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Biomedical subjects

C Waterhouse

Publications and source records attributed to C Waterhouse.

At least 37 records · Page 2Linked to original sources
PubMed1979

Lactic acidosis and liver disease.

Both acute and chronic hepatic insufficiency can result in lactate accumulation and lactic acidosis; data from both types of patients were compared. In the chronic group, an acute precipitating event was identified in seven of nine subjects. Four had sepsis and three had gastrointestinal hemorrhage. In these patients, results from most tests of hepatic function were not altered dramatically. There were no long-term survivors in this group. In contrast, patients with acute hepatic failure had striking alterations in their results of hepatic function tests. Notable prolongation of the prothrombin time was always present initially and antedated other abnormalities of hepatic function. Three of seven patients in this group survived. Hypoglycemia was seen in both groups and in two subjects with acute hepatic insufficiency, glucose administration alone resulted in rapid lowering of lactate levels.

Acidosis↗
PubMed1978

Peripheral amino acid levels in patients with cancer.

Peripheral arterial and venous whole blood amino acid concentrations were determined in four groups of subjects after an overnight fast 1) normal people, 2) patients with cancer who had not lost body weight, 3) subjects with cancer who had lost more than 20% of body weight and 4) patients who had lost more than 20% of body weight from diminished intake due to cause other than cancer. Comparison of the arterial blood levels in the four groups showed that patients with cancer and weight loss had amino acid patterns different from patients who were malnourished for other reasons. Branched chain amino acids were normal in patients with malignant disease. Some gluconeogenic amino acids were reduced as in other subjects with weight loss but the characteristic rise in glycine seen with malnutrition was not present. Arterio venous differences in whole blood across the forearm showed no evidence of increase in venous excess in patients with progressive malignant disease, indicating no excessive protein catabolism in muscle tissue. The data are consistent with increased gluconeogenesis in malnourished cancer subjects, probably due to intrinsic change in hepatic metabolism.

Amino Acids↗
PubMed1978

Treatment of alcoholic acidosis: the role of dextrose and phosphorus.

We have made serial metabolic observations in 18 acute episodes of alcoholic ketoacidosis in ten patients. Data from patients treated with only saline initially were compared to data from patients who received modest amounts of intravenous dextrose (7.0 to 7.5 gm/hr). More rapid improvement in the acidotic state was seen in the latter group (P less than .001). The quicker decline in absolute levels and ratio of beta-hydroxybutyrate to acetoacetate when glucose was given suggests that this treatment induced mitochondrial oxidation of the reduced form of nicotinamide adenine dinucleotide (NADH). Since phosphorus is a critical cofactor necessary for NADH oxidation and the glucose-induced correction of the acidosis was associated with a rapid decline in serum phosphorus from an initial mean of 6.79 +/- .82 mg/100 ml SEM to 0.96 +/- 0.12 mg/100 ml in 24 hours, we propose that glucose enhanced the mitochondrial capacity to oxidize NADH by increasing hepatocyte phosphorus. This effect combined with decline in free fatty acid levels results in reversal of acidosis. Our data suggest that glucose provides the safest, most effective treatment for this disorder; addition of either insulin or bicarbonate is usually unnecessary.

Acetoacetates↗
PubMed1978

The contribution of glucose to alanine metabolism in man.

We have studied by tracer technique the interconversion of the carbon skeleton of alanine with that of glucose. The data analysis is in terms of renewal theory rather than traditional compartmental analysis. This eliminates the need for estimation of compartment size, which is particularly difficult to determine in the case of alanine. In addition, the conversion rates between the two substances are found by considering the two components which are responsible for the determined radioactivity curves, namely, the first conversion of the labeled carbon and its subsequent movement in the product compound. The subjects of the study were for the most part underweight but had been hospitalized and eating a standard hospital diet for at least 3 days prior to the studies. Our data indicate that nearly twice as much carbon from glucose is cycled to alanine as is recycled from alanine back to glucose after a 14 hr overnight fast. Small amounts of glucose suppress the alanine-glucose arm of the cycle but probably do not change the glucose-alanine conversion. The contribution of glucose carbon to alanine metabolism is significant and appears to be immediately influenced by the magnitude of glycolysis.

Adult↗
PubMed1976

Vitamin D resistance in magnesium deficiency.

Four patients with gastrointestinal disorders, and one patient with chronic alcoholism presented with both hypocalcemia and hypomagnesemia. Pharmacological doses of either ergocalciferol or dihydrotachysterol did not correct the hypocalcemia except in one patient who had a minimal rise in serum calcium. Parathormone levels were high in three patients and exogenous parathormone given to the fourth subject failed to elicit a rise in serum calcium, implying impairment of the calcemic response to parathormone. Magnesium repletion simultaneously corrected the hypomagnesemia and hypocalcemia. Balance data suggested that the rise in serum calcium was in part, at least, due to increased mobilization of minerals from bone. While the mechanism remains speculative, it appears that magnesium facilitates the release of calcium from bone in the presence of adequate amounts of vitamin D and parathormone.

