Patient-reported outcome measures obtained via E-Health tools ease the assessment burden and encourage patient participation in cancer care (PaCC Study).

Patient-reported outcome measures obtained via E-Health tools ease the assessment burden and encourage patient participation in cancer care (PaCC Study) BACKGROUND: E-health based patient-reported outcome measures (PROMs) have the potential to automate early identification of both nutrition status and distress status in cancer patients while facilitating treatment and encouraging patient participation. This cross-sectional study assessed the acceptability, accuracy, and clinical utility of PROMs collected via E-Health tools among patients undergoing treatment for stomach, colorectal, and pancreatic tumors. RESULTS: Eight-nine percent mostly, or completely, agreed that PROMs via tablets should be integrated in routine clinical care. Men were significantly more likely to require help completing the questionnaires than women (inv.OR= 0.51, 95% CI=(0.27, 0.95), p = 0.035). The level of help needed increased by 3% with each 1-year increase in age (inv. OR=1.03, 95% CI=(1.01, 1.06), p = 0.013). On average, a patient tended to declare weight which was 0.84 kg inferior to their true weight (Bland and Altman 95 % CI=(-3.9, 5.6); SD: 2.41) and a height which was 0.95 cm superior to their true height (Bland and Altman 95 % CI=(-5, 3.1); SD 2.08). Patient-reported nutrition status was significantly associated with the professionally generated assessment (95% CI=(2.27, 4.15), p < 0.001). As nutrition status declined, the distress score increased (95%CI=(0.88, 1.68), p < 0.001). Of the patients, 48.8% who were both distressed and malnourished requested supportive care to address their problems. CONCLUSION: Patient-reported assessments utilizing E-health tools are an accurate and efficient method to encourage patient participation in cancer care while simultaneously ensuring that regular assessment of psycho-social and nutritional aspects of care are efficiently integrated in the daily clinical routine.

[Cancer and nutrition - a paradigma shift]. / Krebs und Ernährung ­ ein Paradigmenwechsel.

Substantial international differences in the prevalence of cancer disease suppose that nutrition may be an important factor in the development of cancer. Many experts believe, that nutritional factors may contribute up to 35 % to the development of malignant tumors. Many patients have lost substantial body weight already at the time of the diagnosis of the disease as consequence of undernutrition and malnutrition, respectively. During the course of the disease the nutritional status often is deteriorating further. Caused by both the cancer disease itself and the treatment, loss of appetite, changes in taste, nausea and vomiting may additionally contribute to undernutrition. Undernutrition is a relevant factor for the outcome of the disease and for the tolerance of the treatment as well. Therefore, supporting the heavily impaired patients in nutritional intake is of paramount importance and an urgent task for physicians and nurses. In view of physiology, pathophysiology, genetics and molecular biology, metabolic processes in cancer are highly complex regulated and there is increasing evidence that a diet rich in fat and protein is favourable. This, however, implies a paradigma shift away from the "healthy" balanced diet rich in fruit, vegetable and complex carbohydrates. So far, the evidence based data of this new concept is, however, a controversial issue.

Chronic metabolic acidosis decreases albumin synthesis and induces negative nitrogen balance in humans.

Chronic metabolic acidosis has been previously shown to stimulate protein degradation. To evaluate the effects of chronic metabolic acidosis on nitrogen balance and protein synthesis we measured albumin synthesis rates and urinary nitrogen excretion in eight male subjects on a constant metabolic diet before and during two different degrees of chronic metabolic acidosis (NH4Cl 2.1 mmol/kg body weight, low dose group, and 4.2 mmol/kg body weight, high dose group, orally for 7 d). Albumin synthesis rates were measured by intravenous injection of [2H5ring]phenylalanine (43 mg/kg body weight, 7.5 atom percent and 15 atom percent, respectively) after an overnight fast. In the low dose group, fractional synthesis rates of albumin decreased from 9.9 +/- 1.0% per day in the control period to 8.4 +/- 0.7 (n.s.) in the acidosis period, and from 8.3 +/- 1.3% per day to 6.3 +/- 1.1 (P < 0.001) in the high dose group. Urinary nitrogen excretion increased significantly in the acidosis period (sigma delta 634 mmol in the low dose group, 2,554 mmol in the high dose group). Plasma concentrations of insulin-like growth factor-I, free thyroxine and tri-iodothyronine were significantly lower during acidosis. In conclusion, chronic metabolic acidosis causes negative nitrogen balance and decreases albumin synthesis in humans. The effect on albumin synthesis may be mediated, at least in part, by a suppression of insulin-like growth factor-I, free thyroxine and tri-iodothyronine.

