Rates and Predictors of Structural Valve Degeneration and Failure of Trifecta Bioprosthetic Valve Over a 5-year Follow-up Period: A Single-center Experience.

Introduction: The Trifecta bioprosthetic valve has been commonly used for surgical aortic valve replacement (SAVR). Multiple studies have been done to define the rate of structural valve degeneration (SVD) and failure (SVF), but the outcomes are still debatable. Therefore, we aim to conduct this single-center study to estimate the rate and predictors of SVD/SVF. Methodology: This retrospective observational cohort single-center study was conducted between 2014 and 2019 among Trifecta SAVR patients. Data were patient's characteristics collected from electronic medical records at baseline and follow-up (3-5 years). Statistical analysis was performed with a significance level of P ≤ 0.05. Results: A total of 271 eligible patients were identified. Most of our sample were males (57.9%), with a mean age of 71.1 ± 10.6 years. The mean baseline preoperative ejection fraction (EF) was 53.0%, with no change (P = 0.88) in the immediate postoperative EF (53.6%). A most recent follow-up EF revealed a significant increase of EF (55.2%), P = 0.01. Furthermore, there was a significant increase from peak velocity to PVMRE (mean difference [MD] ± standard error of mean (SEM) [0.15 ± 0.04], P < 0.01), an increase in pressure gradient (PGIPE) to PGMRE (MD ± SEM [1.70 ± 0.49], P < 0.01), and a decrease in Doppler velocity index (DVIIPE) to DVIMRE (MD ± SEM [-0.037 ± 0.01], P = 0.01). Regarding the SVF rate, 13 (4.8%) patients had failed valves requiring replacement throughout the study period. Conclusions: Over a 5-year follow-up period, 4.8% had SVF with an SVD of 23.2%, with the majority of SVD not being clinically significant except in six patients. These results corroborate with a previously published study suggesting a bad clinical outcome of Trifecta valve placement.

Estrogen/estrogen receptor activation protects against DEN-induced liver fibrosis in female rats via modulating TLR-4/NF-kß signaling.

AIM: Men are more susceptible to liver fibrosis (LF) than women. However, the underlying molecular mechanism, especially the role of estrogen/estrogen receptor (ER) activation in this sexual dimorphism is unclear. Therefore, the aim of the current study was to investigate the impact and the underlying molecular mechanisms of estrogen/ER activation on diethyl nitrosamine (DEN)-induced LF. MAIN METHODS: Thirty ovariectomized (OVX) female rats were randomly allocated into five groups (n = 6), and received no treatment, diethyl nitrosamine (DEN), DEN/fulvestrant, DEN/silymarin or DEN/estradiol benzoate (EB). In addition, three sham groups received no treatment, DEN or DEN/fulvestrant, and one control group that neither ovariectomized nor treated. Directly after treatment, liver injury biomarkers were measured. In addition, hepatic tissue hydroxyproline, TNF- α, TGF- ß, and IL-10 were evaluated. Expression of NF-kß, CD68 (a marker for macrophage infiltration), ER-ß and TLR-4 were measured. Finally, liver tissue histopathology was assessed. KEY FINDINGS: Ovariectomy aggravates DEN-induced LF, as it significantly elevated all liver tissue injury biomarkers. This effect has become even worse after blocking ER by fulvestrant, indicating a protective role of estrogen/ER activation against DEN-induced LF. Inhibition of TLR-4/NF-kß signaling pathway contributed to this protective effect, as estrogen deprivation or blocking of ER significantly activates this pathway during the onset of LF. While administration of EB or silymarin (selective ER-ß activator) improved LF indices and deactivated this pathway. SIGNIFICANCE: These results provide new insight into the pivotal role of estrogen/ER activation via modulation of TLR-4/NF-kß, in the alleviation of LF pathogenesis.

Thrombocytopenia secondary to iron deficiency anemia responding to iron therapy.

A broad spectrum of diseases can cause anemia and thrombocytopenia. Some of these diseases are a hematological emergency; others are benign diseases, so early and accurate diagnosis is crucial in managing such patients. Usually, IDA is associated with thrombocytosis or normal platelets; however, in rare cases, IDA can be associated with thrombocytopenia; even though, thrombocytopenia that occurs with IDA responds to iron therapy. Iron therapy rarely causes transient thrombocytopenia per se. We are reporting an African female patient who is found to have thrombocytopenia secondary to iron deficiency anemia (IDA), and she responded to iron replacement therapy initially with a transient drop in platelets, followed by a rapid rise in platelets till platelets reached the normal level.

Paroxysmal Nocturnal Hemoglobinuria with Glucose-6-Phosphate Dehydrogenase Deficiency: A Case Report and Review of the Literature.

In this study, we are describing a female patient with paroxysmal nocturnal hemoglobinuria (PNH) and glucose-6-phosphate dehydrogenase (G6PD) deficiency. Both diseases are known to cause hemolytic anemia that mediates the hemolysis of RBCs through several mechanisms. In PNH the hemolysis is mediated through complement activation and oxidative stress. G6PD enzyme is crucial in preventing damage to cellular structures caused by oxygen-free radicles. In G6PD deficiency the hemolysis is mediated through the oxidative stress created by oxygen-free radicles. Since both diseases mediate hemolysis through the oxidative stress, we hypothesize that both conditions have facilitated an effect on each other and this will reflect on the response to treatment, and this response to treatment could vary based on whether the two mutations occurred in the same gene or in two different X chromosomes. Having diagnosed PNH, the management is very expensive and not all the patients can afford it, especially our patient who is a maid by occupation. So, the real challenge in our case is to monitor her in subsequent visits and to plan the treatment keeping in mind her financial status.