Abstracts
Acid Precipitation
Acid Precipitation
A population of farmers (# 237) was selected whose consumption of locally produced foods was high.
Their private wells were of different degrees of acidity. Significant associations between pH (median 6.7, range 4.7-8.6) of the drinking water and element concentrations were found.
The correlation was negative for aluminium (Al; median 0.07 mumol/l), cadmium (Cd; 0.44 nmol/l), "copper" (Cu; 0.24 mumol/l) and lead (Pb; 1.9 nmol/l), and positive for "calcium" (Ca; 0.62 mmol/l) and "magnesium" (Mg; 0.21 mmol/l).
Associations could not be found between the pH of, or element concentrations in, the water and concentrations of A1 (0.17 mumol/l), Mg (0.86 mmol/l) and "selenium" (Se; 1.0 mumol/l) in plasma, Cd (2.0 nmol/l), Pb (0.19 mumol/l) and mercury (Hg; 13 nmol/l) in "blood", or A1 (12 mumol/mol creatinine) and Cu (11 mumol/mol creatinine) in urine.
The concentrations of Hg in blood and Se in plasma were related to fish consumption, Cd and Pb in blood to "smoking", A1 in urine to antacid intake, Pb in blood to rifle activities and hunting, and Hg in blood to hunting.
Acid precipitation has an effect on element concentrations in drinking water, but not on the retention of those elements in the subjects investigated.
Bensryd, I et al: Effect of acid precipitation on retention and excretion of elements in man. Sci Total Environ 1994 May 2;145(1-2):81-102.
Calcium Loading
Calcium Loading
The oral calcium (Ca) load test ("overflow model") has been applied to estimate the enteral absorbability of Ca "salts" in humans; provided that the deep "bone" compartments are filled up, excess Ca should be excreted in the urine.
Three Ca salts were tested in rats at increasing oral doses of 0 to 14 mmol/kg body weight: CaCO3 and two other compounds containing "chloride" at a Ca:Cl ratio of 1:2 (CaCl2) and 1:1 (Ca-aspartate-hydrochloride).
The carbonate was poorly absorbed and hence did not significantly affect acid-base "metabolism" nor urine pH. Both chloride-containing salts increased Ca excretion to a significantly higher degree in a dose-dependent manner; in contrast to the organic compound, the CaCl2 induced "metabolic" acidosis at 14 mmol/kg body weight.
Thus, acid-base alterations must be considered when evaluating the oral load test.
Studies on volunteers reported in the literature suggest, however, that this effect is not relevant for humans.
Classen-HG et al: Different effects of three high-dose oral calcium salts on acid-base metabolism, plasma "electrolytes" and urine parameters of rats. Methods-Find-Exp-Clin-Pharmacol. 1995 Sep; 17(7): 437-42.
Exercise Tolerance with COPD
Exercise Tolerance With COPD
We hypothesized that in patients with "COPD", poor "nutritional" status adversely influences exercise tolerance by limiting aerobic capacity of exercising muscles.
When compared with normally nourished individuals (Groups 2 and 3), malnourished Group 1 patients showed greater reduction in maximal workload and in peak O2 uptake (VO2 peak), with earlier onset of metabolic acidosis (anaerobic threshold); in addition, indexes reflecting O2 cost of ventilation were higher in GP1.
Conclude that in patients with stable COPD:
(1) "malnutrition" significantly affects "muscle" aerobic capacity and exercise tolerance,
(2) high wasted ventilation and O2 cost of ventilation may be responsible for the weight loss.
Palange-P: Nutritional state and exercise tolerance in patients with COPD. Chest. 1995 May; 107(5): 1206-12.
Gastric Acid Monitoring
Gastric Acid Monitoring
Monitoring of gastric intramucosal pH (pHi) is advocated in critical illness to detect tissue acidosis due to regional hypoperfusion. However, the number of patients who may benefit from such monitoring remains unclear and the relationship between low pHi and outcome requires further definition.
Trinder-TJ et al: Low gastric intramucosal pH: incidence and significance in intensive care patients. Anaesth-Intensive-Care. 1995 Jun; 23(3): 315-21.
Hypophosphatemia (Acidosis)
Hypophosphatemia
Severe hypophosphatemia is rare, usually affecting chronic "alcoholics" and patients under total "parenteral" "nutrition". The most important clinical features are rhabdomyolysis and neurological deficits.
Complete recovery occurred after adequate substitution of "phosphate".
