Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a retrospective analysis to determine whether secondary hyperparathyroidism in uremia has a role in uremic peripheral neuropathy, we simultaneously measured motor-nerve conduction velocity and serum parathormone level in 42 uremic patients. We compared age-matched groups of nondiabetic uremic patients, divided into three groups according to serum parathyroid hormone, for degree of impairment of motor-nerve conduction velocity, and 12 diabetic patients with uremia. The group with highest levels had a significantly (P less than 0.01) lower conduction velocity (25.3 +/- 4.9 m per second) than the group with normal or slightly elevated parathyroid hormone, who had only mild depression of nerve conduction (45.1 +/- 1.3 m per second). Mean serum calcium and creatinine were not significantly different between groups. Nerve conduction velocity was similarly depressed in 17 patients on additional dialysis studied prospectively and divided into groups according to parathyroid hormone levels. These results suggest a relation between high parathormone levels and uremic neuropathy and implicate parathyroid hormone as a uremic toxin.
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PMID:Search for the uremic toxin. Decreased motor-nerve conduction velocity and elevated parathyroid hormone in uremia. 20 86

This study was an attempt to compare psychological and biological variables in 43 obese patients after intestinal bypass surgery. The difficulties in expressing the psychological variables quantitatively are discussed on the basis of the concept of transferability. By use of an expanded version of the Beck Depression Inventory and the Marke-Nyman Temperament Scale we could demonstrate that items concerning asthenia (self-dislike, irritability, work retardation, insomnia, fatigability, somatic preoccupation about aches and pains, loss of libido, headache, vertigo, palpitations, dryness of the mouth, thirst or increased liquid intake) had, when summed up, a score distribution indicating bimodality. The asthenic group of patients (n = 19) when compared with the non-asthenic patients (n = 24) showed metabolic deficiencies related to the vitamin D complex with no response to oral vitamin D3 administration measured by plasma levels of 25-hydroxyvitamin D3. The lack of response was associated with low calcium excretion in the urine, higher plasma alkaline phosphatase, and a tendency to higher blood levels of parathyroid hormone.
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PMID:Depression or asthenia related to metabolic disturbances in obese patients after intestinal bypass surgery. 46 85

In a patient with hyperparathyroidism (HPT) two neck explorations with identification of three normal parathyroid glands were carried out. Cervical and mediastinal vein catheterization with blood sampling for determination of parathyroid hormone (PTH) confirmed drainage of large amounts of PTH to a mediastinal vein. Two thoracic explorations were negative anterior and posterior mediastinum). The operations were performed during 1971 and 1978 and extensive, progrediating decalcification with brown tumour formation was radiologically demonstrated during that time. Diminished renal function, skeleton pain and mental depression necessitated a last exploration, at which a 2 cm large parathyroid adenoma was found in the left carotid sheath just below the left mastoid process. The adenoma was drained into mediastinal veins through long anastomotic branches.
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PMID:Hyperparathyroidism--a life-threatening disease in 1978. A case report. 53 42

Twenty-four lactating cows were fed a normal-calcium (.75% of dry matter) diet plus free-choice dicalcium phosphate supplement for 8 wk, a low-calcium (.25% of dry matter) diet for 9 wk, and a low-calcium (.25% of dry matter) diet plus free-choice supplement for 4 wk. The low-calcium diet did not appear to affect adversely feed intake, milk production, or plasma ions. Depression of plasma calcium by sequestration with a chelating agent was less following low intake of calcium than following adequate calcium intake. Presumably, lower calcium intake increased parathyroid hormone which resulted in a larger and more responsive calcium pool immediately mobilizable. Changes in plasma phosphorus and magnesium were similar among treatments. Low calcium intake for short times apparently will not affect intake or production and may increase resistance to calcium stress such as hypocalcemia and parturient paresis.
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PMID:Effects of a low calcium diet on feed intake, milk production, and response to blood calcium challenge in lactating Holstein cows. 81 74

Within 24 hr after unilateral nephrectomy, fractional excretion of phosphate (FEp) by the remaining kidney is markedly increased. This increase in FEp occurs in throparathyroidectomized rats receiving fixed replacement doses of parathyroid hormone and, therefore, cannot be due to secondary hyperparathyroidism occurring in response to unilateral nephrectomy. In the avsence of any hormone replacement, the increase in FEp is much reduced, but still present. The increase in FEp cannot be ascribed to depression of overall tubular sodium reabsorption because it could be demonstrated in the absence of an increase in FENa. Phosphaturia following unilateral nephrectomy in the rat appears to be part of the complex of events that occur after acute reduction of renal mass; the exact mechanisms of its genesis are uncertain.
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PMID:Compensatory phosphaturia after unilateral nephrectomy in the rat. 99 8

Mg deficiency was produced in rats by feeding a Mg-free diet. Ten days of dietary Mg depletion led to an increase in active duodenal Ca absorption in sham-operated animals, but this increase was abolished by thyroparathyroidectomy (TPTX). In addition, TPTX reduced Ca absorption in control aminals fed a Mg-containing diet. More prolonged Mg deficiency was produced by feeding sham-operated animals the Mg-free diet for 19 days. This condition resulted in more marked hypomagnesemia and a depression of Ca transport rates to the level observed in the TPTX groups. These results are consistent with the concept that adaptation of duodenal Ca transport in response to Mg deficiency occurs through an increase in parathyroid hormone (PTH) secretion; however, direct blood PTH measurements will be required to prove this point.
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PMID:Effects of magnesium deficiency and thyroparathyroidectomy on calcium active transport by rat duodenum. 112 21

