolism.