Increase In Extracellular Fluid Volume Research Articles

Comparison of Serum C-reactive Protein, Parathyroid Hormone, and Calcitonin Levels between Pregnant and Non Pregnant Women from Rural North Gujarat: A Case-control Study

Introduction: Pregnancy requires women to provide calcium to foetus in amounts that may exceed their daily intake. C-reactive protein (CRP) is a susceptible marker of systemic inflammation. Parathyroid hormone (PTH) regulates foeto-placental mineral homeostasis and skeletal development and stimulates placental calcium transfer. The increase in calcitonin and calcitriol levels are significant in the transport of maternal calcium to the fetus and in the anticipation, and revival of maternal bone loss. These changes have direct implications on calcium metabolism and cause decreased albumin level, inflammation, increase in extracellular fluid volume, increase in renal function, and placental calcium transfer. Aim: To assess the serum levels of CRP, calcitonin, and PTH in the first, second, and third trimester of pregnancy and also to compare these parameters with non pregnant women. Materials and Methods: The present case-control study was conducted in the Department of Biochemistry of Nootan Medical College and Research Centre, Visnagar, Gujarat, from June 2021 to October 2021. A total of 150 subjects (75 age-and sex-matched apparently healthy well-nourished non pregnant females, and 75 pregnant females) were included. CRP, PTH, and calcitonin were measured. Statistical analysis was performed using Independent t-test, and Pearson’s correlation coefficient (r). Results: Mean age of participants in case group was 32.16±10.97 (mean±SD). The mean age of control was 30.54±6.63. Serum CRP level of cases was significantly higher 3.2±2.2 than the level in controls 2.3±1.8 (p=0.003). Serum PTH level of cases 31.6±10.4 was significantly lower (p=0.0012) than the level in controls 45.9±9.8. Serum calcitonin level of cases 281±143 was significantly higher (p<0.001) than the level in controls 103±46. Conclusion: There was a significant increase in serum CRP level and serum calcitonin level in cases as compared with controls while there is decrease in serum PTH levels between these two groups.

Delirium in Acute Poisoning with 1,4-Butanediol and Its Correction

Delirium complicating regular use of psychoactive substances remains one of the major issues of critical care, toxicology, and psychiatry. However, the pathogenetic mechanisms of delirium development in patients with 1,4-butanediol poisoning have been poorly studied until now.The aim of the study was to reveal specific patterns of delirium in patients with 1,4-butanediol poisoning as well as to study the changes in systemic hemodynamic parameters, respiratory function, and body fluid compartments during the treatment.Material and methods. The study was prospective and treatment-randomized. Forty-eight male patients aged 20 to 45 years with delirium and acute 1,4-butanediol poisoning were enrolled. Of them, 24 patients were administered with succinate-containing drug 40 ml daily, 24 patients received standard treatment without antihypoxic agents. We studied the evolution of delirium, changes in anaerobic metabolism parameters, systemic hemodynamics, respiratory function, and the volume of fluid compartments. Impedance measurement method adjusted for interference was used in the study.Results. At the «peak» of delirium (days 1–3), the hyperdynamic circulation, increased systemic arterial tone, stroke output, respiratory function parameters, and metabolic lactate acidosis were recorded. A decrease in total fluid volume and extracellular fluid volume was clearly observed during day 1 of intoxication delirium along with increased permeability of cell membranes. On day 3 of delirium, a decrease in intracellular fluid volume and increase in extracellular fluid volume were noted. After the cytoflavin administration, shorter delirium duration (7.5 [6; 8] days), more rapid correction of lactate acidosis, stabilization of respiratory parameters and stabilization of cell membrane permeability by day 5 were found. In the control group, delirium persisted for up to 14 [11; 15] days (z=-5.9; P=0.00011) with more frequent development of complications such as nosocomial pneumonia (χ2=8.4, P<0.001).Conclusion. The severity of delirium in acute poisoning with 1,4-butanediol was associated with metabolic lactate acidosis, changes in systemic hemodynamics and pulmonary function. A positive effect of adjunctive antihypoxic therapy with succinate-containing agent on cardio-respiratory parameters, cell membrane permeability, water balance due to elimination of tissue hypoxia and prompt switching to tissue aerobic metabolism has been found.

