(1/89) Granuloma formation in patients receiving BCG immunotherapy.
Eleven patients with acute myeloblastic leukaemia have received repeated intravenous injections of BCG containing 4-9 X 10(6) live organisms per millilitre. Non-caseating epithelioid granulomas, sometimes with giant-cell formation, have been demonstrated in eight bone marrow aspirates. Seven patients had granulomas in the liver, three in the lung, one in the spleen, one in lymph nodes, and one in a skin biopsy. One patient had a raised serum alkaline phosphatase, but none of the patients had any illness which could be related to the presence of granulomas. Granuloma formation appeared more extensive in four patients who were probably anergic before BCG treatment. Until the significance of this finding becomes clear great care should be taken when giving BCG by the intratumour of intravenous routes to potentially immunoincompetent patients. (+info)
(2/89) Is demodex really non-pathogenic?
Although usually considered a non-pathogenic parasite in parasitological textbooks, Demodex folliculorum has been implicated as a causative agent for some dermatological conditions, such as rosacea-like eruptions and some types of blepharitis. Several anecdotal reports have demonstrated unequivocal tissue damage directly related to the presence of the parasite. However, this seems to be exceedingly rare, in contrast with the marked prevalence of this infestation. We have had the opportunity to observe one of such cases. A 38-year-old woman presented with rosacea-like papular lesions in her right cheek. Histopathological examination revealed granulomatous dermal inflammation with a well-preserved mite phagocytized by a multinucleated giant cell. This finding may be taken as an evidence for the pathogenicity of the parasite, inasmuch as it does not explain how such a common parasite is able to produce such a rare disease. (+info)
(3/89) Intracranial giant cell reparative granuloma arising from the temporal lobe area: MR findings.
SUMMARY: We present an unusual case of a giant cell reparative granuloma arising from the left temporal lobe area of a 38-year-old man and provide clinical and MR findings. Current diagnosis and treatment options are also discussed. (+info)
(4/89) Idiopathic giant cell granulomatous hypophysitis with hypopituitarism, right abducens nerve paresis and masked diabetes insipidus.
A 38-year-old man presented with headache, fever, and double vision associated with right abducens nerve paresis. He had neither nuchal rigidity nor visual field defect. Laboratory data revealed elevated erythrocyte sedimentation rate (ESR), eosinophilia, and lymphocytic pleocytosis in the cerebrospinal fluid (CSF). Provocation tests of pituitary hormones showed partial hypopituitarism. Magnetic resonance imaging (MRI) revealed swelling of the hypophysis and a mass lesion expanding into the right cavernous sinus. The supplement dose of dexamethasone for hypothalamic hypocortisolism manifested diabetes insipidus. Biopsy, carried out through the transsphenoidal approach, revealed giant cell granuloma. Systemic granulomatous diseases were ruled out, and the lesion was considered to be idiopathic giant cell granulomatous hypophysitis. Right abducens nerve paresis, diabetes insipidus and dysfunction of the anterior lobe were amended by the treatment with prednisolone for 4 months, and findings of the pituitary gland and stalk were normalized. The present case shows that glucocorticoid has an effect on amendment of idiopathic giant cell granulomatous hypophysitis. (+info)
(5/89) Odontogenic cysts, odontogenic tumors, fibroosseous, and giant cell lesions of the jaws.
