Tumoral calcinosis is a rare disease involving the ectopic calcifications in the major juxtaarticular sites that was first described by Inclan Alberto in 1943. The etiology of tumoral calcinosis is still obscure. A disturbance of the phosphate metabolism in the kidney has been considered a major cause. However, some patients have no laboratory abnormalities. Tumoral calcinosis in the spine has not been reported in Korea. Recently, we encountered a case of tumoral calcinosis in the lumbar region. The clinical and pathological findings are discussed with a review of the relevant literature.
Calcinosis* ; Humans ; Kidney ; Korea ; Lumbosacral Region* ; Metabolism ; Rare Diseases ; Spine

Tumoral calcinosis is an uncommon disease, characterized by deposits of large, calcified soft tissue masses around major joints in children and young adults. The causes of the lesion have not yet been established, but are presumed an inborn error of metabolism of phosphorus. It has been recommanded medical treatment or surgical excision, but recurrence of the lesion is frequent. We report a case of young female patient who presented with tumoral calcinosis at the age of 10 years.
Calcinosis* ; Child ; Female ; Humans ; Joints ; Knee Joint* ; Knee* ; Metabolism ; Phosphorus ; Recurrence ; Young Adult

OBJECTIVETo observe the alterations of taurine transport, taurine transporter (TAUT) and cysteine sulfinate decarboxylase (CSD) mRNA in the calcification of myocardial cells in vitro.

METHODS3H-taurine measured the amount of taurine uptake. TAUT and CSD mRNA consents were measured using competitive quantitative RT-PCR in cultured and calcified myocardial cells.

RESULTSIn calcification of myocardial cells, taurine concentration was decreased by 27% (P < 0.05), taurine uptake was markedly reduced, Vmax reduced by 39% (P < 0.01), there were no statistical significance of Km values between the two groups. TAUT mRNA decreased by 45% (P < 0.01), but CSD mRNA increased by 25% (P < 0.05).

CONCLUSIONSThe data suggest that there were impediment of taurine transport in calcification of myocardial cells, as TAUT mRNA level was decreased, but CSD mRNA concentration was improved.

Animals ; Biological Transport ; Calcinosis ; metabolism ; pathology ; Calcium ; metabolism ; Carboxy-Lyases ; metabolism ; Cells, Cultured ; Myocytes, Cardiac ; metabolism ; pathology ; RNA, Messenger ; metabolism ; Rats ; Taurine ; biosynthesis ; genetics ; metabolism

Calcinosis ; pathology ; Child ; Humans ; Inhibins ; metabolism ; Male ; S100 Proteins ; metabolism ; Sertoli Cell Tumor ; metabolism ; pathology ; surgery ; Testicular Neoplasms ; metabolism ; pathology ; surgery ; Vimentin ; metabolism

Adult ; Calcinosis ; metabolism ; pathology ; surgery ; Fibrosis ; metabolism ; pathology ; surgery ; Humans ; Male ; Neoplasms, Muscle Tissue ; metabolism ; pathology ; surgery ; Thoracic Neoplasms ; metabolism ; pathology ; surgery ; Vimentin ; metabolism

Adult ; Calcinosis ; metabolism ; pathology ; Diagnosis, Differential ; Fibroma ; metabolism ; pathology ; Gastrointestinal Stromal Tumors ; pathology ; Humans ; Male ; Stomach Neoplasms ; metabolism ; pathology ; Vimentin ; metabolism

The purpose of this review is to investigate the value of the calcification in differentiating malignant thyroid neoplasm and the molecular mechanisms for the formation of the calcification. Many published reports have proved the presence of calcifications in thyroid neoplasm and calcified nodules in these studies are more frequently malignant than noncalcified nodules. Through viewing the related references, we found that psammoma bodies (PBs), Runx2, osteocalcin, osteopontin, CD44v6 play an important role in the molecular mechanisms in the formation of the calcification in PTC. But further study is required for elucidating the mode of action.
Calcinosis ; diagnosis ; pathology ; Core Binding Factor Alpha 1 Subunit ; metabolism ; Humans ; Hyaluronan Receptors ; metabolism ; Osteocalcin ; metabolism ; Osteopontin ; metabolism ; Thyroid Neoplasms ; diagnosis ; pathology ; Thyroid Nodule ; pathology

