Biomedical subjects

A Prigent

Publications and source records attributed to A Prigent.

35 records · Page 2Linked to original sources

PubMed1993

The diagnosis of renovascular hypertension: the role of captopril renal scintigraphy and related issues.

This article reviews the screening and diagnostic tests used in the detection of significant renal artery stenosis and renovascular hypertension. After addressing the pathophysiological considerations necessary for correct diagnostic test interpretation, this review critically surveys the recent advances in, and the limitations of, relevant investigational procedures and in particular focuses on the efficacy and issues of angiotensin-converting enzyme inhibitor renal scintigraphy.

Captopril↗

PubMed1992

Chronic neutral phosphate supplementation induces sustained, renal metabolic alkalosis.

The aim of the present study was to test whether intravenous neutral phosphate supplementation, recently shown in our laboratory to acutely stimulate proton secretion in the distal nephron, was able to induce a sustained metabolic alkalosis. Neutral Na and K phosphate supplementation for seven days, with equivalent reduction in chloride supply and unchanged intake of sodium and potassium, in ADX rats receiving fixed physiological doses of aldosterone and dexamethasone (group 1, N = 7), was responsible for a severe metabolic alkalosis (MA; delta [HCO3] 11 +/- 1.3 mM, and delta pH 0.11 +/- 0.06 unit). Metabolic alkalosis was at least in part of renal origin, since net acid excretion (NAE) transiently increased, principally due to an increment in titratable acid excretion rate. Balances were equilibrated for sodium and negative for chloride and potassium, which may have contributed to the severity of the MA. Chronic i.v. neutral Na phosphate, without change in potassium and chloride supply, in ADX rats receiving the same doses of steroids (group 2, N = 5), was responsible for a less severe MA (delta [HCO3] 7.5 +/- 0.9 mM, and delta pH 0.07 +/- 0.01 unit), also of renal origin. In this group, balances were positive for chloride and sodium and equilibrated for potassium. Finally, neutral Na and K phosphate supplementation with reduction in chloride supply in intact rats (group 3, N = 4) was also able to induce a MA (delta [HCO3] 5.5 +/- 1.8 mM, and delta pH 0.06 +/- 0.01 unit) of renal origin, with balances negative for chloride and equilibrated for potassium and sodium. In all groups, the generation and maintenance of MA probably resulted from stimulated proton secretion in the distal nephron, as suggested by the observed increase of PCO2 over HCO3 concentration ratio in the urine and a fall in urine pH despite augmented urinary buffer content throughout the phosphate infusion period. Glomerular filtration rate did not significantly vary in any group. In conclusion, chronic supplementation of neutral phosphate appears to stimulate per se proton secretion in the distal nephron, independently of sodium, chloride, and potassium balances, and adrenal steroid secretion. Thus neutral phosphate supplementation should be added to the previously known factors able to induce MA.

Acid-Base Equilibrium↗

PubMed1991

[Distal tubular acidosis. Recent data].

Tubular acidosis is diagnosed when hyperchloremic acidosis is associated with inappropriate NH4 excretion (less than or equal to 40 mmol/24 hours). Urinary pH is variable because it depends on the secretion of H+ into the collecting duct and is inversely correlated with the amount of ammonia available in the urine. Administration of NaHCO3 for diagnostic purpose allows to eliminate proximal tubular acidosis and to measure the elevation of urinary PCO2 reflecting the secretion of H+ in the collecting duct. Hypokalemia points towards distal tubular acidosis, either by defect of H(+)-ATPases pumps, or by the incapacity to create a normal gradient of H+. In contrast hyperkalemia suggests distal tubular acidosis associated either with hypoaldosteronism or with diminution of trans-epithelial voltage or with pseudohypoaldosteronism. The incidence of distal tubular acidosis with hyperkalemia is increasing whereas distal tubular acidosis with hypokalemia remain rare.

Acidosis, Renal Tubular↗

PubMed1990

[Renal regulation of the acid-base equilibrium].

