An extrahepatic hydatid cyst with the fat-fluid level

A hydatic cyst is a zoonosis caused by the larva of a tapeworm Echinococcus granulosus. The liver is the most commonly affected organ. Soft tissue localization has been reported in 2.3% of cases. Herein, we present a patient with a fat-containing hydatid cyst located in the left thigh. There are only a few reports in the literature on the presence of the fat-fluid level within a hydatid cyst. Previous studies have suggested that fat-containing hydatid cysts occur due to their cysto-biliary communication in the liver. In our case, we describe a fat-containing hydatid cyst in the extrahepatic location and discuss the pathophysiologic mechanism of fat inside it.

How COVID-19 brought smell disorders in the spotlight

The rapid spread of the COVID-19 infection required prompt recognition and immediate isolation of patients. In the evolution of the disease various symptoms were indicated as suggestive of a SARS-CoV-2 infection, among them being also described anosmia and ageusia. In order to review how olfactory disorders are related to COVID-19 disease, we carried out an analysis by searching PubMed, Science Direct, Springer, and LILACS. The research was made using MeSH descriptors and the Boolean operator, “AND”, for the terms “olfactory disorders” or “olfactory dysfunction” or “anosmia” or “neurologic manifestations” or “ENT symptoms” AND “COVID-19” or “SARS-CoV-2” or “coronavirus infections”, with a filter on the publication date set for 01.01.2020 – 18.06.2021. A total of 956 articles were found in the databases, out of which 14 were included in the study. The statistics suggest that alterations of the chemosensory function are strongly correlated with COVID-19, although the exact pathophysiologic mechanism is not well established. Symptomatology suggestive of chemosensory dys-function (smell primarily and then taste alterations) elevate the degree of suspicion of a SARS-CoV-2 infection and they commend prompt isolation and surveillance measurements.

Obese-Inflammatory Phenotypes in Heart Failure With Preserved Ejection Fraction

Background: Comorbidity-driven microvascular inflammation is posited as a unifying pathophysiologic mechanism for heart failure with preserved ejection fraction (HFpEF). Obesity is proinflammatory and common in HFpEF. We hypothesized that unique obesity-inflammation HFpEF phenotypes exist and are associated with differences in clinical features, fibrosis biomarkers, and functional performance. Methods: Patients (n=301) from 3 HFpEF clinical trials were studied. Unsupervised machine learning (hierarchical clustering) with obese status and 13 inflammatory biomarkers as input variables was performed. Associations of clusters with HFpEF severity and fibrosis biomarkers (PIIINP [procollagen III N-terminal peptide], CITP [C-telopeptide for type I collagen], IGFBP7 [insulin-like growth factor-binding protein-7], and GAL-3 [galectin-3]) were assessed. Results: Hierarchical clustering revealed 3 phenotypes: pan-inflammatory (n=129; 64% obese), noninflammatory (n=83; 55% obese), and obese high CRP (C-reactive protein; n=89; 98% obese). The pan-inflammatory phenotype had more comorbidities and heart failure hospitalizations; higher left atrial volume, NT-proBNP (N-terminal pro-B-type natriuretic peptide), and fibrosis biomarkers; and lower glomerular filtration rate, peak oxygen consumption, 6-minute walk distance, and active hours/day ( P <0.05 for all). The noninflammatory phenotype had the most favorable values for all measures. The obese high CRP phenotype resembled the noninflammatory phenotype except for isolated elevation of CRP and lower functional performance. Hierarchical cluster assignment was independent of CRP genotype combinations that alter CRP levels and more biologically plausible than other clustering approaches. Multiple traditional analytic techniques confirmed and extended the hierarchical clustering findings. Conclusions: Unique obesity-inflammation phenotypes exist in HFpEF and are associated with differences in comorbidity burden, HFpEF severity, and fibrosis. These data support comorbidity-driven microvascular inflammation as a pathophysiologic mechanism for many but not all HFpEF patients.