Role of spironolactone in patients with resistant hypertension

Treatment-resistant hypertension (RH) is defined as uncontrolled blood pressure (BP) despite use of at least three different antihypertensive agents (including angiotensin-converting enzyme inhibitor or angiotensin receptor blocker, calcium channel blocker, and a diuretic) at their optimal doses. It is important to properly diagnose and treat RH because patients are at high risk of end-organ damage. Activated renin-angiotensin-aldosterone system, increased renal sympathetic nervous system activity (increase sodium and water reabsorption and thus increase in extracellular fluid volume), and increased arterial stiffness become the main reason for hypertension. Therefore, a controlled BP can be achieved by the use of mineralocorticoid receptor blockers as add-on treatment to the first-line triple-drug combination therapy. In this review, we provide evidences from various studies comparing spironolactone treatment with other comparators (diuretics or other mineralocorticoid receptor blockers) or placebo signifying spironolactone is beneficial for controlling BP in patients with RH. Furthermore, there is a greater need to increase the use of mineralocorticoid receptor blocker, spironolactone, as fourth-line medication add-on to three drug therapy in patients with RH.

Dapagliflozin effects on haematocrit, red blood cell count and reticulocytes in insulin-treated patients with type 2 diabetes

Recent studies have shown that high-risk patients with type 2 diabetes mellitus (T2DM) treated with sodium glucose cotransporter 2 (SGLT2) inhibitors have improved cardiovascular (CV) outcomes. In an exploratory analysis of data from the EMPA-REG study, elevations in haematocrit were shown to be strongly associated with beneficial CV effects. As insulin treatment has been shown to be antinatriuretic, with an associated increase in extracellular fluid volume, it is important to confirm whether haematocrit increase is maintained with concomitant insulin therapy. Here, we investigate the effect of the SGLT2 inhibitor dapagliflozin on haematocrit, red blood cell (RBC) counts and reticulocyte levels in high-risk patients with T2DM receiving insulin. A 24-week, double-blinded, randomised, placebo-controlled trial (ClinicalTrials.gov: NCT00673231) was reported previously with extension periods of 24 and 56 weeks (total of 104 weeks). Patients receiving insulin were randomised 1:1:1:1 to placebo or dapagliflozin at 2.5, 5 or 10 mg. Haematocrit, RBC and reticulocyte measurements were conducted during this study, and a longitudinal repeated-measures analysis was performed here to examine change from baseline during treatment. Dapagliflozin treatment in combination with insulin resulted in a dose-dependent increase in haematocrit levels and RBCs over a 104 week period. There was a short-term increase in reticulocyte levels at the start of treatment, which dropped to below baseline after 8 weeks. SGLT2 inhibition with dapagliflozin leads to a sustained increase in haematocrit in patients receiving chronic insulin treatment.

SALT-SENSITIVE BLOOD PRESSURE RISE IN TYPE 1 DIABETES IS ACCOMPANIED BY INCAPACITY FOR VASODILATION – A RANDOMIZED EXPERIMENTAL CROSS-OVER STUDY

Objective: Diabetes mellitus type 1 (DM1) is suggested to be associated with salt sensitivity. However, strong evidence to support this is scarce, and the pathophysiology is not known. For a long time, the volume-regulating function of the kidney was thought to be the only important factor in salt-sensitive hypertension. Due to insufficient sodium excretion by the kidney, sodium excess was considered to increase extracellular fluid volume (ECFV) and cardiac output (CO), resulting in a blood pressure (BP) rise. However, recent publications put forward that systemic vascular resistance (SVR) might be central in BP regulation. We hypothesized that in salt-sensitive hypertension in DM1, vasodysfunction rather than increases in ECFV and CO plays a role.Design and method: We included 8 DM1 patients and 12 age-matched healthy controls (HC), with normal BP, body mass index, and kidney function. All subjects adhered to an 8-day low salt diet (LSD) and an 8-day high salt diet (HSD), in randomized order. After each diet, hemodynamic measurements included BP (Omron) and CO (Nexfin™), and SVR was calculated accordingly. To assess volume-dependent changes, ECFV, interstitial fluid volume (IFV) and plasma volume (PV) were calculated by the use of iohexol and 125I-albumin distribution. HC were divided in two subgroups: those with versus those without a BP increase after HSD. Results: After HSD, patients with DM1 showed a BP increase (mean arterial pressure HSD vs LSD (85 (5) mmHg vs. 80 (3) mmHg; P = 0.03) while BP in HC did not rise (78 (5) mmHg vs. 78 (5) mmHg; P = 0.85). The difference in BP response was not accompanied by differences in urinary sodium excretion between the DM1 patients and HC (Figure 1) nor by differences in CO, ECFV or ICF (Table 1). HC without a BP increase after HSD (n = 5) showed a SVR reduction after HSD, while this reduction was not present in the HC with a BP increase after HSD (n = 7) or in the DM1 patients (Figure 2, Table 1). Conclusions: DM1 is associated with increased salt sensitivity compared to HC, coinciding with incapacity for vasodilation.

