scholarly journals Bullous Hemorrhagic Dermatosis Induced By Heparin: An Indonesian Case Report

2021 ◽  
pp. 8-12
Author(s):  
Syahfori Widiyani ◽  
Irsalina Rahmawati ◽  
W. Yohannes Widodo ◽  
Dian Zamroni ◽  
Fajar L. Gultom ◽  
...  
Keyword(s):  
Skin Lesions ◽  
Low Molecular Weight ◽  
Heparin Induced Thrombocytopenia ◽  
Clinical Disorder ◽  
Heparin Treatment ◽  
Life Threatening ◽  
Topical Treatments ◽  
Lesion Regression ◽  
The Right ◽  
Related Reaction

Introduction: Bullous haemorrhagic dermatosis is a rare clinical disorder which is usually related to a treatment with unfractionated heparin (UFH) or low molecular weight heparin (LMWH), characterized by multiple intra-epidermal haemorrhages distant from the site of injection. Presentation of Case: A 62-year-old male patient with coronary heart disease who received heparin treatment experienced several tense, haemorrhagic bullae located on the right arm area, close to the injection site, and followed by the formation of several hematomas on his back trunk 2 days after he had received UFH. The lesions regressed after discontinuation of heparin and supportive topical treatments. Discussion: The lesions in this patient have similar characteristic with heparin-induced skin necrosis and demonstrate thrombocytopenia probably related to heparin. There are some proposed hypotheses of pathophysiology which include hypersensitivity reaction and idiosyncratic dose-related reaction. Given the clinically course, the discontinuation of heparin treatment was essential for lesion regression in addition other supportive measures. Conclusion: Heparin-induced skin lesions may indicate the presence of life-threatening heparin-induced thrombocytopenia. An early diagnosis is crucial to enable discontinuation of heparin if required.

scholarly journals An Ovarian Cancer Patient Presenting Heparin - Induced Thrombocytopenia after use of Low - Molecular - Weight Heparin: A Case Report of Rare Condition

2018 ◽  
pp. 1
Author(s):  
Yasin Durmuş ◽  
Yalin Ay Karyal ◽  
Cigdem Kilic ◽  
Caner Cakir ◽  
Dilek Yuksel ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Low Molecular Weight Heparin ◽  
Ovarian Cancer Patient ◽  
Rare Condition ◽  
Low Molecular Weight ◽  
Heparin Induced Thrombocytopenia ◽  
Normal Limits ◽  
Heparin Treatment ◽  
Threatening Condition ◽  
Life Threatening

<p>Heparin-induced thrombocytopenia is a rare and life-threatening condition of exposure to heparin. A case of heparin-induced thrombocytopenia due to the low molecular weight heparin was presented. Pulmonary emboli and progressively decreased number of thrombocytes developed during the low molecular weight heparin treatment. For that reason, the heparin-induced thrombocytopenia was diagnosed. The heparin was ceased and fondaparinux treatment initiated. Platelet levels returned to normal limits within six days. The delaying in diagnosis of heparin-induced thrombocytopenia causes serious outcomes. The physician must be careful and keep in mind be developed of this clinical condition in patient under heparin treatment.</p>

Primary cutaneous nocardiosis of the head and neck in an immunocompetent patient

2021 ◽  
Vol 14 (5) ◽  
pp. e241217
Author(s):  
Claudio Tirso Acevedo ◽  
Frank Imkamp ◽  
Ewerton Marques Maggio ◽  
Silvio Daniel Brugger
Keyword(s):  
Head And Neck ◽  
Skin Lesions ◽  
Immunocompetent Patient ◽  
Rrna Gene ◽  
Gene Sequence Analysis ◽  
Rare Manifestation ◽  
Life Threatening ◽  
Amoxicillin Clavulanic Acid ◽  
Disseminated Nocardiosis ◽  
The Right