Adolescent↗
PubMed1975

The effect of potassium loading on sodium excretion and plasma renin activity in Addisonian man.

Potassium has been shown to suppress plasma renin activity (PRA). This study was designed to study the role of increased aldosterone production in the mediation of such a response. Five patients with adrenal insufficiency were placed on a diet of 60 meq potassium and 100-150 meq of sodium while receiving a constant amount of cortisone acetate and Florinef. Upright PRA was determined each day for 2-3 days in the control period and then for 3-4 days after potassium intake had been increased to 200-300 meq/day. Potassium loading induced a natriuresis. Hence, patients were either sodium replaced (six studies in four patients) or allowed to become sodium depleted (three patients). Potassium loading without replacement was associated with a decrease in weight, negative sodium balance, hyperkalemia, and a positive potassium balance. PRA rose during the experimental period. Potassium loading with sodium replacement was associated with little change in weight or sodium balance. Hyperkalemia and positive potassium balance were present to the same degree as found in the studies without sodium replacement. When all PRA values are considered (both morning and evening values) there was no significant change with potassium loading (+ 1.31 ng/ml per h; range + 6.9 to -2.0). We conclude that hyperkalemia or a positive potassium balance did not suppress PRA in Addisonian man in these studies when sodium balance was maintained, nor did it prevent a rise in PRA when sodium balance was negative.

Addison Disease↗
PubMed1975

GammaG-globulin production and light-chain metabolism in patients with metastatic cancer.

GammaG-Globulin and excess light-chain metabolism were studied in eight subjects with progressive metastatic malignant disease by determining the plasma radioactivity curves following the administration of appropriately labeled substances. In addition to the plasma die-away curves, which required about 3 weeks for full expression for gamma-globulin, but only 3 to 4 days for light-chain, urinary excretion of the label from metabolized protein was determined. The data are compared to similar studies in control individuals. The metabolism of excess light chain was similar to normal in all respects. The total synthesis of gammaG-globulin was increased with a mean value about twice normal. The mean survival time of a circulating immunoglobulin molecule was short, indicating rapid loss from the system. Other aspects of immunoglobulin metabolism were similar to normal with a normal percentage of the labeled protein appearing in the urine, suggesting no abnormality in the utilization pattern but simply an increased rate of turnover. The capability of malnourished patients with cancer to produce large quantities of immunoglobulin is not specific for this disease, since similar patterns may be seen in response to infections in protein-depleted individuals. However, there is the possibility that the cancer itself acts as an inciting agent in these subjects. Furthermore, such sustained protein synthesis may place an additional burden on already compromised host metabolism.

Humans↗
PubMed1973

The relationship between L-chain synthesis and gamma-globulin production.

The simultaneous administration of labeled human gammaG globulin and L-chains to subjects has allowed examination of the metabolic relationship between a component part and the whole immunoglobulin molecule. Studies were carried out in a series of control subjects and in a group of patients where substandard production of gamma-globulin was anticipated, i.e., patients with the nephrotic syndrome on chronic Imuran therapy and patients with uremia. Full expression of the plasma decay curve was obtained for both substances, that for L-chain requiring only 4-5 days except in uremic subjects and that for gamma-globulin requiring up to 30-40 days. Urinary excretion of inorganic iodide was also quantitated for 20-30 days. Equilibrium of the extravascular, vascular, and urinary radioactivity from the labeled gammaG globulin was usually not seen during this time interval suggesting more than one site of catabolism of the protein. Excess L-chain poduction was about 45% of the total L-chain production and probably in no instance could account for the low gamma-globulin production seen in certain patients with renal disease.

Adult↗
PubMed1972

Concentration gradient electrophoresis of plasma from patients with hyperbetalipoproteinemia.

A modification of the Pratt and Dangerfield technique of acrylamide gel concentration gradient electrophoresis has been used to study low density lipoproteins from fasting human beings. Prestained plasma from normal subjects and from patients with Fredrickson's type II hyperbetalipoproteinemia was electrophoresed in continuous gradient gel columns (approximately 3.5-8%). Reproducible low density lipoprotein patterns were obtained, and two major bands of low density lipoproteins as well as trace amounts of two to five other low density lipoproteins were seen in normal plasma. Plasmas from patients with hyperbetalipoproteinemia were more heterogeneous. Abnormal plasmas showed as many as six major low density lipoprotein bands and six minor bands. Patterns were constant for an individual but varied between patients. The major bands frequently had obviously different mobilities from those in normal plasma. Extensive experiments, using a large number and variety of mixed plasmas (normal, type II, and others) or plasmas run separately in divided gel columns, led to a numbering system of the low density lipoproteins comprised of 15 discrete bands. In addition to the changes seen in the low density lipoproteins in patients with hyperbetalipoproteinemia, reduced amounts of high density lipoproteins were consistently found.

Acrylamides↗