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PubMed1983

[Problem of adaptive hyperparathyroidism in chronic renal failure].

It is reported on a case of adaptive hyperparathyroidism (HPT) with diffuse hyperplasia of the adrenal glands including formation of an adenoma, in which during the first 5 weeks of the dialytic therapy massive pulmonary, vascular and periarticular calcifications developed. The previously existing untreated HPT and factors specific for dialysis (composition of the dialysate, heparin therapy) are made responsible for this course of the disease. Within one year the parathyroidectomy led to the regression of the calcifications. Prophylactic and therapeutic possibilities in the adaptive HPT are shown.

Adult↗
PubMed1978

Congenital calcifying hamartoma. A resolving lesion producing gastrocnemius contracture--report of a case.

An 18-month-boy developed a calcifying mass in the gastrocnemius muscle. The lesion presented on the day of birth and resolved completely within 5 months leaving only a fibrous cord replacing the medial head of the gastrocnemius. There were no facts in the history to suggest the etiology of this lesion. Calcification of a vascular hamartoma with subsequent fibrosis is proposed as a possible explanation. The benign course of this lesion is evidence of the value of conservative treatment.

Calcinosis↗
PubMed1977

[Cryogenic injuries of the rabbit abdominal aorta and the iliac artery].

In rabbits, cryogenic injuries of the walls of abdominal aorta and iliac arteries were histologically examined after application of a cryoprobe ob -160 degrees C for 1 minute. Seven days thereafter the animals were killed. Extended partial and circular necroses and calcifications of the vascular walls were found. The alterations were less expressed when the blood stream was maintaimed during the freezing. Maximal changes occured at additional centripetal pinching the vessels.

Animals↗
PubMed1995

[Histogenesis of central neurocytoma: an immunohistochemical and electronmicroscopic study of four cases].

Four intraventricular central neurocytomas were studied histopathologically and intriguing findings were obtained with regard to the histogenesis of this tumor. The cases included 3 males and 1 female aged 17-25. The tumors had developed in the regions from the lateral to the third ventricles and were surgically removed in all the cases. A honeycomb appearance was recognized on H&E staining, and the calcification and latticed vascular findings closely mimicked the appearance of oligodendroglioma. A characteristic wide eosinophilic fibrous stroma was observed frequently. Immunohistochemically, all four cases were NSE-positive and strongly synaptophysin-positive, and by electronmicroscopy, neurosecretory granules and microtubules were observed in all cases and typical synapse structures in 2 cases. GFAP immunoreactivity and glial differentiation, including ependymal cells were exhibited electronmicroscopically, such as glial fibrils, basal bodies, centrioles and 9 + 1 patterned cilia-like structures in 2 cases. These findings suggest that central neurocytoma is an embryonal tumor in the wide sense, originating from the germinal matrix cell of the lateral ventricles and possessing multipotency, with potent differentiation from mature neurons.

Adolescent↗
PubMed1976

Diffuse cavernous hemangioma of the spleen.

Diffuse hemangioma of the spleen occurred in a 59-year-old man. The presenting features were a dull ache and heaviness in the left upper quadrant for 3 weeks, severe left-sided pain and fever immediately before hospitalization, and a tender mass in the left upper quadrant. The condition was diagnosed at laparotomy; splenectomy was performed. In this case intrahemangiomatous hemorrhage had occurred, but not rupture of the spleen, which is a potentially lethal complication. Other complications of diffuse splenic hemangioma are thrombosis, infarction, infection with abscess formation, and partial calcification of the vascular spaces. The condition is rare; only 56 cases have been reported.

Hemangioma, Cavernous↗
PubMed1997

[Calciphylaxis in a patient on long-term dialysis].

Calciphylaxis is a special form of soft tissue calcification (in particular blood vessels), affecting specially patients with chronic renal insufficiency and associated secondary hyperparathyroidism. Most severely affected are small arteries with a diameter of 0.2-0.5 mm at the interface of the corium and subcutaneous layer. Calcification of the vascular media with subsequent narrowing of the lumen causes ischaemic changes manifested by the development of painful reddish-violet spots on the skin with necrosis and ulcerations. The authors describe the case of a 73-year-old diabetic female patient with regular dialyzation treatment. The patient developed reddish-violet spots on the lower extremities shortly before admission to hospital. At the site of the spots rapidly progressing necroses developed. The cause of these ischaemic changes were calciphylactic changes confirmed on post-mortem examination and by histological examination.

