Periarticular Calcifications Research Articles

A Radiological Approach to the Systemic and Neurologic Features of Hyperparathyroidism

Parathyroid hormone (PTH) affects the nervous system directly and indirectly. The induced pathology may present typical imaging findings in neuroradiology. The hormone controls the physiological level of blood calcium. Increased serum PTH causes pathological features in the kidneys and especially in the skeleton where most calcium is situated. Primary hyperparathyroidism is due to hyperplasia or to adenomatous or carcinomatous degeneration of glandular tissue. It causes relapsing nephrolithiasis and, more seldon, nephrocalcinosis. Bone shows increased osteoclastic activity with various aspects of diffuse demineralization. In severe cases pathological fractures and sub-periosteal, sub-chondral reabsorptions appear, especially at the tendon and capsuloligamentous insertions. In even more severe disease fibrous osseous cysts and brown tumours may be found in bone. In the central nervous system, clinical symptoms, such as mental confusion, lethargy and exceptionally coma may appear. Radiologically, bone resorption can be observed in the skull as microlacunar confluent osteolysis (salt and pepper skull). Body fractures may develop in the spine. Secondary hyperparathyroidism is due principally to renal failure. Both hypocalcaemia and hyperphosphoraemia cause the hormone secretion increase. In this case, other pathologic features are associated with the typical manifestations of primary hyperparathyroidism. The uraemic kidney is inable to synthetize active vitamin D, leading to rickets in the young and osteomalacia in adults. Hyperphosphoraemia causes ectopic periarticular calcifications. Furthermore, the lack of degradation of an endogenous protein (beta 2 microglobulin) by the kidney and its poor elimination by dialytic treatment, cause chronic retention and consequent systemic amyloidosis which induces intraosseous cystic lesions and severe destructive arthropathy. All these aspects, together, are known as renal osteodystrophy. The radiological features of secondary hyperparathyroidism are the same as those observed in the primary form. In addition, all the lesions of renal osteodystrophy may be associated, further worsening the disease. In the secondary form, mild hypocalcaemia, if present, rarely leads to the neurological manifestations of the primary disease. Frequently carpal tunnel syndrome arises due to local amyloid infarction. Chronic aluminium retention may produce neurological aspects of dementia. Finally, the decrease of PTH hormone blood levels, as in hypoparathyroidism and the consequent hypocalcaemia may determine neurologic symptoms such as paresthaesias, and in severe disease, tetanic contractions. Radiologically, typical micronodular calcifications can be observed in the brain basal ganglia.

Hydroxyapatite pseudopodagra in a young man: Acute calcific periarthritis of the first metatarsophalangeal joint

Pain and swelling at the first metatarsophalangeal joint can be caused by acute calcific periarthritis (ACP), an inflammatory condition resulting from deposition of hydroxyapatite crystals. A case is reported of a 23-year-old man in whom ACP was initially mistaken for gout, septic arthritis, and cellulitis. The diagnosis of ACP is based on the finding of inflammation around a joint along with radiographic evidence of periarticular soft tissue calcifications. Calcifications may disappear over time, as they did in this case. Failure to recognize this condition can lead to unnecessary testing and inappropriate treatment.

