scholarly journals Treatment of Posaconazole-Induced Peripheral Neuropathy With Methylprednisolone and Magnesium Infusions: A Case Report

2019 ◽  
Vol 6 (2) ◽  
Author(s):  
Sadia Hussain ◽  
Susan Nissen ◽  
Steven M Holland ◽  
Paola Sandroni ◽  
Michail S Lionakis
Keyword(s):  
Case Report ◽  
Peripheral Neuropathy ◽  
Potential Role ◽  
Tablet Formulation

Abstract The tolerability of long-term posaconazole use remains poorly defined. We present a patient who developed peripheral neuropathy following long-term exposure to the tablet formulation of posaconazole, which was treated with methylprednisolone and magnesium infusions. The potential role of methylprednisolone and magnesium infusions in managing this potentially irreversible triazole-associated complication requires further study.

Treatment strategies for chemotherapy-induced peripheral neuropathy: potential role of exercise

2010 ◽  
Vol 4 (2) ◽  
pp. 117-125 ◽  
Author(s):  
Karen Y. Wonders ◽  
Beverly S. Reigle ◽  
Daniel G. Drury
Keyword(s):  
Peripheral Neuropathy ◽  
Potential Role ◽  
Treatment Strategies

Prevention of Cardiac Hypertrophy in Experimental Chronic Renal Failure by Long-Term ACE Inhibitor Administration: Potential Role of Lysosomal Proteinases

1995 ◽  
Vol 15 (2) ◽  
pp. 129-136 ◽  
Author(s):  
Hiroaki Suzuki ◽  
Liliana Schaefer ◽  
Hong Ling ◽  
Roland M. Schaefer ◽  
Jobst Dämmrich ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Cardiac Hypertrophy ◽  
Potential Role ◽  
Ace Inhibitor ◽  
Lysosomal Proteinases

scholarly journals Duodenal Dysbiosis and Relation to the Efficacy of Proton Pump Inhibitors in Functional Dyspepsia

2021 ◽  
Vol 22 (24) ◽  
pp. 13609
Author(s):  
Lucas Wauters ◽  
Raúl Y. Tito ◽  
Matthias Ceulemans ◽  
Maarten Lambaerts ◽  
Alison Accarie ◽  
...  
Keyword(s):  
Functional Dyspepsia ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Potential Role ◽  
Short Term ◽  
Beneficial Effects ◽  
Rrna Sequencing ◽  
Before And After

Proton pump inhibitors (PPI) may improve symptoms in functional dyspepsia (FD) through duodenal eosinophil-reducing effects. However, the contribution of the microbiome to FD symptoms and its interaction with PPI remains elusive. Aseptic duodenal brushings and biopsies were performed before and after PPI intake (4 weeks Pantoprazole 40 mg daily, FD-starters and controls) or withdrawal (2 months, FD-stoppers) for 16S-rRNA sequencing. Between- and within-group changes in genera or diversity and associations with symptoms or duodenal factors were analyzed. In total, 30 controls, 28 FD-starters and 19 FD-stoppers were followed. Mucus-associated Porphyromonas was lower in FD-starters vs. controls and correlated with symptoms in FD and duodenal eosinophils in both groups, while Streptococcus correlated with eosinophils in controls. Although clinical and eosinophil-reducing effects of PPI therapy were unrelated to microbiota changes in FD-starters, increased Streptococcus was associated with duodenal PPI effects in controls and remained higher despite withdrawal of long-term PPI therapy in FD-stoppers. Thus, duodenal microbiome analysis demonstrated differential mucus-associated genera, with a potential role of Porphyromonas in FD pathophysiology. While beneficial effects of short-term PPI therapy were not associated with microbial changes in FD-starters, increased Streptococcus and its association with PPIeffects in controls suggest a role for duodenal dysbiosis after long-term PPI therapy.

scholarly journals Neuroinflammation and Its Impact on the Pathogenesis of COVID-19

2021 ◽  
Vol 8 ◽  
Author(s):  
Mohammed M. Almutairi ◽  
Farzane Sivandzade ◽  
Thamer H. Albekairi ◽  
Faleh Alqahtani ◽  
Luca Cucullo
Keyword(s):  
Immune System ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Immune Cell ◽  
Clinical Manifestations ◽  
Cell Infiltration ◽  
Cellular Mechanisms ◽  
Cytokine Levels

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The clinical manifestations of COVID-19 include dry cough, difficult breathing, fever, fatigue, and may lead to pneumonia and respiratory failure. There are significant gaps in the current understanding of whether SARS-CoV-2 attacks the CNS directly or through activation of the peripheral immune system and immune cell infiltration. Although the modality of neurological impairments associated with COVID-19 has not been thoroughly investigated, the latest studies have observed that SARS-CoV-2 induces neuroinflammation and may have severe long-term consequences. Here we review the literature on possible cellular and molecular mechanisms of SARS-CoV-2 induced-neuroinflammation. Activation of the innate immune system is associated with increased cytokine levels, chemokines, and free radicals in the SARS-CoV-2-induced pathogenic response at the blood-brain barrier (BBB). BBB disruption allows immune/inflammatory cell infiltration into the CNS activating immune resident cells (such as microglia and astrocytes). This review highlights the molecular and cellular mechanisms involved in COVID-19-induced neuroinflammation, which may lead to neuronal death. A better understanding of these mechanisms will help gain substantial knowledge about the potential role of SARS-CoV-2 in neurological changes and plan possible therapeutic intervention strategies.