Approach to Hyponatremia in Cirrhosis.

The patient in the case presented with hypervolemic hyponatremia associated with ascites and edema. The sNa concentration of 120 mmol/L is bordering severe hyponatremia and is associated with renal insufficiency. The management of this patient includes free water restriction, holding diuretics, and consideration of albumin infusion (Fig. ​(Fig.1).1). Tolvaptan is not recommended in patients with liver disease. Furthermore, hyponatremia and renal dysfunction are associated with poor prognosis. If the hyponatremia is persistent, liver transplant evaluation should be considered. Open in a separate window Figure 1 Algorithm depicting suggested management of hyponatremia in the patient with cirrhosis.

Gastrorenal communication: sniffing and tasting.

A video slideshow introduction to the Symposium by organiser Pedro A. Jose can be found here.

Salt and sugar: their effects on blood pressure.

Both dietary salt and sugar are related to blood pressure (BP). The evidence for salt is much stronger, and various types of studies have consistently shown that salt is a major cause of raised BP, and a reduction from the current intake of ≈ 9-12 g/day in most countries of the world to the recommended level of 5-6 g/day lowers BP in both hypertensive and normotensive individuals, in men and women, in all age groups and in all ethnic groups. Countries such as Finland and the UK that have successfully reduced salt intake have demonstrated a reduction in population BP and cardiovascular mortality, with major cost savings to the health service. The mechanisms whereby salt raises BP are not fully understood. The traditional concepts focus on the tendency for an increase in extracellular fluid volume. Increasing evidence suggests that small increases in plasma sodium may play an important role. There are several other factors that also increase BP, one of which is added sugars. The current high intake of added sugars increases obesity which, in turn, raises BP. Recent studies also suggest that added sugars, particularly those in soft drinks, may have a direct effect on BP. However, the relationship between soft drink consumption and BP could be, at least partially, mediated by the effect of salt intake on increasing soft drink consumption. Actions to reduce salt and sugar intake across the whole population will have major beneficial effects on health along with major cost savings.

Role of the Kidneys in Resistant Hypertension

Resistant hypertension is a failure to achieve goal BP (<140/90 mm Hg for the overall population and <130/80 mm Hg for those with diabetes mellitus or chronic kidney disease) in a patient who adheres to maximum tolerated doses of 3 antihypertensive drugs including a diuretic. The kidneys play a critical role in long-term regulation of blood pressure. Blunted pressure natriuresis, with resultant increase in extracellular fluid volume, is an important cause of resistant hypertension. Activation of the renin-angiotensin-aldosterone system, increased renal sympathetic nervous system activity and increased sodium reabsorption are important renal mechanisms. Successful treatment requires identification and reversal of lifestyle factors or drugs contributing to treatment resistance, diagnosis and appropriate treatment of secondary causes of hypertension, use of effective multidrug regimens and optimization of diuretic therapy. Since inappropriate renal salt retention underlies most cases of drug-resistant hypertension, the therapeutic focus should be on improving salt depleting therapy by assessing and, if necessary, reducing dietary salt intake, optimizing diuretic therapy, and adding a mineralocorticoid antagonist if there are no contraindications.

Effects of acute dilutional hyponatremia on acid-base changes and electrolyte concentrations in rats with bilateral renal pedicle ligation