Nocardiosis is known to be an opportunistic infection most commonly affecting immunocompromised patients that can lead to life-threatening conditions. Primary cutaneous disease remains a rare manifestation and unlike pulmonary or disseminated nocardiosis, it usually affects immunocompetent individuals. We present a case of a primary cutaneous nocardiosis of the head and neck after an insect bite in a healthy 50-year-old woman who had recently travelled from Greece. She presented with a painful right-sided swelling of her face and neck and an ulcerated plaque over the right temple. Biopsy of the plaque revealed inflammation with abscess formation indicating underlying infection. Culture from the biopsy showed growth of Nocardia spp and 16S rRNA gene sequence analysis identified Nocardia brasiliensis. The patient was treated with trimethoprim/sulfamethoxazole and subsequently switched to amoxicillin/clavulanic acid due to a drug eruption. Antibiotic therapy was continued for a total of 3 months with complete resolution of the skin lesions.

scholarly journals Case Report of Necrotizing Fasciitis Associated withStreptococcus pneumoniae

2016 ◽  
Vol 2016 ◽  
pp. 1-4 ◽  
Author(s):  
Lei Jiao ◽  
Zain Chagla ◽  
Reham Mohammedsaeed Kaki ◽  
Gabriela Gohla ◽  
Marek Smieja
Keyword(s):  
Case Report ◽  
Streptococcus Pneumoniae ◽  
Necrotizing Fasciitis ◽  
Neutrophil Infiltration ◽  
Skin Lesions ◽  
Blood Samples ◽  
Surgical Exploration ◽  
Lower Back ◽  
Life Threatening ◽  
The Right

Necrotizing fasciitis, caused byStreptococcus pneumoniae, is an extremely rare and life-threatening bacterial soft tissue infection. We report a case of early necrotizing fasciitis associated withStreptococcus pneumoniaeinfection in a 26-year-old man who was immunocompromised with mixed connective tissue disease. The patient presented with acute, painful, erythematous, and edematous skin lesions of his right lower back, which rapidly progressed to the right knee. The patient underwent surgical exploration, and a diagnosis of necrotizing fasciitis was confirmed by pathological evidence of necrosis of the fascia and neutrophil infiltration in tissue biopsies. Cultures of fascial tissue biopsies and blood samples were positive forStreptococcus pneumoniae. To our knowledge, this is the first report of necrotizing fasciitis resulting fromStreptococcus pneumoniaediagnosed at early phase; the patient recovered well without surgical debridement.

Heparin-Induced Thrombocytopenia: Prevalence in a Large Cohort of Patients and Confirmed Role of PF4/Heparin Complex as the Main Antigen for Antibodies

1997 ◽  
Vol 3 (3) ◽  
pp. 203-209 ◽  
Author(s):  
Fabrizio Fabris ◽  
Immacolata Cordiano ◽  
Federica Salvan ◽  
Leopoldo Saggin ◽  
Giuseppe Cella ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Platelet Count ◽  
Platelet Factor 4 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Low Molecular Weight ◽  
Dependent Manner ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Heparin Treatment ◽  
Daily Dose

We performed a retrospective study on the prevalence of heparin-induced thrombocytopenia (HIT) in 233 patients receiving hog mucosa heparin therapy. Of these, 82 patients received s.c. calcium heparin, 130 patient received unfractionated (UF) i.v. heparin, and 21 patients received low molecular weight heparins (LMWH). An additional four patients, referred to our consultation and diagnosed by us as having clinically active type II HIT (HIT-II) were also studied. The mean platelet count of the 233 patients receiving heparin showed a significant decrease after 2 days of heparin treatment and a following significant increase 6 days later (basal: 257 ± 147 x 109 platelets/L; day 2: 239 ± 122, p < 0.0002; day 6: 286 ± 119, p < 0.004). Of the 212 patients receiving UF heparin, 13 (6%) fulfilled the criteria for HIT-II: seven of these had received i.v. heparin (mean daily dose 26,600 ± 4,082 IU ± SD) and six had received s.c. heparin (mean daily dose 21,428:t 6,900 IU). Their mean basal platelet count was 226 ± 100 SD × 109 platelets/L and the nadir during heparin treatment was 78 ± 39 x 10 9 platelets/L. Thrombotic complications occurred in four (30.7%) of the 13 patients with HIT-II. Since the immunological mechanism has been demonstrated for HIT-II and since platelet factor 4 (PF4) was identified as the co-factor for the binding of heparin-related antibodies, we set up our own enzyme-linked immunosorbent assay (ELISA) for testing antibodies against PF4/heparin complex bound through electrostatic bridges to the solid phase. The highest binding capacity of HIT-related IgG to the multimolecular complex was obtained at 20 μg/ml for PF4 and 3 μg/ml for heparin, corresponding to 250 ng of PF4 and 42 ng of heparin in each microtiter well. Such binding was inhibited in a dose-dependent manner by increasing amounts of heparin, protamine hydrochloride, and a monoclonal antibody anti-human PF4 clone 1OB2. We observed that HIT-related antibodies bound also to PF4/LMWH complexes but the optimal PF4/glycosaminoglycan ratio appeared more critical for LMWH (enoxaparin, fraxiparin, and pamaparin) than for UF heparin. Sera from eight patients with HIT-II were tested by PF4/heparin ELISA; six of these had IgG against the complex PF4/heparin and three also had IgM. The persistence of HIT-related antibodies was investigated in three patients: in one such antibodies were still detectable 3 years after the acute episode, while in the other two, they disappeared after 6 months and 1 year, respectively. Key Words: Heparin-related anti body—Platelet factor 4 (PF4)—Heparin—Low molecular weight heparin—Thrombocytopenia—Thrombosis.

