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S O Thier

Publications and source records attributed to S O Thier.

At least 37 records · Page 2Linked to original sources
PubMed1986

Anticystinuric effects of glutamine and of dietary sodium restriction.

We studied four patients with cystinuria to assess the effects of glutamine and dietary sodium on the urinary excretion of dibasic amino acids. In Patient 1, at an ad libitum dietary sodium intake of about 300 mmol per day, oral administration of glutamine led to reproducible and marked anticystinuria and antiornithinuria, whereas the excretion of lysine and arginine was not significantly affected. In Patient 2, at an ad libitum dietary sodium intake of about 150 mmol per day, no effect of glutamine could be demonstrated in studies lasting up to three weeks. Since the principal difference between Patients 1 and 2 was their dietary intake of sodium, Patient 3 was studied during dietary sodium intakes of 150 and 300 mmol per day. His cystine excretion was found to be higher at 300 than at 150 mmol per day. Glutamine suppressed his cystine excretion at a sodium intake of 300 mmol per day but had no effect at 150 mmol per day. When the effect of a further reduction in sodium intake alone was studied in a fourth patient, a decrease of 150 to 50 mmol per day was found to reduce cystine excretion markedly within 17 days. The low-sodium diet alone also reduced the excretion of lysine, arginine, and ornithine. We conclude that glutamine may reduce the excretion of dibasic amino acids at a high sodium intake but not at an intake of about 150 mmol per day. However, since a sodium-dependent excretion of the dibasic amino acids occurs at an intake down to about 50 mmol of sodium per day, dietary restriction of sodium can provide a safe approach to the treatment of cystinuria.

Administration, Oral↗
PubMed1986

Potassium physiology.

Potassium is the most abundant exchangeable cation in the body. It exists predominantly in the intracellular fluid at concentrations of 140 to 150 meq/liter and in the extracellular fluid at concentrations of 3.5 to 5 meq/liter. The maintenance of the serum potassium concentration is a complex bodily function and results from the balance between intake, excretion, and distribution between intracellular and extracellular space. Ingested potassium is virtually completely absorbed from and minimally excreted through the intestine under nonpathologic circumstances. Renal excretion of potassium, which is the major chronic protective mechanism against abnormalities in potassium balance, depends on filtration, reabsorption, and a highly regulated distal nephron secretory process. Factors regulating potassium secretion include prior potassium intake, intracellular potassium, delivery of sodium chloride and poorly reabsorbable anions to the distal nephron, the urine flow rate, hormones such as aldosterone and beta-catecholamines, and the integrity of the renal tubular cell. The maintenance of distribution between the inside and outside of cells depends on the integrity of the cell membrane and its pumps, osmolality, pH, and the hormones insulin, aldosterone, beta 2-catecholamines, alpha-catecholamines, and prostaglandins. Both distribution across cell membranes and/or renal excretion of potassium may be altered by pharmacologic agents such as diuretics, alpha- and beta-catechol antagonists and agonists, depolarizing agents, and digitalis. Problems with hypokalemia and hyperkalemia can be analyzed on the basis of potassium physiology and pharmacology; proper treatment depends on an accurate analysis.

Aldosterone↗
PubMed1983

Pemphigus foliaceus and proteinuria induced by alpha-mercaptopropionylglycine.

Pemphigus foliaceus and proteinuria occurred in a patient with cystinuria treated with alpha-mercaptopropionylglycine. This drug is similar to D-penicillamine in structure and function, and it is being used in patients who are unable to tolerate D-penicillamine. Although side effects of D-penicillamine are common, no major adverse reactions have been reported previously with alpha-mercaptopropionylglycine. Pemphigus foliaceus and proteinuria occurring during therapy with alpha-mercaptopropionylglycine and D-penicillamine are discussed.

Amino Acids, Sulfur↗
PubMed1981

Mixed acid base disturbances: a clinical approach.

