Subarachnoid hemorrhage caused by ruptured dissecting aneurysm arising from the extracranial distal posterior inferior cerebellar artery--case report.

A 50-year-old man presented with a dissecting aneurysm arising from the extracranial portion of the right posterior inferior cerebellar artery (PICA) causing subarachnoid hemorrhage (SAH) and manifesting as sudden onset of disturbed consciousness. Computed tomography showed SAH with ventricular reflux predominantly in the posterior fossa. Angiography revealed a fusiform aneurysm of the right PICA originating extracranially from the right vertebral artery. The aneurysm was isolated and excised. Histological examination showed dissection of the aneurysm wall. Dissecting aneurysm arising from the extracranial portion of the PICA is extremely rare.

Primary malignant hepatic glucagonoma: an autopsy case.

A 73-year-old woman was admitted to our department for treatment of diabetes (plasma glucose 289 mg/dl, HbA(1C) 7.1%, and glycated albumin 34.9%). She displayed the signs and symptoms of glucagonoma syndrome, including necrolytic migratory erythema (NME), low aminoacidemia, and a marked increase of the serum glucagon level (4,940 pg/ ml). Thus, we suspected a glucagonoma causing secondary diabetes. However, we could not detect any mass in the pancreas or the gastrointestinal tract, and only found a liver lesion resembling a hemangioma. Her NME improved markedly after intravenous infusion of amino acids, and her plasma glucose was controlled reasonably well by intensive insulin therapy. However, her general condition deteriorated and she died on day 57 after hospitalization. At autopsy, the only tumor detected was the liver mass. This was a large solid tumor (8 x 6 x 5 cm) with a pattern of white and dark brown stripes located in the left lobe, while two white nodules were also found in the right lobe. Based on the histopathological and immunohistochemical findings, the liver lesion was shown to be a malignant glucagonoma with intrahepatic metastases. Since primary malignant hepatic glucagonoma has not been reported before, we present this extremely rare case of primary malignant glucagonoma of the liver.

The early effects of urinary tract obstruction on glomerulogenesis.

PURPOSE: Our obstructive uropathy model in fetal lambs showed that renal cystic changes appeared 3 weeks after obstruction. In this study, the authors investigated the changes resulting from complete urinary tract obstruction in the first 7 days after obstruction. METHODS: An obstructive uropathy was created in fetal lambs at 60 days' gestation by ligating the urethra and urachus. They were delivered 48 hours, 3 days, 5 days, and 7 days later by cesarian section. The kidneys were removed and processed for histologic examination. RESULTS: Eighteen fetuses were operated on and 15 (4 at 48 hours, 4 at 3 days, 2 at 5 days, and 5 at 7 days; 83%) survived. Macroscopically, bladder dilatation and slightly dilated ureters were identified from 48 hours. Microscopically, dilatation of proximal tubules started from 48 hours after obstruction and increased by 7 days. Glomerular cysts in the nephrogenic zone also were identified from 48 hours. Dysplastic changes were not found. CONCLUSIONS: The first areas in the developing kidney that suffer damage after obstructive uropathy are the proximal tubule and the nephrogenic zone. This change started 48 hours after obstruction. Shunting procedures need to be performed considerably earlier than previously thought.

Adrenal black adenoma associated with preclinical Cushing's syndrome.

A black adenoma of the adrenal gland was laparoscopically removed from a 60-year-old man who presented with severe hypertension. Although laboratory findings were indicative of preclinical Cushing's syndrome, there were no clinical features characteristic of Cushing's syndrome. Microscopically, the tumor showed a proliferation of polygonal cells containing numerous brown-pigmented granules. Special staining studies revealed these granules to be lipofuscin. Electron microscopy also identified lipofuscin and lysosomes in these cells. The morphological appearance of the tumor and the adjacent atrophic non-tumorous adrenal cortex supports the assumption that the black adenoma caused preclinical Cushing's syndrome.