Retrograde ejaculation owing to ectopic erectile tissue.
We report a case of retrograde ejaculation caused by ectopic erectile tissue in the posterior urethra. Transurethral resection of the tissue resulted in antegrade ejaculation.
Biomedical subjects
Publications and source records attributed to J M Heaton.
We report a case of retrograde ejaculation caused by ectopic erectile tissue in the posterior urethra. Transurethral resection of the tissue resulted in antegrade ejaculation.
Four manoeuvres advocated for the assessment of thoracic outlet compression were performed on 64 randomly chosen volunteers. Although only 17% had any symptoms of thoracic outlet compression, 58% had a positive result in at least one of the manoeuvres. Only 2% were positive for more than two manoeuvres. We suggest this low specificity devalues these tests in clinical practice. We were unable to correlate our clinical results with the findings of digital photoplethysmography.
A 40-year-old man, with a history of vasectomy 11 years previously, presented with a tumour in his right testis. At orchidectomy a seminoma was found, together with a nodule on the vas deferens. Histological examination of this area in the vas identified the lesion of vasitis nodosa and also showed it to be the site of proliferating germ cells. The pathogenesis of this lesion is discussed.
Renal biopsy material was examined from 13 patients who had a history of pre-eclampsia and who were biopsied after delivery. The characteristic 'endotheliosis' associated with pre-eclampsia appeared to resolve at varying rates and was not seen in biopsies taken more than 1 month after delivery. Four of the biopsies showed residual focal segmental glomerular lesions which are described. Focal global glomerular sclerosis (eight biopsies), focal interstitial scarring (seven biopsies) and arteriolo-sclerosis (nine biopsies) were also identified. These findings support those earlier reports which indicated that pre-eclampsia is capable of producing persistent renal damage in a small but significant percentage of cases.
This study of thirteen cases of chordoma serves to emphasize the occurrence of three different histological patterns; classical, seven; chondroid, three; and intermediate or mesenchymal, three. The study also suggests that more adequate sampling of these tumours detects the chondroid variant more readily. These varying patterns of differentiation in tumours of notochordal origin suggest that the parent tissue may have the potential to develop along similar lines in the embryo. Thus mesenchymal and cartilaginous tissue formed from notochordal cells could contribute to the formation of the nucleus pulposus and inner portion of the intervertebral disc cartilages. This concept contrasts with the previously held view that the notochord atrophies at an early stage in embryonic development.
An evaluation of the use of horseradish peroxidase labelled antisera against IgG, IgM, IgA and C3 compared with corresponding antisera labelled with fluorescein isothiocyanate has been carried out on renal biopsy material from 200 patients with renal disease. A disparity between the two methods was observed in 10-19% of the readings according to the antigen being demonstrated. The majority of differences recorded would not have influenced the executive diagnosis. Where the immunological results could have influenced the executive diagnosis, 5 probable false results were obtained using innumofluorescence and 4 with immunoperoxidase. Immunoperoxidase has the advantage over immunofluorescence in that it provides a permanent preparation which can be reviewed months or years later. In addition it provides more accurate localization of the immune deposits since the section can be counterstained with Mayer's hemalum and viewed by conventional light microscopy. In view of these advantages we recommend that serious consideration should be given to using immunoperoxidase in place of immunofluorescence for the examination of renal biopsy material.
All the survivors of a series of 88 patients with Henoch-Schönlein nephritis were examined after a follow-up of six and a half to 21 years (mean 9-9). Sixty-one patients had no demonstrable abnormality; six had minor urinary abnormalities; five had hypertension without urinary abnormally or renal dysfunction; four had heavy proteinuria; eight were in chronic renal failure, three of whom were on regular dialysis; and four patients had died within 25 months of onset. Neither corticosteroids nor immunosuppressive drugs alone or in combination appeared to influence the outcome. A clinical presentation with a combination of acute nephritis and a nephrotic syndrome and a high proportion of crescents in renal biopsy specimens was associated with a poor outcome. Neither the clinical presentation nor the renal morphology were, however, precise determinants of outcome. Outcome was not related to age, associated streptococcal infection, or recurrences of the rash. The clinical state two years after presentation was compared with the state six and a half years or more after presentation in 76 patients. The clinical state had changed in 32 patients, in 17 of whom it had deteriorated. It was not possible to identify with any certainty the patients who would deteriorate (or improve). Patients who have had Henoch-Schönlein nephritis should be followed up for at least five years.
Twenty-five renal biopsies from patients with Henoch--Schönlein nephritis were examined using light microscopy, immunofluorescence, 1 micrometer plastic-embedded sections and electron microscopy. The 1 micrometer plastic-embedded sections and electron microscopy showed deposits in mesangial, subendothelial and subepithelial sites. Some of the latter were very large and similar to those which have been described as "humps" in acute proliferative glomerulonephritis. Immunofluorescence showed the mesangial deposition of IgG, IgA and C3 with extension into a peripheral position in some cases. Fibrin was frequently found associated with crescents. The case for Henoch--Schönlein disease being mediated, in part at least, by immune complex deposition, is presented.
The renal papilla has a double blood supply - from both the vasa recta and the calyceal arteries. The importance of the latter supply is not established. A case of polyarteritis associated with papillary necrosis is reported, in which the calyceal vessels, supplying the area, show acute necrotizing arteritis and occlusion. The pathophysiological and clinical implications are discussed.
The clinical and histological findings are described of a patient who presented with the nephrotic syndrome and was found at necropsy to have a bronchial carcinoma. Amyloidosis, renal vein thrombosis, and neoplastic infiltration of the kidneys were excluded. The kidneys showed a diffuse glomerulonephritis of mesangiocapillary type. The possible aetiological association between these two conditions is discussed.
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