scholarly journals Clinical Appearance and Diagnosis of Heparin Induced Thrombocytopenia

2021 ◽  
pp. 466-471
Author(s):  
Gunduz T ◽  
Cakir M ◽  
Bakirci EM ◽  
DEGIRMENCI H
Keyword(s):  
Molecular Weight ◽  
Unfractionated Heparin ◽  
Low Molecular Weight Heparin ◽  
Low Molecular Weight ◽  
Heparin Induced Thrombocytopenia ◽  
Clinical Appearance ◽  
Treatment Management ◽  
Life Threatening ◽  
Life Threatening Complication

Heparin-İnduced Thrombocytopenia (HIT) is a life-threatening complication that occurs in a small percentage of exposed patients (e.g. unfractionated heparin, Low Molecular Weight Heparin [LMWH]) regardless of dose and treatment management.

Heparin-induced skin lesions

Phlebologie ◽  
2010 ◽  
Vol 39 (01) ◽  
pp. 5-11 ◽  
Author(s):  
M. Schindewolf ◽  
B. Kahle ◽  
E. Lindhoff-Last ◽  
R. J. Ludwig
Keyword(s):  
Clinical Importance ◽  
Skin Lesions ◽  
Delayed Type Hypersensitivity ◽  
Medical Patients ◽  
Heparin Induced Thrombocytopenia ◽  
Immune Mediated ◽  
Prospective Epidemiological Study ◽  
Therapeutic Procedures ◽  
Life Threatening ◽  
Cutaneous Reactions

SummaryCutaneous reactions to subcutaneous heparin injections have been described first in 1952. These reactions may be caused by several mechanisms such as immediate or delayed-type hypersensitivity responses, or by life-threatening immune-mediated heparin-induced thrombocytopenia (HIT). In contrast to bleeding, induction of osteoporosis and hair loss, no data on the incidence and causes of heparin-induced skin lesions had been available until recently. In a large prospective epidemiological study, the incidence of heparin-induced skin lesions was as high as 7.5% in medical patients, far exceeding the expected incidence. As heparin-induced skin lesions may be the sole clinical manifestation of immune HIT, rapid and valid diagnosis of heparin-induced skin lesions is of utmost clinical importance. Therefore, we have reviewed all known causes of heparin-induced skin lesions, and propose diagnostic and therapeutic procedures.

