Fatal cutaneous necrosis mimicking calciphylaxis in a patient with type 1 primary hyperoxaluria

Somach, S. C.

doi:10.1001/archderm.131.7.821

Cited by 12 publications

(9 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…62 As the kidneys fail, systemic calcium oxalate levels begin to increase and crystals eventually deposit in extrarenal tissues. 62,63 It is believed that the deposition of these crystals results in intravascular obstruction, end organ damage, and cutaneous ischemia manifesting as LR. 64,65 Secondary hyperoxaluria conditions exist and although no cases have been reported associating it with LR, it is reasonable to think one may be found through a mechanism similar to that of primary hyperoxaluria.…”

Section: Autoimmunementioning

confidence: 99%

“…On a hematoxylineosin stain, calcium oxalate crystals of primary hyperoxaluria do not stain and appear as birefringent yellow-brown crystals within vessel walls, whereas calcium salts of calciphylaxis appear as basophilic deposits within vessel walls. 63 Early diagnosis and treatment are important as both calciphylaxis and primary hyperoxaluria carry a grim prognosis if untreated. 59,66 Primary hyperoxaluria is treated by combined liver-kidney transplants in patients with advanced kidney disease.…”

Section: Autoimmunementioning

confidence: 99%

See 1 more Smart Citation

Livedo reticularis: An update

Gibbs

English

Zirwas

2005

Journal of the American Academy of Dermatology

120

121

View full text Add to dashboard Cite

Section: Autoimmunementioning

confidence: 99%

Section: Autoimmunementioning

confidence: 99%

Livedo reticularis: An update

Gibbs

English

Zirwas

2005

Journal of the American Academy of Dermatology

120

121

View full text Add to dashboard Cite

“…342,343 Regardless of underlying etiology, excessive oxalate in the body precipitates as calcium oxalate initially in the kidneys and ultimately in other tissues, causing damage and subsequent disease. 344,345 Skin manifestations of hyperoxalosis are not common. Cutaneous disease associated with PH results from vascular deposition and includes vascular complications such as livedo, acrocyanosis, and peripheral gangrene.…”

Section: Oxalate Crystalsmentioning

confidence: 99%

“…346 In cases with livedo reticularis or cutaneous necrosis, oxalate crystals may be found in blood vessels in the subcutis. 345 Fiberglass Fiberglass dermatitis is caused by penetration of small fragments of fiberglass in the cornified layer of the skin. It was one of the most common forms of occupational dermatoses from mechanical irritation but is rarely seen these days.…”

Section: Oxalate Crystalsmentioning

confidence: 99%

Cutaneous Deposits

Molina-Ruiz

Cerroni

Kutzner

et al. 2014

The American Journal of Dermatopathology

View full text Add to dashboard Cite

: The cutaneous deposition disorders are a group of unrelated conditions characterized by the accumulation of either endogenous or exogenous substances within the skin. These cutaneous deposits are substances that are not normal constituents of the skin and are laid down usually in the dermis, but also in the subcutis, in a variety of different circumstances. There are 5 broad categories of cutaneous deposits. The first group includes calcium salts, bone, and cartilage. The second category includes the hyaline deposits that may be seen in the dermis in several metabolic disorders, such as amyloidosis, gout, porphyria, and lipoid proteinosis. The third category includes various pigments, heavy metals, and complex drug pigments. The fourth category, cutaneous implants, includes substances that are inserted into the skin for cosmetic purposes. The fifth category includes miscellaneous substances, such as oxalate crystals and fiberglass. In this article, the authors review the clinicopathologic characteristics of cutaneous deposition diseases, classify the different types of cutaneous deposits, and identify all the histopathologic features that may assist in diagnosing the origin of a cutaneous deposit.

show abstract

“…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

View full text Add to dashboard Cite

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.

show abstract

Fatal cutaneous necrosis mimicking calciphylaxis in a patient with type 1 primary hyperoxaluria

Cited by 12 publications

References 0 publications

Livedo reticularis: An update

Livedo reticularis: An update

Cutaneous Deposits

Oxalate crystal deposition disease

Contact Info

Product

Resources

About