scholarly journals Differential diagnosis of obstetric thrombotic microangiopathy: a review

2021 ◽  
Vol 8 (2) ◽  
Author(s):  
Polina I. Kukina ◽  
Anastasiya V. Moskatlinova ◽  
Irina M. Bogomazova ◽  
Elena V. Timokhina
Keyword(s):  
Differential Diagnosis ◽  
Hemolytic Anemia ◽  
Thrombotic Microangiopathy ◽  
Hellp Syndrome ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Target Organ ◽  
Microangiopathic Hemolytic Anemia ◽  
Atypical Hus ◽  
Obstetric Practice

Thrombotic microangiopathy (TMA) is a clinical and morphological syndrome, which is based on damage of the endothelium. Clinically, TMA is characterized by a triad of symptoms: thrombocytopenia, microangiopathic hemolytic anemia, and target organ damage. In obstetric practice, TMA most often occurs with preeclampsia or HELLP syndrome, atypical HUS, TTP. The review presents the basic differential criteria for the diagnosis of TMA during pregnancy and after childbirth, as well as the management of patients.

Thrombotic Microangiopathy in Cancer

2019 ◽  
Vol 45 (04) ◽  
pp. 348-353 ◽  
Author(s):  
Ilene Ceil Weitz
Keyword(s):  
Platelet Count ◽  
Cancer Treatment ◽  
Hemolytic Anemia ◽  
Cancer Chemotherapy ◽  
Thrombotic Microangiopathy ◽  
Organ Damage ◽  
Microangiopathic Hemolytic Anemia ◽  
Therapeutic Modalities

AbstractThrombotic microangiopathy (TMA) is a rare but often devastating complication of cancer and cancer treatment. The syndrome is defined by thrombocytopenia (i.e., a platelet count of < 150,000/mcL or > 30% decrease from baseline), microangiopathic hemolytic anemia, and some evidence of organ damage. Among the nine recognized groups of disorders causing TMA, the focus of this article will be on cancer and cancer treatment-related causes of TMA. This review will discuss the pathophysiology of TMA in cancer, chemotherapy-associated TMA, transplant-associated TMA, and newer therapeutic modalities.

Inflammation and Target Organ Damage in Hypertension With or Without Metabolic Syndrome

2005 ◽  
Vol 12 (3) ◽  
pp. 175
Author(s):  
A. Ferrucci ◽  
S. Sciarretta ◽  
V. Venturelli ◽  
G. M. Ciavarella ◽  
P. De Paolis ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Target Organ

Nocturnal Hypertension, Nondipping Phenomenon and Target Organ Damage in Obstructive Sleep Apnea Patients - The Bad and the Worse

2015 ◽  
Vol 10 (3) ◽  
pp. 182-188 ◽  
Author(s):  
Radostina Vlaeva Cherneva ◽  
Ognian Borisov Georgiev ◽  
Daniela Stoichkova Petrova ◽  
Emil Ivanov Manov ◽  
Dinko Georgiev Valev ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Target Organ ◽  
Nocturnal Hypertension ◽  
Obstructive Sleep

scholarly journals Effects of irbesartan on phenotypic alterations in monocytes and the inflammatory status of hypertensive patients with left ventricular hypertrophy

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jingsi Zhang ◽  
Lina Yang ◽  
Yanchun Ding
Keyword(s):  
Ventricular Hypertrophy ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Hypertensive Patients ◽  
Inflammatory Status ◽  
Tnf Α

Abstract Background Circulating monocytes and tissue macrophages play complex roles in the pathogenesis of hypertension and the resulting target organ damage. In this study, we observed alterations in the monocyte phenotype and inflammatory state of hypertensive patients with left ventricular hypertrophy (LVH) and studied the effects of irbesartan in these patients. This study might reveal a novel mechanism by which irbesartan alleviates LVH, and it could provide new targets for the prevention and treatment of hypertensive target organ damage. Methods CD163 and CD206 expression on monocytes and IL-10 and TNF-α levels in the serum of hypertensive patients with or without LVH and of healthy volunteers were detected. Furthermore, we treated monocytes from the LVH group with different concentrations of irbesartan, and then, CD163, CD206, IL-10 and TNF-α expression was detected. Results We found, for the first time, that the expression of CD163, CD206 and IL-10 in the LVH group was lower than that in the non-LVH group and healthy control group, but the TNF-α level in the LVH group was significantly higher. Irbesartan upregulated the expression of CD163 and CD206 in hypertensive patients with LVH in a concentration-dependent manner. Irbesartan also increased the expression of IL-10 and inhibited the expression of TNF-α in monocyte culture supernatants in a concentration-dependent manner. Conclusions Our data suggest that inflammation was activated in hypertensive patients with LVH and that the monocyte phenotype was mainly proinflammatory. The expression of proinflammatory factors increased while the expression of anti-inflammatory factors decreased. Irbesartan could alter the monocyte phenotype and inflammatory status in hypertensive patients with LVH. This previously unknown mechanism may explain how irbesartan alleviates LVH. Trail registration The study protocols were approved by the Ethical Committee of the Second Affiliated Hospital of Dalian Medical University. Each patient signed the informed consent form.

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