Clinical Presentation, Temporal Relationship, and Outcome in Thirty-Three Patients With Type 2 Heparin-Induced Thrombocytopenia After Cardiotomy

2006 ◽  
Vol 82 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Calvin Wan ◽  
Margaret Warner ◽  
Benoit De Varennes ◽  
Patrick Ergina ◽  
Renzo Cecere ◽  
...  
2017 ◽  
Vol 117 (10) ◽  
pp. 1868-1874 ◽  
Author(s):  
Jo-Ann Sheppard ◽  
Theodore Warkentin ◽  
Andrew Shih

SummaryOne of the standard distinctions between type 1 (non-immune) and type 2 (immune-mediated) heparin-induced thrombocytopenia (HIT) is the transience of thrombocytopenia: type 1 HIT is viewed as early-onset and transient thrombocytopenia, with platelet count recovery despite continuing heparin administration. In contrast, type 2 HIT is viewed as later-onset (i. e., 5 days or later) thrombocytopenia in which it is generally believed that platelet count recovery will not occur unless heparin is discontinued. However, older reports of type 2 HIT sometimes did include the unexpected observation that platelet counts could recover despite continued heparin administration, although without information provided regarding changes in HIT antibody levels in association with platelet count recovery. In recent years, some reports of type 2 HIT have confirmed the observation that platelet count recovery can occur despite continuing heparin administration, with serological evidence of waning levels of HIT antibodies (“seroreversion”). We now report two additional patient cases of type 2 HIT with platelet count recovery despite ongoing therapeutic-dose (1 case) or prophylactic-dose (1 case) heparin administration, in which we demonstrate concomitant waning of HIT antibody levels. We further review the literature describing this phenomenon of HIT antibody seroreversion and platelet count recovery despite continuing heparin administration. Our observations add to the concept that HIT represents a remarkably transient immune response, including sometimes even when heparin is continued.


2021 ◽  
Author(s):  
Fabian Rossi ◽  
Joe Ma ◽  
Nina Tsakadze ◽  
Lourdes Benes-Lima ◽  
Julio Araque Gonzalez ◽  
...  

Abstract BackgroundSpinocerebellar Ataxia type 2 is a slowly progressive adult onset ataxia with a broad clinical presentation. Case presentationWe describe a man with Spinocerebellar Ataxia type 2 with chronic, severe, and recurrent rhabdomyolysis, as part of the cerebellar ataxia genetic spectrum. Initially rhabdomyolysis was refractory to multiple medications, but entirely resolved and remained in chronic remission with pregabalin. ConclusionThis is the first report of Spinocerebellar Ataxia type 2 associated with chronic, severe, recurrent rhabdomyolysis as part of its genetic phenotype responsive to pregabalin.


2014 ◽  
Vol 8 (1) ◽  
pp. 43-47 ◽  
Author(s):  
Graham J Fent ◽  
Hazlyna Kamaruddin ◽  
Pankaj Garg ◽  
Ahmed Iqbal ◽  
Nicholas F Kelland ◽  
...  

A diagnosis of myocardial infarction is made using a combination of clinical presentation, electrocardiogram and cardiac biomarkers. However, myocardial infarction can be caused by factors other than coronary artery plaque rupture and thrombosis. We describe an interesting case presenting with hypertensive emergency and type 2 myocardial infarction resulting from Pheochromocytoma associated with Capnocytophaga canimorsus infection from a dog bite. We also review current literature on the management of hypertensive emergency and Pheochromocytoma.


Endocrines ◽  
2021 ◽  
Vol 2 (4) ◽  
pp. 485-501
Author(s):  
Zoltan Antal

Maturity Onset Diabetes of the Young (MODY) encompasses a group of rare monogenic forms of diabetes distinct in etiology and clinical presentation from the more common forms of Type 1 (autoimmune) and Type 2 diabetes. Since its initial description as a clinical entity nearly 50 years ago, the underlying genetic basis for the various forms of MODY has been increasingly better elucidated. Clinically, the diagnosis may be made in childhood or young adulthood and can present as overt hyperglycemia requiring insulin therapy or as a subtle form of slowly progressive glucose impairment. Due to the heterogeneity of clinical symptoms, patients with MODY may be misdiagnosed as possessing another form of diabetes, resulting in potentially inappropriate treatment and delays in screening of affected family members and associated comorbidities. In this review, we highlight the various known genetic mutations associated with MODY, clinical presentation, indications for testing, and the treatment options available.


2015 ◽  
Vol 25 (05) ◽  
pp. e135-e138 ◽  
Author(s):  
Jun Watanabe ◽  
Shigeto Miyasaka ◽  
Keisuke Morimoto ◽  
Takafumi Hamasaki ◽  
Shingo Ishiguro ◽  
...  

2015 ◽  
Vol 11 (2) ◽  
pp. 112
Author(s):  
Eugene Sobngwi ◽  
Jean Claude Mbanya ◽  
◽  

There is growing evidence for an etiological interaction between infectious diseases and diabetes, as well as for bidirectional influence of clinical presentation, spread, and outcomes. Some HIV treatments increase diabetes risk, and some infectious diseases may determine unique phenotypes of diabetes. Individuals who have type 2 diabetes have increased risk for tuberculosis and viral hepatitis and have poorer treatment outcomes. Joint noncommunicable diseases (NCDs) and infectious diseases clinics are the ideal method of tackling the double burden of these diseases in developing countries.


2009 ◽  
Vol 54 (4) ◽  
pp. 563-572 ◽  
Author(s):  
Marie Meeths ◽  
Yenan T. Bryceson ◽  
Eva Rudd ◽  
Chengyun Zheng ◽  
Stephanie M. Wood ◽  
...  

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