Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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.
 ...
PMID:Search for the uremic toxin. Decreased motor-nerve conduction velocity and elevated parathyroid hormone in uremia. 20 86

Parathormone (PTH) excess limits renal bicarbonate reabsorption. This may aggravate the acidosis in patients with renal insufficiency and secondary hyperparathyroidism. Why parathormone, the primary action of which is thought to be stabilization of the inonized fraction of calcium, affects acid-base balance remains uncertain. Parathormone not only promotes the release of calcium from bone but also mobilizes salts, including bicarbonate and phosphate. Accumulation of these anions in the extracellular fluid would limit the ionization of calcium. Teleologically it is not unexpected to find that, coincident with evolution of a mechanism which permits rapid mobilization of calcium from bone, a system had to develop which removed the byproducts of bone dissolution. If this concept is valid, parathormone-induced depression of renal bicarbonate reabsorption in uremia represents an undesired side effect of an adaptive mechanism. This would extend Bricker's "trade-off" hypothesis which ascribes metabolic bone disease due to PTH-induced phosphate loss to include metabolic acidosis resulting from diminished renal bicarbonate regeneration. Parathyroidectomy or phosphate restriction have been proposed for correction of the side effects of secondary hyperparathyroidism. These therapeutic manipulations cannot be recommended for general use. A more rational apprach for prevention of secondary hyperparathyroidism is the combined use of phosphate restriction with a short-acting vitamin D derivative.
 ...
PMID:Parathyroid hormone and the regulation of acid-base balance. 110 50

Psychiatric symptoms are well recognized as a feature of patients with primary hyperparathyroidism. We have applied a standardized psychiatric interview to 15 patients before and after surgery. Thirteen had a lower 'psychiatric score' (less psychiatric morbidity) after surgery and improvements were particularly seen in symptoms of fatigue, depression, irritability, sleep disturbance and lack of concentration. The levels of intellectual impairment and of anxiety were unchanged after surgery. The 'psychiatric scores' in an additional group of 21 hyperparathyroid patients, in whom a decision to treat conservatively had been made independently, were similar to those in the surgically treated patients after surgery. Among all the untreated patients no relationship was found between overall 'psychiatric score' and serum levels of calcium or parathyrin.
 ...
PMID:Psychiatric morbidity in primary hyperparathyroidism. 260 90

Sixty-one consecutive patients were examined to determine the current mode of presentation of primary hyperparathyroidism (pHPT). Of these patients, 37.7% were asymptomatic, and the initial indication of pHPT was hypercalcemia, which was found unexpectedly on biochemical screening of the serum in elderly patients. Hypertension was twice as common among patients with pHPT as in the general population (36.1%). The next most common presentations were urinary calculi (18%) and mental depression (18%). The most useful discriminant laboratory tests were serum calcium, phosphorus, chloride, and parathormone (PTH). The calculated coefficient of correlation of PTH to land weight was high (r = 0.571, p less than 0.001). There was very significant correlation between PTH and seriousness of bone disease (r = 0.620, p less than 0.001). After parathyroidectomy, 3.3% of patients remained hypercalcemic, 93% were normocalcemic, and 1.6% were hypocalcemic.
 ...
PMID:Clinical and biochemical features in primary hyperparathyroidism. 291 78