Aged↗
PubMed1988

Response of the cubital vein to occlusion and calcification of the abdominal aorta in patients with chronic renal failure on maintenance hemodialysis.

Dysfunction of vascular endothelial cells and accelerated calcification of the abdominal aorta were found in patients on maintenance hemodialysis. Indicators of vascular wall function, expressed as the amount of plasminogen activator and von Willebrand factor released during venous occlusion, suggested that the cubital venous wall in patients has normo- or hyper-responsiveness to occlusion. Calcification of the abdominal aorta on CT scan image was observed in most of patients including those of the ages of twenties years. The mean aortic calcification index (ACI), as an indicator of organic changes in vascular wall, was significantly higher in dialysis patients than in the nondialysis subjects. However, the mean values of indicators for vascular wall function decreased and ACI increased, as the period of treatment with hemodialysis became longer. A significant negative correlation was found between the mean ACI and most indicators of vascular wall function. The function of cubital vein was suggested to decrease in association with the progress in mural calcification of the abdominal aorta. We conclude that the alteration of the coagulation-fibrinolysis system induced by repeated hemodialysis may result from and continue to exacerbate endothelial damage, the consequence of which may be atherosclerosis.

Adult↗
PubMed2003

Cartilaginous metaplasia in calcified diabetic peripheral vascular disease: morphologic evidence of enchondral ossification.

The mechanism of arterial calcification is not clear. We examined histological sections of major arteries from lower extremities of two patients with longstanding type II (or non-insulin-dependent) diabetes mellitus, and found morphological evidence of cartilaginous metaplasia and ectopic ossification with associated severe medial arterial calcification and atherosclerosis. Hematoxylin and eosin, alcian blue, and toluidine blue stains were applied for the demonstration of cartilage cells and their specific matrix proteins, and immunohistochemical studies for type II collagen. To our knowledge, cartilaginous metaplasia has not previously been described in medium-sized human muscular arteries. This observation supports the hypothesis that active enchondral ossification may be a pathway leading to arterial calcification in diabetic obstructive peripheral vascular disease.

Arteries↗
PubMed2005

Osteogenic PTHs and vascular ossification-Is there a danger for osteoporotics?

Inflammation in vascular (mostly arterial) walls and heart valves triggered by the trans-endothelial influx of LDL particles and the action of subsequently modified (e.g., by oxidation) LDL particles can trigger true bone formation by valvar fibroblasts, by a subpopulation of re-differentiation-competent VSMCs (vascular smooth muscle cells) or by vascular pericytes. Vascular ossification can lead to heart failure and death. Elderly osteoporotic women who need osteogenic drugs to restore their lost skeletal bone are paradoxically prone to vascular ossification-the "calcification paradox." The recent introduction into the clinic of a potently osteogenic parathyroid hormone peptide, Lilly's rhPTH-(1-34)OH (Forteotrade mark), to reverse skeletal bone loss raises the question of whether this and other potently osteogenic PTHs still in clinical trial might also stimulate vascular ossification in such osteoporotic women. Indeed the VSMCs in human and rat atherosclerotic lesions hyperexpress PTHrP and the PTHR1 (or PTH1R) receptor as do maturing osteoblasts. And the evidence indicates that endogenous PTHrP with its NLS (nuclear/nucleolar localization sequence) does stimulate VSMC proliferation (a prime prerequisite for atheroma formation and ossification) via intranuclear targets that inactivate pRb, the inhibitory G1/S checkpoint regulator, by stimulating its hyperphosphorylation. But neither externally added full-length PTHrP nor the NLS-lacking PTHrP-(1-34)OH gets into the VSMC nucleus and instead they inhibit proliferation and calcification by only activating the cell's PTHR1 receptors. No PTH has an NLS and, as expected from the observations on the externally added PTHrPs, hPTH-(1-34)OH inhibits calcification by VSMCs and cannot stimulate vascular ossification in a diabetic mouse model. Encouraging though this may be for osteoporotics with their "calcification paradox," more work is needed to be sure that the skeletally osteogenic PTHs do not promote vascular ossification with its cardiovascular consequences.

