Benign intracranial hypertension and recombinant growth hormone therapy in Australia and New Zealand

Benign intracranial hypertension (BIH) is reported in three children from Australia and one from New Zealand, who were being treated with recombinant human growth hormone (rhGH). Three males and one female, aged between 10.5 and 14.2 y, developed intracranial hypertension within 2 weeks to 3 months of starting treatment. A national database, OZGROW, has been prospectively collecting data on all 3332 children treated with rhGH in Australia and New Zealand from January 1986 to 1996. The incidence of BIH in children treated with growth hormone (GH) is small, 1.2 per 1000 cases overall, but appears to be greater with biochemical GHD (<10IUml ^-1), i.e. 6.5/1000 (3 in 465 cases), relative risk 18.4, 95% confidence interval 1.9-176.1, than in all other children on the database. The incidence in patients with Turner's syndrome was 2.3/1000 (1 in 428 cases). No cases in patients with partial GHD (10–20 IUml ^-1) or chronic renal failure were identified. Possible causative mechanisms are discussed. The authors'practice is now to start GH replacement at less than the usual recommended dose of 14IUm-² week^-1 in those children considered to be at high risk of developing BIH. Ophthalmological evaluation is recommended for children before and during the first few months following commencement of rhGH therapy and is mandatory in the event of peripheral or facial oedema, persistent headaches, vomiting or visual symptoms. The absence of papilledema does not exclude the diagnosis.     

A prospective radiologic and neurologic follow-up study of 61 HIV-1 -infected subjects: early beginning and slow progression of brain atrophy

The course of the organic brain disease caused by human immunodeficency virus (HIV-1) was evaluated in a follow-up study. The primary material included 200 consecutive HIV-1 infected persons. Sixty-one subjects, in whom other brain-affecting factors were excluded, consented to the follow-up. They underwent 278 radiologic examinations: computed tomography, magnetic resonance imaging, or a combination of both (mean 4.6 examinations/subject). Clinical neurologic status and, in 40 subjects, cognitive performance were repeatedly evaluated. Sixteen subjects were followed up until death and 11 of them were autopsied. Median follow-up time was 27 mo (range 2.5–66 mo). The most common radiologic finding was atrophy, found in 19 subjects at study entry and developing in 10 subjects during the study. Twenty-four subjects (39%) showed the development and/or progression of atrophy. Atrophic changes progressed most rapidly in acquired immunodeficiency syndrome (AIDS), but mild developing/progressive atrophy was found even in 33% of asymptomatic or neurologically intact subjects. Cognitive and radiologic worsening were simultaneous in 6/7 subjects with declining neuropsychologic test performance. Signal intensity changes including HIV-1 leukoencephalopathy appeared in AIDS patients with clear cognitive decline.     

O,O′-二烷基-O″-(5-取代-3-苯并噻吩乙腈肟)磷酸酯及硫代磷酸酯的合成

合成了18个O,O′-二烷基-O″-(5-取代-3-苯并噻吩乙腈肟)磷酸酯及硫代磷酸酯类化合物(Ⅰ_1～18)。初步杀螺试验结果表明,其中5个化合物,即Ⅰ_2,3,7,11,12有明显的杀螺增效作用。     

Closed cervicocranial trauma, "false aneurysm" of the internal carotid artery and brain infarction

A 17-year-old man developed acute hemiparesis 6 months after a motor cycle accident. In the accident he had a closed trauma on the contralateral side of the head and the neck, with multiple bone fractures. Aortocervical angiography, performed after the infarction, revealed a 2.5 cm long aneurysmatic dilatation in the internal carotid artery, the presumably source of embolic infarction. This and the 24 other cases gathered from the literature support the notion that closed neck trauma may create "false aneurysm" which again may cause neurological deficits.     

Radiological signs in newborns exposed to primary Toxoplasma infection in utero

A total of 44 181 serum samples from 16 733 pregnant women were analyzed for findings suggesting primary Toxoplasma infection. Thirty-seven newborns exposed to maternal primary Toxoplasma infection in utero were studied prospectively with ultrasound, CT, and MRI for signs of intrauterine infection. Their mothers had been treated during pregnancy, and all infants were treated. The children were assigned to three groups according to their mothers' serological status, and the radiological results were compared with the clinical outcome. Although radiological signs were scarce, ultrasound findings combined with maternal serology were found to be significantly related to clinical outcome. Received: 19 October 1994 Accepted: 28 April 1996     

Sera from patients with heparin-induced thrombocytopenia generate platelet-derived microparticles with procoagulant activity: an explanation for the thrombotic complications of heparin-induced thrombocytopenia

Heparin-induced thrombocytopenia is characterized by moderate thrombocytopenia and thrombotic complications, whereas quinine/quinidine-induced thrombocytopenia usually presents with severe thrombocytopenia and bleeding. Using flow cytometry and assays of procoagulant activity, we investigated whether sera from patients with these immune drug reactions could stimulate normal platelets to generate platelet-derived microparticles with procoagulant activity. Sera or purified IgG from patients with heparin-induced thrombocytopenia stimulated the formation of platelet-derived microparticles in a heparin-dependent fashion. Further studies showed that heparin-induced thrombocytopenia sera also produced a marked increase in procoagulant activity. In contrast, sera from patients with quinine- or quinidine-induced thrombocytopenia did not generate platelet-derived microparticles nor generate increased procoagulant activity. However, quinine/quinidine-induced thrombocytopenia sera produced a significant increase in the binding of IgG to platelets in a drug-dependent fashion, whereas sera from patients with heparin-induced thrombocytopenia demonstrated no drug-dependent binding of IgG to platelets. We also observed increased levels of circulating microparticles in patients with acute heparin-induced thrombocytopenia compared with control patients. Our observations indicate that the generation of procoagulant platelet-derived microparticles in vivo is a plausible explanation for the thrombotic complications observed in some patients with heparin-induced thrombocytopenia.