Tumoral Calcinosis Research Articles

Tenosynovitis With Psammomatous Calcifications: A Distinctive Trauma-Associated Subtype of Idiopathic Calcifying Tenosynovitis With a Predilection for the Distal extremities of Middle-Aged Women-A Report of 23 Cases.

The term "idiopathic calcifying tenosynovitis" (ICT) refers to a clinically and radiologically defined syndrome of pain and tendinous calcifications, most often involving the shoulder joint. A distinctive subset of ICT cases, termed "tenosynovitis with psammomatous calcifications" (TPC), occurs in the distal extremities and shows characteristic morphology, in particular psammomatous calcifications. As only 14 cases have been reported to date, TPC remains poorly recognized by both pathologists and clinicians. Twenty-three well-characterized cases of TPC along with all available radiologic and clinical information, including follow-up, were collected. Cases occurred in 21 females and 1 male (1 patient of unknown sex), aged 16 to 75 years (mean: 41), and almost exclusively involved the fingers and toes, except for one case in the elbow and one in the knee joint. The lesions ranged from 2 to 30 mm in size (mean: 10 mm). Pain was the most common presenting symptom (12/16 patients). A history of trauma or repetitive activity was present in 6 of 15 patients. None of the individuals was known to have disorders in calcium or phosphate metabolism. Radiographic studies showed a nonspecific, calcified mass. Typical morphologic features of TPC were invariably present, with degenerating tendinous tissue containing psammomatous calcifications, surrounded by a variably cellular, CD68/CD163/CD4-positive histiocyte-rich granulomatous host reaction. HUMARA assay in one case showed a polyclonal pattern. Clinical follow-up (19 patients; mean: 5.2 y; range: 1 to 14 y) showed no local recurrences. In this, the largest study of TPC to date, we confirm striking predilection of this distinctive pseudoneoplasm for the fingers and toes of young to middle-aged women. TPC should be rigorously distinguished from other forms of ICT, which typically involve large, proximal joints, and show simply dystrophic calcification involving tendinous tissues, and from tumoral calcinosis, which also involves large joints and often is associated with calcium and/or phosphate abnormalities. TPC appears to be related to trauma and/or repetitive activity and is cured with simple excision.

Hyperphosphatemic Tumoral Calcinosis: a Rare Clinico-pathological Disorder

Tumoral calcinosis (TC) is a rare clinic-pathological entity characterised by neoplasm-like (tumoral) calcium phosphate deposition (calcinosis) in the periarticular soft tissues. We report a case of a 24-year-old male who presented with a spontaneous onset, gradually increasing swelling in his left buttock since 3 years. On examination, a huge soft tissue mass involving the entire left gluteal region and thigh was present. After thorough workup including tissue biopsy, radiological imaging, and biochemical investigations, his swelling was diagnosed as tumoral calcinosis. TC is often misdiagnosed as soft tissue sarcoma but presence of several calcified masses with chronic inflammatory reaction clinches the diagnosis. He underwent complete surgical excision and was put on low phosphorus diet and phosphate binder (Sevelamer Carbonate 400–800 mg TDS orally with phosphate-binding antacids) referred to as phosphorous deprivation therapy. He showed a remarkable post-operative recovery with gain in weight and no recurrence after 1 year of follow-up.

Tumoral calcinosis of the lumbar and cervical spine

BackgroundTumoral calcinosis has been defined as a pathological condition which presents as calcified masses around juxta-articular structures. The etiology of this pathology is still not well understood but degenerative spine diseases seem to play a role. The diagnosis of tumoral calcinosis preoperatively can prevent intraoperative confusion from unexpected findings, especially in cases where removal of the calcified mass is essential to treating the patient’s symptoms, i.e. nerve compression causing radiculopathy. Case descriptionWe present two cases of patients who presented with spinal radiculopathy and mechanical pain. Both patients were found to have a calcified facet joint mass and underwent surgical resection of the mass combined with spinal fusion resulting in excellent symptom relief post-surgery. ConclusionFor accurate diagnosis and management of tumoral calcinosis, a high index of suspicion together with neuro imaging remains a good place to start. Intra-operative visualization of the pathology as well as permanent pathology reports is a good adjunct to confirming the diagnosis.

Isolated Tumoral Calcinosis in the Hip Mimicking Peri-articular Infection: A Case Report and Literature Review

Introduction: Tumoral calcinosis is a rarely described metabolic condition, characterized by the accumulation of calcium hydroxyapatite crystals in the soft tissues. The purpose of this paper is to present a case of a tumoral calcinosis with uncommon characteristics in order to discuss the diagnosis and treatment options. Case report: We report the case of a 65 years-old patient with a multifactorial avascular necrosis of the femoral head, to which a hip replacement was planned. Due to the images observed preoperatively, infection was ruled out and after the studies; an isolated tumoral calcinosis was identified and confirmed with histopathological findings. Conclusion: Tumoral calcinosis is a benign pathology that can create confusion due to the nonspecific characteristics. Metabolic profile studies and multimodal imaging are recommended to diagnose this condition adequately. In some cases, biopsy or aspiration can also be helpful to confirm the diagnosis.

FGF23 and Bone and Mineral Metabolism.