Adherence to Guidelines for Monitoring for Heparin-Induced Thrombocytopenia in Patients Treated with Low Molecular Weight Heparin

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 1282-1282
Author(s):  
Maarten ten Berg ◽  
Patricia Van den Bemt ◽  
Albert huisman ◽  
Fred Schobben ◽  
Toine Egberts ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Platelet Count ◽  
Clinical Guidelines ◽  
Low Molecular Weight Heparin ◽  
Low Molecular Weight ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Alternative Anticoagulation ◽  
Life Threatening ◽  
Platelet Count Monitoring

Abstract Laboratory monitoring for early detection of adverse drug reactions is recommended for many drugs. For patients treated with low molecular weight heparin (LMWH), the Summary of Product Characteristics (SPC) and clinical guidelines recommend to monitor the platelet count for heparin-induced thrombocytopenia (HIT), a potentially life-threatening adverse event, characterised by a typical drop in platelet count. When the platelet count drops without obvious explanation in these patients, testing for heparin-platelet factor 4 antibodies (HPF4-Ab) and initiating alternative anticoagulation are advised. In the current study adherence to recommended platelet count monitoring in clinical patients without thrombocytopenia-associated diseases treated with LMWH for at least five days at our institution, and adherence to recommended testing for HPF4-Ab and initiation of alternative anticoagulation in patients with potential HIT (defined as a drop of at least 50% in platelet count between days 5 and 14 following the start of LMWH treatment, or stopdate, whichever occurred first, compared to the highest platelet count within days 1–4) were investigated. Data from the Utrecht Patient Oriented Database (UPOD) were used for this retrospective cohort study. Inpatients exposed to the LMWHs dalteparin or nadroparin for at least five days during the period 2004–2005 were included. Patients with thrombocytopenia-related diseases were excluded. Firstly, adherence to recommended platelet count monitoring, based on recommendations from SPCs and clinical guidelines, was investigated. Secondly, the association between patient- and treatment characteristics and obtaining at least 2 platelets counts during treatment was investigated. Thirdly, adherence to recommended testing for HPF4-Ab and initiating treatment with danaparoid was investigated in patients with potential HIT. 6,804 patients with 7,770 episodes of LMWH treatment of at least five days were included. Adherence to the recommendations for platelet count monitoring from the SPC of nadroparin and dalteparin was 36.5% and 26.3% respectively. Adherence to the different platelet count monitoring recommendations from the 2002 clinical guideline on HIT was 23.0% and 41.5%. Obtaining at least 2 platelet counts during treatment was found to be strongly associated with ICU admission, previous UFH exposure, and a treatment duration of at least 10 days. There were 98 patients with potential HIT. Adherence to testing for HPF4-Ab in patients with potential HIT was 6.1%. Adherence to starting alternative anticoagulation in patients with potential HIT treatment was 0%. The results of this study suggest that adherence to recommendations for monitoring for HIT with LMWH is low at our institution. The results of this study justify to say that there is a need to think of appropriate actions for improving the awareness of HIT as an adverse reaction to LMWH, and to secure the safe use of LMWH.

scholarly journals A complicated case of pulmonary embolism in a patient with renal failure

2015 ◽  
Vol 4 (3S) ◽  
pp. 47-54
Author(s):  
Fulvio Pomero ◽  
Chiara Brignone ◽  
Giovanni Gollè ◽  
Alberto Silvestri ◽  
Elena Migliore ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Renal Failure ◽  
Low Molecular Weight ◽  
Antithrombotic Drugs ◽  
Low Molecular Weight Heparins ◽  
Heparin Induced Thrombocytopenia ◽  
Complicated Case ◽  
High Prevalence ◽  
Life Threatening ◽  
Life Threatening Complication

We describe a case of pulmonary embolism with instable hemodynamics in a patient with renal failure; the case is complicated by heparin-induced thrombocytopenia (HIT). Renal failure has a high prevalence in hospitalized patients and is a restriction on administration of low molecular weight heparins (LMWH) and fondaparinux. HIT is a potentially life-threatening complication, therefore a precocious diagnosis is essential. Therapy consists in the immediate stop of heparin’s administration and in the administration of non-heparin antithrombotic drugs.

