Primary oxalosis with livedo reticularis

Greer, K. E.

doi:10.1001/archderm.116.2.213

Cited by 14 publications

(12 citation statements)

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“…However, the diagnosis must be further supported by a bone biopsy and immunohistochemical analyses. 2,7,13 The history of neprolithiasis, chronic renal failure and the type of the skeletal findings seems to be favouring the diagnosis of primary hyperoxaluria. However, in cases with chronic renal failure, a secondary oxalosis can develop from haemodialysis.…”

Section: Discussionmentioning

confidence: 99%

A case of late‐onset primary hyperoxaluria

Çalışır

Yavas

2007

Australasian Radiology

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Primary hyperoxaluria is a rare autosomal recessive disorder resulting in diffuse deposition of insoluble oxalate crystals in multiple organs. Two-thirds of patients have nephrolithiasis by 5 years of age and 80% die of renal failure by 20 years of age. Rarely, the disease will present in adulthood, with the onset of symptoms occurring as late as the sixth decade. Oxalosis is a condition in which the highly insoluble calcium oxalate crystals are deposited in extrarenal tissue. Pathologic involvement of bone is recognized as osteosclerosis on radiograph. Oxalosis should be considered in patients with osteosclerotic bone changes and chronic renal failure and should not be misinterpreted as renal osteodystrophy. We describe here a case of oxalosis in a 33-year-old man.

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Section: Discussionmentioning

confidence: 99%

A case of late‐onset primary hyperoxaluria

Çalışır

Yavas

2007

Australasian Radiology

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“…1A), vascular calcifications [1,2•] (Fig. 1B), arterial spasm leading to chronic peripheral vascular insufficiency and gangrene [20][21][22], thromboembolic stroke [23], small intestine infarction [24], livedo reticularis [21,25,26•,27,28], reversible arterial spasm [27], acute livedo racemosa [28], cardiomyopathy [29,30], complete heart block [31], pleuropericarditis [26•], polyradiculopathy [32], peripheral neuropathy and mononeuritis multiplex [33], livedo and flecked retinopathies [34][35][36], pancytopenia [37,38], hypothyroidism [39], skin necrosis with or without calciphylaxis [20,22,40], nasal granulomas [41], and a black liver [42•].…”

Section: Oxalate and Calcium Oxalate Deposition Diseasesmentioning

confidence: 99%

Oxalate crystal deposition disease

Maldonado¹,

Prasad²,

Reginato

2002

Curr Rheumatol Rep

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In addition to monosodium urate, calcium pyrophosphate dihydrate, and apatite crystals, oxalate crystals are less often found in synovial fluids in association with acute or chronic arthritis. Oxalate crystal deposition disease is seen in patients with primary hyperoxaluria types 1 and 2 (PH1 and 2) and in patients with end-stage renal disease managed with long-term dialysis. Oxalate crystal deposits are found mainly in kidneys, bone, skin, and vessels, and less often inside the joints. Musculoskeletal and systemic manifestations of oxalate crystal deposition disease may be confused with those observed with the other most common types of crystal deposition diseases. Clinical and radiographic features include calcium oxalate osteopathy, acute and chronic arthropathy with chondrocalcinosis, synovial calcification, and miliary skin calcium oxalate deposits and vascular calcifications that affect mainly the hands and feet. Systemic life-threatening cardiovascular, neurologic, and hematologic manifestations are rare. Genomic DNA studies have identified those genetic defects of PH1 and PH2 that allow a precise early diagnosis. Kidney transplantation has poor outcome as a result of graft oxalosis. Combined liver and kidney transplantation is the treatment of choice in patients with PH1 and advanced renal failure. Pre-emptive isolated liver transplantation is the preferred treatment in patients who develop the disease during infancy with progressive manifestations of oxalosis. These novel findings in the understanding of the molecular and enzymatic aspects of primary hyperoxalurias have provided a more rational basis for the management and prevention of oxalate crystal deposition disease. This information may lead to a better understanding and effective management of other common calcium-containing crystal deposition diseases.

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“…Thus these patients have LR. Embolic processes such as numerous cholesterol emboli (33,34), primary and secondary oxalosis (35,36), and systemic air emboli (37) can also lead to a decrease in blood fiow and concomitant LR.…”

Section: Livedo Reticularis Symptomaticamentioning

confidence: 99%