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García, F.R.; Martínez, R.J.G.; Camarasa, F.J.H.; Cerdá, J.C.M.; Messeguer, F.L.; Gallardo, M.L. Adults Supplemental Parenteral Nutrition at End of Life. Encyclopedia. Available online: https://encyclopedia.pub/entry/53763 (accessed on 02 May 2024).
García FR, Martínez RJG, Camarasa FJH, Cerdá JCM, Messeguer FL, Gallardo ML. Adults Supplemental Parenteral Nutrition at End of Life. Encyclopedia. Available at: https://encyclopedia.pub/entry/53763. Accessed May 02, 2024.
García, Francisco Rivas, Rafael Jesús Giménez Martínez, Felipe José Huertas Camarasa, Joan Carles March Cerdá, Fuensanta Lloris Messeguer, Margarita López-Viota Gallardo. "Adults Supplemental Parenteral Nutrition at End of Life" Encyclopedia, https://encyclopedia.pub/entry/53763 (accessed May 02, 2024).
García, F.R., Martínez, R.J.G., Camarasa, F.J.H., Cerdá, J.C.M., Messeguer, F.L., & Gallardo, M.L. (2024, January 11). Adults Supplemental Parenteral Nutrition at End of Life. In Encyclopedia. https://encyclopedia.pub/entry/53763
García, Francisco Rivas, et al. "Adults Supplemental Parenteral Nutrition at End of Life." Encyclopedia. Web. 11 January, 2024.
Adults Supplemental Parenteral Nutrition at End of Life
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This entry is adapted from the peer-reviewed paper 10.3390/ph17010065

“End of life” is a stage defined by the existence of an irreversible prognosis that ends with a person’s death. One of the aspects of interest regarding end of life focuses on parenteral nutrition, which is usually administered in order to avoid malnutrition and associated complications.

parenteral nutrition critical illness terminally ill parenteral nutrition solutions supplemental parenteral nutrition clinical nutrition nutritional support

1. Introduction

“End of life” (EL) is a process that will lead to death due to an illness and/or clinical circumstance with no possible therapeutic alternative. The approach to EL must guarantee physical and mental well-being, which palliative care offers, to reduce the symptoms caused by malnutrition such as edema, nausea, vomiting and reduced appetite. Parenteral nutrition (PN) must be included within the framework of such care as a support whereby hydration and nutrition are guaranteed in EL. PN has been characterized by a rapid technology and formulation evolution since its origin in 1968 in order to cover basic daily nutritional requirements [1][2]. PN is a nutritional strategy that consists of the administration of the nutrients required by the body through the circulatory system. Indications for use of PN include paralytic ileus, intestinal obstruction, short bowel syndrome, acute pancreatitis, intestinal fistulas, very severe previous malnutrition, ulcerative colitis, Crohn’s disease, severe preoperative malnutrition and major surgery. It is contraindicated when the expected intake is less than 5 days, when there is a functioning digestive system and a prognosis that will not improve with PN, and in uncontrolled metabolic alterations. The ultimate objective of PN is the maintenance of an adequate nutritional state, so all the necessary nutrients must be provided to the body in the appropriate proportion [3]. Depending on their nutritional contribution, these nutrients are classified into three large groups as caloric source, protein source and micronutrients. The first group is made up of carbohydrates and fats; the second group is administered through mixtures of amino acids and is quantified in grams of nitrogen; the third group is made up of minerals, trace elements and vitamins. Notwithstanding, PN involves a high financial cost and many complications, as follows.
(A)
Thrombotic complications: frequent in 50% of cases and arising from the catheter used, the duration of the procedure, the puncture site and/or the composition of the mixture.
(B)
Infectious complications: generated by contamination of the solution, infection of the catheter insertion point, primary contamination and secondary contamination of the catheter.
(C)
Metabolic complications: these are diverse and include hyperglycemia, hypoglycemia, hypertriglyceridemia, liver complications, dyslipidemia, bone problems, refeeding syndrome, hypophosphatemia, fat overload syndrome, essential fatty acid deficiency, hyperammonemia and metabolic acidosis [4][5].
The use of PN in EL must be assessed on a case-by-case basis for its impact on the quality of life of the patient. Even though there is controversy about the use of PN in EL since there are positions that justify its use and others that propose its withdrawal or non-establishment because it generates more complications than benefits, there is not enough evidence of the benefits, and the existing benefits are questionable and relate to earlier stages of EL [6].