Blood Pressure Monitoring in Hemiplegic Patients

To the Editor: We are frequently asked which arm should be used to measure blood pressure in patients with hemiplegia. We have observed that blood pressure measurements from the hemiplegic arms of post-stroke patients do not correlate well with measurements from the nonhemiplegic arm. The following two cases illustrate that finding. Patient 1 is a 69-yr-old male who suffered a stroke 2 yr prior to sustaining a femoral neck fracture. Residuals from the stroke included mild dementia and right hemiparesis with spasticity. The blood pressure in the hemiparetic arm was 114/68 mm Hg, whereas the blood pressure in the nonparetic arm was 157/73 mm Hg. The radial pulse was also weaker in the paretic arm than the nonparetic arm. Patient 2 is a 75-yr-old male who presented for colon resection. He had suffered a stroke with residual right hemiparesis 2 yr prior to the current surgery. Blood pressure was 100/60 mm Hg in the paretic arm and 150/74 mm Hg in the nonparetic arm. Yagi et al. [1] measured blood pressure, both noninvasively and invasively, in 47 patients after stroke. They found that blood pressure was significantly higher in the paretic arm than in the nonparetic arm. Panayiotou et al. [2] measured blood pressure in 15 patients with acute hemiparesis and flaccidity and found the systolic and diastolic blood pressures to be higher in the paretic arm in 8 of 15 patients and lower in 7 of the 15 patients. Dewar et al. [3] measured blood pressure in 103 hemiplegic patients and found blood pressure in the paretic arm to be higher if it was spastic and lower if it was flaccid. They concluded that muscle tone influences extremity blood pressure. A number of investigators, including Broe and Ofner [4], have described vasomotor changes affecting the upper extremities in patients after a stroke. These changes may affect the paretic arm, the nonparetic arm, or both. We measured blood pressure in 14 patients with hemiplegia. Nine patients had spasticity on the affected side and five had flaccidity. All five of the patients with flaccid arms had lower blood pressure in the flaccid arm compared with the normal arm. Five of the nine patients with spasticity had higher blood pressure in the paretic arm, four had lower blood pressure in the paretic arm, and one patient had equal blood pressures. Two patients in whom we invasively measured blood pressure in the paretic arm demonstrated blood pressure that was not different from the blood pressure measured noninvasively in the unaffected arm. A large number of chronic changes such as clubbing, retardation of nail growth, edema, osteoporosis, fractures, arthritis, shoulder dislocation, frozen shoulder, periarticular calcification, muscle wasting, temperature differences, and deep vein thrombosis can occur in paretic extremities after a stroke. Interestingly, some pathologic changes such as rheumatoid arthritis and gouty tophi do not affect paretic limbs after a stroke [5]. Because of the large and inconsistent differences in blood pressure in the arms of patients with hemiparesis, we suggest that measuring blood pressure in the nonparetic arm of poststroke patients will provide a more reliable monitor of blood pressure during anesthesia. S. S. Moorthy, MD Larry Davis, MS R. V. Reddy, MD Stephen F. Dierdorf, MD Departments of Anesthesia and Neurology Indiana University School of Medicine Indianapolis, IN 46202

Fluorose osseuse au niveau de la main. A propos de deux observations

Skeletal fluorosis is well known, particularly in the spine, pelvis and forearm. However, the hand may also be involved. The authors report two cases of this site in endemic areas in Senegal, after ingestion of large amounts of fluoride in the water. Fluorosis consisted of deforming metacarpal and phalangeal osteoperiotitis in one case and peri-articular ossifications and calcifications of the attachments of the ligaments and capsule in the other case. They review the literature concerning skeletal fluorosis and discuss the rarity of hand involvement its clinical features and particularly its radiological features. Lastly, they emphasize the differential diagnosis with certain metabolic, infectious and neoplastic diseases.

Progressive Subcutaneous and Periarticular Calcifications in a Patient with Spinal Muscular Atrophy Type III

We describe a boy, diagnosed to have spinal muscular atrophy type III at 3 years, who developed as yet unexplained progressive subcutaneous and periarticular calcified nodules at the age of 5 years.