Evaluation of back pain secondary to spinal epidural hematoma associated with aspirin intake and a partial platelet glycoprotein Ia/IIa deficiency.

We report a case of spontaneous spinal epidural hemorrhage with three unusual features: (1) the hemorrhage was associated with aspirin ingestion and a reduced level of platelet glycoprotein Ia/IIa; (2) the patient presented with typical severe back pain but without neurologic dysfunction; and (3) the patient initially recovered without surgical decompression but suffered from recurrent epidural hematoma.

Influence of dietary protein intake on whole-body protein turnover in humans.

Methods for measuring rates of protein synthesis and degradation in the whole body of humans with isotopes of carbon and nitrogen are described and attention is drawn to their relative merits and drawbacks for studying the nutritional control of protein metabolism. A review of published work on dietary protein and protein metabolism leads to the conclusion that protein is the major dietary determinant of whole-body protein turnover rates, and that energy intake is comparatively unimportant. Dietary protein affects protein turnover at two levels: an immediate response to the intake of protein in meals and a longer-term adaptation after a change in protein intake. An increase in the level of dietary protein enhances the response to meals, which mainly consists of a decrease in the rate of protein degradation. The adaptation to higher protein intakes involves an increase in the basal (postabsorptive) rates of both synthesis and degradation. Suggestions for future investigation include more detailed studies of the acute and adaptive responses, to facilitate understanding of dietary protein requirements, and the effects of very-high-protein intakes with continued development of techniques for studying protein turnover in individual tissues in humans.

[Eating and drinking during aging]. / Essen und Trinken.

The retirement is a good moment in life to mirror one's health behaviour in regard to eating habits and physical activity. Based on the literature we recommend the Mediterranean "diet" in all ages. This diet is characterized by the intake of fresh fruit, vegetables, cereals, olive oil, fish, little meat, legumes, spices and herbs such as basil and garlic. A glass wine a day is legitimate. In increasing age total energy needs are decreasing. Therefore the energy intake has to be adjusted. Caloric restriction per se is a powerful means to reduce cardiovascular morbidity and mortality. However, not only the eating habits but also the entire lifestyle are important factors to influence cardiovascular mortality. Thus, the "low risk factors", i.e. Mediterranean diet, moderate alcohol consumption, physical activity and non-smoking must be controlled to improve health. In the HALE project the control of these factors reduced over-all mortality by 65 percent!

[Antioxidant vitamin supplementation in the prevention of cardiovascular disease]. / Antioxidanzien und Vitamine in der Prävention von kardiovaskulären Erkrankungen.

Oxidative stress, in particular oxidative modification of LDL-cholesterol, appears to be of great importance in the pathogenesis of atherosclerosis. Various observational epidemiological studies have suggested that antioxidant vitamin intake is associated with reduced cardiovascular morbidity and mortality. Also, experimental studies in animals have demonstrated that antioxidant vitamins slow the progression of atherosclerosis. However, prospective controlled clinical trials have failed to demonstrate a benefit of antioxidant vitamin supplementation in primary or secondary prevention of cardiovascular disease. Thus, the use of antioxidants and vitamin supplements as a preventive or therapeutic intervention can not be recommended.

Acute suppression of albumin synthesis in systemic inflammatory disease: an individually graded response of rat hepatocytes.

The effects of an inflammatory insult on albumin of the rat liver were investigated at the cellular level and were correlated with serum albumin concentration. After SC injection of turpentine, the livers were perfused and fixed in vivo; serial liver sections were stained using a streptavidin-ABC-immunoperoxidase technique with an antibody to rat albumin. Albumin and total protein were measured at intervals after turpentine injection in whole livers and in serum. Fibrinogen was determined in plasma only. Twenty-four hours after turpentine injection serum albumin had dropped by 25% and was at 50% of its initial value at Day 3. Serum fibrinogen increased 2.4-fold within 24 hr and decreased thereafter. Liver homogenates showed no significant changes in albumin concentration. Immunohistochemically, all hepatocytes stained positive for albumin in normal animals. During inflammation, the immunostainable albumin content vanished entirely in a majority of all hepatocytes while remaining unchanged in other cells, thus producing a strikingly patchy staining pattern. No signs of resumption of albumin accumulation in depleted hepatocytes were seen after 8 days, despite a clear trend towards normalization of serum albumin concentration. These results suggest that individual hepatocytes differ widely in their response to agents that suppress albumin synthesis in an acute-phase reaction.