To describe the effects of increasing the extracellular fluid (ECF) volume by approximately 20% on acid-base changes and electrolyte concentrations in anesthetized rats. 18 adult male Sprague-Dawley rats. Rats were assigned to a control group (n = 6 rats) and a treatment group (12). All rats were anesthetized, and instrumentation and bilateral renal pedicle ligation were performed. The treatment group was infused IV with sterile water throughout a 30-minute period. Acid-base variables and concentrations of electrolytes, lactate, albumin, phosphorus, and hemoglobin were measured before (baseline) and 30 and 60 minutes after onset of infusion. Anion gap, strong ion difference, strong ion gap, and contributions of sodium, chloride, albumin, phosphorus, and lactate concentrations to base excess were calculated at each time point. Infusion of sterile water led to an increase in ECF volume of approximately 18%. This had no effect on acid-base balance, compared with that in control rats. Infusion of sterile water caused a significant decrease in sodium, chloride, ionized calcium, lactate, and albumin concentrations, compared with concentrations in the control group. Anion gap and calculated effects of sodium, chloride, albumin, and lactate concentrations on base excess at 60 minutes differed significantly between infused and control rats. Infusion of sterile water did not cause clinically relevant dilutional acidosis. The acidotic impact of water administration was offset by generation of new bicarbonate via carbonic acid equilibration and intracellular buffering in combination with the alkalotic effects of decreases in albumin, phosphorus, and lactate concentrations.

Hiponatremia en la cirrosis hepática: patogenia y tratamiento

Hyponatremia is the most common electrolyte disorder in patients with cirrhosis. This disorder can be a result of substantial loss of extracellular fluid “hypotonic or hypovolemic hyponatremia” or develop in the context of an increase in extracellular fluid volume and in the absence of major sodium losses; this situation occurs in patients with advanced cirrhosis and is known as “dilutional or hypervolemic hyponatremia”. In dilutional or hypervolemic hyponatremia, serum sodium concentration is reduced, plasma volume is increased (although the effective plasma volume is decreased due to marked arterial vasodilation in the splanchnic circulation) and extracellular fluid volume is increased, with ascites and edema in the absence of signs of dehydration. This is a result of the marked deterioration in renal excretion of solute-free water, leading to disproportionate water retention in relation to sodium retention. Hypotonic hyponatremia represents 10% of all hyponatremias in patients with cirrhosis. Since hypervolemic hyponatremia is by far the most frequent form of this disorder, the present chapter will concentrate specifically on hypervolemic hyponatremia in cirrhosis.

Aldosterone Modulates Steroid Receptor Binding to the Endothelin-1 Gene (edn1)

Aldosterone and endothelin-1 (ET-1) act on collecting duct cells of the kidney and are important regulators of renal sodium transport and cardiovascular physiology. We recently identified the ET-1 gene (edn1) as a novel aldosterone-induced transcript. However, aldosterone action on edn1 has not been characterized at the present time. In this report, we show that aldosterone stimulated edn1 mRNA in acutely isolated rat inner medullary collecting duct cells ex vivo and ET-1 peptide in rat inner medulla in vivo. Aldosterone induction of edn1 mRNA occurred in cortical, outer medullary, and inner medullary collecting duct cells in vitro. Inspection of the edn1 promoter revealed two putative hormone response elements. Levels of heterogeneous nuclear RNA synthesis demonstrated that edn1 mRNA stimulation occurred at the level of transcription. RNA knockdowns corroborated pharmacological studies and demonstrated both mineralocorticoid receptor and glucocorticoid receptor participated in this response. Aldosterone resulted in dose-dependent nuclear translocation and binding of mineralocorticoid receptor and glucocorticoid receptor to the edn1 hormone response elements. Hormone receptors mediated the association of chromatin remodeling complexes, histone modification, and RNA polymerase II at the edn1 promoter. Direct interaction between aldosterone and ET-1 has important implications for renal and cardiovascular function.

Discovery of (2R)-2-(3-{3-[(4-Methoxyphenyl)carbonyl]-2-methyl-6-(trifluoromethoxy)-1H-indol-1-yl}phenoxy)butanoic Acid (MK-0533): A Novel Selective Peroxisome Proliferator-Activated Receptor γ Modulator for the Treatment of Type 2 Diabetes Mellitus with a Reduced Potential to Increase Plasma and Extracellular Fluid Volume

Peroxisome proliferator-activated receptor gamma (PPARgamma) agonists are used to treat type 2 diabetes mellitus (T2DM). Widespread use of PPARgamma agonists has been prevented due to adverse effects including weight gain, edema, and increased risk of congestive heart failure. Selective PPARgamma modulators (SPPARgammaMs) have been identified that have antidiabetic efficacy and reduced toxicity in preclinical species. In comparison with PPARgamma full agonists, SPPARgammaM 6 (MK0533) displayed diminished maximal activity (partial agonism) in cell-based transcription activation assays and attenuated gene signatures in adipose tissue. Compound 6 exhibited comparable efficacy to rosiglitazone and pioglitazone in vivo. However, with regard to the induction of untoward events, 6 displayed no cardiac hypertrophy, attenuated increases in brown adipose tissue, minimal increases in plasma volume, and no increases in extracellular fluid volume in vivo. Further investigation of 6 is warranted to determine if the improvement in mechanism-based side effects observed in preclinical species will be recapitulated in humans.