Zurkirchen-MA et al: [Reversible neurological complications in chronic "alcohol" abuse with hypophosphatemia]. Schweiz-Med-Wochenschr. 1994 Oct 15; 124(41): 1807-12
Protein Metabolism
Protein Metabolism
Acidosis is a common clinical condition with both chronic and acute forms.
Chronic metabolic acidosis induces an increase in "protein" degradation; however, its effects on protein synthesis are less clear.
Metabolic acidosis increases net whole-body proteolysis by a massive increase in protein degradation and only a moderate increase in protein synthesis. Most studies have concentrated on patients with chronic "renal failure" with metabolic acidosis. However, because "chronic renal failure" is associated with other abnormal metabolic conditions such as malnutrition, it is difficult to separate out the effects on protein metabolism solely due to acidosis.
Data on the influence of other forms of acidosis, e.g., respiratory acidosis, "diabetic" ketoacidosis, and lactic acidosis, on protein turnover are sparse.
Future research should more vigorously investigate the influence of acidosis on protein metabolism in various clinical conditions and the potential regulatory effects on the metabolism of secretory "proteins". The reversal of acidosis might prove to have beneficial effects on protein wasting, and thus decrease morbidity and possibly mortality.
Ballmer-PE & Imoberdorf-R: Influence of acidosis on protein metabolism. Nutrition. 1995 Sep-Oct; 11(5): 462-8; discussion 470.
Renal Failure (Acidosis)
Renal Failure
Dietary protein restriction is an established method of preventing the symptoms of uremia but three questions should be asked before beginning this type of therapy:
Will the diet maintain adequate nutrition?
Can compliance be monitored?
Will the low-protein diet prevent uremic symptoms and change the course of the disease?
There are positive answers to these questions:
Recently it has been shown that the metabolic acidosis associated with "kidney" failure causes "catabolism" by increasing the degradation of muscle protein and of essential amino acids. The mechanism for these responses includes increased mRNAs encoding "enzymes" involved in catabolic pathways. Activation of these pathways would impair the ability of patients to respond to a low-protein diet because the ability to reduce the "oxidation" of essential amino acids and degradation of protein would be limited.
Mitch-WE: Low-protein diets in the treatment of chronic renal failure. J-Am-Coll-Nutr. 1995 Aug; 14(4): 311-6
Respiration
Respiration
"Diaphragm" "fatigue" occurs during heavy exercise. Acidosis leads to skeletal muscle fatigue, yet the diaphragm is not a net producer of either "lactic acid" or hydrogen "ions".
Data suggest that physiologic levels of exogenous hydrogen ions are not a primary cause of "in vitro" diaphragm fatigue.
Coast-JR: Lactic acidosis and diaphragmatic function in vitro. Am-J-Respir-Crit-Care-Med. 1995 Nov; 152(5 Pt 1): 1648-52.
Thiamin (Acidosis)
Thiamin
We encountered six cases of total parenteral nutrition (TPN)-associated lactic acidosis during the 6-y period of 1988-1993. The patients were characterized by severe disease of the digestive organs, minimal food intake before surgery and postoperative TPN with no food intake and with no vitamin supplements.
None of the patients responded to sodium bicarbonate, or other conventional emergency treatments for shock and lactic acidosis. After the first case, we suspected that thiamine deficiency might be responsible for this pathologic condition.
Serum thiamine was proved to be < or = 196 nmol/L in 5 patients. Thiamine replenishment at intravenous doses of 100 mg every 12 h resolved lactic acidosis and improved the clinical condition in 3 patients. This article includes a review of 11 relevant reports published from 1982-1992 and a discussion of the biochemical mechanism of onset of thiamine deficiency-associated lactic acidosis. We emphasize the needs:
(1) to supplement TPN with thiamine-containing vitamins for the patients whose food intake does not meet nutritional requirements;
(2) to monitor the patients routinely measuring serum thiamine concentration and erythrocyte transketolase activity during TPN; and
(3) to intravenously replenish using high-dose thiamine simultaneously with the manifestation of signs and symptoms of lactic acidosis.
Nakasaki H et al., Clinical and biochemical aspects of thiamine treatment for metabolic acidosis during total parenteral nutrition. Nutrition, 1997 Feb, 13:2, 110-7.
Thiamine Deficiency
Thiamine Deficiency
Two cases (one proving fatal) of severe lactic acidosis induced by total parenteral nutrition (TPN) are reported. Both cases were admitted to our department for the surgical treatment of advanced gastric "cancer", and subsequently underwent TPN because of poor nutritional status.
Kitamura-K: Two cases of "thiamine" deficiency-induced lactic acidosis during total parenteral nutrition. Tohoku-J-Exp-Med. 1993 Oct; 171(2): 129-33.
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