The analysis of a mixed acid-base disturbance begins with the history and physical examination from which data can be derived that make the clinician suspect a specific disturbance(s). The electrolytes are then evaluated with emphasis on the meaning of the values for serum bicarbonate, potassium and chloride concentration and on the level of the anion gap. Other laboratory data such as serum creatinine or glucose concentrations, blood cultures, and so forth, should also be reviewed for further clues to a possible disturbance(s). When it is clinically indicated, values for pH and Pco2 are obtained by blood gas determination. If the evidence up to this point indicates the presence of at least one disturbance, the data are examined to see if compensation for this disturbance is appropriate. If not, a mixed disturbance must be present. A normal pH in the setting of an abnormal serum HCO3(-) concentration or Pco2 also suggests a mixed disturbance since compensation rarely corrects the pH back to normal. Of course, a pH deviated in the opposite direction than that expected for a known primary disturbance makes the diagnosis of a mixed disturbance certain. The diagnosis of a mixed acid-base disturbance is therefore based on an analysis of all the clinical data and not just the blood gas measurements. Treatment of the disorders should be directed at maintaining a normal or near normal pH. Some combined acid-base disorders are important to recognize because they can result in a severe deviation in blood pH that demands immediate, specific therapy. Other mixed disturbances result in a pH which is near normal but are important to recognize since they can alert the clinician to the possibility of certain clinical derangements such as septic shock or drug ingestion. Careful analysis of mixed acid-base disturbances in this way is not peutic information to be used in caring for his (her) patients.

Acid-Base Equilibrium↗
PubMed1979

Effect of acute metabolic acidemia on renal electrolyte transport in man.

The effect of acute NH4C1-induced metabolic acidemia on renal electrolyte excretion was examined in nine healthy subjects during steady state water diuresis. Following oral NH4C1, venous pH and bicarbonate concentration declined significantly (p less than 0.01) while inulin and PAH clearances remained unchanged. Mean sodium excretion (UNaV) increased from 142 +/- 16 mueq/min (mean +/- SEM) to 310 +/- 49 mueq/min (p less than 0.01) at 8 hr without change in plasma aldosterone or renin levels. Urine flow remained unchanged while CH2O/(CH2O + CCl) declined significantly, suggesting that acute metabolic acidemia inhibits sodium transport in the distal nephron. Similar results were observed in two subjects with central diabetes insipidus. Three subjects restudied following the ingestion of an equivalent amount of chloride administered as NaCl, failed to demonstrate a significant rise in UNaV. UKV fell acutely from 91 +/- 13 to 45 +/- 5 mueq/min (p less than 0.001) despite an increase in serum potassium concentration. No change in plasma insulin was observed. UCaV rose from 66 +/- 15 to 143 +/- 18 microgram/min and fractional excretion of calcium increased from 0.55 +/- 0.13 to 1.24 +/- 0.21% (p less than 0.001). Total serum calcium fell slightly, but ionized calcium rose from 3.99 +/- 0.05 to 4.30 +/- 0.03 mg/dl (p less than 0.001). No change in nephrogenous cyclic (cAMP) excretion was observed. In conclusion, acute metabolic acidemia in man (1) inhibits sodium reabsorption in the distal nephron independent of changes in plasma aldosterone concentration, filtered chloride load, or volume expansion; (2) inhibits potassium excretion despite a rise in serum potassium concentration; and (3) inhibits tubular calcium reabsorption independetn of changes in parathyroid hormone (as reflected by urinary cAMP).

Acidosis↗
PubMed1979

Continuing education network builds on physician acceptance.

In 1975, the Department of Internal Medicine at Yale and nine community hospitals in southwestern Connecticut began a continuing medical education program, the Yale Affiliated Hospital Program (YAHP). Physicians from Yale and the community hospitals were involved in the planning and organization of the YAHP from the beginning, since the authors believe that physician acceptance is necessary for the success of a program between a university medical center and community hospitals. The attention to physician acceptance has fostered a cooperative spirit and trust among members of the group so that issues in addition to education, such as house staff and faculty recruitment, program content, and regional planning, can be dealt with.

Connecticut↗