Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes 21 cases of nodular regenerative hyperplasia (NRH) and its clinical and radiologic features. NRH of the liver is an established pathologic entity that should not be confused with focal nodular hyperplasia, hepatocellular adenoma, or the regenerative nodules associated with cirrhosis. Correct diagnosis will prevent an unnecessary hepatic lobectomy should NRH be mistaken for hepatocellular adenoma. Unlike focal nodular hyperplasia, NRH may bleed, may be associated with portal hypertension in one-half of cases, and is often associated with a systemic disease such as a myelo- or lymphoproliferative disorder. Correct diagnosis is important because the prognosis in patients with NRH and portal hypertension is better than that in patients with portal hypertension due to cirrhosis. Radiologically, multiple nodules, large masses, or an apparently normal liver (containing nodules less than 0.5 cm in diameter) were visible. The nodules may take up technetium sulfur colloid and have variable echogenicity on sonography. They are often hypodense on CT without significant enhancement. The nodules may fill from the periphery on angiography, are vascular, and sometimes contain small hypovascular areas due to hemorrhage. A large nodule may rupture and cause hemoperitoneum. These findings may resemble some features of focal nodular hyperplasia, hepatocellular adenoma, or metastases. NRH is probably underdiagnosed owing to a lack of recognition of the entity and limited sampling of liver tissue by needle biopsy. Scintigraphy, sonography, and CT of the liver should be performed in cases of idiopathic portal hypertension to detect NRH. In cases with compatible findings, multiple needle biopsies or a laparoscopically guided needle biopsy or wedge liver biopsy should be recommended for definitive diagnosis.
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PMID:Nodular regenerative hyperplasia of the liver: clinical and radiologic observations. 354 83

Rare cases of myelolipomas associated with adrenocortical lesions responsible for Cushing or Conn syndromes have been described. We report two additional cases of extensive lipomatous changes in incidentally discovered adrenocortical adenomas, which were preoperatively interpreted as myelolipomas on the basis of radiologic findings. Microscopically, the adenomas were composed of sheets and nests of adrenocortical cells, and extensive areas of mature adipose tissue admixed with a bland stromal infiltration of small cells. The impression was that myeloid cells were present, featuring a myelolipoma associated with a clear cell adenoma of the adrenal cortex, but specific immunocytochemical markers of myeloid lineage were not reactive in the small cell component, and these cells consisted of small lymphocytes. The lipomatous tissue may represent a degenerative phenomena within an adrenocortical adenoma or may be an additional neoplastic component of the tumor. Irrespective of their origin, extensive (myelo)lipomatous changes in adrenocortical tumors can lead to misinterpretations in the preoperative work-up of patients with adrenal masses.
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PMID:Lipomatous Changes in Adrenocortical Adenomas: Report of Two Cases. 1211 35

Pituitary adenoma with ossification is a rare histological variant. Previously there have been four cases reported in the literature. Here a case of pituitary prolactin-producing adenoma with bone formation in a 21-year-old woman is described. The patient had irregular menstruation for three years. MRI revealed an unusual 1.5 cm(3) ovoid nodule with partial shell-like structure showing heterogeneous signals. The pre-operative prolactin serum level was 258.78 ng/mL. The patient was operated through the trans-sphenoidal pathway under general anesthesia. Histologically, the tumor was parenchymal and mostly replaced by the well-differentiated lamellar bony tissue. Sheets of tumor cells interweaved with the mature lamellar bone trabeculae showing no cellular atypia. The cytoplasm of the adenoma cells was slightly eosinophilic and the myelo-adipose metaplastic foci were also found within the parenchyma. Immunohistochemical staining of tumor cells showed positive expressions of prolactin, synaptophysin and chromogranin A in the cytoplasm of the tumor cells. Meanwhile, negative expressions of S-100, epithelial membrane antigen, GFAP and other pituitary hormones were also demonstrated. As a rare histological variant of pituitary adenoma, the current case of pituitary prolactin producing adenoma with ossification is reported. It is speculated that the ossification may be derived from the osteo-metaplasia of mesenchymal fibroblasts resulting from the effects of both secondary ischemia by the outgrowth of the tumor and/or the autocrine effect of prolactin in this case. The bony shell structure may limit the growth of pituitary adenoma.
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PMID:Pituitary prolactin producing adenoma with ossification: a rare histological variant and review of literature. 1973 58