Aims: Traditionally, advanced stage ovarian carcinoma is treated by debulking surgery followed by chemotherapy. However, in some circumstances preoperative chemotherapy may be given before optimal surgical debulking. This study aims to describe the morphological features found in ovarian carcinoma after chemotherapy because these have not been detailed previously. Methods: Histological sections were examined from 18 cases of ovarian carcinoma that had been treated by preoperative chemotherapy. The morphology was compared with any pre-chemotherapy biopsies that had been performed. Tumours were classified as showing morphological features suggesting a good response to chemotherapy (n = 14) or as showing little or no response (n = 4). Serum CA125 values before and after chemotherapy were compared. In all cases, the mitotic activity index (MAI), volume percentage of epithelium (VPE), and mean nuclear area (MNA) of tumour cells were calculated. Results: The preoperative biopsies were all typical ovarian serous or endometrioid adenocarcinomas. Morphological features present in the group responding to chemotherapy included the presence of small groups or single tumour cells in a densely fibrotic stroma. Tumour cells were characterised by both nuclear and cytoplasmic alteration, making accurate tumour typing and grading impossible. Nuclear features included the presence of bizarre enlargement with hyperchromatism, irregularity of outline, and chromatin clumping or smudging. Cytoplasmic alterations included intense eosinophilia, vacuolation, or foam cell change. There were pronounced stromal changes of fibrosis, inflammation, collections of foamy histiocytes, cholesterol cleft formation, haemosiderin deposition, fat necrosis, and dystrophic calcification, including the presence of many free psammoma bodies. There was no correlation between morphological response and biochemical response, as determined by serum CA125 values. In all nine cases in which pre-chemotherapy and post-chemotherapy biopsies were available, the MNA increased post-chemotherapy (p = 0.007, paired Wilcoxon test) and in six of nine cases the MAI decreased (p = 0.093). Conclusions: Because preoperative chemotherapy is being used increasingly in the management of ovarian cancer, pathologists should be aware of the resultant morphological effects. Accurate tumour typing and grading is impossible. In some cases, it may be difficult to confirm the presence of residual tumour, making it imperative that pre-chemotherapy tissue biopsies are obtained. Definite confirmation of residual tumour may require the examination of multiple histological sections from areas showing pronounced stromal changes, sometimes with multiple levels and immunohistochemistry. In the absence of definite residual tumour, the report should state that the features are consistent with the prior presence of tumour.
SUMMARY A 30-year-old woman presented with dilated episcleral vessels in the right eye which were found to be associated with an underlying ciliary body tumour. Contact lens examination, transpupillary transillumination, ultrasonography, computerised tomography, magnetic resonance imaging, and fine needle aspiration biopsy produced apparently conflicting and inconclusive results, and the eye was enucleated. Light and electron microscopy showed the lesion to be a neurilemmoma (schwannoma), of which very few cases have been reported. The clinical and pathological features are described and discussed.
Three patients presented with orbital cysts lined with upper respiratory tract epithelium. In each case there was no evidence of an associated mucocele. Two patients had a past history of orbital trauma, and the third had had preceding sinus surgery. It is postulated that these cysts were caused by traumatic herniation of nasal sinus epithelium cells into the orbit.
SummaryAn experimental model of qumme induced blindness is presented. Elec trophysiological, angiographical and morphological examinations were made. The occurrence of blindness and any recovery from blindness was dependent upon the dose of quinine taken. As no evidence of acute retinal ischaemia was found it is concluded that quinine is retinotoxic.Despite the many clinicaP and experimentaF reports of quinine blindness providing much detailed evidence and analysis, the first line of clinical therapy continues to be directed at preventing retinal vasoconstriction either using vasodilator drugs or interfering with the sympathetic nerve supply by blocking a stell ate ganglion.3,4 Our experiment was designed to create an animal model which would allow us to study the genesis of quinine blindness electrophysiologically, fluorescein angio graphically and morphologically. Our inten tion was that by correlating these findings we might identify the site and mode of action of quinine, so that rational therapeutic regimens could be designed and tested. We present some of our preliminary observations. Additional observations included blood pressure, heart rate and respiratory rate. All observations and recordings were made at half hourly intervals.Fourteen cats were anaesthetised and ERG and VER recordings were made to determine the normal range of the ERG A and B waves and the morphology of the VER (Fig. 1). The cats were allowed to recover and at a later date were given oral doses of quinine sulphate. After 2 hours they were anaesthetised and observations commenced.During the acute experiments, when quinine was given, flourescein angiography was performed on the right eye.After the acute experiment the cats were allowed
Iris atrophy, of unknown origin and believed to be secondary to the vaso-occlusive process of sickle cell disease, has been observed in 25 eyes of 22 patients (two SS disease, 20 SC disease). The crude prevalence was highest in males with SC disease, in whom 14.7% of patients were affected. Iris atrophy was closely associated with proliferative sickle retinopathy in the same eye. Analysis of haematological indices failed to reveal any significant differences between patients with and without iris atrophy. The characteristics and distribution of iris atrophy are described as well as the histopathology in one 68-year-old male patient with SS disease.
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