Familial Hydroxyapatite Chondrocalcinosis with Spondyloepiphyseal Dysplasia

We describe the course of the articular manifestations in a kindred with familial hydroxyapatite chondrocalcinosis and because of an associated spondyloepiphyseal dysplasia (SED) have investigated the linkage between the disease and markers in the type II procollagen gene (COL2A1). Twenty-seven family members from a large pedigree underwent musculoskeletal and radiographic examinations. In 12 patients, the progression of the disease was evaluated by comparative radiographic surveys obtained 12 years apart. Seven of the 12 family members who were studied in 1978 had severe progression of erosive hand osteoarthritis, whereas there was only minimal progression of the previously observed intervertebral disc or periarticular calcifications. The disease was recognized in seven other siblings from the third generation at a mean age of 24 years. Mild SED was present in several previously and newly diagnosed patients. Nevertheless, no genetic linkage between the disease and COL2A1 polymorphic markers was found. Hydroxyapatite chondrocalcinosis in this kindred displays a variable spectrum of phenotypic manifestations, which include spondyloepiphyseal dysplasia, precocious and progressive erosive hand osteoarthritis, and intervertebral disc and costal cartilage calcification. The gene responsible for the occurrence of hydroxyapatite chondrocalcinosis, osteoarthritis, and mild epiphyseal dysplasia in this family must be one that encodes a protein other than type II procollagen. The mild SED was most easily detected by examining younger affected members. The apatite deposits in this family seem to be secondary to the SED and should be distinguished from those in primary hydroxyapatite disease as in calcific periarthritis.

Alkalosis and hypomagnesaemia: unwanted effects of a low-calcium CAPD solution

We studied 43 CAPD patients for 4 months during the change from a high-calcium dialysis fluid (Baxter PD1) to a low-calcium fluid (Baxter PD4), which also contained low magnesium (0.25 mmol/l) and high lactate concentrations (40 mmol/l). Serum calcium fell significantly as did the incidence of hypercalcaemia, whilst the proportion of patients taking calcium-containing phosphate binders increased. There was a non-significant increase in serum i-PTH levels but the proportion with i-PTH > 150 pg/ml (normal range 10-65 pg/ml) increased significantly. There was a significant fall in serum magnesium level and seven patients developed hypomagnesaemia. Serum bicarbonate increased significantly and progressively and 17 patients were alkalotic at 4 months, five severely (bicarbonate 35-40 mmol/l). One patient developed recurrent episodes of painful subcutaneous and periarticular calcification, which may have been related to the alkalosis. Initial serum bicarbonate levels correlated significantly with dialysis adequacy assessed by daily Kt/V (r = 0.458, P = 0.002). The relationship to adequacy was abolished during the period of use of the high-lactate dialysis fluid. Use of low-magnesium CAPD fluids must be supported by regular monitoring of serum magnesium levels. The high lactate concentration in such fluids may not be appropriate and is potentially hazardous when individualization of dialysis dose demands the use of relatively high exchange volumes. Low serum bicarbonate levels in CAPD patients reflect inadequate dialysis, which use of these fluids serves to mask.

Acute Calcium Pyrophosphate Dihydrate Crystal-Induced Tenosynovitis

Calcium pyrophosphate dihydrate crystal deposition in tendon sheaths is a rare cause of acute and chronic tenosynovitis. An elderly patient with acute wrist pyrophosphate tenosynovitis and transient periarticular calcification is described.

Post-traumatic dynamic change of carboxyterminal propeptide of type I procollagen, alkaline phosphatase and its isoenzymes as predictors for enhanced osteogenesis in patients with severe head injury.

Patients suffering from severe head injury and fractures of long bones or large joints often show enhanced osteogenesis, with hypertrophic callus formation and/or heterotopic ossifications. The advantage of this phenomenon is early consolidation of the fractures. An extreme disadvantage is extensive periarticular calcification, resulting in complete ankylosis of the affected joint. In spite of numerous efforts aimed at clarifying the way in which severe head injury can influence osteogenesis at a distant site, this phenomenon is still not understood. The process, once started, seems irreversible, but if diagnosed in time, could be prevented with non-steroid anti-inflammatory drugs that inhibit development of heterotopic ossifications. The major prerequisite for testing this possibility is to define parameters of an early diagnosis of enhanced osteogenesis. Thus, the aim of this study was to test whether serum values of some parameters related to bone regeneration could allow an early prediction of enhanced ossification following bone fracture in patients with severe head injury. Samples of sera were obtained from three groups of injured patients: fractures of long bones or large joints only (n = 6), severe head injury only (n = 8), severe head injury and fractures of long bones and large joints (n = 7) and from a group of apparently healthy volunteers (n = 10). The values for alkaline phosphatase (ALP), the bone isoenzyme, and the carboxy terminal propeptide of type I procollagen (PICP) were significantly higher (5-20 times as high) in patients with severe head injury and bone or joint fractures than in any other group. Significantly increased concentrations of PICP were already found in the 1st week after injury, and those of ALP and of the bone isoenzyme increased during the 2nd week after injury. Results show that these parameters are helpful for an early diagnosis of enhanced osteogenesis and heterotopic ossifications in patients with severe head injury and bone fractures. Further studies are necessary to verify these findings, while analysis of reasons for the specific patterns of dynamic change of these parameters could lead to better understanding of the mechanisms underlying the uncontrolled bone formation.

