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.     

Prostanoid stimulation of anion secretion in guinea-pig gastric and ileal mucosa is mediated by different receptors.

1. The receptors that mediate stimulation of anion secretion by prostanoids in isolated preparations of guinea-pig gastric and ileal mucosa have been compared by use of selective prostanoid agonists and antagonists. 2. In gastric mucosa, the relative potency of agonists suggested that the control of anion secretion in this tissue was complex and may be mediated by EP2, EP3, and TP receptors. A role for TP receptors was confirmed with the TP-selective antagonist AH23848 which inhibited short circuit current responses to the TP receptor agonist U-46619 with a pA2 value of 8.44 but was without effect on responses to prostaglandin E2 (PGE2) or the EP selective agonist, sulprostone. 3. In ileal mucosa, the relative potency of agonists differed from that observed in gastric mucosa and was consistent with the view that anion secretion in this region of intestine was controlled by DP and EP2 receptors. 4. These studies suggest that anion secretion in gastric and ileal mucosa is controlled by different prostanoid receptor subtypes and so provide important information for the design of prostanoids which may protect gastric mucosa and that are free from side effects such as diarrhoea.     

How do clinicians learn to request permission for autopsies?

A postal survey of 434 clinicians at four local hospitals was undertaken in order to identify the methods by which clinicians learn how to request permission for hospital autopsies and to assess the preferred techniques and timing of relevant communication skills training. The majority of 128 responding clinicians had learnt through personal experience with some assistance from senior colleagues and peers. Few clinicians appeared to have learnt through formal training. The preferred methods for the provision of communication skills training were training in small groups (such as seminars or tutorials) and observation of clinicians at work. The most desirable time for the provision of this training was considered to be between the beginning of the final undergraduate year and the end of the pre-registration house officer year. The communication skills training provided within medical education is in need of improvement. More emphasis should be given to clinical-task- or situation-specific applications such as requesting permission for autopsies.     

Presence of 3-fucosyl-N-acetyllactosamine shown by monoclonal antibody AGF 4.48 in Reed-Sternberg cells.

A series of 50 specimens of Hodgkin's disease and 10 of reactive follicular hyperplasia were examined by means of indirect immunoperoxidase staining with a monoclonal antibody AGF 4.48: this is known to bind to 3-fucosyl-N-acetyllactosamine, which, in particular, is expressed by granulocyte series cells. Most Reed-Sternberg and many Hodgkin's cells were labelled by the antibody after pretreatment with neuraminidase. Routinely processed paraffin wax embedded sections proved suitable for staining. The findings were comparable with those reported by others with monoclonal antibodies to various other granulocyte markers. This technique is of potential diagnostic value.     

Interaction of Angiotensin with Disseminated Intravascular Coagulation: A Possible Mechanism in the Genesis of Acute Renal Failure

Because of the importance of the renin-angiotensin system in renal homeostatic mechanisms, the effect of angiotensin administration upon disseminated intravascular coagulation has been studied in rabbits. An infusion of angiotensin II (0.1 μg/kg/min for 2 hours) produced neither histologic abnormalities in the kidneys nor an elevation of creatinine. After an infusion of thrombin (2.0 units/kg/min for 2 hours) only 3 of 10 rabbits, when sacrified 24 hours later, showed histologic lesions comprised of occasional fibrin thrombi and foci of tubular necrosis. Creatinine levels did not rise. In contrast, the combination of angiotensin and thrombin resulted in renal lesions in 12 of 14 animals. Four had frank cortical necrosis, while combinations of tubular necrosis, glomerular thrombosis and segmental glomerular infarction occurred in the others, together with elevated creatinine levels. Blockade of α-adrenoreceptors with phenoxybenzamine in 12 animals did not prevent either these histologic changes or creatinine elevation, showing that the effect of angiotensin was independent of α-adrenoreceptor stimulation. The synergistic interaction between angiotensin and disseminated intravascular coagulation was not explained by differences in the consumption of plasma fibrinogen but apparently was due to localization of fibrin thrombi within glomerular capillaries by the vasomotor actions of angiotensin, as has previously been shown to occur with α-adrenoreceptor simulation. Such a mechanism might contribute to renal glomerular deposition of fibrin in acute ischemic renal failure.