Animals↗
PubMed1988

Comparison of BAY e 5009 (nitrendipine) with dihydralazine in Wistar rats with experimentally induced nephritis.

Chronic administration of nitrendipine (N) prevented the development of serious renal damage in Wistar rats with experimental glomerulonephritis. This effect is in sharp contrast with the action of dihydralazine (D). In the two treated groups, the blood pressure levels were in the same range and had returned to values of about 140 mm Hg. The heart rate and the increase in body weight were identical. Daily urinary protein excretion was significantly lower in the N-treated rats (p less than 0.001). During the experiment, 4 of the 12 D-treated and 6 of the 12 untreated animals died. In contrast, all of the N-treated rats survived. Their blood urea nitrogen and serum creatinine levels were significantly lower (p less than 0.01). Histologically, all untreated nephritic animals and three of eight D-treated rats revealed severe arteriopathy in the large vessels of the kidney and focal calcification of the glomerular and tubular basement membranes. Neither vascular changes nor basement membrane calcification were found in the kidneys of the N-treated group. These results suggest the direct renal prophylactic effect of N by prevention of the cellular calcium overload and the extracellular deposition of calcium.

Animals↗
PubMedDate not supplied

MRI of tuberculous cervical lymphadenopathy.

PURPOSE: The purpose of the study was to document the range of appearances of tuberculous cervical lymphadenopathy (TCL) on MRI. METHOD: The MR images of nine patients who were subsequently found to have TCL were retrospectively reviewed. All patients were scanned on a 1.5 T unit using a neck coil (nine patients) and a surface coil (five patients). Each abnormal region was assessed separately for maximum size, pattern of disease, necrosis, calcification, soft tissue edema, muscle involvement, and vascular compression. RESULTS: There were 17 abnormal regions. The posterior triangle was most frequently involved (six patients) followed by the supraclavicular fossa (five patients). There were three patterns of disease, comprising discrete nodes, matted nodes, and confluent masses. Necrosis occurred in 10 of the 17 abnormal regions; necrotic areas were located peripherally in 7 of these 10. The percentage of necrotic to solid areas ranged from <25 to >75% and was not related to the pattern of disease. Edema was present in four patients and was seen with matted nodes and confluent masses. Muscle involvement and vascular compression occurred in three regions. Calcification was not identified. CONCLUSION: MRI revealed three patterns of disease in TCL: discrete nodes, matted nodes, and confluent masses. Necrotic foci, when present, were more frequently peripheral rather than central, and this together with the soft tissue edema may be of value in differentiating TCL from metastatic nodes.

Contrast Media↗
PubMed2000

[Arteriosclerosis and media sclerosis. A comparison of 2 calcifying vascular diseases].

PATHOGENESIS: Arteriosclerosis and Mönckeberg's mediasclerosis are vascular diseases associated with calcification of the artery wall. While mediasclerosis in most cases develops in type 2 diabetic patients, arteriosclerosis is the result of a combination of different vascular risk factors. Mönckeberg's mediasclerosis typically involves the tunica media, whereas arteriosclerosis-associated calcifications primarily involve the intima. CLINICS: Isolated mediasclerosis does not cause narrowing of the blood vessel. The disease is usually asymptomatic, specific therapy has not yet been established. The involvement of the intima in arteriosclerosis finally leads to a decreased circulation.

Arteriosclerosis↗
PubMed2002

Cells, rather than extracellular matrix, nucleate apatite in glutaraldehyde-treated vascular tissue.

