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PubMed1990

A case of POEMS syndrome associated with essential thrombocythaemia and dermal mastocytosis.

We describe a case of POEMS syndrome presenting with the recognized features of polyneuropathy, organomegaly, endocrine abnormalities, monoclonal protein, skin changes and anasarca. The patient was found to have both a solitary sclerotic plasmacytoma of the pelvis and evidence of Castleman's disease of lymph nodes. A number of unusual and unique features are also documented. Histological examination of affected skin demonstrated changes similar to urticaria pigmentosa including local oedema and mast cell infiltration. There was marked thrombocythaemia which has been seen in only one previous case and in addition the patient developed diffuse vascular calcification in the absence of recognized aetiological factors. Radiotherapy of the pelvic lesion and chemotherapy to control the myeloproliferative disorder gave rise to significant improvement in neuropathy. Control of anasarca required steroid therapy in addition to diuretics. The significance of these observations is discussed in relation to previous reports.

Adult↗
PubMed1991

Complications of radiation therapy: CT evaluation.

Radiation therapy is an important technique for treating cancer. In the evaluation of the results of radiation therapy with computed tomography (CT), radiation-induced injuries to normal tissues are often detected. Common complications include pneumonitis, calcified lymph nodes, gastric ulceration, enteritis, hepatitis, cystitis, nephritis, osteitis, and insufficiency fractures. Rare complications include spontaneous pneumothorax, thymic cysts, vascular calcifications, and osseous sarcomas. Radiation-induced injury can usually be diagnosed from characteristic CT appearances and knowledge of the radiation port, radiation dose, and time interval since therapy. CT findings that cannot be explained on the basis of radiation therapy or that are suggestive of recurrent disease must be further evaluated.

Adult↗
PubMed1993

Musculoskeletal manifestations of chronic renal insufficiency.

Abnormalities involving the musculoskeletal system are numerous and frequent in patients with chronic renal insufficiency (CRI). The most common radiologic manifestations of CRI are those referred to collectively as renal osteodystrophy: the findings seen in secondary hyperparathyroidism (bone resorption, periosteal reaction, and brown tumors), osteoporosis, osteosclerosis, osteomalacia, and soft-tissue and vascular calcification. Bone resorption, the most frequent alteration of CRI, occurs in several locations (subperiosteal, subchondral, trabecular, endosteal, and subligamentous), whereas brown tumors and periosteal reaction are much less common. Osteosclerosis primarily affects the axial skeleton and may be the only sign of CRI. Osteoporosis and osteomalacia cause osteopenia and are not infrequent changes of CRI. The prevalence of calcifications increases with the duration of hemodialysis. The other major group of musculoskeletal abnormalities attributable to CRI includes aluminum deposition, amyloid deposition and destructive spondyloarthropathy, tendon rupture, crystal deposition, infection, and avascular necrosis. These changes are less common than those of renal osteodystrophy and are more frequently seen in patients who have undergone long-term hemodialysis or renal transplantation. Recognition of musculoskeletal manifestations is important in the clinical management of patients with CRI.

Bone Diseases↗
PubMed2003

The iceman: discovery and imaging.

The anatomic features of a 5,300-year-old mummy, the iceman, were documented with conventional radiographic, portable computed radiographic, and conventional and spiral computed tomographic images obtained between September 1991 and June 2001. A team of scientists and radiologists from Austria, Italy, and the United States supervised the examinations and interpreted the images. The images demonstrated excellent preservation of the mineralized skeleton with profound dehydration of the soft tissues. The skeleton exhibited several types of trauma, including (a) healed rib fractures, (b) hairline skull fractures and a compression deformity of the thorax, probably acquired while encased in the glacier, and (c) damage acquired during the effort to recover the corpse. Skeletal variants were present, as was evidence of degenerative arthritis, frostbite, vascular calcification, and adaptation to cultural and geographic influences. In terms of anatomy and apparent health-related conditions, the iceman was very similar to modern humans. An arrowhead lodged between the rib cage and the left scapula was the probable cause of the iceman's death. Study of the images also provided insight regarding postmortem processes that led to the iceman's mummification.

Animals↗
PubMed1987

Episternal ossicles.

Eight hundred computed tomographic (CT) scans of the chest were reviewed, and 12 cases of episternal ossicles were found. Eight persons had paired ossicles, and four had unilateral ossicles. The overall frequency in the study population was 1.5% (men, 1.4%; women, 1.7%). Episternal ossicles represent a normal variant and should be distinguished from fracture fragments, sequestra, foreign bodies, calcified lymph nodes, or vascular calcifications.

