Role of Membranes in Calcification

Kim, Kookmin M.

doi:10.1159/000154993

Cited by 2 publications

(3 citation statements)

References 34 publications

(61 reference statements)

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“…MG bodies are an example of dystrophic calcification. 13 Calcium salt deposition at sites of local tissue damage may be augmented by hyperphosphatemia that occurs in renal failure. Since our patient and the patient described by Blumberg et al 9 had renal failure and transient hyperphosphatemia, it is possible that the mechanism of augmented dystrophic calcification might have played a role in the pathogenesis of cerebral malacoplakia in these cases.…”

Section: Discussionmentioning

confidence: 99%

Michaelis-Gutmann bodies in a healing brain infarct.

Gal¹,

Gukovsky-Oren²,

Sandbank³

et al. 1987

Stroke

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A case of Michaelis-Gutmann bodies in a healing brain infarct is described. Morphologically this was consistent with cerebral malacoplakia. There are only 6 previously reported cases of cerebral malacoplakia, and only 1 of them was a consequence of postpartum stroke. The histologic and ultrastructural features of the malacoplakic lesion are reported and compared with the previously reported cases. (Stroke 1987;18:947-950) T he accumulation of histiocytes containing Michaelis-Gutmann (MG) bodies is rare. MG bodies are calcified, laminated, periodic acidSchiff (PAS)-positive inclusions that were first described by Michaelis and Gutmann in 1902.' Malacoplakia usually involves the urinary bladder, but involvement of other sites has been reported. 2 "* Cerebral malacoplakia seems to be very rare. In a search of the literature we located only 6 previously reported cases of cerebral malacoplakia. Most were in children in association with neonatal herpes infection, 5 " 8 and 1 case was in a young woman who died as a consequence of postpartum stroke. 9 We report the histochemical and ultrastructural findings of MG bodies in a healing brain infarct. To the best of our knowledge, our 72-year-old patient is the oldest case of cerebral malacoplakia reported in the literature. Report of a CaseA 72-year-old man was admitted to the hospital because of sudden onset of confusion and dysarthria. Past medical history included congestive heart failure and chronic atrial fibrillation. Physical examination on admission revealed a right central facial palsy.Laboratory findings were 80 mg% urea, 1.5 mg% creatinine, 10 mg% calcium, and 4.1 mg% phosphate; electrocardiogram showed atrial fibrillation. Chest xray examination displayed enlargement of the heart, mild pulmonary congestion, and a small pleural effusion. The electroencephalogram revealed slow wave activity in the left temporal region. The diagnosis of a thromboembolic event in the form of a cerebrovascular "accident" was made.On the seventh day of hospitalization the patient began complaining of abdominal pain. Serum urea rose to 110 and creatinine to 2.4 mg%, while calcium

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Section: Discussionmentioning

confidence: 99%

Michaelis-Gutmann bodies in a healing brain infarct.

Gal¹,

Gukovsky-Oren²,

Sandbank³

et al. 1987

Stroke

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“…AP is present in blood extracellular fluid and urine; therefore, AP could be readily adsorbed on and absorbed into many implantable biomaterials. Calcification of bioprosthesis may occur in association with the deposition of devitalized cells and cellular debris (6,8) and perhaps adherent blood platelets, which also contain high levels of AP activity. In this case, PEG grafting on BP in combination with aspirin/heparin delivery can substantially inhibit the cellular attachment and subsequently their extrinsic calcification.…”

Section: Discussionmentioning

confidence: 99%

“…It is also proposed that the nucleus of calcification appears as a result of adhesion and death of cells that contain calcium, phosphate, phospholipids, lipoproteins, and enzymes (6,7). Hence, as a result of cell death, membrane fragments forming a vesicular matrix appear in the media, and calcium phosphate crystals are formed in this matrix (8).…”

mentioning

confidence: 99%

Synergistic Effect of Released Aspirin/Heparin for Preventing Bovine Pericardial Calcification

et al. 2000

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Calcification is a frequent cause of the clinical failure of bioprosthetic heart valves fabricated from glutaraldehyde pretreated bovine pericardium (GATBP). Aspirin, a potent antiplatelet drug, and heparin, an anticoagulant, are commonly used for postimplant complications such as thrombosis and thromboembolism. Aspirin and heparin were embedded in chitosan/polyethylene vinylacetate co-matrix to develop a prolonged release form. The effect of these drugs towards the bioprosthetic calcification was investigated by in vitro and in vivo models. In vitro and in vivo evaluation suggest that the released aspirin/heparin from the co-matrix had a synergistic effect in inhibiting GATBP calcification. In vivo subcutaneous co-implantation was performed with PEG-20,000 grafted bovine pericardium (PEG-GABP), aspirin, and heparin. Biochemical, histological, and scanning electron microscopic evaluation of retrieved samples demonstrated a significant reduction in calcium deposition and alkaline phosphatase activity on PEG-GABP compared to GATBP. It seems that the aspirin/heparin combination synergistically inhibits the pericardial calcification in addition to their antithrombotic function.

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Role of Membranes in Calcification

Cited by 2 publications

References 34 publications

Michaelis-Gutmann bodies in a healing brain infarct.

Michaelis-Gutmann bodies in a healing brain infarct.

Synergistic Effect of Released Aspirin/Heparin for Preventing Bovine Pericardial Calcification

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