Increased sympathetic responses induced by chronic obstructive sleep apnea are caused by sleep fragmentation

Obstructive sleep apnea causes a hyperactive chemoreflex, with increased sympathetic activation. However, it is not clear whether this pathophysiologic mechanism is due to repeated hypoxia or to sleep disruption. The present study suggests that sleep fragmentation contributes importantly to increased sympathetic activation after chemoreceptor stimulation. This suggests that sleep fragmentation has an important role in the sympathetic activation seen in sleep apnea patients.

Association between psoriasis and migraine: what should we expect from a meta-analysis?

Background Although many studies have demonstrated the commodity of psoriasis with migraine and indicated that they may have similar susceptibility genes and pathophysiologic mechanism, the clinic association between the migraine and psoriasis remains unclear. Methods We have already searched Pubmed, Embase, and Web of Science for case–control, cross-sectional, or cohort studies, and extract rate, odds or risk of migraine in subjects with psoriasis or without psoriasis. Using defined inclusion and exclusion criteria, finally include nine studies. Pooling of the suitable data was applied when necessary. Results Five cross-sectional studies included 6355 psoriasis patients and 934413 controls, migraine highly occurred in psoriasis patient (pooled OR 1.64; 95% confidence interval [1.28; 2.11]). In addition, with 4375 psoriasis patients provided, the rate of migraine occurred in psoriasis patient (pooled rate 0.21; 95% confidence interval [0.13; 0.35]). Conclusion Migraine and psoriasis present a clear co-occurrence and similar pathophysiologic mechanism, which lead to the assumption that the two diseases might be linked. Screening and selection of proper assessment of migraine among psoriasis patients are warranted and needed.

Postural Orthostatic Tachycardia Syndrome: Mechanisms and New Therapies

Postural orthostatic tachycardia syndrome (POTS) is a clinically heterogeneous disorder with multiple contributing pathophysiologic mechanisms manifesting as symptoms of orthostatic intolerance in the setting of orthostatic tachycardia (increase in heart rate by at least 30 beats per minute upon assuming an upright position) without orthostatic hypotension. The three major pathophysiologic mechanisms include partial autonomic neuropathy, hypovolemia, and hyperadrenergic state. Patients often will exhibit overlapping characteristics from more than one of these mechanisms. The approach to the treatment of POTS centers on treating the underlying pathophysiologic mechanism. Stockings, abdominal binders, and vasoconstrictors are used to enhance venous return in partial neuropathic POTS. Exercise and volume expansion are the main treatment strategies for hypo-volemic POTS. For hyperadrenergic POTS, beta-blockers and avoidance of norepinephrine reuptake inhibitors is important. Attempts should be made to discern which pathophysiologic mechanism(s) may be afflicting patients so that treatment regimens can be individualized.

Trying to understand preeclampsia. A rocky road

This narrative is not a review, it is just a personal account of a series of pivotal studies that directly influenced my evolving research interest in the pathogenesis and prevention of preeclampsia since the early 1980s’.Studying in Leiden (The Netherlands) in the early 1970’s, my introduction into obstetrics was not very positive. The obstetrical teaching, we received, as 3rd year medical students was boring. The focus was very much on the individual plusses and minuses of types of obstetrical forceps. Preeclampsia was a disease caused by ‘salt excess’, strict salt restriction the key concept in prevention of preeclampsia in The Netherlands.One of my lecturers told us that disseminated intravascular coagulation (DIC) was the key causal pathophysiologic mechanism in preeclampsia. At this stage one did not realize that the ‘DIC’ observations were all based on autopsy findings in women dying of eclampsia and/or HELLP (although that acronym was only introduced by Weinstein1 in 1982). It was Prof Jack Pritchard2 who – already in these years – made the observation that we ‘never die alone – DIC is always there’. For me the ‘DIC’ lectures certainly triggered my interest in the haemostatic system.