Modelling volume‐loading hypertension with Guyton's model: role of whole body blood flow autoregulation

Computer simulations offer a unique way to test the role of whole body blood flow autoregulation (WBFAR) in the pathogenesis of volume‐loading hypertension since it is not possible to block WBFAR experimentally. Using Guyton's large circulatory model, we analyzed, in the presence or absence of WBFAR, the hemodynamic and fluid volume changes in three classical models of volume‐loading hypertension. In the first model, hypertension was induced by reducing renal mass to 30% of normal and increasing salt intake by 6‐fold. In the presence of WBFAR, the development of hypertension (+30 mmHg) was characterized by an initial increase in cardiac output (CO) by ~30% followed by a secondary increase in vascular resistance (+25%). In the absence of WBFAR, there was a similar long‐term increase in blood pressure (BP). However, a nearly 2‐fold increase in CO and an increase in extracellular fluid volume by more than 30% were observed whereas vascular resistance decreased by 30% owing to the mechanical distension of blood vessels by the increased BP. Qualitatively similar results were obtained in two other models of volume‐loading hypertension: aldosterone infusion and Goldblatt 1 kidney ‐ 1 clip hypertension. From the simulations one may conclude that autoregulation limits the amount of fluid retention required to increase BP in order to achieve salt balance, but does not affect the final level of BP. (Supported by HL‐51971)

MRI assessment of drug-induced fluid accumulation in humans: validation of the technology

The purpose of this study was to evaluate the feasibility of using proton and sodium magnetic resonance imaging (MRI) to detect fluid accumulation produced by fludrocortisone and nifedipine - two drugs known to cause salt/water retention by different mechanisms. Twelve young healthy male subjects were randomly assigned to one of two groups and treated with either fludrocortisone or nifedipine for 14 or 25 days, respectively. The change in sodium MRI, as well as in proton T(2) value and T(1)-weighted signal intensity in the calf following postural change [referred to here as 'postural delta signal'(PDS)], was evaluated before, during and after drug administration. The changes in MRI PDS were compared to conventional physiological parameters, including body weight, calf volume and pitting edema. When compared to the baseline pretreatment values, the subjects treated with fludrocortisone showed a 5.5% increase in sodium MRI PDS (P=.01), a 2-ms increase in proton T(2) PDS of the gastrocnemius muscle (P=.06) and a body weight gain of 2.3% (P=.001) within 1 week. In the nifedipine-treated subjects, the sodium MRI PDS increased by 6% versus baseline (P=.03), while the proton T(2) PDS of the gastrocnemius muscle increased by 3.7 ms (P=.01), associated with a 0.5% weight gain (P=.55), within 3 weeks. No significant changes were noted in the T(1)-weighed images following postural change. Measurements of calf circumference, volume and pitting edema did not show consistent changes associated with the drug administration. The postural change in sodium MRI and proton T(2) signals provides a sensitive method for detecting the fluid accumulation produced by fludrocortisone and nifedipine. The MRI results are consistent with treatment-induced increases in extracellular fluid volume and correlate well with the observed weight gain. These findings support the potential utility of MRI for the evaluation of medication-induced fluid retention.

Plasma sodium and hypertension

Dietary salt is the major cause of the rise in the blood pressure with age and the development of high blood pressure in populations. However, the mechanisms whereby salt intake raises the blood pressure are not clear. Existing concepts focus on the tendency for an increase in extracellular fluid volume (ECV), but an increased salt intake also induces a small rise in plasma sodium, which increases a transfer of fluid from the intracellular to the extracellular space, and stimulates the thirst center. Accordingly, the rise in plasma sodium is responsible for the tendency for an increase in ECV. Although the change in ECV may have a pressor effect, the associated rise in plasma sodium itself may also cause the blood pressure to rise. There is some evidence in patients with essential hypertension and the spontaneously hypertensive rat (SHR) that plasma sodium may be raised by 1 to 3 mmol/L. An experimental rise in sodium concentration greater than 5 mmol/L induces pressor effects on the brain and on the renin-angiotensin system. Such a rise can also induce changes in cultured vascular tissue similar to those that occur in the vessels of humans and animals on a high sodium diet, independent of the blood pressure. We suggest that a small increase in plasma sodium may be part of the mechanisms whereby dietary salt increases the blood pressure.