The kidney controls extracellular bicarbonate concentration and the pH of the body by modulating neat acid excretion (ammonium plus titratable acidity minus bicarbonate) according to the systemic acid-base balance. Proton, bicarbonate and phosphate transport and ammonium synthesis in the proximal tubules change in a homeostatic manner. The intercalycial A (proton secreting) and B cells (bicarbonate secreting) of the distal tubule and cortical collecting ducts have a high capacity of adaptation. The wide ascending branch of the loop of Henle also plays an important role in the bicarbonate and ammonium transport. Recent data suggest a pluri-hormonal regulation of urinary acidification. Therefore, the precision of the renal response to metabolic acidosis depends on the coordinated regulation of different segments of the nephron by the parathyroid hormone, aldosterone and the glucocorticosteroids.

Acid-Base Equilibrium↗

PubMed1990

[Renal acidosis].

Normal adults with normal protein intakes have a urinary NH4 excretion of 40 to 50 mmol/24 hours and a variable urinary pH. In cases of metabolic acidosis a urinary pH less than 5.5 suggests an extra-renal origin whilst a urinary pH greater than 5.5 is in favour of renal acidosis, but there are many exceptions to this rule. On the other hand, urinary NH4 excretion is always greater than 70 mmol/24 hours in the first case and less than 40-50 mmol/24 hours in the second; and the use of the urinary anionic gap (Na + K - Cl), negative in the first case and positive in the second, enables the two situations to be distinguished. The acidosis of nephron reduction is easily recognised in cases of severe renal failure with an increase in unmeasured plasma anions whilst tubular acidoses are accompanied by a hyperchloremia. Measurement of fractional HCO3 excretion after an oral loading dose of NaHCO3, preferably by TmCHO3 with respect to GFR, distinguishes proximal tubular acidosis (low TmHCO3) from distal tubular acidosis (normal or high TmHCO3). In the latter case, the presence of hypokalemia suggests a distal tubular acidosis either due to deficiency of the H(+)-ATPase pumps (absence of increased urinary pCO2 after oral loading dose of NaHCO3) or to the inability of the kidney to maintain a normal H+ gradient (normal increase of urinary pCO2. The presence of hyperkalemia suggests diseases associated with hypoaldosteronism (low or inappropriate serum aldosterone concentrations), abnormal transepithelial voltages or with a pseudo-hypoaldosteronism syndrome (high plasma aldosterone concentration). The prevalence of distal tubular acidosis with hyperkalemia is on the increase whilst tubular acidosis with hypokalemia remains rare.

Acid-Base Equilibrium↗

PubMed1989

Effects of glucagon on H(+)-HCO3- transport in Henle's loop, distal tubule, and collecting ducts in the rat.

Paired micropuncture experiments were carried out in somatostatin-infused volume-expanded rats to examine the effects of a glucagon infusion (0.05 ng.min-1.g body wt-1) on urinary acidification and tubular handling of bicarbonate. Whole kidney and single-nephron glomerular filtration rate were not affected by glucagon. In thyroparathyroidectomized (TPTX) rats, glucagon inhibited the reabsorption of total CO2 in Henle's loop. In intact animals, however, the latter effect was not observed. In the distal tubule accessible to micropuncture, net total CO2 absorption was observed during volume expansion plus somatostatin infusion, which reversed to net total CO2 secretion during glucagon infusion in Wistar rats; thus the late distal delivery of total CO2 increased almost 80%. Marked inhibition of urinary acidification occurred in all animals as evidenced by a rise in urine pH and bicarbonate excretion. Conversely, a somatostatin infusion, which decreased the plasma glucagon concentration, stimulated net total CO2 absorption along the distal tubule and augmented final urine acidification in Wistar rats. Finally, urine-minus-blood PCO2 during alkaline diuresis was significantly reduced by glucagon infusion in bicarbonate-loaded TPTX rats. We conclude that 1) glucagon inhibits bicarbonate absorption in superficial Henle's loop in TPTX but not in intact rats, and 2) glucagon stimulates bicarbonate secretion and/or inhibits proton secretion in the distal tubule and collecting ducts, which leads to reduced urinary acidification.

Animals↗

PubMed1989

Determinants of parathormone secretion in primary hyperparathyroidism.