FGF23 is a phosphotropic hormone produced by the bone. FGF23 works by binding to the FGF receptor-Klotho complex. Klotho is expressed in several limited tissues including the kidney and parathyroid glands. This tissue-restricted expression of Klotho is believed to determine the target organs of FGF23. FGF23 reduces serum phosphate by suppressing the expression of type 2a and 2c sodium-phosphate cotransporters in renal proximal tubules. FGF23 also decreases 1,25-dihydroxyvitamin D levels by regulating the expression of vitamin D-metabolizing enzymes, which results in reduced intestinal phosphate absorption. Excessive actions of FGF23 cause several types of hypophosphatemic rickets/osteomalacia characterized by impaired mineralization of bone matrix. In contrast, deficient actions of FGF23 result in hyperphosphatemic tumoral calcinosis with high 1,25-dihydroxyvitamin D levels. These results indicate that FGF23 is a physiological regulator of phosphate and vitamin D metabolism and indispensable for the maintenance of serum phosphate levels.

Three cases of carpal tunnel syndrome due to tumoral calcinosis

Three cases of carpal tunnel syndrome due to tumoral calcinosis

Hyperphosphataemic tumoral calcinosis

Hyperphosphataemic tumoral calcinosis

A case report of tumoral calcinosis in the forearm

A case report of tumoral calcinosis in the forearm

Extensive Tumoral Calcinosis of Elbow

Extensive Tumoral Calcinosis of Elbow

A rare development of tumoral calcinosis of the ear auricle.

Tumoral calcinosis is a condition characterized by deposition of calcium salts in the skin and sub- cutaneous tissue, commonly found around the joints. However, tumoral calcinosis of the auricle is extremely rare. We present the case of a 13-year-old boy with tumoral calcinosis of the helix of the ear auricle. A 13-year-old boy presented with a 10-year history of an enlarging mass on the left auricle. The mass was hard, non-tender, and non-compressible. The patient had no history of trauma. Complete surgical excision and pathological examination of the specimen was performed. The final diagnosis of the excised mass was tumoral calcinosis. After 9 months of follow-up, there were no signs of recurrence of the tumor and the patient was satisfied with the surgical results. Tumoral calcinosis of the auricle is extremely rare and may be misdiagnosed as other tumors. Pathological examination is essential for definitive diagnosis and complete surgical excision should be considered as the treatment of choice.

Hyperphosphatemic Familial Tumoral Calcinosis in Two Siblings with a Novel Mutation in GALNT3 gene: Experience from Southern Turkey

Hyperphosphatemic Familial Tumoral Calcinosis in Two Siblings with a Novel Mutation in GALNT3 gene: Experience from Southern Turkey

A Novel Mutation in FGF23 Causing Severe Manifestation of Hyperphosphataemic Familial Tumoral Calcinosis

We present a 16-year girl, second issue of a consanguineous couple presented with painless symmetrical bony swellings around hips for 3 years. She lost 25 kg weight due to profound anorexia in the first year of illness and developed secondary amenorrhea. Last 7 months she had repeated generalized tonic clonic seizure due to hypocalcaemia. The bony swellings were located in both gluteal regions and were 30x35 cm2, hard and non tender. Mobility of hip joints were restricted. Except for severe wasting as a part of generalized cachexia other systemic examination was unremarkable. Investigations revealed anaemia (Hb-E trait), low albumin, low corrected calcium (during convulsions) otherwise normal, persistently high phosphate & vitamin-D level, normal iPTH & alkaline phosphatase (ALP), low serum ascorbic acid, normal ESR & CRP. X-ray & CT scan of pelvis showed large calcified mass in periarticular soft tissues. Biopsy confirmed presence of dystrophic calcification. Diagnosis of tumoral calcinosis was based on biochemical parameters, imaging and biopsy findings. A homozygous novel mutation in FGF homology domain: B-21 mutated from G to A at 232 in exon 2. As a result glutamic acid is replaced by lysine. Phosphate restricted diet and phosphate lowering agent improved biochemical paramaters. Surgical excision has been withheld. Contemporary manifestation of hFTC and Hb E trait; two disease of autosomal recessive inheritance in an individual makes it extremely rare. High index of suspicion is needed for early diagnosis and treatment.

131I uptake in tumoral calcinosis in a patient on hemodialysis treated for thyroid cancer

131I uptake in tumoral calcinosis in a patient on hemodialysis treated for thyroid cancer

787 Generation and characterization of a mutant rat with targeted ablation in Samd9, the gene responsible for normophosphatemic familial tumoral calcinosis

787 Generation and characterization of a mutant rat with targeted ablation in Samd9, the gene responsible for normophosphatemic familial tumoral calcinosis

Fever as a Presentation of Tumoral Calcinosis: A Case Report

Fever as a Presentation of Tumoral Calcinosis: A Case Report

Choroidal Neovascular Membrane Association with Tumoral Calcinosis, a Case Report

Choroidal Neovascular Membrane Association with Tumoral Calcinosis, a Case Report

Choroidal Neovascular Membrane Association with Tumoral Calcinosis, a Case Report

Choroidal Neovascular Membrane Association with Tumoral Calcinosis, a Case Report

Tumoral Calcinosis in a Patient with Sarcoidosis

Tumoral Calcinosis in a Patient with Sarcoidosis

Tumoral calcinosis misdiagnosed

Tumoral calcinosis misdiagnosed

A case report of tumoral calcinosis in the epiduralspace of the sacrum of hemodialysis patient

A case report of tumoral calcinosis in the epiduralspace of the sacrum of hemodialysis patient