Glutaraldehyde (GA) causes a large increase in [Ca(2+)](i) and [P(i)](i) and calcification of porcine aortic valve fibroblasts. Calcification in GA-treated vascular tissue is likely to begin intracellularly, but the potential role of extracellular matrix has not been taken into account in earlier studies. To compare the role of cells and matrix in calcification, intestinal pouches made of a lipid-extracted rat small intestine were prepared. Lipid-extracted porcine aortic valves, or cells cultured from those same valves, were placed in intestinal pouches, sealed, fixed with GA, and grafted in rat subcutis. Cells in the pouches calcified in 3 weeks whereas the valvular matrix did not calcify for 9 weeks. Cellular calcification spread to the wall of the intestinal pouches and grew heavier after 9 weeks. Similarly, smooth muscle cells calcified exclusively in GA-treated rat aorta grafted in rat subcutis for 3 weeks. Calcification of extracellular matrix was seen after 9 weeks. Cells initiate calcification and extracellular matrix serves as a substrate for the subsequent growth of apatite in GA-treated vascular tissue.

Animals↗
PubMed2000

Testicular regression syndrome: a clinical and pathologic study of 11 cases.

CONTEXT: The vanishing or regressed testis is an entity well known to urologists and pediatric surgeons, affecting approximately 5% of patients with cryptorchidism. However, there is little review and discussion of this entity among pathologists with only 2 of 40 published reviews of testicular regression syndrome (TRS) found in the pathologic literature. OBJECTIVES: To assess recognition of TRS among a subset of pathologists and to determine the applicability of histologic criteria for TRS as published. DESIGN: An 8-year retrospective review of cases submitted as atrophic or regressed testis was performed. Original diagnosis and diagnosis after review were compared to assess pathologic recognition of TRS. Pathologic assessment included identification of vas deferens, epididymis, dystrophic calcification, hemosiderin, dominant vein, pampiniform plexus-like vessels, and vascularized fibrous nodule formation. At minimum, the presence of a vascularized fibrous nodule (VFN) with calcification or hemosiderin or VFN with cord element(s) was required for diagnosis. SETTING AND PARTICIPANTS: Medical records and pathologic specimens of patients undergoing surgery for cryptorchidism or with specimens reviewed at a medium-sized university hospital were analyzed. RESULTS: The original diagnosis in 3 (23%) of 13 cases was that of TRS. On secondary review, 11 (85%) of 13 cases showed features consistent with TRS. The diagnoses both before and after review showed a concurrence of 23% (3/13 cases). Two (15%) of 13 cases were correctly recognized and diagnosed as TRS at primary review; 1 case originally thought to represent TRS was not confirmed. Pathologic features correlated well with those reported in the literature. Among all 13 cases, the 11 confirmed TRS cases showed VFN in 11 (85%), intranodular calcification in 8 (62%), intranodular hemosiderin in 9 (69%), vas deferens in 9 (69%), epididymal structures in 5 (38%), and a dominant venous structure in 11 (85%). The average size of the VFN was 1.1 cm. CONCLUSION: A urologic and pediatric surgical problem, TRS may be unrecognized by many practicing pathologists. In the typical situation in which a blind ending spermatic cord is submitted for tissue analysis, characterization of such cases as consistent with regressed testis is desirable and achievable in a high percentage of cases. Pathologists may play a pivotal role in management of these patients since histologic confirmation of the testis as regressed reassures the surgeon and the family of the correctness of diagnosis and can eliminate the necessity for further intervention.

Adolescent↗
PubMed2006

Soft tissue calcifications in the lower extremities of severely diabetic patients simulating venous stasis or collagen vascular disease.

The purpose of this work is to report soft tissue calcifications in severely diabetic patients that simulate venous stasis or scleroderma, without other stigmata of these diseases. Findings from lower extremity radiographs were reviewed on two patients with severe diabetes mellitus and abnormal soft tissue calcifications. Findings were correlated with clinical history, physical exam findings, and laboratory values. Both patients in this study demonstrate radiographic findings of lower extremity soft tissue calcifications similar to those seen in venous stasis or scleroderma. Clinical history, physical examination, and laboratory values support severe diabetes mellitus, with no evidence of these other disease entities. Patients with severe diabetes mellitus may exhibit soft tissue calcifications of their lower extremities that may simulate the changes of venous stasis or scleroderma. This association has not been previously described.

Adult↗