Skin lesions, hypereosinophilia, and subcutaneous heparin

Bircher, A.J.; Itin, P; Büchner, S.

doi:10.1016/s0140-6736(94)92067-2

Cited by 20 publications

(8 citation statements)

References 4 publications

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“…Isolated reactive peripheral hypereosinophilia after subcutaneous heparin application has been reported. Possibly an activation of CD4 as well as interleukin (IL)‐3 and IL‐5 secretion can stimulate formation and activation of eosinophils (17, 18).…”

Section: Eosinophiliamentioning

confidence: 99%

See 1 more Smart Citation

Hypersensitivity reactions to anticoagulant drugs: diagnosis and management options

Bircher¹,

Harr²,

Hohenstein³

et al. 2006

Allergy

136

118

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Anticoagulants, including heparins, coumarins, hirudins, and some of the previously used plasma volume expanders, belong to the most widely used drugs. Hypersensitivity reactions from these agents are uncommon. However, they may have a considerable impact on patient safety and treatment decisions. Therefore, early diagnosis of potentially life‐threatening adverse events and identification of alternatives is clinically important. This review contains an update on current knowledge about hypersensitivity reactions caused by the different anticoagulants. In addition, it discusses pathophysiologic mechanisms, diagnostic possibilities, and management options. The most common hypersensitivity reactions are erythematous plaques, occurring with a delay after subcutaneous application of heparins. Seldom they turn into maculopapular exanthema. Other hypersensitivity reactions are rare but may be life‐threatening, e.g. skin necrosis because of heparin‐induced thrombocytopenia. Skin and provocation tests with immediate and late readings are the most reliable diagnostic tools for heparin‐ or hirudin‐induced urticaria/anaphylaxis or heparin‐induced delayed plaques. If necrosis from heparins or coumarins is suspected, skin tests are contraindicated. In anaphylactic reactions caused by dextrans or hydroxyethyl starch skin tests are useless. Most in vitro tests have a low sensitivity and are not generally available. Therefore, in some anticoagulant‐associated hypersensitivity reactions detailed allergologic investigation may help to identify safe treatment alternatives. However, several tests may be needed, and the procedures are usually time‐consuming.

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Section: Eosinophiliamentioning

confidence: 99%

“…3). It may initially be confounded with plaques in cell‐mediated hypersensitivity (9, 17). Heparin necrosis is the cutaneous manifestation of the severe form of HIT II.…”

Section: Heparin Necrosis and Thrombocytopeniamentioning

confidence: 99%

Hypersensitivity reactions to anticoagulant drugs: diagnosis and management options

Bircher¹,

Harr²,

Hohenstein³

et al. 2006

Allergy

136

118

View full text Add to dashboard Cite

show abstract

“…Possibly an activation of CD4+ T cells inducing IL-5 secretion can stimulate formation and activation of eosinophils [24,25].…”

Section: Eosinophiliamentioning

confidence: 99%

“…It may initially be confounded with plaques in cell-mediated hypersensitivity [17,24]. Heparin necrosis is thought to be the cutaneous manifestation of the severe form of heparin-induced thrombocytopenia (HIT II).…”

Section: Heparin Necrosis and Thrombocytopeniamentioning

confidence: 99%

Hypersensitivity Reactions to Anticoagulant Drugs

Scherer¹,

Tsakiris²,

Bircher³

2008

CPD

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Drugs with anticoagulant activity, including heparins, hirudins, coumarins, and platelet aggregation inhibitors belong to the most widely used drugs. Hypersensitivity reactions from these agents are rare. However, due to their widespread use, they may have a considerable impact on patient safety and treatment. Accurate diagnosis of potentially life-threatening adverse events and identification of alternatives is mandatory. We review hypersensitivity reactions caused by the different groups of anticoagulant agents and discuss the pathophysiological mechanisms, diagnostic possibilities and management options. According to patients histories the most common hypersensitivity reaction is intolerance to acetylsalicylic acid (ASA). Also localized erythematous plaques, occurring to subcutaneous application of heparins are rather common. Other hypersensitivity reactions are rare but may be life-threatening, e.g. skin necrosis due to heparin-induced thrombocytopenia. Rarely anaphylactoid reactions have been observed to ASA, heparin, and hirudin. Skin and provocation tests with immediate and late readings are the most reliable diagnostic tools for heparin- or hirudin-induced urticaria/anaphylaxis or heparin-induced delayed plaques. Provocation tests may be used to identify safe alternatives. In cases of necrosis from heparins or coumarins, all in vivo tests are contraindicated. Most in vitro tests are not universally available, and with the exception of platelet aggregation tests, they have a low sensitivity. In some anticoagulant-associated hypersensitivity reactions detailed allergologic investigation may help to identify safe treatment alternatives. Typically, several tests are needed, and therefore the test procedures are time consuming.

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“…HEPARIN AND EOSINOPHILIA Eosinophilia occurs in 5% to 10% of patients receiving unfractionated or low molecular weight heparin therapy (17,18,64). The eosinophilia is asymptomatic.…”

Section: Altered Liver Function Testsmentioning

confidence: 99%

Aberrations of the Tissue Factor Pathway in Patients Positive for Lupus Anticoagulant

Wakita¹,

Wada

Nakase

et al. 1999

Clin Appl Thromb Hemost

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To evaluate the relationship between the tissue factor (TF) pathway and lupus anticoagulant (LA), in the present study, we measured the plasma levels of TF antigen and TF pathway inhibitor (TFPI) antigen in patients positive for LA. Plasma TF and TFPI levels in LA-positive patients were significantly higher than levels in healthy volunteers (p < 0.01). In LA-positive patients, there were no significant differences in plasma TF and TFPI levels between patients with and without thrombosis. In patients with thrombosis, there was no significant difference in the plasma TF level between LA-positive and LA-negative patients; however, the plasma TFPI level in LA-positive patients was significantly lower than that in LA-negative patients (p < 0.01). We also examined the TF pathway in human umbilical venous endothelial cells (HUVEC) incubated with plasma of LA-positive patients, LA-negative patients, and healthy volunteers. TF activity was significantly higher (p < .05) in HUVECs incubated with the plasma of LA-positive patients than in cells incubated with the plasma of the other two groups (p < .01). However, there was no significant difference in TFPI antigen levels among the media of HUVECs incubated with the plasma of all groups. The viability of HUVEC incubated with the plasma of LA-positive patients with thromboses, LA-positive patients without thromboses, and LA-negative patients with thromboses were significantly lower than that of HUVECs incubated with the plasma of healthy volunteers (p < .01). These findings suggest that abnormalities of the TF pathway plays an important role in the mechanism of hypercoagulability in LA-positive patients. LA may affect vascular endothelial cells causing thrombogenesis.

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Skin lesions, hypereosinophilia, and subcutaneous heparin

Cited by 20 publications

References 4 publications

Hypersensitivity reactions to anticoagulant drugs: diagnosis and management options

Hypersensitivity reactions to anticoagulant drugs: diagnosis and management options

Hypersensitivity Reactions to Anticoagulant Drugs

Aberrations of the Tissue Factor Pathway in Patients Positive for Lupus Anticoagulant

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