Acute metabolic acidosis decreases muscle protein synthesis but not albumin synthesis in humans.

Chronic metabolic acidosis induces negative nitrogen balance by either increased protein breakdown or decreased protein synthesis. Few data exist regarding effects of acute metabolic acidosis on protein synthesis. We investigated fractional synthesis rates (FSRs) of muscle protein and albumin, plasma concentrations of insulin-like growth factor-I (IGF-I), thyroid-stimulating hormone (TSH), and thyroid hormones (free thyroxin [fT(4)] and triiodothyronine [fT(3)]) in seven healthy human volunteers after a stable controlled metabolic period of 5 days and again 48 hours later after inducing metabolic acidosis by oral ammonium chloride intake (4.2 mmol/kg/d divided in six daily doses). Muscle and albumin FSRs were obtained by the [(2)H(5)ring]phenylalanine flooding technique. Ammonium chloride induced a significant decrease in pH (7.43 +/- 0.02 versus 7.32 +/- 0.04; P < 0.0001) and bicarbonate concentration (24.6 +/- 1.6 versus 16.0 +/- 2.7 mmol/L; P < 0.0001) within 48 hours. Nitrogen balance decreased significantly on the second day of acidosis. The FSR of muscle protein decreased (1.94 +/- 0.25 versus 1.30 +/- 0.39; P < 0.02), whereas the FSR of albumin remained constant. TSH levels increased significantly (1.1 +/- 0.5 versus 1.9 +/- 1.1 mU/L; P = 0.03), whereas IGF-I, fT(4), and fT(3) levels showed no significant change. We conclude that acute metabolic acidosis for 48 hours in humans induces a decrease in muscle protein synthesis, which contributes substantially to a negative nitrogen balance. In contrast to prolonged metabolic acidosis of 7 days, a short period of acidosis in the present study did not downregulate albumin synthesis.

Depletion of plasma vitamin C but not of vitamin E in response to cardiac operations.

The whole-body inflammatory response produced by cardiopulmonary bypass is an important cause of perioperative morbidity after cardiac operations. This inflammatory response produces reactive oxygen species and other cytotoxic substances, such as the cytokines. The generation of reactive oxygen species might deplete principal antioxidant micronutrients, that is, vitamins C and E and the carotenoids. Therefore, we have investigated the time course of the plasma concentrations of vitamins C and E and the carotenoids in 18 patients undergoing coronary bypass operations after randomization for previous vitamin E supplementation (300 mg dl-alpha-acetyl-tocopherol 3 times daily for 4 weeks) or placebo. Supplementation with alpha-tocopherol doubled the lipid-standardized plasma vitamin E concentration to 63.7 +/- 14.5 mumol/L when compared with that of the control subjects (31.2 +/- 9.0 mumol/L) before the operation. The plasma concentrations of vitamin C (36.0 +/- 19.0 mumol/L and 44.0 +/- 21.7 mumol/L, respectively) and of the carotenoids were not statistically different between the two groups at baseline. The absolute plasma concentrations of both vitamin E and the carotenoids decreased during and after cardiopulmonary bypass, but after correction for hemodilution the plasma concentrations of vitamin E and the carotenoids showed no decrease. The vitamin E concentrations in the erythrocytes did not change either. In contrast, the plasma concentration of vitamin C decreased in all subjects within 24 hours after the operation by roughly 70%. Correction for hemodilution still revealed a significant decrease in plasma vitamin C that persisted in most patients up to 2 weeks. In conclusion, the vitamin E and the carotenoid plasma concentrations are of no major concern during and after cardiac operations. In contrast, the serious depletion of vitamin C may deteriorate the defense against reactive oxygen species-induced injury during cardiac operations.

Urinary leukotriene E(4) levels are not increased prior to high-altitude pulmonary edema.