Animal experimental studies conducted at the turn of the century resulted in the use of magnesium sulphate as an anticonvulsant in humans. In U.S. clinics, parenteral administration of magnesium sulphate became a routine procedure in the treatment of eclampsia and pre-eclampsia. This treatment has proved very effective in treating convulsions in pregnancy provided an adequate dosage was given amounting to up to 60 g daily. Mother and infant mortality were largely eliminated. Numerous clinical studies showed a negligible side effect rate. Side effects in the foetus: These are due to penetration of magnesium into the foetal blood circulation. Reports on an inhibition of cardiac rate fluctuation and changes in calcium levels have been contradictory, and hence not generally accepted. It is claimed that the parathormone level may drop slightly. Isolated reports on foetal magnesium intoxications associated with depression of breathing, slackness and hyporeflexia often prompt the conclusion that this disease pattern had been due to immaturity and asphyxia. Generally, foetal magnesium blood levels do not correlate well with signs of magnesium intoxication. Urine excretion is greatly slowed down in foetal immaturity. Side effects in the mother: Short-term relaxing action on the uterus has been described frequently. High dosages have been successfully used in arresting labour if there is a tendency to premature birth. Increase in uterine blood flow was seen after administration of magnesium sulphate in animal experiments. Magnesium is said to reduce blood coagulation by influencing fibrinolysis and thrombocyte resistance. However, a somewhat enhanced loss of blood during birth is said to be more likely due to relaxation of the uterus than to a disturbance of blood coagulation. Rapid intravenous injection causes short-term flushing, nausea and vomiting. Short-acting drops in blood pressure are possible. The cardiac output is said to increase at the conventional dosage level whereas the peripheral resistance drops due to vasodilation. Increases and decreases in heart rate have been reported, but in most cases no changes were seen. Changes in ventricular action time occur with toxic doses only, which can lead to cardiac arrest in the diastole. Other toxic signs are hyporeflexia, depressed breathing and CNS depressions which may result in coma. Hyporeflexia always occurs before the other toxic signs appear, so that it can be used as a clinical control criterion. Calcium gluconate, given via the IV route, is a good and rapid-acting antidote.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[Use of magnesium sulfate as an anticonvulsant in severe pregnancy toxemia and eclampsia]. 655 75

Rapid immobilization after acute spinal cord injury (SCI) leads to increased bone resorption, net calcium efflux from the bone, hypercalciuria, depressed parathormone (PTH) and increased calcitonin release. However, the effects, if any, of long-standing SCI on calcium regulatory system is not well understood. We measured plasma concentrations of 25 hydroxy (OH) vitamin D, 1,25(OH)2 vitamin D (calcitriol), intact PTH molecule, calcitonin, ionized calcium [Ca++] and phosphorus in 40 clinically stable men with long-standing SCI of 3-year to 50-year duration (22 persons with paraplegia and 18 persons with quadriplegia). The results were compared with those obtained in 14 able-bodied control men. Plasma PTH concentration in the SCI group was significantly lower than that found in the able-bodied controls despite virtually identical concentrations of ionized calcium. Likewise, plasma calcitriol concentration in the SCI group was significantly lower than the value found in the able-bodied control group and lower in persons with quadriplegia than in those with paraplegia. In contrast, plasma calcitonin concentration in the quadriplegic group was significantly higher than that in persons with paraplegia and insignificantly higher than that in the control group. No significant difference was noted in serum ionized calcium between the study groups. PTH and calcitriol levels were positively related to one another (r = 0.35, p < .01) and negatively related to the level of injury (r = -0.43, p < .002 and r = -0.54, p < .001, respectively). In conclusion, long-standing SCI is associated with significant depression of calcitriol and PTH concentrations despite normal ionized calcium concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Vitamin D, parathormone, and calcitonin profiles in persons with long-standing spinal cord injury. 802 22

Idiopathic basal ganglia calcifications is a heterogeneous entity characterized by the association of bilateral and symmetric calcifications of the basal ganglia and the dentae nuclei in the cerebellum, polymorphous neuropsychiatric symptomatology. It is rare, of unknown etiology and often hereditary. We report the case of a 48 years old man, who presented with melancholic depression which has been steadily worsening for more than a year and which had led to a serious suicide attempt. Clinical observation revealed apragmatism, affective dullness and impoverished spontaneous expression; the theme of incapacity predominated but guilt feelings were absent. Neurologic examination was normal except for extra-pyramidal signs. CT-scan revealed the presence of bilateral and extensive calcifications of caudate nuclei, lenticular nuclei and thalamus, which indicated a diagnosis of idiopathic basal ganglia calcification characterized by depression. Moreover, MRI revealed an hypersignal of the white periventricular substance. Phospho-calcic results and the parathormone dosage were normal. Psychometric tests showed that although intellectual capacity seemed to be intact, it was not utilised in practice. Unresponsive to antidepressants and sismotherapy, the patient is still the same one and a half year later, and needs to remain in an institution. Subsequent tests indicate that intellectual deterioration has begun. This case poses the problem of the relationship between depressive syndrome and basal ganglia lesions. We look at studies bearing on this subject and on other clinically similar syndromes (athymhormia, loss of psychic self-activation), in which the interruption or cortico-striato-pallido-thalamo-cortical circuits (particularly the limbic loop), is a physiopathologic mechanism currently invoked.
 ...
PMID:[Depression and calcinosis of the basal ganglia: apropos of a case]. 870 22