Familial spondyloepiphyseal dysplasia tarda, brachydactyly, and precocious osteoarthritis associated with an arginine 75-->cysteine mutation in the procollagen type II gene in a kindred of Chiloe Islanders. I. Clinical, radiographic, and pathologic findings.

To characterize a kindred of Chiloe Islanders with spondyloepiphyseal dysplasia tarda (SEDT), brachydactyly, precocious osteoarthritis (OA), and intraarticular calcification. Sixteen family members underwent a complete physical examination, anthropometric measurements, radiographic studies of the spine and peripheral joints, and analysis of the type II procollagen gene (COL2A1). Seven family members presented with SEDT, brachydactyly, precocious OA, and periarticular calcification while 2 others had the same syndrome but without brachydactyly. The inheritance was autosomal dominant, and the disease cosegregated with a base substitution in the COL2A1 gene. The syndrome o SEDT, precocious OA, and brachydactyly in a kindred of Chiloe Islanders is associated with a point mutation in 1 allele of the COL2A1 gene. The relationship of this type of SEDT to familial calcium pyrophosphate dihydrate deposition disease and idiopathic hip dysplasia, both endemic in Chiloe Islanders, needs to be further investigated.

Intramedullary reduction and stabilisation of adult radial neck fractures

We report the treatment of six adult patients with displaced fractures of the radial neck by intramedullary reduction and stabilisation. Nine months after operation all the patients had good joint function, little or no pain, complete healing and no significant periarticular calcification. This simple semi-closed procedure may help to avoid resection of the radial head in some cases.

Dialysis-associated arthropathy — Role of age

Skeletal and joint disorders are the most common medical problem in long term survivors of maintenance dialysis [1, 2]. These disorders can take various clinical and radiological forms. Renal osteodystrophy, periarticular calcifications, tendon rupture, microcrystalline arthropathies, and infectious arthritis are already well known. Since dialysis has become widely available for patients with chronic renal disease and regularly dialyzed patients are surviving for prolonged periods, a new type of arthropathy has been reported. This new entity has not yet been adequately defined. Several authors (including our group) considering the relationship between such clinical and radiological features as carpal tunnel syndrome (CTS), tenosynovitis of the finger flexors, and destructive arthropathies of the limbs and spine have identified what has been called dialysis-associated arthropathy (DAA) [2-5] and have suggested a common pathophysiological pathway. The presence of amyloid deposits consisting mainly of [32 microglobulin, ([3am) in carpal tunnel synovial tissue, capsule, and subchondral bone of the major limb joints and in the intervertebral disks [6] has led many authors to think of the condition as a dialysis-related amyloidosis [7-9]. This review discusses the criteria and the diagnostic tools for a diagnosis of DAA, and its relationship to [32m amyloidosis. The factors thought to contribute to the pathogenesis of DAA and [32m amyloidosis are analyzed, and therapeutic approaches are discussed. The duration of dialysis and the age of the patient appear to be significant factors predisposing to the development of DAA. Elderly people, most of them with a life expectancy of several years, constitute an increasing proportion of patients receiving chronic hemodialysis and peritoneal dialysis, and this population is probably prone to rapidly develop joint anomalies linked to dialysis.