STUDY OBJECTIVE: To examine whether increased urinary cysteinyl-leukotriene E(4) (LTE(4)) excretion, which has been found to be elevated in patients presenting with high-altitude pulmonary edema (HAPE), precedes edema formation. DESIGN: Prospective studies in a total of 12 subjects with susceptibility to HAPE. SETTING: In a chamber study, seven subjects susceptible to HAPE and five nonsusceptible control subjects were exposed for 24 h to an altitude of 450 m (control day), and exposed for 20 h to 4,000 m after slow decompression over 4 h. In a field study, prospective measurements at low and high altitude were performed in five subjects developing HAPE at 4,559 m. PARTICIPANTS: Mountaineers with a radiographically documented history of HAPE and control subjects who did not develop HAPE with identical high-altitude exposure. INTERVENTIONS: 24-h urine collections. MEASUREMENTS AND RESULTS: In the hypobaric chamber, none of the subjects developed HAPE. The 24-h urinary LTE(4) did not differ between HAPE susceptible and control subjects, nor between hypoxia and normoxic control day. In the field study, urinary LTE(4) was not increased in subjects with HAPE compared to values obtained prior to HAPE at high altitude and during 2 control days at low altitude. CONCLUSIONS: These data do not provide evidence that cysteinyl-leukotriene-mediated inflammatory response is associated with HAPE susceptibility or the development of HAPE within the context of our studies.

The influence of extracorporeal circulation on erythrocytes and flow properties of blood.

The influence of extracorporeal circulation on red blood cells and flow properties of blood was studied in 10 patients undergoing aorta-coronary bypass grafting. Blood samples were drawn on admission, under general anesthesia before the operation, during extracorporeal circulation, immediately after extracorporeal circulation, and 24 hours after extracorporeal circulation. Echinocytes were found during and shortly after extracorporeal circulation, but disappeared within 24 hours. Washing the cells in buffer restored the normal discocytic shape, which indicated that a plasma factor was responsible. Red cell membrane lipids were not affected. Analysis of the membrane proteins revealed a decrease of ankyrin after extracorporeal circulation, which was prevented by protease inhibitors during preparation. This suggests an increased proteolytic activity of the plasma after extracorporeal circulation. Red cell deformability was not altered. Plasma viscosity and hematocrit were markedly reduced by hemodilution with the priming solution. Their low levels resulted in a low blood viscosity during extracorporeal circulation, which was even lower at 26 degrees C than before or after the operation at 37 degrees C. We conclude that the red cell is affected by extracorporeal circulation. The flow properties of blood, however, are not impaired, but are improved by hemodilution.

Quantification and predictors of plasma volume expansion from mannitol treatment.

OBJECTIVE: To determine the effects of acute hypertonic mannitol infusion on intravascular volume expansion and to identify potential predictors of hypervolemia. DESIGN: Measurements of plasma volume and volume regulatory hormones were performed in healthy volunteers before and over 90 min after acute infusion of 20% mannitol solution in a therapeutic dose of 0.5 g/kg body weight, equalling an average infusion volume of 180 ml. SETTING: Clinical research unit in an 800-bed teaching hospital in the eastern part of Switzerland. PARTICIPANTS: Eight normal male volunteers. MEASUREMENTS AND RESULTS: Baseline plasma volume was determined by the indocyanine green dye dilution technique. Serial plasma protein measurements were performed after mannitol infusion to calculate intravascular volume changes. Mannitol administration resulted in a plasma expansion that persisted for more than 90 min and peaked at 112% of the baseline plasma volume 15 min after infusion. Concomitantly, an increase in systolic blood pressure and a fall in plasma sodium concentration occurred. Pharmacokinetic analyses of mannitol distribution and elimination revealed a close relation between plasma volume expansion and mannitol serum concentrations. While renin activity and aldosterone concentrations were suppressed proportionally to the intravascular volume increase, antidiuretic hormone was increased despite notable volume expansion and hyponatremia. Similarly, a rise in atrial natriuretic peptide was detected. CONCLUSIONS: Therapeutic doses of hypertonic mannitol cause substantial plasma volume expansion, resulting in increased blood pressure. Plasma volume expansion is related to mannitol serum concentrations and mannitol clearance determines the time required to restore normovolemia. ADH and ANP are potentially aggravating factors of mannitol-induced hyponatremia.

Determination of plasma volume by indocyanine green--validation of the method and use in patients after cardiopulmonary bypass.

