Thrombocytopenia (TP) affects 7-10% of pregnant women. It occurs 4 times more frequently in pregnancy than in the non-pregnant women population. Women with thrombocytopenia in pregnancy are a heterogeneous and poorly known group. There are several possible causes of thrombocytopenia in pregnancy. The most common are: gestational thrombocytopenia (GE) (60-75%), preeclampsia (PE) and HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome associated TP (21%), and idiopathic immune thrombocytopenia (ITP) (3-10%). Although thrombocytopenia diagnosed in pregnancy in most cases has a mild course, it has also been reported to be associated with a higher rate of preterm birth and premature detachment of the placenta. Some cases of severe thrombocytopenia with systemic involvement are associated with high risk of serious perinatal complications and require early diagnosis, careful clinical monitoring and medical treatment. The differential diagnosis and proper assessment of clinical risk of TP during pregnancy may be of great concern. The article discusses these issues, focusing on pathophysiology of TP in pregnancy.
Primary hyperaldosteronism (PHA) is the most common form of secondary hypertension of hormonal origin. It affects about 10% of all hypertensive patients. It is connected with increased morbidity and mortality from cardiovascular diseases (CVD) compared to patients with essential hypertension of a similar age. Usually, it is an effect of bilateral adrenal hyperplasia (BAH) or aldosterone-producing adenoma (APA), more rare causes of PHA are: unilateral adrenal hyperplasia, aldosterone-producing adrenocortical carcinoma, ectopic aldosterone-producing tumors and familial hyperaldosteronism. Recent genetic studies have thrown a new light on the pathogenesis of PHA, classifying it as a channelopathy. Several mutations within the ion channels encoding genes have been identified. A possible link between primary hyperaldosteronism and polymorphism of aldosterone synthase gene and ion channel genes is still being investigated. In this manuscript, we focus on genetic aspects of primary hyperaldosteronism, and present an up-to-date compilation of available data with the widened pathogenetic approach.
Obstructive sleep apnea (OSA) and sleep bruxism (SB) may appear concomitantly. Data on the relationship between OSA and SB are limited. It was shown that in a population with an increased risk of OSA, OSA was dependently correlated with SB on the degree of OSA severity only in mild and moderate cases of OSA. We aimed to confirm this relationship and affecting factors in a group of dental office patients in a prospective, observational study. Adult patients (n = 119) were evaluated using respiratory polygraphy. The risk of OSA was assessed using a STOP-Bang questionnaire (SBQ). The episodes of bruxism and respiratory events were scored according to the standards of the American Academy of Sleep Medicine. The prevalence of OSA and SB was found to be 63.02% and 41.17%, respectively. The bruxism episode index (BEI) was increased in the group with a higher risk of OSA (SBQ ≥ 3) compared to the group with a lower risk of OSA (3.49 ± 3.63 vs. 2.27 ± 2.50, p = 0.03). The sensitivity and specificity of the SBQ were not sufficient to predict SB. A positive linear correlation between AHI and BEI in the group with AHI < 23/h was found. The study confirmed that OSA was associated with SB in the group of patients with OSA and/or SB risk. The relationship between OSA and SB depended on the degree of severity of OSA and occurred in mild and moderate cases of OSA.
Hypertension is the most common chronic cardiovascular disease in adults in all Western societies. Unfortunately, hypertension treatment is still often insufficient and in most countries the majority of patients still have inadequately controlled blood pressure. In recent years, dietary modifications and supplementations, including polyunsaturated fatty acids (PUFA), have attracted considerable interest as a potentially complementary therapy for the treatment of hypertension. The reduction of blood pressure due to PUFA supplementation may be a consequence of promoting nitric oxide-induced endothelial relaxation, a reduced vasoconstrictive response to catecholamines and angiotensin II, improved vasodilatory responses, arterial compliance and reduced oxidative stress. It has been clearly demonstrated that PUFA decreases blood pressure in experimental studies, animal models and clinical trials, especially in higher doses (more than 3g/day). Thus, PUFA consumption might be useful, particularly in the control of patients with 1st degree hypertension or as a complementary method in treating patients with antihypertensives. The consumption of fishes, the main source of PUFA, needs to be recommended for all the hypertensives to reduce cardiovascular risk. Because of the dose-dependent effect differences, the choice of a correct dose of PUFA may be difficult and controversial. Therefore, a qualified healthcare provider should be consulted prior to starting treatment with PUFA supplements.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.