Cushing's Syndrome from an Ectopic Pituitary Adenoma with Peliosis: A Histological,Immunohistochemical, and Ultrastructural Study and Review of the Literature

Ectopic pituitary adenoma (EPA) is rare and, to the authors’ knowledge, its association with peliosis has not yet been described. The case of a 38-yr-old woman with clinical and biochemical evidence of Cushing’s syndrome is reported. Magnetic resonance imaging (MRI) disclosed a normal pituitary and a separate mass in the sphenoid sinus. The surgically remove’s hyaline change in the corticotrophs, indicating exposure to glucocorticoid excess. By histology, the mass in the sphenoid sinus was a congested, chromophobic, partly basophilic, periodic acid-Schiff (PAS)-positive pituitary adenoma composed of pleomorphic, adrenocorticotropic hormone (ACTH)-positive, corticotrophs. There was focal immunopositivity for MIB-1 and proliferating cell nuclear antigen (PCNA). Electron microscopy confirmed the diagnosis of corticotroph adenoma. A striking finding, consistent with the diagnosis of peliosis, was the presence of multiple large blood-filled spaces lacking an endothelial lining. The capillaries were dilated, but often appeared empty and the fenestrated endothelium exhibited discontinuities. The cause of peliosis is obscure. It may be that the venous outflow was impaired in this case leading to capillary dilation, congestion, hyperpermeability, rupture, and accumulation of blood in extravascular spaces.     

The Effect of Neonicotinoids Exposure on Oreochromis niloticus Histopathological Alterations and Genotoxicity

This study aimed to examine the side effects of selected neonicotinoids (Acetamiprid, Aceta, and Imidacloprid, Imid) on Oreochromis niloticus juveniles. The acute toxicity, Probit method, revealed an LC₅₀ of 195.81 and 150.76 ppm for Aceta/96 h and Imid/72 h respectively. The fish were divided into three groups that were exposed, for 21 days (n?=?5/replicate), to 1/10 of the LC₅₀ of either neonicotinoids, however, the third was an unexposed control group. Results of erythrocytic micronucleus (MN), and nuclear abnormalities (NA) showed that Aceta and Imid exposure caused a significant (p?<?0.05) increase in MN by?~?2.2 and?~?10 folds, respectively relative to control. NAs occurred at the order of kidney-shaped?>?budding?>?binucleated in Aceta, however, budding?>?binucleated?>?kidney-shaped was noticed in the Imid group. Histopathological changes in gills, liver, and muscles were observed significantly in both exposed groups with more severity in the Imid group. Collectively, Aceta and Imid have potential genotoxicity and histopathological alterations in O. niloticus.

     

Positron emission tomography in breast cancer: a clinicopathological correlation of results

We conducted a retrospective study to evaluate the sensitivity, specificity and accuracy of positron emission tomography (PET) scans in 109 patients with primary recurrent or metastatic breast cancer. All patients had a PET scan, X-ray or CT scan of the chest, an ultrasound or CT scan of the liver and a bone scan. Mammography was available for 86 patients. Correlation between the PET scan result and histological findings were made. The sensitivity, specificity and accuracy of the PET scan were calculated for both the primary tumour (T) and lymph nodes (N). In patients with metastasis (M) the accuracy of the PET scan was compared with other imaging modalities. Histological results of the site in question were available in only 105 patients. Information for the primary tumour was available for 93 patients and for nodes in 74. The PET scan was accurate in 89.2% for (T), with 3.2% false positive and 7.6% false negative. For (N) the PET scan was accurate in 90.5% with 9.5% false negative. In the 86 patients who underwent both mammography and PET scanning, the PET scan was more accurate in 89.5% versus 72% (p = 0.0003). In the 19 patients with metastasis, the PET scan was in agreement with other imaging modalities in 100% of cases. PET scanning is the only non-invasive imaging procedure that will detect tumours in the breast, lymph nodes, lung, liver, bone and bone marrow with high sensitivity, specificity and accuracy. It is a valuable tool in the management of patients in all stages of breast cancer for diagnosis, staging and following treatment response.     

Preventive effects of cannabis on neurotoxic and hepatotoxic activities of malathion in rat

Objective: To investigate the effect of Cannabis sativa extract on the development of neuroand hepato-toxicity caused by malathion injection in rats. Methods: The extract of Cannabis sativa was obtained from the plant resin by chloroform treatment. Δ~9-Tetrahydrocannabinol content of the extract(20%) was quantified using gas chromatography–mass spectrometry. The doses of cannabis extract were expressed as Δ~9-tetrahydrocannabinol content of 10 or 20 mg/kg. Malathion(150 mg/kg) was intraperitoneally administered followed after 30 min by the cannabis extract(10 or 20 mg/kg, subcutaneously). Rats were euthanized 4 h later. Malondialdehyde(MDA), reduced glutathione(GSH), nitric oxide and paraoxonase-1(PON-1) activity were determined in brain and liver. Brain 5-lipoxygenase and butyrylcholinesterase(BChE) activity were measured as well. Histopathological examination of brain and liver tissue was also performed. Results: Compared to controls, malathion resulted in increased oxidative stress in brain and liver. MDA and nitric oxide concentrations were significantly increased(P0.05) and GSH significantly decreased with respect to control levels(P0.05). Malathion also significantly inhibited PON-1 and BChE activities but had no effect on brain 5-lipoxygenase. Brain MDA concentrations were not altered by cannabis treatment. Cannabis at 20 mg/kg, however, caused significant increase in nitric oxide and restored the GSH and PON-1 activity. Brain BChE activity significantly decreased by 26.1%(P0.05) after treatment with 10 mg/kg cannabis. Cannabis showed no effect on brain 5-lipoxygenase. On the other hand, rats treated with cannabis exhibited significantly higher levels of liver MDA, nitric oxide and PON-1 activity compared with the malathion control group. Rats treated with only malathion exhibited spongiform changes, neuronal damage in the cerebral cortex and degeneration of some Purkinje cells in the cerebellum. There were also hepatic vacuolar degeneration and dilated and congested portal vein. These histopthological changes induced by malathion in brain and liver were reduced to great extent by cannabis administration at 20 mg/kg. Conclusions: Our data suggest that acute treatment with cannabis alleviates the malathion-induced brain and hepatic injury in rats possibly by maintaining the levels of GSH and PON-1 activity.