Effect of phenobarbitone and pre-eclamptic toxaemia on neonatal jaundice.
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Biomedical subjects
Publications and source records attributed to B Wood.
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The normal human neonate has a copper profile indistinguishable from Wilson's disease, and we have previously postulated that this disease is caused by genetic failure to switch from the fetal to adult mode of copper metabolism. This study validates the developing guinea pig as a suitable animal in which to study copper ontogeny. At birth, liver copper concentrations are 7 times higher than in adults and serum copper and ceruloplasmin are 27 and 21% of adult values, respectively. A 53% fall in liver copper occurs in the 4 days after birth. This is associated with a marked increase in bile copper output, which does not parallel increasing bile flow. Liver copper falls, and serum copper and ceruloplasmin increase to near adult levels in the 30 days after birth. Until the sixtieth day of gestation, liver copper was significantly increased in copper-stressed littermates, although paradoxically at birth, concentrations were significantly lower. In copper-stressed fetal animals, bile copper output increased markedly before birth. Metallothionein was the dominant copper-binding protein in the fetal liver but a minor component in the adult. Superoxide dismutase activity only developed after birth. We conclude that the postnatal switch from the fetal to adult mode of copper metabolism involves activation of biliary excretion and ceruloplasmin export as well as changes in the association of copper with hepatic copper proteins. Similarities between the fetus and Wilson's disease suggest that this disease is caused by failure of this postnatal adaptation process.
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The technique of epiglottic laryngoplasty, previously described for reconstruction following near total laryngectomy for glottic carcinoma, has been used in selected patients with severe glottic and subglottic stenosis. Our experience in four patients suggests that it is useful for 1) laryngeal stenosis in which there is loss or collapse of the external cartilaginous framework, and 2) laryngeal stenosis which is refractory to the usual forms of therapy. The technique is a technically simple, one-stage procedure which provides its own endolaryngeal mucosal lining, as well as autogenous cartilaginous support. It has been successful in restoring adequate airway and preserving voice without interfering with deglutition or laryngeal competence in most patients.
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To determine whether any potentially reversible variables are related to the development of hand gangrene in diabetic patients on dialysis, the authors compared 15 patients with hand gangrene (group A) to three control groups of diabetics on dialysis: 20 patients with foot gangrene (group B); 31 patients without gangrene of the extremities (group C); and 20 patients without hand arterial calcifications (group D). All patients in groups A-C had medial arterial calcifications of the hands. Group A patients started dialysis at an earlier age (p less than 0.05), were treated for end-stage renal disease (ESRD) for a longer time period (p less than 0.05), and had a lower mean serum albumin concentration during the dialysis period (p less than 0.05) than the patients in the control groups. Hand gangrene also appeared to be associated with the presence of a functioning arterio-venous fistula in the extremity with the gangrene, with loss of function of renal transplant, and with hyperaluminemia. Other variables, including serum parathormone, were not different for the four groups. Logistic regression showed that the following were risk factors for hand gangrene: hypoalbuminemia, long duration of ESRD treatment, hyperphosphatemia, high insulin dose, hypercholesterolemia, and hypoglycemia. In diabetics on dialysis, gangrene develops in hands with medial arterial calcifications, but does not correlate with measures of calcium or phosphorous metabolism. Predictors of hand gangrene include certain potentially reversible clinical and biochemical variables.
The purpose of this preliminary study is to evaluate the effectiveness of the titanium hemi-great toe implant. The device is found to be successful in helping to treat painful degenerative joint disease of the first and second metatarsophalangeal joints. The implant's most promising application appears to be use in patients below the age of 50 years manifesting metatarsophalangeal joint dystrophy, with subsequent clinical debilitation, who become surgical candidates.
This is the first report of brachial plexus inflammation associated with clinical herpes zoster paresis. A 78-year-old female with a 3-week history of herpes zoster of the C4, C5, and C6 dermatomes developed left upper arm monoplegia. She died from an acute myocardial infarction. Post-mortem provided a rare opportunity to study the neuropathology of herpes zoster motor involvement. Histology of the brachial plexus showed extensive lymphocytic infiltration, myelin breakdown, and preservation of axons without vasculitis. The cervical spinal cord showed perivascular lymphocytic cuffing and no anterior horn necrosis. We suggest, the brachial plexus inflammation was a distal extension of a dorsal ganglionitis. Brachial plexus neuritis may be a direct cause of reversible upper limb paresis in herpes zoster. We demonstrate the motor neuropathy is an inflammatory demyelinative process consistent with the recovery observed in a number of patients. We postulate post-herpetic neuralgia may be related to an ongoing inflammatory process.