Tumour tissue monitoring during photodynamic and hyperthermic treatment using bioimpedance spectroscopy

Electrical bioimpedance spectroscopy is a fast and relatively easily applicable method for tissue characterization. In the frequency range up to 10 MHz, current conduction through tissue is mainly determined by tissue structure, i.e. the extra- and intra-cellular compartments and the insulating cell membranes. Therefore, changes in the extra- and intra-cellular fluid volumes are reflected in the impedance spectra. Investigations of tumours (DS sarcoma, implanted on the hind foot dorsum of rats) during treatment with localized hyperthermia (HT), photodynamic therapy (PDT) and the combination of these two components were carried out using impedance spectroscopy in the frequency range of 37 Hz to 3.7 MHz. Data collected reveal totally different, but characteristic, behaviour patterns for the three treatments. HT caused a slow increase in conductance at high frequencies (GHF) and in the extracellular space index (ECSI), indicating an increase in extracellular fluid volume and in total fluid content. With PDT, GHF increased immediately upon commencement of irradiation and was accompanied by a distinct decrease in ECSI, indicating the development of a pronounced intracellular oedema.

Macro minerals deficiencies in pregnant Mauritian women

During pregnancy there is usually a fluctuation in the levels of trace elements in the body. The level of copper for example may rise whilst that of zinc may fall. Plasma zinc and copper levels were measured in pregnant and non-pregnant women (mean age 25±6 and 23±5 years respectively). A commercially available kit was used for the direct determination of zinc while copper assay was performed by atomic absorption spectrophotometry. Total plasma proteins, albumin and globulin levels were also measured by colorimetric method using commercially available kits. Plasma zinc and copper levels in pregnant women were found to be 99.3 ± 10.8 g/dl and 180 ± 31.4 g/dl respectively compared to mean values of 111.8 ± 7.2g/dl for zinc and 153.2 ± 15.2 for copper g/dl in the non-pregnant group. Plasma proteins were also significantly lower (p<0.05) in the pregnant individuals. Mean values of 63 ± 8.7g/l for total plasma proteins, 37.2 ± 4.7 g/l for albumin and 25.8 ± 10.7g/l for globulin were obtained for the pregnant women. In the controls, total protein level was 79.6± 3.8 g/l, albumin level was 43.4 ±2.6 g/l and globulin 36.1 ± 5 g/l. In conclusions, our findings indicate that high level of copper during pregnancy may be responsible for the lowering of zinc level since these two metals are known antagonists. In addition, lower levels of albumin and globulin that are all carriers of zinc in the body may also be implicated in the lower zinc level during pregnancy. Key words : zinc, copper, total proteins, pregnancy, albumin, globulin.

Role of Digitalis-Like Substance in the Hypertension of Streptozotocin-Induced Diabetes and Simulated Weightlessness in Rats

We have examined the role of plasma Na+-K+pump inhibitor (SPI) in the hypertension of streptozotocin induced insulin dependent diabetes (IDDM) in reduced renal mass rats. The increase in blood pressure (BP) was associated with an increase in extracellular fluid volume (ECFV), and SPI and a decrease in myocardial Na+,K+ATPase (NKA) activity, suggesting that increased SPI, which inhibits cardiovascular muscle (CVM) cell NKA activity, may be involved in the mechanism of IDDM-hypertension. In a second study, using prolonged suspension resulted in a decrease in cardiac NKA activity, suggesting that cardiovascular deconditioning following space flight might in part result from insufficient SPI

Assessing the efficacy of nutritional support

This review outlines the conventional methods of assessing nutritional status and their limitations in the presence of acute trauma and sepsis. It also discusses the problems of attempting to improve or at least maintain nutritional status in the presence of an inflammatory stimulus. Most of the conventional markers of nutritional status are altered in trauma and sepsis with decreases in plasma protein concentrations and muscle strength, an apparent depression of immune function and an increase in extracellular fluid volume. It also appears to be impossible to improve nutritional status in the presence of a severe inflammatory stimulus, and the most one can hope for is to attenuate the rate of decline. The evidence for these observations is discussed.