We studied the effects of acute modifications in plasma calcium on parathormone (PTH) secretion in 23 patients with primary hyperparathyroidism (PHPT). In 12 patients, PTH hypersecretion was autonomous, and basal plasma calcium concentration was positively correlated with maximal serum PTH(1-84) reached during Na2EDTA infusions. In 11 patients, PTH hypersecretion remained suppressible, but with elevated set point value, and basal plasma calcium concentration was positively correlated with set point. Thus, the degree of hypercalcemia seems mainly determined by the magnitude of maximal PTH secretion and set point error in autonomous and suppressible PHPT, respectively. We have previously suggested that high serum calcitriol levels might chronically inhibit PTH hypersecretion in PHPT. We showed that hyperparathyroid patients with renal stone presentation exhibited an abnormally high value of circulating calcitriol and a moderately elevated PTH activity, while patients with severe bone disease presentation displayed a low to normal calcitriol value and a dramatically increased PTH activity. The hypothesis was supported by a recent study from our Unit in one hyperparathyroid patient with severe bone disease and normal serum calcitriol level. Increment of serum calcitriol after daily intravenous Rocaltrol for 5 days directly suppressed PTH hypersecretion without change in plasma ionized calcium.

Calcitriol↗

PubMed1989

Marked direct suppression of primary hyperparathyroidism with osteitis fibrosa cystica by intravenous administration of 1,25-dihydroxycholecalciferol.

A marked direct suppression of primary hyperparathyroidism with osteitis fibrosa cystica has been achieved by the intravenous administration of 1,25-dihydroxycholecalciferol [1,25(OH)2D]. In a recent survey of 306 patients with primary hyperparathyroidism (PHPT), we hypothesized that the far higher degree of parathyroid hormone (PTH) hypersecretion in PHPT with osteitis fibrosa cystica than in PHPT without overt bone disease might be due to the absence of suppression of hormonal hypersecretion by the low-to-normal circulating 1,25(OH)2D reflecting a relative vitamin D deficiency. To test this hypothesis, a patient having hypercalcemic PHPT with florid osteitis fibrosa cystica and normal serum 1,25(OH)2D was given increasing daily doses of intravenous calcitriol (0.5-2 micrograms) for several days. Doubling the level of circulating 1,25(OH)2D from 48 to 100-114 pg/ml was accompanied by a marked decline (46%) in serum iPTH(1-84), without a change in the serum calcium concentration. A lowered set point of parathyroid cells for calcium, and a diminished maximum secretory rate of PTH, may contribute to the marked suppression of PHPT.

Calcitriol↗

PubMed1988

Maximal PTH secretory rate and set point for calcium in normal subjects and patients with primary hyperparathyroidism. In vivo studies.

The characteristics of PTH secretion, which have been extensively studied in vitro with dispersed cells of normal and abnormal parathyroid glands, remain poorly studied in vivo. We performed ethylenediamine tetraacetate (EDTA) intravenous infusions in 12 normal subjects and 5 patients with hypercalcemia (serum ionized calcium between 2.72 and 2.89 mEq/l) and surgically proven primary hyperparathyroidism (PHPT) to establish the relationship between nephrogenous cyclic AMP (NcAMP) used as an index of PTH secretion and serum ionized calcium. We determined the maximal NcAMP taken as an index of maximal secretory rate for PTH, the set point and sensitivity of parathyroid cells for calcium. In normal subjects, mean values (+/- SD) were 4.04 +/- 0.47 nmol/dl glomerular filtrate (GF) for maximal NcAMP, 2.23 +/- 0.04 mEq/l for set point, and -250 +/- 58 for sensitivity when NcAMP was expressed in percent of maximal value and serum calcium in mEq/l. In patients with PHPT, the differences between maximal and basal values of NcAMP represented 50% or more of maximal NcAMP, indicating that PTH secretion was suppressible. Sensitivity values were within normal limits in all patients. Calculated set point values were abnormally elevated (between 2.64 and 2.83 mEq/l) in all patients. Maximal NcAMP values ranged from low to normal (2.77 nmol/dl GF) to abnormally high (6.64 nmol/dl GF), and a positive linear correlation was observed with parathyroid cell mass. Basal serum calcium concentrations were not correlated with either parathyroid cell mass or maximal NcAMP values, and were close to calculated set point values for each patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1986

Effects of increase in plasma calcium concentration on renal handling of NaCl and NaHCO3.