A study of bone and joint changes secondary to burns

A clinical and radiological study of 80 postburn patients to determine the extent of bone and joint changes is presented. The group comprised 38 males and 42 females, with ages ranging from 2 to 60 years. The time since burning ranged from 6 to 12 months in 40, from 1 to 5 years in 24 and over 5 years in 16 patients. Clinically bone and adjoining tissue involvement were seen in 32 patients (40 per cent), while radiological changes were seen in 49 (61.25 per cent). Radiological changes noted included osteoporosis 56.25 per cent, stunted growth (phalanges and limbs) 27.5 per cent, osteomyelitis 2.5 per cent, partial resorption of terminal phalanges and ankylosis 1.25 per cent each. Periarticular, pericapsular and tendon calcification were each seen in 1.25 per cent of the patients. Bone and joint changes were encountered only in major burns, and these could be minimized by proper early surgical care and long-term rehabilitation.

Tumoral calcifications in hemodialysis patients: possible role of aluminum intoxication.

Uremic patients may develop extraskeletal calcifications. Among the latter, periarticular tumoral calcifications (TC) represent massive, multiloculated calcium-phosphate deposits. The aim of this report was to analyze a series of 10 cases of TC in hemodialysis patients who were admitted at the Necker Hospital between 1974 and 1988. They were all male. An increased plasma calcium x phosphorus product was observed in 8 of the 10 patients. Plasma calcium level was increased in only 2 patients. In contrast, hyperphosphatemia was a constant feature in all the patients, as was the absence of an increase in plasma alkaline phosphatase activity. Using the bone histomorphometry technique, osteitis fibrosa of mild degree was observed in 2 patients, of moderate degree in 2 and of severe degree in 2 others. Evidence of aluminum (Al) overload was found in the 8 patients in whom it was searched based on bone histomorphometry, bone histochemistry, bone Al content and increased serum Al levels either in the basal state or after a deferoxamine test. In addition, Al overload was strongly suspected in the 2 remaining patients because of prolonged exposure to Al-contaminated dialysate. Various treatment strategies, including parathyroidectomy (PTx), were undertaken that remained unsuccessful in modifying the course of TC to a significant extent. Remarkably, TC occurred for the first time after PTx in 1 patient and worsened after PTx in 2 others. In conclusion, overt secondary hyperparathyroidism appears not to be an essential prerequisite for TC development in hemodialysis patients, and PTx must not be performed in such patients on the sole basis of the presence of TC.(ABSTRACT TRUNCATED AT 250 WORDS)

Uremic Tumoral Calcinosis: Preliminary Observations Suggesting an Association With Aberrant Vitamin D Homeostasis

Periarticular tumoral calcification is a unique form of soft tissue calcification that occurs infrequently in patients with end-stage renal disease. The mechanism underlying such massive periarticular calcifications is unknown. The radiographic similarity between uremic tumoral calcifications and those found in hereditary tumoral calcinosis, a disorder of calcitriol and phosphorus homeostasis, caused us to examine whether abnormalities in vitamin D metabolism were associated with uremic calcinosis as well. We examined two uremic subjects with massive periarticular tumoral calcifications and found that they had inappropriately high serum calcitriol levels for the degree of renal function, hyperparathyroidism, and hyperphosphatemia. The source of calcitriol could not be identified in one subject, but likely was derived from granulomatous tissue in the other. In the subject with marrow granulomas, we found that calcitonin administration further stimulated calcitriol production. Although epidemiological studies are needed to confirm this preliminary association between calcitriol and uremic tumoral calcinosis, our observations suggest that normal serum calcitriol levels in association with hyperphosphatemia may be a contributing factor in the development of this rare disorder.

