Cutaneous reactions secondary to heparin injections

Tuneu, Anna; Moreno, Abelardo; Moragas, José M. de

doi:10.1016/s0190-9622(85)70135-1

Cited by 58 publications

(24 citation statements)

References 7 publications

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“…It is a thrombotic manifestation of the HIT syndrome and is characterized by the presence of platelet thrombi within the dermal microvasculature. It occurs in approximately 10-20% of patients with HIT antibodies and interestingly, as in this case, generally occurs in the absence of thrombocytopenia [2,3]. Other thrombotic manifestations such as deep vein thrombosis, pulmonary embolism and adrenal infarction are also seen in patients with heparin-induced skin necrosis [4].…”

Section: Discussionmentioning

confidence: 62%

Heparin-Induced Skin Necrosis in a Patient with End-Stage Renal Failure and Functional Protein S Deficiency

2001

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Skin ulceration is a well-characterized thrombotic complication of the heparin-induced thrombocytopenia (HIT) syndrome. We present the case of a 73-year-old diabetic woman nearing end-stage renal failure who developed extensive upper thigh, abdominal and buttock ulceration following initiation of subcutaneous heparin for prophylaxis against deep vein thrombosis. A preliminary diagnosis of calciphylaxis was made based on the classical distribution and macroscopic appearance of the ulceration in a patient with end-stage renal failure and secondary hyperparathyroidism. However skin biopsy showed complete absence of calcium deposits in the dermal microvasculature. The presence of extensive microthrombi within dermal vessels prompted serologic testing to detect a prothrombotic state. We identified the combined presence of heparin-dependent platelet activating (HIT) antibodies and functional protein S deficiency. To our knowledge this is the first reported case of a dialysis patient presenting with skin ulceration induced by heparin and protein S deficiency. This case highlights the importance of a skin biopsy and testing for a hypercoaguable state in patients with end-stage renal disease and skin ulceration. We suggest that HIT antibodies should be requested in all dialysis patients presenting with skin ulceration.

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Section: Discussionmentioning

confidence: 62%

Heparin-Induced Skin Necrosis in a Patient with End-Stage Renal Failure and Functional Protein S Deficiency

2001

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“…It is a thrombotic manifestation of the HIT syndrome and is characterized by the presence of platelet thrombi in the dermal microvasculature. It occurs in 10-20% of all patients with HIT antibodies, and generally in the absence of severe thrombocytopenia [4,5].…”

Section: Discussionmentioning

confidence: 99%

Heparin‐induced skin necrosis associated with thrombocytopenia and acquired protein C and protein S deficiency

Prasad

Govindarajan

2007

American J Hematol

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We have described a patient with colon cancer and liver metastases who developed heparin-induced thrombocytopenia and skin necrosis. We believe that the skin necrosis caused by the heparin/platelet factor 4 antibody was exacerbated by the acquired protein C and protein S deficiency. After the heparin was discontinued and infection treated, the skin necrosis and thrombocytopenia resolved. This case illustrates the fact that, in patients with heparin-induced skin necrosis, a search must be undertaken for an underlying pro-thrombotic state, which may precipitate the microthrombosis responsible for skin necrosis. We could not find any previous case reports of heparin-induced skin necrosis associated with isolated protein C deficiency, or combined protein C and protein S deficiency. Am. J. Hematol. 82:1116Hematol. 82: -1117Hematol. 82: , 2007

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“…Although no prospective studies have been performed, this complication appears to be extremely rare, since only a limited number of cases of UFH-induced skin necrosis and seven cases (including our case) after LMWH have been reported. In addition, a number of cases of erythematous skin reactions after administration of UFH [9,10,21,23,24] and LMWH [9,10,13,18,21] have been described. In the seven cases of LMWH skin necrosis (Table 1) the lesion developed after about 1 week of treatment, starting with painful erythema and progressing within a short time to necrosis.…”

Section: Discussionmentioning

confidence: 99%

Low-molecular-weight heparin-induced skin necrosis

Füreder

Kyrle

Gisslinger

et al. 1998

Annals of Hematology

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We report a case of low-molecular-weight heparin (LMWH)-induced skin necrosis in a patient with chronic lymphatic leukemia. The patient had heparin-PF4 antibodies and the heparin-induced platelet activation (HIPA) test was positive, but platelet counts remained normal. Analysis of seven cases of LMWH-induced skin necrosis revealed that this complication occurred mostly in patients previously exposed to heparin, and that severe problems such as thrombocytopenia or thromboembolic complications were rare. This is in contrast to skin necrosis induced by unfractionated heparin (UFH), where a substantially higher number of patients suffered from thrombocytopenia and thromboembolism. In addition, most patients with UFH-induced skin necrosis were not pretreated with heparin. Therefore, it is possible that LMWH is less immunogenic than UFH and requires repeated exposure for induction of skin necrosis.

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Cutaneous reactions secondary to heparin injections

Cited by 58 publications

References 7 publications

Heparin-Induced Skin Necrosis in a Patient with End-Stage Renal Failure and Functional Protein S Deficiency

Heparin-Induced Skin Necrosis in a Patient with End-Stage Renal Failure and Functional Protein S Deficiency

Heparin‐induced skin necrosis associated with thrombocytopenia and acquired protein C and protein S deficiency

Low-molecular-weight heparin-induced skin necrosis

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