Recollection micropuncture experiments were carried out in thyroparathyroidectomized volume-expanded rats to examine the effects of CaCl2 infusion on the renal and nephronal segmental handling of chloride and bicarbonate. In group 1A, a 0.23 mM increase in plasma calcium concentration [delta(Ca)P] reduced urinary total CO2 (tCO2) excretion from 401 +/- 90 to 166 +/- 43 nmol X min-1 X g kidney wt-1 (P less than 0.05), whereas tCO2 filtered load was slightly diminished from 34,086 +/- 3,627 to 28,904 +/- 2,496 nmol X min-1 X g kidney wt-1 (NS). In group 1B [delta(Ca)P, 0.73 mM], whole kidney filtered loads were significantly lowered, as was urinary tCO2 excretion; however, urinary excretion of sodium, chloride, and water remained constant. Calcium infusion inhibited the proximal reabsorption of chloride 25% and water 16%; however, calcium infusion caused the end-proximal tCO2 concentration to significantly decrease so that the absolute and fractional tCO2 reabsorption remained constant. In group 2 [delta(Ca)P, 0.43 mM], whole kidney filtered load was unchanged for chloride and water but decreased for bicarbonate; urinary tCO2 excretion was reduced, whereas chloride and water excretion increased. In this group, early distal micropunctures evidenced that superficial single-nephron filtered loads were significantly reduced during calcium infusion; early distal chloride delivery was enhanced from 348 +/- 32 to 441 +/- 36 pmol X min-1 X g kidney wt-1 (P less than 0.05), whereas tCO2 delivery decreased from 47 +/- 5 to 38 +/- 4 pmol X min-1 X g kidney wt-1 (P less than 0.05). In group 3 of time control animals, whole kidney and early distal data were unchanged during second period. In group 4, H+ secretion in the collecting duct, as assessed by analyzing the relationship between urine-minus-blood PCO2 and urinary bicarbonate concentration in maximally alkaline urine, was not modified during CaCl2 infusion [delta(Ca)P, 0.79 mM]. We conclude that increase in plasma calcium concentration inhibits proximal NaCl and water reabsorption, whereas it stimulates the bicarbonate transport relative to that of chloride, leading to an enhanced proximal and renal bicarbonate-to-chloride reabsorptive ratio that could generate metabolic alkalosis; and decreases urinary bicarbonate excretion by also lowering the bicarbonate filtered load.

Absorption↗

PubMed1986

Effects of parathyroid hormone and urinary phosphate on collecting duct hydrogen secretion.

Urine-minus-blood PCO2 (U - B PCO2) during alkaline diuresis (urinary pH greater than 7.8) was determined in paired experiments using bicarbonate-loaded rats to assess the effects of parathyroid hormone (PTH) and urinary phosphate concentration [( Pi]u) on collecting duct H+ secretion. U-B PCO2 was higher for any value of urinary bicarbonate concentration ([HCO3]u) in the presence of PTH [intact rats and thyroparathyroidectomized (TPTX) PTH-infused rats] than in its absence (calcium-infused intact rats and TPTX rats). However, when [Pi]u was maintained constant by prior phosphate infusion, PTH administration in TPTX rats failed to elevate U-B PCO2. When PTH was infused in TPTX rats to maintain constant the plasma PTH level, subsequent phosphate infusion increased [Pi]u and elevated U-B PCO2 for any value of [HCO3]u. Moreover, when the data were pooled, there was a positive linear relationship between U-B PCO2 factored for [HCO3]u and [Pi]u (P less than 0.001). In all experiments, other factors that may affect U-B PCO2, such as plasma acid-base status, urinary osmolality, and extracellular fluid volume, did not vary. We conclude that PTH stimulates collecting duct H+ secretion indirectly via the increase in [Pi]u.

Animals↗

PubMed1986

Pseudohypoaldosteronism type II: proximal renal tubular acidosis and dDAVP-sensitive renal hyperkalemia.