scholarly journals Case Report: Clostridium neonatale Bacteremia in a Preterm Neonate With Necrotizing Enterocolitis

2021 ◽  
Vol 9 ◽  
Author(s):  
Nadim Cassir ◽  
Isabelle Grandvuillemin ◽  
Manon Boxberger ◽  
Priscilla Jardot ◽  
Farid Boubred ◽  
...  
Keyword(s):  
Necrotizing Enterocolitis ◽  
Potential Role ◽  
Preterm Neonate ◽  
Gastrointestinal Disorder ◽  
Etiologic Agent ◽  
Preterm Neonates ◽  
Environmental Cleaning ◽  
Life Threatening

Necrotizing enterocolitis is a life-threatening acquired gastrointestinal disorder among preterm neonates and is associated with a high mortality rate and long-term neurodevelopmental morbidity. No etiologic agent has been definitively established; nonetheless, the most implicated bacteria include members of the Clostridium genus. We reported here on a case of Clostridium neonatale bacteremia in a preterm neonate with necrotizing enterocolitis, providing more information regarding the potential role of this bacterium in pathogenesis of necrotizing enterocolitis. We emphasized the sporulating form of C. neonatale that confers resistance to disinfectants usually applied for the hospital environmental cleaning. Further works are needed to establish the causal relationship between the occurrence of NEC and the isolation of C. neonatale, with promising perspectives in terms of diagnostic and therapeutic management.

Radiotherapy after Prostatectomy

2002 ◽  
Vol 88 (6) ◽  
pp. 445-452 ◽  
Author(s):  
Giuseppe Sanguineti ◽  
Paola Franzone ◽  
Laura Culp ◽  
Michela Marcenaro ◽  
Salvina Barra ◽  
...  
Keyword(s):  
High Risk ◽  
Radical Prostatectomy ◽  
Adjuvant Radiotherapy ◽  
Potential Role ◽  
Specific Antigen ◽  
Salvage Treatment ◽  
Salvage Radiotherapy ◽  
Risk Of Failure

Aims and background The role of radiotherapy after prostatectomy is controversial. This paper tries to give some guidelines for everyday practice through an analysis of literature data. Methods The potential role of radiotherapy in the adjuvant and salvage setting is discussed. We also report and interpret available literature data for both settings. Results As regards an increase in or detectable prostate-specific antigen (PSA) after radical prostatectomy, about 40–50% of patients are rendered bNED with local salvage radiotherapy, but only 10–50% are long-term (5 years) biochemically controlled. A timely salvage treatment is crucial to optimize control probability. As regards adjuvant radiotherapy for undetectable postoperative PSA in patients at high risk of failure as judged on pathology, results are more encouraging. Recent data report bNED rates ≥70% at 5 years. Conclusions Although results are far from satisfactory, salvage radiotherapy should be considered for every patient with an increased or detectable PSA after surgery. Adjuvant radiotherapy seems preferable to salvage radiotherapy for patients at high (>30%) risk of failure.

scholarly journals Amyloid Proteins and Peripheral Neuropathy

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1553 ◽  
Author(s):  
Mohammed M. H. Asiri ◽  
Sjoukje Engelsman ◽  
Niels Eijkelkamp ◽  
Jo W. M. Höppener
Keyword(s):  
Peripheral Neuropathy ◽  
Potential Role ◽  
Inflammatory Diseases ◽  
Amyloid Proteins ◽  
Chronic Inflammatory Diseases ◽  
Histopathological Feature ◽  
Common Diseases ◽  
Biological Defects

Painful peripheral neuropathy affects millions of people worldwide. Peripheral neuropathy develops in patients with various diseases, including rare familial or acquired amyloid polyneuropathies, as well as some common diseases, including type 2 diabetes mellitus and several chronic inflammatory diseases. Intriguingly, these diseases share a histopathological feature—deposits of amyloid-forming proteins in tissues. Amyloid-forming proteins may cause tissue dysregulation and damage, including damage to nerves, and may be a common cause of neuropathy in these, and potentially other, diseases. Here, we will discuss how amyloid proteins contribute to peripheral neuropathy by reviewing the current understanding of pathogenic mechanisms in known inherited and acquired (usually rare) amyloid neuropathies. In addition, we will discuss the potential role of amyloid proteins in peripheral neuropathy in some common diseases, which are not (yet) considered as amyloid neuropathies. We conclude that there are many similarities in the molecular and cell biological defects caused by aggregation of the various amyloid proteins in these different diseases and propose a common pathogenic pathway for “peripheral amyloid neuropathies”.

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