Female↗
PubMed2004

The calcium-sensing receptor: a key factor in the pathogenesis of secondary hyperparathyroidism.

Serum calcium levels are regulated by the action of parathyroid hormone (PTH). Major drivers of PTH hypersecretion and parathyroid cell proliferation are the hypocalcemia and hyperphosphatemia that develop in chronic kidney disease patients with secondary hyperparathyroidism (SHPT) as a result of low calcitriol levels and decreased kidney function. Increased PTH production in response to systemic hypocalcemia is mediated by the calcium-sensing receptor (CaR). Furthermore, as SHPT progresses, reduced expression of CaRs and vitamin D receptors (VDRs) in hyperplastic parathyroid glands may limit the ability of calcium and calcitriol to regulate PTH secretion. Current treatment for SHPT includes the administration of vitamin D sterols and phosphate binders. Treatment with vitamin D is initially effective, but efficacy often wanes with further disease progression. The actions of vitamin D sterols are undermined by reduced expression of VDRs in the parathyroid gland. Furthermore, the calcemic and phosphatemic actions of vitamin D mean that it has the potential to exacerbate abnormal mineral metabolism, resulting in the formation of vascular calcifications. Effective new treatments for SHPT that have a positive impact on mineral metabolism are clearly needed. Recent research shows that drugs that selectively target the CaR, calcimimetics, have the potential to meet these requirements.

Calcium↗
PubMed2000

Diffuse calcinosis cutis in a patient with congenital leukemia and leukemia cutis.

We report an unusual case of congenital leukemia with leukemia cutis (LC) and diffuse calcinosis cutis. A newborn girl presented with widespread dusky red and yellowish cutaneous nodules and papules. Bone marrow morphology was consistent with the diagnosis of acute monocytic leukemia of the FAB M5 type. Skin biopsy specimens confirmed the presence of a leukemic infiltrate and revealed calcium salt deposition in the papillary and reticular dermis. Calcinosis was diffuse in the whole skin but spared other organs. Vascular calcification was not present. Serum calcium levels oscillated between 2.5 and 2.86 mmol/l, and phosphorus, parathyroid hormone and 25-hydroxyvitamin D(3) levels were normal. There were diffuse osteoporosis and spontaneous fractures of small tubular bones. The patient responded to chemotherapy but, following consolidation treatment, developed sepsis and died at 120 days of age. Congenital leukemia is rare and LC is uncommon. Hypercalcemia may be a complication of leukemia, which leads to multiorgan metastatic calcification. Despite the absence of frank hypercalcemia, the presence of bone lesions suggests that the patient's calcinosis cutis was of the metastatic type. However, the cutaneous leukemic infiltrate may also represent a triggering factor for calcium deposition in the skin.

Acute Disease↗
PubMed2003

Management of secondary hyperparathyroidism: the importance and the challenge of controlling parathyroid hormone levels without elevating calcium, phosphorus, and calcium-phosphorus product.

Secondary hyperparathyroidism (HPT) is a common complication of chronic kidney disease (CKD) that can lead to clinically significant bone disease. Additional consequences of secondary HPT, such as soft-tissue and vascular calcification, cardiovascular disease, and calcific uremic arteriolopathy, may contribute to the increased risk of cardiovascular morbidity and mortality among CKD patients. Secondary HPT arises from disturbances in calcium, phosphorus, vitamin D and parathyroid hormone metabolism, which develop early in the course of CKD and become more prominent as kidney function declines. The standard therapies currently recommended to correct mineral metabolism and bone disease in these patients include calcium supplementation, dietary phosphorus restriction, phosphate-binding agents, and treatment with vitamin D sterols. However, such medications often have significant effects on the serum levels of calcium and phosphorus, which result in exacerbation of the disease and significant extraskeletal morbidity and mortality. Thus, there is a need to identify more effective treatment approaches. This review discusses the pathophysiology of secondary HPT, the challenges faced in the management of this disorder, and the impact of current treatment options on patients' risks of morbidity and mortality. In addition, the development of new, more physiologically relevant therapies, which may lead to successful management of secondary HPT, is reviewed.

Calcitriol↗
PubMed2005

C-reactive protein in end-stage renal disease: are there reasons to measure it?