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3-6.9 mmol/l), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mmol/l), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/h), high plasma aldosterone level (32-100 ng/dl), and normal glomerular filtration rate (131 ml/min/1.73 m2). During the hyperkalemic period, urine was highly acidic (pH 4.6-5.0), urinary NH4 excretion (10-13 microEq/min) and urinary net acid excretion (19-24 microEq/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, the maximal tubular HCO3 reabsorption was markedly diminished (19.8 mmol/l glomerular filtrate), and the fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized was 20%. Urine minus blood PCO2 increased normally during NaHCO3 infusion (31 mm Hg), and the urinary pH remained maximally low (less than 5.3) when the buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while the urinary pH remained maximally low (4.9-5.2), the maximal tubular HCO3 reabsorption returned to normal values (24.8 mmol/l glomerular filtrate), and FE HCO3 at normal plasma HCO3 was 1%. Nasal insufflation of 1-desamino-8-D-Arginine Vasopressin (dDAVP) resulted in an acute normalization of the renal handling of K and in an increase in net urinary acid excretion. We conclude that: the effect of dDAVP on renal handling of K may be explained by the reversal of the distal chloride shunt and/or an increase in luminal membrane conductance to K; the distal acidification seems to be normal which in the event of distal chloride shunt impairing distal hydrogen secretion might be explained by the presence of systemic acidosis which is a potent stimulus of hydrogen secretion, and metabolic acidosis in the steady state was accounted for by the diminution of bicarbonate reabsorption and ammonia production in the proximal tubule secondary to chronic hyperkalemia.

Acid-Base Equilibrium↗

PubMed1985

Hydrogen transport in papillary collecting duct of rabbit kidney.

To examine the cellular mechanisms of H+ transfer in rabbit papillary collecting duct (PCD), the 5,5-[14C]dimethyloxazolidine-2,4-dione-derived cell pH (pHi), the [3H]triphenylmethylphosphonium-derived membrane potential (Em), the lumen-to-cell Na+ concentration gradient [( Na+]o/[Na+]i), and cell potassium and chloride concentrations were studied at 37 degrees C in separated PCD from rabbits pretreated with deoxycorticosterone acetate. The variations in cell pH values were used as an index of changes in H+ secretion. Under standard conditions pHi was 7.30 +/- 0.04, [Na+]o/[Na+]i was 2.46 +/- 0.43, Em was 78 +/- 7 mV (cell negative), [K+]i was 105 +/- 10 mM, and [Cl-]i was 33 +/- 6 mM; the value of pHi thus remained higher than expected if H+ ions were passively distributed (6.13). Acetazolamide, 10(-4) M, alkalinized the cells. When [Na+]o/[Na+]i was reduced (low-Na+ medium or 10(-3) M ouabain), the cells did not acidify, suggesting that net H+ secretion did not decrease; also, pHi was not linked to the variations in the transmembrane chloride concentration gradients. When the cells were depolarized (low-Na+ medium), they became more alkaline; when the cells were hyperpolarized (10(-4) M amiloride), they became more acid; minor change in Em (ouabain) was associated with no change in pHi. It is concluded that: 1) H+ is actively secreted into the lumen; 2) active H+ secretion may not be secondary, via electroneutral Na+:H+ countertransport or HCl cotransport, but probably occurs via a primary H+ pump; 3) variations in Em probably affect pHi by acting on both the active H+ transport system and passive movements of HCO-3 (or its equivalent).

Acetazolamide↗

PubMed1985

[Type II pseudohypoaldosteronism: proximal tubular acidosis and distal tubular hyperkalemia corrected by DDAVP].

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3 to 6.8 mM), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mM), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/hr), high plasma aldosterone (32 to 100 ng/dl), normal GFR (131 +/- 2.5 ml/min/1.73 m2). During hyperkalemic period, urine was highly acidic (pH 4.6 to 5.0), urinary NH4 excretion (13 mumoles/min) and urinary net acid excretion (24 mumoles/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, maximal tubular HCO3 reabsorption (Tm HCO3) was markedly diminished (19 mmoles/liter GF), fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized, was 20%. Urine-minus-blood PCO2 increased normally (31 mmHg) during NaHCO3 infusion, and urinary pH remained maximally low (less than 5.3) when buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while urinary pH remained maximally low (4.9 to 5.2), Tm HCO3 returned to normal value (24.8 mmoles/liter GF), and FE HCO3 became nil. The renal handling of K was improved with acute NaHCO3 loading and normalized after DDAVP nasal insufflation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗

PubMed1983

Na:H exchange and the primary H pump in the proximal tubule.

