Phosphorus Deprivation Treatment of Tumoral Calcinosis

Mozaffarian, G.; Nakhjavani, M; Hedayati, Masoud; Shamekh, S.

doi:10.7326/0003-4819-86-1-120_2

Cited by 13 publications

(8 citation statements)

References 1 publication

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“…Classically, dietary phosphate deprivation is combined with aluminum and magnesium based phosphate binders often using high doses. Although several case reports have demonstrated successful decrease in serum phosphate concentrations [71–75] and regression of hFTC lesions [71, 73, 74, 76, 77] with a low phosphate diet combined with phosphate binders (mostly aluminum hydroxide), the results have been inconsistent. However, in many cases these measures have still failed to resolve hFTC lesions, and the response in terms of serum phosphate is highly variable [64, 75, 78–80].…”

Section: Therapeutic Avenuesmentioning

confidence: 99%

Hyperphosphatemic familial tumoral calcinosis (FGF23, GALNT3 and αKlotho)

Farrow

Imel

White

2011

Best Practice & Research Clinical Rheumatology

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Familial Tumoral calcinosis (TC) is a rare disorder distinguished by the development of ectopic and vascular calcified masses that occur in settings of hyperphosphatemia (hFTC) and normophosphatemia (nFTC). Serum phosphorus concentrations are relatively tightly controlled by interconnected endocrine activity at the level of the intestine, kidney, and skeleton. Discovering the molecular causes for heritable forms of hFTC has shed new light on the regulation of serum phosphate balance. This review will focus upon the genetic basis and clinical approaches for hFTC, due to genes that are related to the phosphaturic hormone Fibroblast growth factor-23 (FGF23). These include FGF23 itself, an FGF23-glycosylating enzyme (GALNT3), and the FGF23 co-receptor α-Klotho (αKL). Our understanding of the molecular basis of hFTC will, in the short term, aid in understanding normal phosphate balance, and in the future, provide potential insight into the design of novel therapeutic strategies for both rare and common disorders of phosphate metabolism.

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Section: Therapeutic Avenuesmentioning

confidence: 99%

Hyperphosphatemic familial tumoral calcinosis (FGF23, GALNT3 and αKlotho)

Farrow

Imel

White

2011

Best Practice & Research Clinical Rheumatology

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“…Mozaffarian et al [13] reported in his study the effect of calcium-phosphorus diet with oral doses of aluminum hydroxide containing antacids in a patient with tumoral calcinosis, and they showed significant improvement in the clinical and radiological evaluation. Kirk and Simon [14] reported one case of tumoral calcinosis who had a large painful mass lesion on the shoulder with a limited range of motion.…”

Section: Discussionmentioning

confidence: 99%

Tumoral Calcinosis Presentation in Operated Developmental Dysplasia of the Hip: A Case Report and Review of Literature

AlRumaih¹,

Alotaibi²,

Alshammari³

2020

Cureus

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Tumoral calcinosis has long been a disputed clinical-pathological subject. It has been characterized by the deposition of calcium salt and hydroxyapatite in different periarticular soft tissue regions. It is most commonly seen in adults, and rarely seen in children. In this report, we present the case of a six-year-old girl referred to our institution for one year with a history of left hip pain and swelling. The patient underwent an open reduction of left hip and acetabuloplasty for developmental dysplasia of the hip (DDH) at the age of two years. Systematic investigations were performed and showed that the patient had abnormal calcifications and large, ill-defined lesions with an irregular margin on the left hip extended to the left gluteal area with skin ulceration suggestive of primary tumor calcinosis. Medical therapy has started, and a follow-up appointment was given to her in a pediatric metabolic clinic. In addition, we present a brief literature review of the effect of medical and surgical treatments on tumor calcinosis.

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“…Clinical and radiographical improvement has been reported after phosphorus deprivation therapy [ 9 ]. Surgical excision is the recommended management for removing abnormal tissue to prevent recurrence and improve limited motion [ 10 , 11 ]. However, incomplete resection is associated with higher rates of recurrence [ 6 , 12 ].…”

Section: Discussionmentioning

confidence: 99%

Hyperphosphatemic Tumoral Calcinosis after Total Knee Arthroplasty

Mochizuki¹,

Ikari

2017

Case Reports in Orthopedics

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We report a case of hyperphosphatemic tumoral calcinosis (TC) that occurred after total knee arthroplasty. A 64-year-old Japanese man presented with painful swellings in both shoulders, the left elbow, and the right hip that developed after he underwent total knee arthroplasty (TKA). The pathology of the patient's bone at the time of TKA included a thick osteoid seam with calcareous deposition at the margin of the trabecular bone, which is not generally seen in osteoarthritis. Computed tomography scans of the swollen joints demonstrated leaflet and amorphous calcification masses around the joints. We diagnosed the patient with TC. The present case highlights that TC lesions are rare but should be considered in the differential diagnosis of subcutaneous soft and hard masses around the joint.

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Phosphorus Deprivation Treatment of Tumoral Calcinosis

Cited by 13 publications

References 1 publication

Hyperphosphatemic familial tumoral calcinosis (FGF23, GALNT3 and αKlotho)

Hyperphosphatemic familial tumoral calcinosis (FGF23, GALNT3 and αKlotho)

Tumoral Calcinosis Presentation in Operated Developmental Dysplasia of the Hip: A Case Report and Review of Literature

Hyperphosphatemic Tumoral Calcinosis after Total Knee Arthroplasty

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