2. Impact of Disease and Treatments on Nutritional Status at the End of Life

2.1. Nutritional Status and EL

EL is considered a critical status where nutritional support must be aimed at redirecting the metabolic state in order to avoid malnutrition that affects physical health, reduces quality of life and increases morbidity and mortality [7].
The malnutrition accompanying EL occurs mainly with loss of weight and muscle mass, i.e., sarcopenia, with or without loss of fat mass. Malnutrition and weight loss can lead to cachexia, which is a negative predictor of morbidity and mortality in terms of lower tolerance of treatments, higher rate of toxicity and prevalence of infections, worse quality of life and longer duration of hospitalization with increased financial costs [8][9]. Nevertheless, the overall malnutrition status causes a reduction in the capacity to mobilize bronchial secretions and intestinal flora, as well as interstitial edema, atrophy of epithelial cells of the digestive system, decreased ventilatory drive or damage of the cardiac muscles, delay in wound healing, or impairment of cellular and humoral immunity [10][11][12][13].
EL involves an increase in catabolic hormones (catecholamines, corticosteroids and glucagon), which—together with other humoral mediators (IL-1, IL-6, IL-8, TNF-α)—cause alterations in carbohydrate, lipid, and protein metabolism that in turn entails, among other metabolic effects, hypermetabolism, mobilization of energy substrates, blockage of hepatic ketogenesis, and hypercatabolism [14][15].
Hypercatabolism caused by cachexia derives mainly from a systematic inflammatory response that increases the body’s metabolic needs, decreases appetite, and drives catabolism of muscle proteins. Thus, patients with malnutrition exhibit an increase in inflammatory markers (IL6, CRP, β2 microglobulin) due to the presence of an inflammatory state that is associated with malnutrition and cachexia [16].
During EL, a metabolic response to stress is developed aiming to produce the energy required to sustain vital functions, inflammatory response, immune function and tissue repair. Two phases can be distinguished during metabolic stress: hypometabolism and the hypermetabolism phase, which temporally follows the earlier phase [17].
Below are the main metabolic characteristics of EL and their relationship with nutritional status. This outline assumed that EL corresponds to a critical state as addressed by the existing scientific literature.
(a)
Carbohydrate Metabolism. Several events to be considered take place, as follows.
  • High catabolism without an excessive increase in energy expenditure. There is an increase in hepatic gluconeogenesis (the substrates used in gluconeogenesis include lactate, alanine and glycerol) and peripheral resistance to the action of insulin, despite the existence of high levels of circulating insulin. These metabolic alterations result in hyperglycemia, which inhibits hepatic glucose production and stimulates its peripheral uptake in order to reduce blood glucose levels [18].
    The high amount of gluconeogenic substrates and the increase in counterregulatory hormones (epinephrine, cortisol and insulin), together with the action of inflammatory mediators, are determining factors for the increase in hepatic glucose production [18][19].
  • Inflammatory mediators (TNF-α and interleukins) antagonize the action of insulin and produce hyperglycemia. Hyperglycemia is common in critically ill patients, even in those patients who have not previously been diagnosed with diabetes. The development of hyperglycemia during EL increases morbidity and mortality, as well as hospital stay days and mechanical ventilation days [20].
  • Hyperlactatemia. Pyruvate and lactate plasma levels are very high during EL. This phenomenon results in a greater conversion of pyruvate to lactate and is more intense at the muscle than at the hepatic level. In this sense, severe hyperlactatemia is associated with extremely high mortality in the intensive care unit (ICU), hence the importance of knowing the variables derived from lactate (timing and persistence of severe hyperlactatemia, maximum level and 12 h clearance) that are associated with mortality [21].
(b)
Protein metabolism
Protein metabolism is quite complex in these circumstances, since on the one hand, there is an increase in protein catabolism, and on the other, a decrease in protein synthesis, both in total and visceral proteins. However, hepatic uptake of amino acids and protein synthesis is increased. Numerous events take place and include the following.
  • Activation of gluconeogenesis to mobilize proteins. There is a massive mobilization of body nitrogen and an increase in protein catabolism, which is evidenced by increased excretion of urinary nitrogen [22].
  • Hypoalbuminemia. The majority of critically ill patients exhibit an inflammatory response that causes endothelial damage and increased capillary permeability, with the ensuing extravasation of fluids and albumin. Hypoalbuminemia represents a marker of increased vascular permeability rather than a marker of albumin itself that is associated with the appearance of edema. In EL, hepatic albumin synthesis would decrease, and both TNF and IL-6 would contribute to this process. Hypoalbuminemia can lead to unnecessary administration of albumin or excessive administration of macronutrients in nutritional regimens, generating possible adverse effects and additional costs, and hence the importance of adequate assessment [23].
  • Excessive catabolism of body proteins that affect skeletal muscle, visceral proteins of connective tissue and circulating proteins. Nutritional support is essential in critically ill patients, and thus great caution must be exercised during the catabolic phase. The use of hypercaloric and hyperprotein nutrition is justified in situations involving marasmus, COPD, respiratory distress syndrome, sepsis with hemodynamic instability, hypercapnia, hyperglycemia and hypertriglyceridemia [24].
  • Reduction in amino acid metabolism. It is necessary for nutritional support to maintain adequate metabolic pathways without causing redistributions that compromise the functionality and structure of the organs. The importance of protein intake has been observed in EL patients, resulting in reduction in infectious complications, hospital stay, morbidity associated with energy excess, and in turn reduced mortality in cases of sepsis [25].
(c)
Lipid metabolism
Modifications in lipid metabolism are related to the metabolic stress phase. The increase in lipolysis and mobilization of fats causes triglycerides to be released, which are hydrolyzed to free fatty acids and glycerol. Free fatty acids can follow different metabolic pathways, such as: (a) oxidation in skeletal muscle; (b) oxidation in the liver, promoting gluconeogenesis by providing energy and cofactors necessary for glucose synthesis; (c) reesterification in the liver towards triglycerides, resulting in an increase in triglycerides plasma levels. In the event of carnitine deficiency, either prior or acquired, this condition can worsen. Hyperinsulinism, where insulin decreases hepatic ketone production, increases peripheral utilization of fatty acids. This is compounded with a deficiency of long-chain fatty acids, which can lead to an increase in the metabolism of arachidonic acid and appearance of its metabolites with inflammatory properties (prostaglandins and thromboxanes) [26][27][28].
Taking into consideration EL, nutritional support would attenuate metabolic stress, reduce the inflammatory response and avoid malnutrition. Indeed, the use of supplements with immunomodulatory function (Glu, Arg, nucleotides, w-3 and its metabolites and L-carnitine) has shown effectiveness in reducing oxidative damage and a decrease in the metabolic response to stress, although further studies are needed since there are no conclusive data on a reduction in mortality and prevention of PN complications [29][30][31].