Cell pH (pHi) transients were monitored at 5-min intervals with the weak acid 5,5-[14C]dimethyloxazolidine-2,4-dione and membrane potentials were estimated from the distribution of [3H]triphenylmethylphosphonium ion in separated proximal tubules (SPT) or rabbit kidney. SPT suspensions were gassed at 37 degrees C first with 5% CO2 and then with 15% CO2. Under normal conditions, pHi rapidly fell during initial 15% CO2 acid loading and then recovered within 20 min. In the presence of 10(-3) M ouabain, which eliminated Na:H exchange as a driving force for H+ secretion, initial cell acidification was still followed by cell pH recovery, which demonstrated a sodium gradient-independent H+ extruding mechanism. In the presence of 10(-3) M ouabain plus 10(-4) M potassium cyanide, there was no pHi recovery following initial cell acidification but, on the contrary, further progressive cell acidification occurred, which is compatible with passive diffusion only of HCO-3 out of the cell. From the cyanide experiments, an apparent permeability coefficient for HCO-3 of the basolateral cell membrane was calculated; this latter result allowed the calculation of rates of passive HCO-3 diffusion and of active H+ extrusion under normal conditions and in the presence of 10(-3) M ouabain. We conclude that in the proximal tubule 1) there is a primary H+ pump additional to Na:H exchange; and 2) this primary H+ pump is responsible for about 25% of active H+ extrusion following acute CO2 cellular acid loading.

Animals↗

PubMed1983

Unilobar small hepatic vein obstruction: possible role of progestogen given as oral contraceptive.

The case of a 33-yr-old woman with an obstruction of small hepatic veins limited to the right lobe of the liver is reported. Abdominal pain, fever, absence of ascites, and normality of liver biochemical tests were the most striking features. Abnormalities characteristic of lesions were observed on surgical wedge liver biopsy, hepatic phlebography, and computerized tomography. None of the usual causes of small hepatic vein obstruction were found. This patient had been taking an oral progestative compound as contraceptive therapy for 7 mo before evaluation. Because progestogens have recently been incriminated in the occurrence of vascular alterations, the possible role of this drug in our case is discussed.

Adult↗

PubMedDate not supplied

[Present status of primary hyperparathyroidism].

The availability of accurate and inexpensive methods for measuring serum calcium levels has resulted in a rapid increase in the number of diagnoses of primary hyperparathyroidism, notably in its asymptomatic hypercalcemic forms. In addition, the development of a radioimmunoassay of the parathyroid hormone and, more recently, measurements of nephrogenous cyclic AMP during fasting and after calcium loading have led to the recognition of clinical variants of the disease, such as intermittent or borderline hypercalcemia and pure hypercalciuria with normal calcemia. The degree of hypercalcemia in stable primary hyperparathyroidism depends on renal tubular reabsorption of calcium rather than on bone resorption. The poor correlation observed between calcium tubular reabsorption rate and magnitude of parathyroid hormone hypersecretion suggests that as yet undetermined factors interfere with the effects of parathyroid hormone on renal tubules and probably account for the fluctuations in calcemia reported during serial determinations in patients. The sigmoid relationship between parathyroid hormone release and extracellular calcium concentrations has been analyzed from recent in vitro studies with dispersed parathyroid cells. In primary hyperplasia of the parathyroid glands hypersecretion of parathyroid hormone seems to depend principally upon the increase in tissue mass with normal sensitivity to calcium at cellular levels, whereas in adenoma the primary abnormality responsible for hypersecretion of parathyroid hormone would be an alteration in cell sensitivity to calcium, as indicated by an elevated "set point". Finally, while complicated primary hyperthyroidism requires surgery, our limited knowledge of the natural history of asymptomatic forms makes it impossible to decide which of these patients will ultimately need to be operated upon.

Calcium↗