Heparin induces neutrophil elastase-dependent vital and lytic NET formation

2019 ◽  
Vol 32 (5) ◽  
pp. 359-368 ◽  
Author(s):  
Patrick M Lelliott ◽  
Masatoshi Momota ◽  
Takayuki Shibahara ◽  
Michelle S J Lee ◽  
Nicholas I Smith ◽  
...  
Keyword(s):  
Neutrophil Elastase ◽  
Biological Effects ◽  
Extracellular Dna ◽  
Low Molecular Weight ◽  
Oxygen Species ◽  
Heparin Induced Thrombocytopenia ◽  
Extracellular Traps ◽  
Dna Strands ◽  
Life Threatening ◽  
Dose Dependent

Abstract Heparin is used extensively as an anticoagulant in a broad range of diseases and procedures; however, its biological effects are not limited to coagulation and remain incompletely understood. Heparin usage can lead to the life-threatening complication known as heparin-induced thrombocytopenia (HIT), caused by the development of antibodies against heparin/PF4 complexes. Here, we demonstrate the ability of heparin to induce neutrophil extracellular traps (NETs). NETs occurred with cell lysis and death, but live neutrophils releasing extracellular DNA strands, known as vital NETs, also occurred abundantly. Formation of NETs was time and dose dependent, and required reactive oxygen species and neutrophil elastase. Other compounds related to heparin such as low molecular weight heparin, fondaparinux and heparan sulfate either failed to induce NETs, or did so to a much lesser extent. Our findings suggest the ability of heparin to directly induce NET formation should be considered in the context of heparin treatment and HIT pathogenesis.

Defining the Role of Monocytes in Heparin-Induced Thrombocytopenia (HIT): Insights from a Murine HIT Model.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 280-280
Author(s):  
Lubica Rauova ◽  
Douglas B. Cines ◽  
Mortimer Poncz
Keyword(s):  
Platelet Surface ◽  
Heparin Induced Thrombocytopenia ◽  
Life Threatening ◽  
Low Levels ◽  
Novel Target ◽  
The Right ◽  
Iatrogenic Disorder

Heparin-induced thrombocytopenia (HIT) is an iatrogenic disorder seen in 1–5% of patients exposed to unfractionated heparin. One unusual feature of HIT is that affected patients often have only moderate thrombocytopenia yet suffer severe, life-threatening thrombosis. We have previously defined the importance of PF4:glycosaminoglycan (GAG) antigenic complexes on the surface of circulating platelets in the development of thrombocytopenia using mice that express varying levels of human PF4 (hPF4+/+) as well as Fc γRIIA on the platelet surface after infusing the animals with a monoclonal antibody (KKO) that demonstrates HIT-like properties. Because HIT antibodies have been reported to activate monocytes to produce tissue factor in vitro, we further examined their role both in vitro and in vivo in the murine HIT model. Monocytes bind PF4 onto their surface forming antigenic PF4:GAG complexes recognized by KKO. Monocytes express antigenic complexes at low levels of PF4, a setting in which none can be demonstrated on platelets. Furthermore, monocytes express antigenic complexes at heparin concentrations that completely dissociate antigen from the surface of platelets. We then investigated the role of monocytes in a murine model of HIT. Monocytes were depleted by IV injection of 200 μL of clodronate-containing liposomes (Encapsula Nano Sciences) 12 hrs prior to IP injection of 200 μg of KKO. Over 92% of circulating monocytes were depleted for >24 hrs with a return to near baseline by 72 hrs. In co-transgenic hPF4+/+/FcγRIIA mice, clodronate did not cause a significant fall in platelet count at 4 hrs, but counts fell to 30 ± 14% of baseline by 24 hrs vs. 70 ± 23% of baseline after injection of control liposomes or no liposomes (p<0.001), thrombocytopenia persisted for 72 hrs. Nevertheless, monocyte depletion inhibited thrombosis in the HIT model. Rose Bengal (500 mg/kg) was injected and the right carotid artery injury was exposed to 3 mW green (540 nm) light for 5 min followed by an IV injection of KKO (500 μg/kg). 4 of 5 mice that did not receive liposomes and 4 of 5 mice that received control liposomes 16–24 hrs prior to KKO developed thrombosis, in contrast to 1 of 5 clodronate liposome-treated mice (p<0.01 vs. all controls) in spite of having platelet counts of 860,000 ± 185,000/μL. These studies show that antibody mediated activation of monocytes contributes to the initiation of HIT, while intravascular activation of platelets contributes to the development of thrombocytopenia. These studies also suggest that depletion of monocytes may be a novel target for therapeutic intervention in the early stages of the disease.

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