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)

Hypocalcemia, although a relatively uncommon sequela of operations for carcinoma of the larynx and pharynx, often presents as an acute medical emergency. In its chronic form, hypocalcemia may be a difficult disorder to control. Understanding the etiologic basis of hypocalcemia secondary to operations for carcinoma of the head and neck requires knowledge of the pathophysiology of the preoperative and postoperative factors affecting calcium homeostasis. These factors include thyroidectomy, hypoparathyroidism, hypomagnesemia, anticonvulsant therapy, estrogen replacement therapy, oral contraceptives, blood transfusions, hyperventilation alkalosis, hypoalbuminemia, corticosteroid therapy, depression, emotional stress and diet. Often the onset of symptoms and signs of hypocalcemia occurs within 24 to 48 hours after the operation. The symptoms may include mental depression, headache, tingling of the hands and perioral region and abdominal pain. Unrecognized chronic hypocalcemia may lead to the development of cataracts, convulsions and psychosis.
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PMID:Etiologic factors in hypocalcemia secondary to operations for carcinoma of the pharynx and larynx. 67 61

Idiopathic hypoparathyroidism in a 3-year-old dog was manifested clinically as periodic episodes of depression, vomiting, and tetanic convulsions. Hypocalcemia and hyperphosphatemia were detected late in the course of the illness, but the dog died before corrective measures could be instituted. The pathologic features were similar to those reported in dogs in which hypoparathyroidism was induced by injection of homologous parathyroid tissue, thus suggesting an auto-immune pathogenesis.
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PMID:Idiopathic hypoparathyroidism in a dog. 126 51

The mechanical and electrical effects of hypoparathyroidism (Px), hypothyroidism (Tx), and hypothyroidism combined with hypoparathyroidism (TPx) were investigated by comparing simultaneously recorded transmembrane action potentials and isometric and isotonic contractions recorded from the myocardium. Left ventricular papillary muscles from male Wistar rats were studied electrically and mechanically in a muscle bath at 30 degree C, stimulated at 0.1 Hz and external calcium = 2.4 mM. No significant difference was found between control (C), Px, Tx, and TPx preparations with regard to resting tension and developed tension. However, time to peak tension, time to one half relaxation and time to peak shortening were significantly increased in preparations from animals that were Px, Tx, and TPx as compared with age-matched controls. Maximum velocities of shortening (Vs) and relengthening (Vr) at all relative loads studied were significantly depressed in Px preparations when compared with those of C muscles. A greater depression was found in the Tx muscle and still greater depression of these indices was noted in TPx muscles. No significant difference was found between C, Px, Tx, and TPx action potential with regard to resting membrane potential (RMP), action potential amplitude (AMP), overshoot (OS), or maximum rate of rise of the upstroke (Vmax).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of hypothyroidism and hypoparathyroidism on rat myocardium: mechanical and electrical alterations. 370 91

In previous work we found that vitamin D-deficient and also calcium-deficient rats developed hypocalcemia and an impairment of bone formation and mineralization. The present study of thyroparathyroidectomized (TPTX) rats was undertaken to determine the effect of hypocalcemia without secondary hyperparathyroidism. TPTX rats fed a normal diet developed hypocalcemia and hyperphosphatemia in association with impairment of osteoblastic bone matrix formation and of mineralization of newly formed matrix. The serum calcium x phosphorus product was not decreased. The decreased formation was largely due to a reduction in matrix apposition indicating decreased synthetic activity of individual ostcoblasts. In contrast to the above results, when TPTX rats were fed a high-calcium diet to prevent hypocalcemia, no impairment of either formation or mineralization was found. From the results of these two experiments, it is reasonably certain that hypocalcemia was responsible for the inhibition of formation and mineralization. Moreover, based on the magnitude of the changes in serum calcium and bone parameters in TPTX rats, hypocalcemia could have accounted for the inhibition of formation and mineralization in calcium-deficient as well as vitamin D-deficient rats. In TPTX rats the mineralization defect was manifested by decreases in both the rate of osteoid maturation (indicating a delayed onset of mineralization) and the rate of mineralization. A strong correlation (r = 0.95, P < 0.001) was observed between these two rates suggesting a tight coupling of these two aspects of mineralization.TPTX rats also had lower bone resorption rates and higher serum phosphorus levels than sham-operated animals when the normal calcium diet was fed but not when the high-calcium diet was fed. Thus the inhibition of bone resorption in TPTX rats was at least partially prevented by correction of hyperphosphatemia. This is consistent with previous work showing an inverse relationship between serum phosphorus and bone resorption. Accordingly, the depression of bone resorption in TPTX rats was probably due to hyperphosphatemia as well as to hypoparathyroidism.
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PMID:Inhibition of bone matrix formation, mineralization, and resorption in thyroparathyroidectomized rats. 470 Apr 83