Cardiovascular disease (CVD) remains the major cause of morbidity and mortality in end-stage renal disease (ESRD) patients. As traditional risk factors cannot alone explain the unacceptable high prevalence and incidence of CVD in this population, inflammation (a common phenomenon in ESRD), and other non-traditional risk factors are likely to contribute. Among several inflammatory biomarkers used to assess inflammation, high-sensitivity C-reactive protein (hs-CRP) has attracted the most interest. Indeed, in the general population the consistency of prognostic data for hs-CRP and the practicality of its use have led to suggestions that CRP should be used as a clinical criterion for global cardiovascular risk prediction. As CRP is so strongly associated with vascular disease, it has been suggested that this protein is not only a marker, but also a mediator, of atherogenesis. Indeed, recent in vitro data from studies on endothelial cells, monocytes-macrophages and smooth muscle cells support a direct role for CRP in atherogenesis. In ESRD, hs-CRP has been proven to be a strong predictor of both cardiovascular and all-cause mortality, and associated with oxidative stress, vascular calcification and endothelial dysfunction. As recent studies suggest that interleukin-6 may be a somewhat better outcome predictor than hs-CRP, comparative studies are needed to evaluate which inflammation biomarker is the most cost-effective predictor of outcome in the ESRD patient population.

Biomarkers↗
PubMed2005

Matrix GLA protein gene polymorphisms: clinical correlates and cardiovascular mortality in chronic kidney disease patients.

BACKGROUND: Increased vascular calcification plays an important role in the pathogenesis of cardiovascular events in chronic kidney disease (CKD) patients. It is the result of an active ossification process counteracted by 'protective' proteins, such as matrix GLA protein (MGP). Polymorphisms of MGP have been identified. METHODS: The aim of this study was to define the distribution of two MGP polymorphisms (-7, -138) in 99 hemodialysis (HD) patients, in 26 patients with CKD stage 3 and in 135 age- and sex-matched healthy controls. Patients were followed up for 12 months to record any cardiovascular deaths. The cause of death was determined by medical doctors, considering the medical history of each patient. The primers were designed with Primer Express software. RESULTS: MGP -138TT homozygotes were more frequent in the HD group versus controls (p = 0.0004). Additionally, the frequency of the T allele was significantly higher in the HD group (p = 0.0006). The frequency of the A allele of MGP-7 was significantly higher both in the HD group (p = 0.033) and in the CKD group (p = 0.0017) versus controls. MGP-7 GG homozygotes were significantly less common in the CKD group than in controls (p = 0.037). Combination -138TT -7AA was significantly more frequent in both CKD patients (p = 0.001) and in HD patients (p = 0.029) than in controls. Seventeen out of 99 HD patients experienced fatal cardiovascular events. Sixteen (94.1%) were -138TT homozygotes and either -7AA homozygotes or -7GA heterozygotes. CONCLUSION: This study suggests that CKD and HD patients have a different distribution of MGP gene polymorphism as compared with the normal population. Altered MGP gene polymorphism may be a negative prognostic factor for the progression to end-stage renal disease and for cardiovascular events in CKD patients.

Aged↗
PubMed2006

Hyperechoic plaque: an ultrasound marker for osteoporosis in acute stroke patients with carotid disease.

BACKGROUND: Osteoporosis is a significant complication of stroke, and hip fracture after a stroke is a frequent problem. Moreover, growing evidence links vascular and bone diseases, in the form of osteoporosis associated with both atherosclerosis and vascular calcification. The aim of our study is to detect bone change in the acute phase of ischemic stroke in patients with carotid disease and to verify the correlation with carotid echogenic plaques. PATIENTS AND METHOD: Out of 245 subjects consecutively admitted to our Stroke Unit for their first ischemic stroke, we selected 49 patients with a first-ever stroke due to carotid atherosclerosis without a previous diagnosis of bone disease. We assessed risk factors for cerebrovascular disease as well as for osteoporosis, the degree of neurological deficit and disability, and bone mineral density that was quantified by bilateral hip dual energy X-ray absorbimetry. Osteoporosis was defined as a T score below -2.5. Carotid ultrasound was used to classify plaques in non-hyperechoic (grade 1) and hyperechoic plaque (grade 2). RESULTS: We found a high prevalence of low bone mass density (BMD) in our patients (18 out of 49=36.7%), without relationship to the side of paresis. According to univariate analysis evidence of osteoporosis was correlated with age (p=0.05), score of Scandinavian Stroke Scale (p=0.01) and grade 2 plaque (p=0.01). According to multivariate analysis, there was a significant positive correlation between grade 2 plaques and osteoporosis (OR=6.58; 95% CI=1.57-27.54; p=0.01), which was stronger in women (OR=18.15; 95% CI=1.80-182.83; p=0.01). The percentage of intraplaque hyperechogenicity was inversely correlated with BMD (r=-0.411, p=0.016). CONCLUSION: Osteoporosis is highly prevalent in acute atherosclerotic stroke patients. Carotid hyperechoic plaque is an independent marker of osteoporosis.