2.2. Interaction between Nutritional Status and Drugs in PN

As various studies have shown, the treatment of EL causes a deterioration in nutritional status with a decrease in appetite and weight (topiramate, zonisamide, zidovudine, bupropion, fluoxetine, paroxetine, digoxin and digitoxin), as well as alteration of the intestinal microbiota (metformin, brivudine, levodopa and proton-pump inhibitors) [32][33] (Table 1). Therefore, malnutrition can be present in PN if the formula requirements are not administered correctly [7]. Further, some medications have been found to affect micronutrients with diuretics and steroids affecting the absorption of sodium and potassium, while amphotericin B and calcium affect the absorption of magnesium and phosphorus, respectively [34].
Table 1. Nutritional status and drugs.

Drugs

Alterations

Topiramate, zonisamide, zidovudine, bupropion, fluoxetine, paroxetine, digoxin, digitoxin

Decrease in appetite and weight

Metformin, brivudine, levodopa and proton-pump inhibitors

Intestinal dysbiosis
It is also worth noting that nutritional status can be affected by pharmacokinetic interactions between nutrients and drugs, which can affect the bioavailability of the nutrient, as well as reduction in the therapeutic action of the drug [32][33].
Pharmacokinetic interactions between drugs and nutrients in PN are the most significant and are limited to the distribution, metabolism and excretion processes of drugs [34]. Thus, an effect of nutrients on the distribution of L-dopa, melphalan, valproic acid, phenytoin, tetracyclines, midazolam, gentamicin and amikacin has been observed, while methotrexate, fluorouracil, lidocaine and theophylline interact during the nutrient metabolism phase [32] (Table 2). Genesis of metabolites from metabolism is to be noted, such as oxalate from the metabolism of ascorbic acid that can interact with calcium and generate insoluble precipitates [34]. A widely debated aspect in the field of nutrient–drug interactions is the influence of amino acid intake on kidney function. Thus, proteins in combination with certain vitamins would affect the metabolism of drugs, causing a delay in their excretion [34].
Table 2. Pharmacokinetic interactions between drugs and nutrients in PN.