The present authors observed and treated a siblings case of normocalcemic tetany, which is considered as belonging to Bartter's syndrome. As far as we know, there are a number of familial cases of tetany in literature, but none of them spreads over more than two generations, so that the tetany appears to be recessive in hereditary characters including our patients. Both of them presented tetanic seizures in the course of Bartter's syndrome and they were regarded as one of various manifestations of the syndrome. In other words, the Bartter's syndrome or the hypopotassemia should be one of the fundamental disorders for developing tetanic symptom. The tetanic symptoms became extinct during the treatment with spironolactone against hypopotassemia. Of the two patients, younger sister had shown an agitated depression developed on her childish and over-sensitive personality, but the depression was improved in parallel to the recovery from tetany and hypopotassemia. Therefore, it appears to be certain that the patients would have some premorbid deviation of personality traits, where symptomatic psychoses could be attributed, in the case of Bartter's syndrome. Generally speaking the psychic disorders, such as personality deviation and psychotic episode, seem to by very important symptoms in patient with Bartter's syndrome as well as in patient with hypocalcemia or hypoparathyroidism.
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PMID:[Development of tetany in siblings suffered from Bartter's syndrome]. 649 22

The basal values of plasma vitamin D metabolites were evaluated in patients with primary hyperparathyroidism (1 degree HPT, n = 31), hypoparathyroidism (HP, n = 7), pseudohypoparathyroidism (PHP, n = 4) and normal controls (n = 21). Plasma 25-hydroxyvitamin D (25-OH-D) in 1 degree HPT (9.0 +/0 7.3 ng/ml, mean SD) was significantly lower than that of normal controls (17.9 +/- 5.5ng/ml)(p less than 0.001), and in particular 1 degree HPT classified as the skeletal type showed extremely low value (4.7 +/- 4.6 ng/ml). Plasma 1, 25-dihydroxyvitamin D [1, 25-(OH)2D] was significantly higher in 1 degree HPT (69.1 +/- 31.4pg/ml)(p less than 0.001) and significantly lower in Hp (15.2 +/- 11.0 pg/ml) (p less than 0.001) compared to normal controls (37.2 +/- 13.8pg/ml), although there was no significant difference in PHP (22.3 +/- 17.5 pg/ml). Plasma 24, 25-dihydroxyvitamin D [24,, 25-(OH)2D] in 1 degree HPT (1.06 +/- 0.55 ng/ml) was significantly lower than that of normal controls (1.73 +/- 0.62 ng/ml) (p less than 0.05), and particularly 1 degree HPT classified as the skeletal type showed a marked low value (0.85 +/- 0.27 ng/ml), whereas no significant differences were seen in HP (1.84 +/- 0.46 ng/ml) or PHP (1.34 +/- 0.22 ng/ml). There were slight but significant correlations between either plasma 25-OH-D and 1, 25-(OH)2D (r = -0.350, p less than 0.05), or plasma 25-OH-D and 24, 25-(OH)2D (r = 0.356, p less than 0.05), or plasma 1, 25-(OH)2D and 24, 25-(OH)2D (r = -0.444, p less than 0.01) in all subjects. In addition, relationships between plasma vitamin D metabolites and other indicators of parathyroid function in all subjects were analyzed. There were positive correlations between plasma 1, 25-(OH)2D and serum Ca (r = -0.621, p less than 0.001) or urinary cAMP (r = -0.671, p less than 0.001) or nephrogenous cAMP (r = -0.689, p less than 0.001), while negative correlations were seen between plasma 1, 25-(OH)2D and serum P (r = -0.680, p less than 0.001) or %TRP (r = -0.663, p less than 0.001). On the other hand, there were negative correlations between plasma 24, 25-(OH)2D and serum Ca (r = -0.457, p less than 0.01) or urinary cAMP (r = -0.562, p less than 0.005) or nephrogenous cAMp (r = -0.561, p less than 0.005), and a positive correlation was seen between plasma 24, 25-(OH)2D and %TRP (r = 0.519, p less than 0.005). After parathyroidectomy, a distinct depression of plasma 1, 25-(OH)2D and reciprocal elevation of plasma 24, 25-(OH)2D were observed in 1 degree HPT. Furthermore, there was a clear elevation of plasma 24, 25-(OH)2D as well as plasma 1, 25-(OH)2D after treatment with maintenance doses of 1 alpha-OH-D3 or 1 alpha, 25-(OH)2D3 in HP and PHP. It is concluded that plasma vitamin D metabolites are very useful as the indicators of parathyroid function.
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PMID:[Plasma vitamin D metabolites in parathyroid diseases (author's transl)]. 698 Jan 45