Absorptiometry, Photon↗
PubMed1994

Histological, radiological, and biochemical features of the adynamic bone lesion in continuous ambulatory peritoneal dialysis patients.

Adynamic bone is being found with increasing frequency in dialysis patients. Little is known about its aetiology, and even less about its natural history. We found 10 cases of asymptomatic adynamic bone among a group of 32 continuous ambulatory peritoneal dialysis patients, most of whom had never been exposed to aluminium-containing phosphate binders. Compared to the remaining 22 patients, they had an older mean age (54 +/- 11.4 vs. 42 +/- 11.8 years; p < 0.05), probably a longer pre-dialysis duration of renal failure (10.9 vs. 7.1 years), higher mean ionized calcium (1.30 +/- 0.04 vs. 1.15 +/- 0.02 mmol/l; p < 0.01), and lower mean intact parathyroid hormone (31.5 vs. 200.3 pg/ml; p < 0.001). The bone density was not different between the two groups, but 9 of the 10 adynamic patients had significant vascular calcification seen on plain radiology as compared with only 7 of 20 in the comparison group (p < 0.05). Follow-up of the adynamic patients showed a close association with serum intact parathyroid hormone and ionized calcium levels. With one exception, adynamic bone did not appear to be associated with lower bone density than other types of osteodystrophy, but a longer-term study is required to determine the complete natural history of this lesion.

Adult↗
PubMed1995

Calciphylaxis in a chronic hemodialysis patient with protein S deficiency.

Vascular calcifications are common in uremic patients whereas calciphylaxis is rare. We report the case of a 45-year-old woman on chronic hemodialysis since 1977. She had a subtotal parathyroidectomy in 1985, aortic and mitral valve replacement in 1986, and has been treated since then with nicoumalone. In June 1991, she presented with repeated, painful cutaneous necrosis suggesting panniculitis. A skin biopsy showed lobular panniculitis and evidence of calciphylaxis. There was an obvious biological hyperparathyroidism. Protein C functional level was in the normal range whereas protein S functional level was low, i.e. 42%. The patient underwent cervical surgery to remove two parathyroid glands, and daily hemodialysis sessions. Despite this treatment, cutaneous necrosis progressed with superinfection. A few weeks later, the patient died from a septic shock after a myocardic infarction. Necropsy was not performed.

Calciphylaxis↗
PubMed1977

Chronic peritoneal dialysis in the management of diabetics with terminal renal failure.

Twelve diabetics with terminal renal failure were maintained on chronic peritoneal dialysis (PD) for 2-28 months (average 10 months). 7/12 survived more than 1 year. Blood glucose levels were well controlled by the use of supplemental, intradialysis, intraperitoneal insulin. The incidence of dialysis-related complications, including peritonitis was not significantly higher than in controls. Neurophysiological studies revealed a high incidence of neuropathy initially with progression in most patients. Radiological studies revealed initial vascular calcifications in 7 out of 12 patients with progression in 4. Retinopathy did not progress significantly. PD is a suitable alternative to hemodialysis in the management of end-stage diabetic nephropathy.

Adult↗
PubMed1983

Parathyroidectomy in chronic renal failure.

Parathyroidectomy was carried out in 26 patients over a 14-year period. Excellent results were obtained in patients with severe hyperparathyroidism. Vascular calcification, hypercalcaemia and pruritus did not justify surgery unless associated with unequivocal hyperparathyroidism. 13 patients required intravenous calcium infusion for up to 2 weeks to control post-operative hypocalcaemia. Calcium requirements could be predicted from the pre-operative plasma alkaline phosphatase level. Following operation continued treatment with vitamin D was necessary to prevent hypocalcaemia. Hyperparathyroidism recurred in 1 patient after 8 years and 4 patients developed osteomalacia. Since parathyroid hormone may have toxic effects other than those on bone, maintenance of normal levels should be a long-term objective in the treatment of patients with chronic renal failure. Where large parathyroid glands are present, surgical reduction in gland mass is a logical prelude to long-term suppression of parathyroid hormone with vitamin D and phosphate-binding agents.