OBJECTIVE: Validation of plasma volume (PV) determination by indocyanine green (ICG) in comparison to the gold-standard method with radioiodinated albumin, and investigation of the effect of commonly used plasma expanders (albumin, hydroxyethyl starch, and polygelatine) on PV in the early postoperative phase in patients undergoing cardiac surgery. DESIGN: Prospective clinical study. SETTING: Department of medicine and intensive care unit at a university hospital. PATIENTS AND PARTICIPANTS: Ten healthy volunteers and 21 patients after elective open-heart surgery. MEASUREMENTS AND RESULTS: PV of subjects was measured by i.v. injecting 5 microCi [125I]albumin (I-ALB). One hour later, PV was determined by a peripheral i. v. injection of 0.25 mg/kg body weight ICG (ICG1). In five subjects PV was measured repeatedly by ICG (ICG2) 1 h after ICG1. Mean PV of I-ALB and ICG1 or ICG2 showed consistent results. Further, we investigated central vs peripheral intravenous injection of ICG in six patients after open-heart surgery compared to [125I]albumin. There was no difference between mean PV measured by [125I]albumin and peripheral ICG (P = 0.40). PV determined by central injection of ICG was significantly higher than by the other methods. In 15 patients PV was determined by [125I]albumin. Thereafter, patients were randomly divided into three groups. Group ALB was infused with 1.75 ml/kg body weight human albumin 20%, group HAES with 5.25 ml/kg body weight hydroxyethyl starch 6%, and group HAEM with 7.0 ml/kg body weight polygelatine 3.5%. PV was measured 1 h and 4 h after infusion by ICG. There were no significant changes in PV between the groups. CONCLUSIONS: PV determination by peripheral i. v. injection of ICG produced reliable and consistent results when a reactive hyperaemia was produced by a tourniquet prior to injection. Therefore, central venous injection of ICG may not be prerequisite for precise measurements of PV. The expected acute increase in PV after infusion of commonly used plasma expanders after cardiac surgery was not found.

Transcapillary escape rate of albumin positively correlates with plasma albumin concentration in acute but not in chronic inflammatory disease.

The relationship among "negative" plasma acute-phase proteins (APP), ie, albumin, prealbumin, and transferrin, and "positive" APP, ie, C-reactive protein (CRP), fibrinogen, and orosomucoid, was investigated in patients with acute infectious disease (n = 8) and in patients with chronic malignant disease (n = 9). In addition, the transcapillary escape rate (TER) and outflux (J(alb)) of albumin were investigated using an intravenous injection of 2 microCi 125I-albumin. Interleukin-6 (IL-6) plasma concentrations were measured with an enzyme immunoassay. In the majority of patients, negative APP were decreased, whereas positive APP were increased. However, in patients with infectious disease, there were no significant correlations between any of the negative and positive APP. Also, in patients with infectious disease, TER was increased to 8.6 +/- 3.4%/h (mean +/- SD), and J(alb) to 114 +/- 60 mg/kg/h, compared with normal values of 4.3 +/- 2.6%/h and 108 +/- 7 mg/kg/h, respectively. Unexpectedly, there was a significant positive correlation between plasma albumin and both TER (r = .8279, P = .011) and J(alb) (r = .8683, P = .005). In patients with malignomas, significant correlations within negative and positive APP and inverse correlations between negative and positive APP resulted. Malignant disease induced only a slight elevation in TER (6.6 +/- 2.4%/h), J(alb) was within normal limits (92 +/- 35 mg/kg/h), and no correlations between plasma albumin concentrations and TER (r = -.0174, P = .97) or J(alb) (r = .4090, P = .27) were found.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence against an increase in capillary permeability in subjects exposed to high altitude.

A potential pathogenetic cofactor for the development of acute mountain sickness and high-altitude pulmonary edema is an increase in capillary permeability, which could occur as a result of an inflammatory reaction and/or free radical-mediated injury to the lung. We measured the systemic albumin escape by intravenously injecting 5 muCi of 125I-labeled albumin and the plasma concentrations of cytokines, F2-isoprostanes (products of lipid peroxidation), and acute-phase proteins in 24 subjects exposed to 4,559 m. Ten subjects developed acute mountain sickness, and four subjects developed high-altitude pulmonary edema. The transcapillary escape rate of albumin was 6.9 +/- 2.0%/h (SD) at low (550 m) and 6.3 +/- 1.9%/h at high (4,559 m) altitude (P = 0.23; n = 24). The subjects with high-altitude pulmonary edema had a modest but insignificant increase in the transcapillary escape rate of albumin (4.6 +/- 1.9%/h at low vs. 5.7 +/- 1.9%/h at high altitude; P = 0.42; n = 4). Plasma concentrations of fibrinogen, alpha 1-acid glycoprotein, C-reactive protein, and interleukin-6 were unchanged in the early phases and significantly increased by the end of the observation period in the subjects with high-altitude pulmonary edema, whereas tumor necrosis factor-alpha and F2-isoprostanes did not change at all. This suggests that the inflammatory reaction was rather a consequence than a causative factor of high-altitude pulmonary edema. In summary, these data argue against a dominant role for increased systemic capillary permeability in the development of acute mountain sickness and high-altitude pulmonary edema.