Hypercalcemia in accelerated phase of chronic myelogenous leukemia (CML) is very rare. Its pathogenesis is considered humoral hypercalcemia of malignancies mediated by parathyroid hormone-related protein (PTHrP). In severe hypercalcemia, calcifications in kidneys, skin, vessels, heart, and stomach may occur. Our two cases were admitted because of severe hypercalcemia in accelerated phase of CML. On Tc-99m methylene diphosphonate (MDP) bone scintigraphies, a marked tracer accumulation was seen in the lung, heart, stomach and kidney. We report increased tracer accumulation of multiple organs on Tc-99m MDP bone scintigraphy in two rare hypercalcemic patients with CML.
Adult ; Bone Diseases/radionuclide imaging* ; Bone Diseases/etiology* ; Calcinosis/radionuclide imaging ; Calcinosis/etiology ; Case Report ; Human ; Hypercalcemia/radionuclide imaging* ; Hypercalcemia/etiology* ; Leukemia, Myeloid, Chronic/metabolism ; Leukemia, Myeloid, Chronic/complications* ; Male ; Middle Age ; Proteins/metabolism ; Technetium/diagnostic use

Advanced atherosclerosis is often associated with dystrophic calcification and remodeling of extracellular matrix of vascular wall. Recently many studies have documented a general relationship between calcification and severity of coronary disease, and discussed the feasibility of electron beam computed tomography for detecting and quantifying the coronary artery calcification in the patients. The present study investigated the expression and the localization of osteopontin, one of noncollagenous bone matrix protein, within the calcified coronary arteries. Autopsy-derived coronary artery specimens were scanned and reconstructed to visualize the pattern of coronary calcification using a novel microscopic computed tomography technique. The localization of the osteopontin were evaluated by immunohistochemial stain with LF7. The present study showed that the pattern of coronary calcification is variable and the expression of osteopontin is localized mainly to calcified lesion. The smooth muscle cells in addition to macrophage expressed osteopontin protein in human coronary atherosclerotic plaques. Soluble osteopontin released near to the sites of vascular calcification may represent an adaptive mechanism aimed at regulating the process of vascular calcification.
Aged ; Calcinosis/metabolism ; Coronary Arteriosclerosis/pathology* ; Coronary Arteriosclerosis/metabolism* ; Coronary Vessels/pathology* ; Coronary Vessels/metabolism ; Coronary Vessels/chemistry* ; Female ; Human ; Immunohistochemistry ; Male ; Middle Age ; Sialoglycoproteins/biosynthesis ; Sialoglycoproteins/analysis*

OBJECTIVETo investigate the morphological features, immunohistochemical phenotype, diagnosis and differential diagnosis of collagenous spherulosis of the breast.

METHODSClinicopathologic observation, immunohistochemistry using EnVision method and histochemical staining were applied in 33 cases of collagenous spherulosis of the breast.

RESULTSCollagenous spherulosis of the breast was a benign lesion, consisting of proliferative myoepithelial and ductal epithelial cells. These cells were arranged in a cribriform pattern with esinophilic, round, oval or star-shaped fibrillary spherules in the lumen.SMA, calponin and p63 by immunohistochemistry identified the proliferative myoepithelium, while E-cadherin identified the proliferative ductal epithelial cells. The esinophilic spherules were stained with collagen type IV, AB-PAS and reticulin. Collagenous spherulosis was often found in sclerosing adenosis.

CONCLUSIONSCollagenous spherulosis of the breast is often associated with other diseases. It has special morphological presentation and is easily confused with malignant tumors such as adenoid cystic carcinoma or cribriform carcinoma in situ, and needs to be differentiated from these disease entities.

Actins ; metabolism ; Adult ; Aged ; Breast ; pathology ; Breast Diseases ; metabolism ; pathology ; Cadherins ; metabolism ; Calcinosis ; Calcium-Binding Proteins ; metabolism ; Collagen ; metabolism ; Collagen Type IV ; metabolism ; Female ; Humans ; Hyperplasia ; Membrane Proteins ; metabolism ; Microfilament Proteins ; metabolism ; Middle Aged