Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A knowledge of the relationship between nutrition and the respiratory system applied in chronic airflow obstruction (BCO) enables a better understanding of the increased frequency (30 to 50%) of protein-energy malnutrition (MEP) in this population. The physiology of the wasting in chronic airflow obstruction seems to relate to hypermetabolism (HMB) which is not compensated by an increased alimentary intake. The HMB is linked to a rise in the work of the respiratory muscles whose efficiency is altered by intrathoracic hyperinfiltration and also the consequences of MEP on the mass and function of the respiratory muscles. In the animal MEP induced by alimentary restrictions leads to a model of pulmonary emphysema and to the diminution of the synthesis of surfactant. This emphysema seems to be principally due to an alteration of the process of protein synthesis and to a diminution of lysyl-oxydase activity. The nutrients (utilised notably by the venous route) have their own pharmacological role, and in addition they have an effect on the natural equilibrium of the energy and nitrogen balance. Lipids (rich in polyunsaturated fatty acids) intervene in the synthesis of prostaglandins, and exercise some effects on the inflammatory process and the activity in the bronchial and vascular smooth muscles. Based on this fact they have been used for their anti-inflammatory role at the pulmonary level in the treatment of mucoviscidosis. The administration of amino acids changes ventilation by acting on the central neuro-muscular command mechanism (VT/TI). The perfusion of amino acids enables a restoration of the chemo-sensitivity to oxygen and to CO2 abolished by the prolonged restricted diet. Finally the partial pressure of oxygen ought to be interpreted with respect to meal times because an oral dose of glucose can provoke an increase in the PaO2 of around 10 mmHg for healthy subjects and those with BCO. A preventive and therapeutic attitude vis a vis BCO should take account of the relationship between nutrition and the respiratory system in parallel with a correction of hypoxaemia in order to avoid the development of wasting.
Rev Mal Respir 1988
PMID:[Malnutrition and chronic obstructive bronchopathies]. 314 Mar 15

Numerous studies have shown that longterm oxygen therapy in hypoxaemic patients with chronic airflow obstruction (BPCO) is capable of improving the prognosis and decreasing the risk of cardio-respiratory decompensation; in addition sometimes physical capacity and intellectual capacity is improved. Another result often noted is a reduction in the mean hospital stay which corresponds to an improvement in the quality of life. A PaO2 constantly below 55 mmHg (7.3 kPa) is defined by the majority of authors as a precarious state. At this level even a small change in alveolar ventilation or disturbance of distribution would lead to an important fall in the oxygen content of the arterial blood. The stability of the PaO2 during the weeks of respiratory reeducation with specially controlled medical treatment, as well as the willing consent of the patient and his family, are indispensable conditions for the prescription of OLT. When hypoxaemia is of moderate severity (PaO2 between 50 and 60 mmHg (6.6-8 kPa), prolonged medical treatment (with abstention from tobacco) for at least two months is advised and a study of complementary criteria to further validate the indications for oxygen. Such features would include a worsening of the hypoxaemia during exercise of 30 to 40 watts (PaO2 less than 50 mmHg, 6.6 kPa), an elevated haematocrit (greater than 55%), a rise of the P (A-a)O2 (greater than 30 mmHg or 4 kPa), a nocturnal desaturation even in the absence of apnoea (oxyhaemoglobin saturation (SaO2) of less than 80% for more than 50% of the time asleep). Added to these criteria are the radiological, echographic and clinical signs of the effect of hypoxaemia on the pulmonary circulation. Frank pulmonary arterial hypertension observed in hypoxaemia of moderate severity when the PaO2 is in the region of 55 mmHg and is an argument for the prescription of OLT. Amongst the developing criteria, exacerbations of respiratory encephalopathy, intellectual deterioration, progressive wasting, permanent ventilatory embarrassment with tachypnoea, should be borne in mind as the occasion arises. A schedule of 18 hours per day (without stopping for more than 3 hours) is necessary to obtain an improved survival and places a great demand on patient co-operation and on their environment. A prolonged educational programme is required. To achieve such a schedule the use of portable oxygen may be justified so that patients can lead a normal social life.(ABSTRACT TRUNCATED AT 400 WORDS)
Rev Mal Respir 1988
PMID:[Critical study of the indications for long-term oxygen therapy. Chronic obstructive bronchopneumopathies]. 314 Mar 16

The relationship between sodium homeostasis and the renin-angiotensin system was assessed through the use of two angiotensin-converting enzyme inhibitors (captopril and enalapril) in the rat. Treatment with captopril (group SQ) or enalapril (group MK) before and during a 6-day period of sodium free diet was associated with sodium wasting; on the sixth day of sodium restriction, sodium excretion was 164 +/- 17 and 144 +/- 10 mumol/24 h in SQ and MK group respectively. In addition, the cumulative Na+ excretion during the 6 day period of sodium-free diet was 1.04 +/- 0.07 mmoles in untreated rats and 1.70 +/- 0.13 and 1.86 +/- 0.14 mmoles in MK and SQ group respectively. At the end of the study, mean arterial pressure was lower in treated than in untreated animals. These findings show that in rats both renal and systemic adaptations to reduced sodium intake are markedly impaired by administration of converting enzyme inhibitors.
Arch Mal Coeur Vaiss 1984 Oct
PMID:[Renal adaptation to a restriction of sodium intake in the rat: effects of inhibition of the renin-angiotensin system]. 609 35

The LMNA gene encodes lamins A and C, components of the nuclear envelope. Its mutations cause a wide range of diseases named laminopathies involving either specific tissues in isolated fashion (cardiac and skeletal muscles, peripheral nerve, adipose tissue) or several tissues in a generalized way (premature ageing syndromes and related disorders). The striated muscle laminopathies include a variety of well clinically characterized disorders where cardiac muscle involvement represents the common feature that coexists with or without skeletal muscle disease. The cardiac disease of LMNA mutated patients is classically defined by conduction system and rhythm disturbances occurring early in the course of the disease, followed by dilated cardiomyopathy and heart failure. These features are life threatening and often responsible of cardiac sudden death. When associated, the skeletal muscle involvement is characterized by muscle weakness and wasting of variable topography with or without early joint contractures and spinal rigidity. Specific management of the cardiac disease to includes antiarrhythmic drugs, cardiac devices such as implantable cardioverter for primary and secondary prevention of sudden death, and heart transplantation at the end stage of heart failure. A large number of LMNA mutations leading to striated muscle laminopathies have been reported without so far any clear and definite phenotype/genotype relation. Finally, among the diverse hypotheses for pathomechanisms of LMNA mutations, the structural hypothesis suggesting a defective role of lamins A/C in maintaining the structural integrity of the nuclear envelope in striated muscles under constant mechanical stress is highly attractive to link the LMNA mutations and the cardiac disease.
Arch Mal Coeur Vaiss 2006 Sep
PMID:Heart involvement in lamin A/C related diseases. 1706 7