Enhanced synthesis of albumin and fibrinogen at high altitude.

The acute effects of active and passive ascent to high altitude on plasma volume (PV) and rates of synthesis of albumin and fibrinogen have been examined. Measurements were made in two groups of healthy volunteers, initially at low altitude (550 m) and again on the day after ascent to high altitude (4,559 m). One group ascended by helicopter (air group, n = 8), whereas the other group climbed (foot group, n = 9), so that the separate contribution of physical exertion to the response could be delineated. PV was measured by dilution of (125)I-labeled albumin, whereas synthesis rates of albumin and fibrinogen were determined from the incorporation of isotope into protein after injection of [ring-(2)H(5)]phenylalanine. In the air group, there was no change in PV at high altitude, whereas, in the foot group, there was a 10% increase in PV (P < 0.01). Albumin synthesis (mg. kg(-1). day(-1)) increased by 13% in the air group (P = 0.058) and by 32% in the foot group (P < 0.001). Fibrinogen synthesis (mg. kg(-1). day(-1)) increased by 40% in the air group (P = 0.068) and by 100% in the foot group (P < 0.001). Hypoxia and alkalosis at high altitude did not differ between the groups. Plasma interleukin-6 was increased modestly in both groups but C-reactive protein was not changed in either group. It is concluded that increases in PV and plasma protein synthesis at high altitude result mainly from the physical exercise associated with climbing. However, a small stimulation of albumin and fibrinogen synthesis may be attributable to hypobaric hypoxia alone.

Does parenteral magnesium sulfate have an antiemetic effect during chemotherapy with cis-platinum?

Cisplatin is a chemotherapeutic agent with a high emetic potential; it can lead to hypomagnesemia, which is caused by a renal wasting. Because of beneficial effects of magnesium in the therapy of motor disorders of the upper gastrointestinal tract and its sedative, anticonvulsive effect in eclampsia, we tested parenteral magnesium sulfate as a potential antiemetic in patients receiving cisplatin. A prospective, randomized, double-blind, cross-over study was carried out in 20 patients receiving greater than or equal to 60 mg/m2 cisplatin. A standard antiemetic regimen consisting of a single dose of 10 mg diazepam and five times 0.5 mg/kg metoclopramide (every 2 h) was used. Simultaneously, 8 g magnesium sulfate or isotonic sodium chloride was infused over 4.5 h. The efficacy of magnesium was analyzed with an emetic score system; no difference was found between magnesium sulfate and sodium chloride. Only two patients were hypomagnesemic, and they had a better emetic score with the magnesium infusion. We conclude that the i.v. administration of magnesium during cisplatin therapy has no antiemetic effect, at least in normomagnesemic patients.

Thiamin deficiency in HIV-positive patients: evaluation by erythrocyte transketolase activity and thiamin pyrophosphate effect.

BACKGROUND AND AIMS: The aim of the study was to determine the thiamin status in HIV-positive patients. METHODS: Measurement of erythrocyte transketolase activity (ETK) and thiaminpyrophosphate (TPP) effect in 55 consecutive HIV-positive patients of a specialized outpatient clinic were grouped into five groups according to their CD4 counts. Comparison of results of HIV-positive patients with age-matched control group of 22 healthy subjects. RESULTS: Of the patients, 27% had a pathologically-increased TPP effect, 18% of the patients had pathologically-low ETK. The percentage of pathological values of TPP effect in the patients was significantly higher compared with the control group. There was no statistically significant correlation between pathological thiamin status and stage of the disease, zidovudine therapy or nutritional status of the patients. CONCLUSIONS: Thiamin deficiency in HIV-positive patients was found in a higher percentage than previously reported. Thiamine deficiency is not only present in advanced stages of HIV-infection, but also in clinically asymptomatic patients.