Adolescent↗
PubMed1988

Pathogenesis of cerebral atrophy in uraemia. State of the art.

This paper discusses the possible pathogenesis of the cerebral atrophy (CA) observed in a large percentage of uraemic patients, taking the form of prevalently cortical damage (cortical atrophy) and/or subcortical enlargement of ventricular cavities (subcortical atrophy). This central nervous system pathology seems to share very little either with the better known 'dialysis encephalopathy' or with the 'acute encephalopathy syndrome', even though sporadic cases of both these forms have shown concomitant CA. Histopathologically it offers the picture of loss of neurons and nerve fibres and can thus be compared with uraemic peripheral nervous system damage. CA is unquestionably important because of its implications in terms of impairment of superior cortical functions, just as in CA of non-uraemic aetiology. A first aetiopathogenic hypothesis might include endogenous uraemic intoxication to the nerve tissue, believed responsible for peripheral uraemic neuropathy, but other possibilities merit consideration: vascular calcification secondary to hyperparathyroidism, blood lipid disorders, and systemic hypertension--factors that contribute to impairing the brain vasculature, with cascade effects on brain tissue oxygenation, neuronal metabolism, and energy exchanges. Tissue oxygenation is already jeopardized in the uraemic patient by the concomitant chronic anaemia and by cardiac insufficiency in cases with hypertensive heart disease. In dialysis patients with volume-dependent hypertension the brain may be further damaged by abrupt pressure changes produced by dialytic ultrafiltration; these constitute a severe challenge to cerebral blood flow autoregulation. Cyclic variations of brain tissue hydration connected with regular dialysis treatment may have adverse effects on neurotransmitter functions, particularly those mediated by neuropeptidergic systems. Chronic intoxication may result from oral Al(OH)3 of phosphorus-chelating agents: in animal studies and clinical observations in non-uraemic populations the neurotoxic potential of Al is indicated by a significant correlation between histological neuronal damage, impaired function, and Al concentration in brain tissues. In addition, a concausal role of malnutrition in central nervous system damage in the uraemic patient cannot be overlooked, since malnutrition is known to give rise to functional and structural alterations in non-uraemic human pathology. In the light of these clinical observations and experimental findings, it would appear that the prevention of CA in uraemia is today feasible.

Aluminum↗
PubMed1989

[Extreme hyperphosphatemia with hypocalcemia within the scope of cell lysis syndrome in a child with T-ALL].

In a 10 3/4-year-old girl suffering from a T-ALL with an extremely high leukocyte blood cell count (400,000/microliters) we observed a tumor-lysis syndrome with hyperphosphatemia and hypocalcemia accompanied by clinical signs of tetany. The therapeutic application of calcium gluconate resulted in vascular calcification by exceeding by far the calcium-phosphate solubility product. The fast lysis of T-lymphoblasts with their high phosphate concentration is etiologically involved in the hyperphosphatemia. Our patient died of multiorganic failure. Regular monitoring of phosphate in urine might be helpful in instituting early therapeutic procedures.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2003

Osteopontin deficiency attenuates atherosclerosis in female apolipoprotein E-deficient mice.

OBJECTIVE: Osteopontin (OPN), a noncollagenous adhesive protein, is implicated in atherosclerosis, in which macrophages within atherosclerotic plaques express OPN. However, it is not known whether the elevated OPN expression is a cause or result of atherosclerosis. METHODS AND RESULTS: We generated mice that lacked OPN and crossed them with apolipoprotein (apo) E-deficient mice and analyzed these mice with a mixed C57BL/6x129 background after 36 weeks on a normal chow diet. In female mice, OP+/-E-/- and OP-/-E-/- mice had significantly smaller atherosclerotic and inflammatory lesions compared with OP+/+E-/- mice, and that was reflected by smaller area of MOMA-2-positive staining. In male mice, however, there was no significant difference in the atherosclerosis lesion areas among 3 genotypes. In both OP-/-E-/- and OP+/+E-/- mice, typical atherosclerotic lesions were detected, which include necrotic core, foamy cell collections, and cholesterol clefts. However, we found that vascular mineral-deposited areas in 60-week-old male OP-/-E-/- mice were significantly increased compared with those in OP+/+E-/- male mice. CONCLUSIONS: These results suggest that OPN plays a promoting effect in atherosclerosis and inhibitory effect in vascular calcification. The suppression of OPN expression in females should be considered a therapeutic possibility in atherosclerosis.

Animals↗