Amino acid clearances were studied in four patients with hypophosphatemic vitamin D resistant rickets. T,e clearances of the single amino acids in the patients did not differ from that of control individuals for all amino acids tested. The reabsorption of amino acids and phosphate was further investigated with the use of calcium infusions. Under these conditions there was a significant decrease in the filtered fraction of phosphate and amino acid excreted in the vitamin D resistant group suggesting a depression of parathyroid hormone secretion. It seems likely, as demonstrated in the vitamin D resistant group, that in this disorder the renal tubule is particularly sensitive to changes in parathyroid hormone secretion in respect to amino acid reabsorption.
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PMID:The effect of calcium infusions on renal handling of amino acids in hypophosphatemic vitamin D resistant rickets. 116 91

The mechanism of inhibition of HCO3 transport by parathyroid hormone (PTH) in the proximal tubule is not clearly defined. Previous studies in vitro have suggested that this effect is mediated via cAMP generation, which acts to inhibit Na/H exchange, resulting in cell acidification. To examine this question in vivo, intracellular pH (pHi) was measured in the superficial proximal tubule of the rat using the pH-sensitive fluoroprobes 4-methylumbelliferone (4MU) and 2',7'-bis(carboxyethyl)-(5, and 6)-carboxyfluorescein (BCECF). PTH was found to alkalinize the cell. This alkalinization suggested inhibition of basolateral base exit, which was confirmed by in situ microperfusion studies: lowering HCO3 in peritubular capillaries acidified the cell, an effect blunted by PTH. Removal of luminal Na promoted basolateral base entry, alkalinizing the cell. This response was also blunted by PTH. Readdition of luminal Na stimulated the luminal Na/H exchanger, causing an alkalinization overshoot that was partially inhibited by PTH. cAMP inhibited luminal H secretion but did not alkalinize the cell. Stimulation of phosphatidylinositol-bis-phosphate turnover by PTH was suggested by the effect to the hormone to increase cell Ca. Blocking the PTH-induced rise in cell Ca blunted the effect of the hormone to alkalinize the cell, as did inhibition of phosphatidylinositol breakdown. Furthermore, stimulation of protein kinase C by a phorbol ester and a diacylglycerol applied basolaterally alkalinized the cell and inhibited luminal H secretion. The findings indicate that both arms of the phosphatidylinositol-bis-phosphate cascade play a role in mediating the effect of PTH on the cell pH. The results are consistent with the view that PTH inhibits base exit in the proximal tubule by activation of the phosphatidylinositol cascade. The resulting alkalinization may contribute, with cAMP, to inhibit apical Na/H exchange and the PTH-induced depression of proximal HCO3 reabsorption.
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PMID:Parathyroid hormone decreases HCO3 reabsorption in the rat proximal tubule by stimulating phosphatidylinositol metabolism and inhibiting base exit. 131 50

Cellular immunity and blood serum levels of parathyroid hormone have been studied in patients with gestoses depending on the disease severity. Progressive immune depression accompanied by a parallel drop in parathyroid hormone level up to critical values has been demonstrated in patients with eclampsia. The patients with pre-eclampsia were treated postoperatively with t-activin. Cellular immunity was compared in patients on and off t-activin. A marked immunostimulating effect of the drug on T-lymphocytes and especially on theophylline-resistant T-lymphocyte subpopulations has been revealed. The effect of t-activin was most marked on the 3rd-5th day of the postoperative period.
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PMID:[The use of T-activin in the intensive therapy of the postoperative period in gestosis patients]. 148 74

Parathyroid hormone and calcitonin, two major calcium-regulating hormones, were measured in the plasma of five experimental groups of rats to evaluate postflight calcium homeostasis after the 14-day COSMOS 2044 flight. Parathyroid hormone values were slightly higher in the flight animals (F) than in the appropriate cage and diet controls (S) (44 +/- 21 vs. 21 +/- 4 pg/ml, P less than 0.05), but they were the same as in the vivarium controls (V), which had different housing and feeding schedules. Neither V nor S showed the increase in plasma creatinine phosphorus and magnesium found in F, features of early renal insufficiency. F showed the lowest mean plasma calcitonin that was statistically different from V only. This difference in F and V (22 +/- 11 vs. 49 +/- 16 pg/ml, P less than 0.05) was most likely due to failure of circulating calcitonin in F to show the normal age-dependent increase we demonstrated in age-matched controls in a separate experiment. Basal values for parathyroid hormone and calcitonin were unchanged after 2 wk of hindlimb suspension, a flight simulation model, in age-matched and younger rats. From a time course experiment serum calcium was higher and parathyroid hormone lower after 4 wk than in ambulatory controls. Postflight circulating levels of parathyroid hormone appear to reflect disturbances in calcium homeostasis from impaired renal function of undetermined cause, whereas levels of calcitonin reflect depression of a normal growth process.
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PMID:Circulating parathyroid hormone and calcitonin in rats after spaceflight. 152 47


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