ABSTRACT
Dyspnoea in chronic respiratory disease is a very frequent symptom with a significant impact on quality of life (QoL). The aim of palliative care is to improve and maintain the QoL of patients with life-threatening diseases and its early implementation is now recommended in many evolving pulmonary diseases. The effectiveness of symptomatic treatments to relieve refractory breathlessness (morphine, oxygen supply, hypnosis, pulmonary rehabilitation) is often limited. These measures are more effective if offered early in the holistic management of the patient. This article illustrates and describes, with the help of a clinical situation, these treatments options and the collaborations established between the palliative care and pneumology divisions.
La dyspnée en lien avec une maladie respiratoire chronique est un symptôme très fréquent avec un impact important sur la qualité de vie (QoL). Les soins palliatifs ont pour objectif d'améliorer la QoL et les symptômes des personnes atteintes de maladies potentiellement mortelles et sont recommandés dans la prise en charge usuelle de nombreuses pathologies pulmonaires évolutives. Les traitements symptomatiques de la dyspnée réfractaire (morphine, oxygène, hypnose, réadaptation respiratoire) ont souvent un effet limité. Ces mesures sont d'autant plus efficaces si elles sont proposées précocement dans la prise en charge holistique du patient. Cet article illustre et décrit, à partir d'une situation clinique, ces modalités thérapeutiques et les collaborations établies entre les soins palliatifs et la pneumologie.
Subject(s)
Palliative Care , Pulmonary Disease, Chronic Obstructive , Humans , Quality of Life , Dyspnea/etiology , Dyspnea/therapy , Dyspnea/diagnosis , Morphine , Pulmonary Disease, Chronic Obstructive/complications , Pulmonary Disease, Chronic Obstructive/therapyABSTRACT
Given reports showing a high prevalence of azole resistance in Aspergillus fumigatus, alternatives to azole therapy are discussed when a threshold of 10% of azole-resistant environmental isolates is reached. This raises the issue of calculation of this threshold, either on the prevalence of azole-resistant isolates as a whole or on the prevalence of azole-resistant cases in populations at risk of invasive aspergillosis (IA). For isolate evaluation, there are high disparities in routine microbiological procedures for the isolation of A. fumigatus and azole resistance detection. There are also huge differences between the microbiological work-up for diagnosing IA. Some centres rely on galactomannan detection alone without actively trying to culture appropriate samples, which affects reliability of the figures on the prevalence of resistance and thus the threshold of resistance. Moreover, reports from the laboratory could mix up figures from completely different patient populations: frequent azole-resistant isolates from pneumology patients and rare azole-resistant isolates from haematology patients. Therefore, to sum isolates from different specimens and different wards can lead to erroneous calculations for the restricted populations at risk of developing IA. In conclusion, assessing the incidence of azole resistance in A. fumigatus should be based on harmonized consensual microbiological methods and reports should be restricted to IA episodes in identified populations at risk of IA when the issue is to define an operational threshold for modifying recommendations.
Subject(s)
Antifungal Agents/pharmacology , Antifungal Agents/therapeutic use , Aspergillus fumigatus/drug effects , Aspergillus fumigatus/isolation & purification , Azoles/pharmacology , Drug Resistance, Fungal , Invasive Pulmonary Aspergillosis/drug therapy , Humans , Incidence , Invasive Pulmonary Aspergillosis/diagnosis , Invasive Pulmonary Aspergillosis/microbiology , Microbial Sensitivity Tests/methods , PrevalenceABSTRACT
Hereditary tyrosinemia type 1 (HT1) is a recessive disease caused by a deficiency of the enzyme fumarylacetoacetate hydrolase (FAH) that catalyzes the conversion of fumarylacetoacetate (FAA) into fumarate and acetoacetate. In mice models of HT1, FAH deficiency causes death within the first 24h after birth. Administration of 2-(2-nitro-4-trifluoro-methylbenzoyl)-1,3 cyclohexanedione (NTBC) prevents neonatal death in HT1 mice, ameliorates the HT1 phenotype but does not prevent development of hepatocellular carcinoma later on. FAA has been shown to deplete cells of glutathione by forming adducts. We tested whether a combination of a cell membrane permeable derivative of glutathione, glutathione monoethylester (GSH-MEE) and vitamin C could provide an alternative effective treatment for HT1. GSH-MEE (10 mmol/kg/j)/vitamin C (0.5 mmol/kg/j) treatment was given orally to pregnant/nursing female mice. While FAH-/- pups died in absence of treatment, all FAH-/- pups survived the critical first 24h of life when the mothers were on the GSH-MEE/vitamin C treatment and showed normal growth until postnatal day 10 (P10). However, after P10, pups showed failure to thrive, lethargy and died around P17. Thus, GSH-MEE/vitamin C supplementation could rescue the mice model of HT1 from neonatal death but it did not prevent the appearance of a HT1 phenotype in the second week after birth.