Nutrients

Drugs

Pharmacokinetic Phase Interaction

Calcium, magnesium, sodium, vitamins (A, D, E, K).

L-dopa, melphalan, valproic acid, phenytoin, tetracyclines, midazolam, gentamicin, amikacin

Distribution, metabolism, excretion

Vitamin B12, calcium, sodium, protein, vitamin D.

Methotrexate, fluorouracil, lidocaine

theophylline

Metabolism
Even though the addition of drugs in PN is not recommended, for any such addition to take place, absence of risk to the preparation such as degradation and/or destabilization of the lipid emulsion is to be ruled out. It should be noted that combinations of two or more drugs should not be administered in a PN bag and so Y-administration is used, which is nonetheless not free of interactions either. Notwithstanding, there are studies and clinical practice guidelines that have described possible interactions with PN in order to provide recommendations to optimize the PN that is administered [33][34][35].
Therefore, for adequate assessment of the stability and compatibility of the PN concerned with the therapeutic treatment, it is necessary to consider the concentration of amino acids, the type of fat that is part of the parenteral emulsion, the concentration of electrolytes, the concentration of amino acids and dextrose, trace elements, pH, Pka and the acid–base nature of the drugs. In this regard, there are numerous known physical interactions vis-à-vis interactions of a chemical nature that must be further explored and researched. The American Society for Parenteral and Enteral Nutrition (ASPEN) recommends consultation of existing data on physicochemical compatibility and aspects related to therapeutic action prior to preparation of PN [33][34][36].
How can interactions that could worsen the state of malnutrition in EL and/or decrease the therapeutic action of drugs be avoided? The following course of action is proposed.
-
Risk assessment through knowledge of all the drugs that the patient is given.
-
Monitoring of pharmacological treatment.
-
Avoid inappropriate PN mixtures, which will require following the relevant clinical guidelines to avoid PN safety issues.
-
Assess the treatment and establish appropriate changes. Establish possible changes in treatment to avoid known interactions that may arise.
-
Adapt PN to the administration of drugs according to the patient’s needs.
Malnutrition derived from EL and therapeutic treatment has direct effects on clinical outcomes and is associated with significant spending on medical care, so better identification and treatment of the factors involved in malnutrition related to EL would entail a benefit for people and a potential reduction in health costs [33][34].

3. The Role of Parenteral Nutrition at the End of Life: Benefit or Harm?

Nutritional support is an essential part of patient care in EL when oral food intake is not possible. This support includes enteral nutrition (EN) and PN, the use of which will depend on the clinical indications in accordance with the patient’s condition.
Hydration and nutrition are culturally understood as symbols of care for life. Anthropologically, food is related to a basic vital need of people since birth, and it is attributed a meaning of respect for life and care for our fellow human beings. There are positions in favor of considering PN basic care that cannot be waived, and other positions that define it as a basic treatment that can in fact be waived [35][36].
Scientific literature describes a series of benefits associated with an adequate nutritional status in EL (Figure 1): (a) modification of the body’s response to the aggression of inflammatory cytokines; (b) reduced malnutrition associated with hypermetabolism; (c) reduced mortality and length of hospital stay; (d) control of adverse effects of polypharmacy; (e) maintenance of muscle mass; (f) preservation of the integrity of intestinal microbiota; (g) improvement in immune function; (h) attenuation of the inflammatory response; (i) reduced vomiting; (j) improved prognosis of patients in the ICU and reduced stay [37][38][39][40]. However, other studies attribute PN a symbolic value and no significant differences with other life support techniques, which, like any other technique, can sometimes be harmful, since they are considered invasive measures that prolong agony, cause refeeding syndrome, do not reduce mortality or shorten the length of hospital stay and give rise to accumulation of fluids such as bronchial secretions, pleural effusion, infections, edema and ascites [41][42][43][44].
Figure 1. Benefits associated with an adequate nutritional status in EL.
Given these conflicting positions on PN, as well as its imprecise and undefined action protocol under clinical practice guidelines, both the ASPEN and the European Society of Parenteral and Enteral Nutrition (ESPEN) recommend withdrawing and/or not instituting PN if the results are doubtful and do not produce any physical and/or psychological benefit, there is a neurodegenerative pathology, life prognosis is less than 3 days, or for uncontrolled refractory symptoms and multiple organ failure [45][46]. However, it is necessary to continue delving into this field since there are significant gaps to fill and regulate in procedures beyond the individualized approach to each case.