Odontogenic cysts that can be problematic because of recurrence and/or aggressive growth include odontogenic keratocyst (OKC), calcifying odontogenic cyst, and the recently described glandular odontogenic cyst. The OKC has significant growth capacity and recurrence potential and is occasionally indicative of the nevoid basal cell carcinoma syndrome. There is also an orthokeratinized variant, the orthokeratinized odontogenic cyst, which is less aggressive and is not syndrome associated. Ghost cell keratinization, which typifies the calcifying odontogenic cyst, can be seen in solid lesions that have now been designated odontogenic ghost cell tumor. The glandular odontogenic cyst contains mucous cells and ductlike structures that may mimic central mucoepidermoid carcinoma. Several odontogenic tumors may provide diagnostic challenges, particularly the cystic ameloblastoma. Identification of this frequently underdiagnosed cystic tumor often comes after one or more recurrences and a destructive course. Other difficult lesions include malignant ameloblastomas, calcifying epithelial odontogenic tumor, squamous odontogenic tumor, and clear-cell odontogenic tumor. Histologic identification of myxofibrous lesions of the jaws (odontogenic myxoma, odontogenic fibroma, desmoplastic fibroma) is necessary to avoid the diagnostic pitfall of overdiagnosis of similar-appearing follicular sacs and dental pulps. Fibroosseous lesions of the jaws show considerable microscopic overlap and include fibrous dysplasia, ossifying fibroma, periapical cementoosseous dysplasia, and low-grade chronic osteomyelitis. The term fibrous dysplasia is probably overused in general practice and should be reserved for the rare lesion that presents as a large, expansile, diffuse opacity of children and young adults. The need to use clinicopathologic correlation in assessing these lesions is of particular importance. Central giant cell granuloma is a relatively common jaw lesion of young adults that has an unpredictable behavior. Microscopic diagnosis is relatively straightforward; however, this lesion continues to be somewhat controversial because of its disputed classification (reactive versus neoplastic) and because of its management (surgical versus. medical). Its relationship to giant cell tumor of long bone remains undetermined. (+info)
(6/89) Large giant cell reparative granuloma of the petrous bone--case report.
A 41-year-old man presented with a large mass bulging over the suprazygomatic temporal region. Neuroradiological examination showed that the huge extra-axial mass with osteolytic character originated from the upper surface of the petrous bone. Preoperative obliteration of the feeding arteries with super-selective intravascular embolization was helpful for the total removal of the tumor. Histological examination revealed that the tumor consisted of massive fibrohistiocytic proliferation with numerous heavily hemosiderin-laden macrophages and numerous multinucleated giant cells. The most probable diagnosis was giant cell reparative granuloma. Therefore, no postoperative irradiation or other adjuvant therapy was given. (+info)
(7/89) Peripheral giant-cell granuloma. Review of 13 cases.
Peripheral giant-cell granuloma is an infrequent exophytic lesion of the oral cavity, also known as giant-cell epulis, osteoclastoma, giant-cell reparative granuloma, or giant-cell hyperplasia. The present study reports 13 cases on patients that visited the Oral Medicine department of the Dental Faculty in the Santiago de Compostela University. We report the location, size, course and treatment of each lesion, comparing the results obtained to those reported in the literature. We discuss differential diagnosis with respect to other entities, in particular brown tumor of hyperparathyroidism, cherubism, and aneurysmal bone cyst, all of which show very similar histological appearance to peripheral giant-cell granuloma. (+info)
(8/89) Trapping of misdirected dendritic cells in the granulomatous lesions of giant cell arteritis.
Immature dendritic cells (DCs) are scattered throughout peripheral tissues and act as sentinels that sample the antigenic environment. After activation, they modify their chemokine receptor profile and migrate toward lymphoid tissues. On arrival, they have matured into chemokine-producing DCs that express co-stimulatory molecules and can prime naive T cells. Normal temporal arteries contain immature DCs that are located at the media-adventitia border. In temporal arteries affected by giant cell arteritis, DCs are highly enriched and activated and have matured into fully differentiated cells producing the chemokines, CCL18, CCL19, and CCL21. In keeping with their advanced maturation, DCs in the granulomatous lesions possess the chemokine receptor, CCR7. CCR7 binds CCL19 and CCL21, causing the highly activated DCs to be trapped in the peripheral tissue site. The co-stimulatory molecule, CD86, which is critical for DC/T-cell interaction, is expressed by a subset of DCs captured in the arterial wall. DC/T-cell interaction does not involve interleukin-12; transcripts for interleukin-12 p40 are absent in the vasculitic infiltrates. We propose that differentiation of DCs and the autocrine and paracrine actions of chemokines in granulomatous lesions misdirect DCs away from their usual journey to lymphoid organs and are critical in maintaining T-cell activation and granuloma formation in giant cell arteritis. (+info)