Biomedical subjects
Publications and source records attributed to N J Mahy.
We report a case of sarcoidosis which was not diagnosed in life for a variety of reasons. In particular the chest was silent despite extensive pulmonary damage, and florid finger clubbing developed within a very short time.
We have examined the relationship between (a) histochemically demonstrable copper using rubeanic acid, (b) copper-associated protein (CAP) using orcein, and (c) immunoreactive metallothionein (MT) using DNP hapten sandwich staining and have correlated these with histological lesions in 95 liver biopsies from patients with conditions associated with hepatic copper retention, 4 fetal livers, and 25 histologically normal adult controls. No copper or CAP was present in normal adult liver but periportal CAP was present in fetal liver. MT was present in hepatocytes of normal livers with a predominantly perivenular (centrilobular) cytoplasmic distribution varying in staining intensity; all fetal hepatocytes stained strongly for MT. Fifty-two of 95 (55 per cent) abnormal livers contained CAP and 42 (44 per cent) contained both CAP and copper. In CAP-positive livers, the commonest histological lesions were piecemeal necrosis and cholestasis. CAP was present in (a) 15/15 cases of primary biliary cirrhosis including early cases with minimal pathology; and (b) 5/5 cases of Wilson's disease, 6/6 cases of biliary atresia, and 3/9 cases of sclerosing cholangitis. In other conditions, it was present in 25-50 per cent of cases. MT distribution was abnormal in most CAP-positive livers. Necrotic hepatocytes were intensely MT-positive and in Wilson's disease had a characteristic appearance.
A multicentre study of 51 cases of lymph-node infarction seen in the 30-year period 1956 to 1985 was conducted in order to assess both the short- and long-term prognostic implications of the condition. In 14 cases malignant lymphoma was found synchronously with the infarct. Of the remaining 37 patients with apparently 'benign' lymph-node infarction only six showed manifestations of malignant lymphoma in the follow-up time studied (mean = 48 months; range 1-156 months). These subsequent malignant lymphomas all occurred within 2 years of the lymph-node infarction. A postal enquiry and collation of other cases in the medical literature indicates that a minority (26 of 81) have developed malignant lymphoma, and that these lymphomas, too, have all appeared within 2 years. Thorough examination of both the infarcted lymph nodes and others resected at the same time is mandatory in order to exclude concomitant or underlying malignant lymphoma. Two years after lymph-node infarction the risk of malignant lymphoma is negligible.
Lymph node lesions attributable to ischaemia are described in the mesenteric nodes from 10 patients with volvulus of the small and large bowel. Frank infarction, the microanatomy of which differs from that seen in superficial lymph nodes, is one of the nodal lesions evoked by ischaemia. Two others in the form of lymphocyte depletion and capsular hypervascularity also appear to result from vascular occlusion. These three lesions were also found in nodes associated with 'primary' venous and arterial infarction of the bowel mucosa, but not in non-vascular diseases of the small bowel or colon. The enhanced frequency of infarction in volvulus with mucosal necrosis, as opposed to cases with 'primary' vascular thromboses suggest that ischaemic lymph node changes are more frequent when several sets of vessels are occluded. Distension of lymph node sinuses, erythrocyte extravasation, and dilatation of small intranodal vessels were not restricted to vascular cases, and appear to be less specific reactions to ischaemia. The range of ischaemia-induced reactions is wider than has hitherto been recognized in human lymph nodes.
Twelve normal volunteers received two doses of 3 g amoxycillin at weekly intervals on up to five occasions. Amoxycillin-resistant oral streptococci were not isolated from any subject beforehand, but they had appeared in all eleven subjects (who could be included in the analysis) by the end of the investigation, and in one subject after one administration of double dose amoxycillin. Resistant streptococci were undetectable in all volunteers 13 weeks after their last dose of amoxycillin. All resistant streptococci identified were Streptococcus sanguis (non-dextran-producing), many were highly resistant to amoxycillin and some were also moderately resistant to erythromycin. The minimum bactericidal concentrations for the most resistant streptococcal strains isolated were less than the peak serum amoxycillin concentrations expected following a 3 g oral dose of amoxycillin. In the majority of volunteers the counts of oral resistant streptococci had greatly declined by about 6 weeks following the last administration of a double dose of amoxycillin. If further dental treatment liable to cause bacteraemia is required within six weeks of double dose amoxycillin prophylaxis an alternative regimen should be sought.