4. Supplements of Interest for Parenteral Nutrition Formulations

Nutritional requirements of PN in EL must be established according to the clinical situation, nutritional status, symptomatology of EL, existence of organ failure and the state of hypermetabolism. Therefore, in general, PN will include the following.
-
Carbohydrates. Carbohydrates constitute the main source of energy. An intake of 4–5 g/kg weight/day is required. Any of the following can be used: (a) glucose solutions that determine osmolarity of the solution and can be used in anhydrous or monohydrate glucose format. Glucose is the preferred carbohydrate due to its usefulness and low cost. It is necessary to ensure that osmolarity does not exceed 1000 Osm/L; (b) glycerol solutions are used mainly in situations where a lower insulin response is desired or there is hyperglycemia due to stress that is difficult to control and thus a glucose substitute is needed. It should be monitored in lipid emulsions that use glycerol since an excess in the formulation can give rise to hemolysis issues; (c) polyols are the least used due to the controversies generated by possible mixture with glucose, fructose, xylitol, sorbitol or glycerol and the relationship with lactic acidosis processes [47].
-
Amino acids. Essential and non-essential amino acids are used in the form of commercial crystalline amino acid solutions. Daily protein requirements will depend on the degree of metabolic stress and may range between 1 and 2 g/kg weight/day. As to the administration of amino acids, some are usually used as precursors to increase solubility in the parenteral solution, such as tyrosine and cysteine, and others are administered as dipeptides (glutamine, tyrosine) to improve stability and solubility of the formula. Use of branched-chain amino acids in PN has been noted to give rise to controversy since there is lack of consensus on their use as an energy substrate, as well as to increase protein synthesis and turnover. Notwithstanding, in severe cases, the amino acids administered must be modified to adequately control those aspects that may cause an increase in aromatic Aa and alteration of mental status [48].
-
Lipids. Lipids are responsible for the reduction in osmolarity of the mixture. The contribution of lipids in the form of an O/W emulsion has an energy supply function and a potential positive modulation of the inflammatory response, which is why 1.5–2.5 g/kg weight/day is required. Lipids are incorporated into PN through the administration of essential fatty acids in the form of triglycerides. Fatty acids can be either long chain (from soybean, safflower or sunflower oil), which tend to be more unstable and easily subject to lipid peroxidation, or 50% long- and short-chain mixtures that have shown to be more stable, with fewer liver complications and better nitrogen balance. Also, it has been observed that in these emulsions, tocopherols are transported with fats (affording protection against cellular oxidative damage) and vitamin K (compatible with olive or soy oil). Lipids are used in the form of a lipid emulsion, and emulsifiers (egg lecithin), isotonizers (glycerol) and stabilizers (sodium oleate) are used for stabilization so that the lipid droplets formed are similar to human chylomicrons, but with different types of fatty acids, less cholesterol, no apoproteins and more phospholipids. Intralipid© (soybean oil), Nutralipid© (80% olive oil and 20% soybean oil), Clinolipid© (80% olive oil, 20% soybean oil), SOLE© (soybean oil), SMO Lipid© (olive oil, fish oil, soybean and medium-chain triglycerides) and Omegaven© (fish oil) are among the most common commercial lipid emulsions. In critical situations, different effects in reduction of sepsis and the ratio of T helper and T suppressor lymphocytes have been observed for SOLE©, as well as in the increase in albumin, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) for mixtures of long/short-chain triglycerides [1][49].
-
Electrolytes. Basal parenteral electrolyte requirements are 1–2 mEq/kg/day of sodium and potassium, 10–15 mEq/day of calcium, 8–20 mEq/day of magnesium, 20–40 mmol/day of phosphate and chlorine and acetate necessary to maintain an acid–base balance. However, the particular EL situation must be assessed, as well as losses that may occur, in order to determine specific daily requirements. Isolated electrolyte preparations comprising sodium, potassium, calcium, chloride, magnesium and phosphorus are used [50].
-
Vitamins. Fat-soluble vitamins (A, D, E, K) and water-soluble vitamins (B1, B2, B6, B9, B12) are included. It is common to have to add supplements based on the recommended needs and requirements of each terminally ill patient [47].