The authors reached the suppression of serum intact parathormone (iPTH) by calcitriol therapy in chronic hemodialyzed patients with secondary hyperparathyroidism. Parallel with the depression of iPTH levels it was enough a lower doses of recombinant human erythropoietin (Rh-EPO) to maintain the target hematocrit, while on two patients non-treated with Rh-EPO they founded an improvement in moderate anemia. Their data confirm that the calcitriol is an effective drug in the treatment of secondary hyperparathyroidism. The results speak in favour that in the improvement of renal anemia on regular hemodialysis patients play an important role the suppression of serum iPTH levels too.
 ...
PMID:[The effect of calcitriol on renal anemia in patients under chronic hemodialysis]. 917 68

The main forms of renal osteodystrophy are secondary hyperparathyroidism, aluminum-induced bone disease and adynamic bone disease without aluminum intoxication. Aluminum intoxication has become rare because of control of the dialysate solution and avoidance of aluminum containing phosphate binders. Secondary hyperparathyroidism still develops early in the course of renal failure and remains the most frequent form of osteodystrophy in patients treated by maintenance hemodialysis. Several factors, including hyperphosphatemia and deficient synthesis of 1,25-dihydroxyvitamin D are involved in its pathogenesis. Secondary hyperparathyroidism is symptomatic only in severely affected patients. Prevention depends on control of serum phosphorus +/- prescription of 1-alpha-hydroxylated vitamin D derivatives or may require subtotal parathyroidectomy when hyperparathyroidism is refractory.Adynamic bone disease not related to aluminum intoxication has been increasingly recognized in recent years and is presently the most frequent form of osteodystrophy in continuous ambulatory peritoneal dialysis patients. This condition, characterized by low bone turnover and depression of bone formation, appears to be associated with an increased risk of bone fracture. The main pathophysiologic feature is excessive treatment of hyperparathyroidism leading to hypoparathyroidism. Serum immunoreactive 1,84-parathormone levels should therefore be kept at a level of 1.5-fold to 3-fold the upper limit of normal in patients treated by maintenance hemodialysis.
 ...
PMID:Renal osteodystrophy. 1907 65

The correlation between vitamin D deficiency and depression has recently been put forward and resulted in controversial findings. The present study was conducted to find out the effect of 2 single injections of 150,000 and 300,000 IU of vitamin D on improving the depression in depressed patients with vitamin D deficiency.This clinical trial study was carried out during 2011-2012 in Yazd, Islamic Republic of Iran. A total of 120 patients who had a Beck Depression Inventory II score of 17+ and were affected with vitamin D deficiency were randomly assigned to 3 groups of 40. They included G300, G150, and NTG. G300 and G150 received an intramuscular single dose of 300,000 and 150,000 IU of vitamin D, respectively, and the NTG group received nothing. After 3 months of intervention, the depression state, serum vitamin D, calcium, phosphorus, and parathormone were measured.The median of serum vitamin D after intervention were 60.2, 54.6, and 28.2 nmol/L (P < 0.001) for the G300, G150, and NTG, respectively. Percentages of vitamin D deficiency after intervention were 18, 20, and 91.2 for the groups, respectively. The serum calcium mean showed a statistically significant increase in just the 2 test groups receiving vitamin D. There was only significant difference in mean of Beck Depression Inventory II test score between G300 and NTG (P = 0.003).The results of the study revealed that first, the correction of vitamin D deficiency improved the depression state, and second, a single injection dose of 300,000 IU of vitamin D was safe and more effective than a 150,000-IU dose.
 ...
PMID:The effect of 2 different single injections of high dose of vitamin D on improving the depression in depressed patients with vitamin D deficiency: a randomized clinical trial. 2360 90


1 2 Next >>