Idiopathic infantile arterial calcification: Unusual features

Idiopathic infantile arterial calcification (IIAC) is a rare disease of unknown etiology, which causes widespread arterial calcification and usually leads to early death from coronary arterial occlusion. Periarticular calcification has been reported in some cases. Two new cases are reported. In addition to the usual features of the disease, one was found to have ear-lobe calcification and the other an aortic aneurysm and coarctation of the aorta. Therapy with diphosphonate was apparently successful in one patient.

Simultaneous Occurrence of Calcium Pyrophosphate Dihydrate and Basic Calcium Phosphate (Hydroxyapatite) Crystals in a Knee

An 82-year-old man developed periarticular roentgenographic calcifications of the knee joint. Fragments of meniscus and peritendinous tissue were collected during total knee arthroplasty. Crystals were released from tissues by collagenase digestion. Calcium pyrophosphate dihydrate crystals were identified in the meniscus, and basic calcium phosphate crystals were identified in the peritendinous tissue. Methods of crystal identification included compensated polarized light microscopy, scanning electron microscopy with X-ray energy dispersive analysis, and X-ray diffraction.

Radiographic followup of joints injected with triamcinolone hexacetonide for the management of childhood arthritis

Evidence of deleterious effects following intraarticular injection of triamcinolone hexacetonide was sought through a review of radiographs of 145 joints of 55 children with chronic arthritis. Possible deleterious effects were noted in 16 joints of 11 patients. These effects included: small patella (2 joints), patellar osteochondritis dissecans (1 joint), periarticular calcification (9 joints), intraarticular tibial bony spur (1 joint), avascular necrosis of the distal radial epiphysis (2 joints), and avascular necrosis of the proximal femoral epiphysis (1 joint). Only the latter possible complication was symptomatic. Serial radiographs of 76 joints of 30 children showed mild progressive changes compatible with the underlying disease, except in the hip joint, where changes were more severe. The intraarticular injection of triamcinolone hexacetonide is a procedure that appears to be associated with an acceptably low frequency of radiologic abnormalities for many joints in children with chronic arthritis, but its effects on the hip joint remain uncertain.

Flurbiprofen inhibits heterotopic bone formation in total hip arthroplasty

A double-blind prospective parallel group study comparing slow-release flurbiprofen with placebo in the control of ectopic bone formation was carried out in 68 patients undergoing total hip arthroplasty. Eight weeks after surgery there was evidence, significant at the 1% level, that the incidence and extent of periarticular calcification was lower in the flurbiprofen group. At an early phase, serum calcium level decreased and after 8 weeks serum alkaline phosphatase level increased more in the placebo group than in the flurbiprofen group, indicating an effect of flurbiprofen on bone mineral metabolism. Six patients were withdrawn in each treatment group, four due to side effects in the flurbiprofen group and three due to side effects in the placebo group. Overall, five patients in each group reported side effects, the nature and severity of the side effects being very similar in each group. We conclude that flurbiprofen is an efficient and safe drug in limiting ectopic bone formation following total hip arthroplasty. Heterotopic bone formation is a frequent complication after total hip replacement. Heterotopic bone reduces the extent of hip motion, reduction being more evident in cases with extensive ectopic bone formation around the hip joint. Various treatment regimens have been proposed for discouraging heterotopic bone formation. Anti-inflammatory agents such as indomethacin and ibuprofen have turned out effective. Local irradiation also prevents ectopic bone formation, but diphosphonates seem not be effective in this respect. The aim of the present study was to assess the efficacy of flurbiprofen, a new anti-inflammatory agent, in limiting heterotopic bone formation, and to note the frequency and severity of any side effects of the treatment.

ARTHRITIS MUTILANS, TUMORAL CALCINOSIS, RAYNAUD'S PHENOMENON AND SJÖGREN'S SYNDROME

We report a female patient who over 25 years developed a progressive deforming arthropathy involving both hands without anatomical or functional abnormalities of other joints. Raynaud's phenomenon, lung fibrosis and Sjögren's syndrome. She had multiple soft tissue and periarticular calcification particularly evident in the lower extremities, shoulders, hands, fingers and back.