-
Trace elements. This group includes copper, cobalt, chromium, fluorine, iodine, manganese, molybdenum, nickel, selenium and zinc. Trace element deficiency is associated with various functional and structural abnormalities as they play an important role as enzymatic cofactors. Currently, it is not possible to individualize the prescription of trace elements, but preparations of trace elements already exist [47].
-
Drugs. The addition of drugs to PN should be avoided whenever possible. However, there are cases in which such addition can be very useful, but drugs can only be added to the bag as long as they do not degrade or destabilize the lipid emulsion and the pharmacokinetics are adequate during administration. In this sense, some of the most commonly used drugs in PN include the following: (a) insulin, which may be necessary in situations of hyperglycemia in patients with preexisting diabetes or in hyperglycemia due to stress; (b) H2 antihistamines (ranitidine and famotidine), which tend to be more stable if the PN includes lipids; (c) octreotide and somatostatin, with stability reduced to 24–48 h in the parenteral formulation bag and longer periods leading to adherence to the bag and, consequently, decreased bioavailability; (d) heparin, the addition of which to PN generates controversy since—even though the risk of thrombophlebitis is reduced in people undergoing PN—the interaction that can develop between the negative and positive charges of heparin and calcium from the fat droplets can lead to destabilization and separation of the phases of the emulsion that constitutes the PN, and this needs to be monitored. The fact that the administration of two or more drugs with PN should be avoided should not be ignored [51].
-
Water. Sterile water is used for injectables, adding just enough to obtain the right volume of the final mixture. A daily amount of water of 30–40 mL/kg weight/day is required [47].
However, SPN involves the addition of nutrients, in standard or individualized formulations, according to the needs of patients and is defined as nutritional support that can be administered when, after individualized patient assessment, the energy and protein intake cannot be covered by PN to guarantee daily requirements [52].
Thus, in EL, SPN would be useful when, after monitoring and assessing the patient, the following is determined: (a) objectives are not achieved with PN and there are increased nutrient requirements; (b) there are nutrient losses; (c) problems arise in absorption and use of nutrients, together with insufficient caloric protein intake; (d) drug–nutrient interactions; (e) hemodynamic instability; (f) hypermetabolism; (g) prolonged use of vasopressor and inotropic medication; (h) intestinal ischemia and high abdominal pressure; and (i) malabsorption. Notwithstanding, SPN must be monitored, as it can cause hyperglycemia, liver dysfunction, and respiratory problems that require the use of mechanical ventilation. It should be noted that SPN is not recommended in the 48 h preceding death [53].
At present, there are no conclusive studies on the use of SPN and its usefulness in EL. Certain studies associate SPN with a decrease in mortality and the risk of infections, while others show that SPN does not reduce the length of stay in the ICU or provide benefits in people who have a low risk of malnutrition [54].

5. Compatibility and Stability of Nutrients in Parenteral Nutrition of Interest for SPN

Relevance of compatibility and stability, which are two different aspects in PN, are to be noted. Stability refers to possible physical, chemical or microbiological degradation, while compatibility comprises everything related to loss of the properties of the parenteral formulation, both in terms of nutrients and the possible toxicity that may be generated. Consequently, the requirements of PN stability and compatibility must persist over time from preparation to administration to guarantee its safety and effectiveness [55]. There are diverse factors that affect the compatibility and stability of PN that are also applicable to SPN.

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Subjects: Critical Care Medicine
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Francisco Rivas García
,
Rafael Jesús Giménez Martínez
,
Felipe José Huertas Camarasa
,
Joan Carles March Cerdá
,
Fuensanta Lloris Messeguer
,
Margarita López-Viota Gallardo
View Times: 159
Revisions: 4 times (View History)
Update Date: 20 Feb 2024
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