At the origin, idiopathic hypercalciuria has been described as a syndrome consisting of normocalcemia, low plasma phosphate levels and abnormally high urinary calcium excretion. The cause of this syndrome was subject to many investigations throughout the years. Two main pathophysiologic hypotheses have been proposed: a) primary intestinal hyperabsorption of calcium, leading to depression of parathyroid hormone (PTH) secretion ("absorptive" hypercalciuria); and b) primary renal tubular leak of calcium which stimulates PTH secretion (secondary hyperparathyroidism). Most of the published studies indicate that intestinal hyperabsorption of calcium with subsequent relative hypoparathyroidism is the primary event causing idiopathic hypercalciuria, and that this occurs as a consequence of increased production of 1,25(OH)2-vitamin D3 (calcitriol). Fasting hypercalciuria, originally taken as evidence for a "renal leak" of calcium, appears to be, at least in part, the consequence of relative hypoparathyroidism.
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PMID:The tale of parathyroid function in idiopathic hypercalciuria. 831 9

Thyroid hormones affect the functions of several organs including the heart and kidney. Using isolated left papillary muscles we have investigated the action of thyroid hormones on the mechanical and electrical properties of the heart. We found that pure hypothyroidism causes a depression in contractile and electrical parameters, but we noticed that superimposed hypoparathyroidism accounts for the marked prolongation in contractile kinetics and action potential duration. At kidney level we have shown that thyroid hormones affect proximal tubular sodium transport and this effect is only partially mediated by the action of thyroid hormones on Na-K-ATPase activity. Using the micropuncture technique, we hypothesized that the early effect of thyroid hormone action is on the potassium permeability of proximal tubular cell membrane. This latter effect would explain the increase in isotonic fluid reabsorption through an increase in the driving force for sodium. Finally, hypothyroid patients have a decrease in glomerular filtration rate and renal plasma flow that are completely reversed by thyroxine administration. On the other hand, hyperthyroid subjects exhibit a significant increase in both parameters.
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PMID:Effects of thyroid hormones on heart and kidney functions. 1020 61

The exact cause of depression in cases of hypoparathyroidism is not known. We report the first case of an elderly patient with a long history of major depression as a complication of an undiagnosed chronic hypoparathyroidism following surgery on a parathyroid adenoma. Her depression was completely eliminated by calcium supplementation therapy to restore the calcium homeostasis in serum. As it is well known that disturbances in the endocrine hypothalamus-pituitary-thyroid system might be consistent findings of depressive disorders concerning neuroendocrinological alterations, this case report and review of literature strongly supports our claim that also parathyroid diseases like chronic hypoparathyroidism, even in its latent form, might be a relevant factor in the development of depressive symptoms.
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PMID:Depression as a manifestation of latent chronic hypoparathyroidism. 1736 54

Frontal-subcortical dementias are a heterogeneous group of disorders that share primary pathology in subcortical structure and a characteristic pattern of neuropsychologic impairment. Their clinical presentation is characterized by memory disorders, an impaired ability to manipulate acquired knowledge, important changes of personality (apathy, inertia, or depression), and slowed thought processes (or bradyphrenia). It also has marked frontal dysfunction. Classic frontal-subcortical dementias include Huntington chorea, Parkinson disease dementia, progressive supranuclear palsy, thalamic degeneration, subcortical vascular dementia, multiple sclerosis, the acquired immunodeficiency syndrome dementia complex, depressive pseudodementia, and some other rare dementias like spinocerebellar degenerative syndromes, Hallervorden-Spatz disease, choreoacanthocytosis, idiopathic basal ganglia calcification, Guamanian parkinsonism-dementia complex, corticobasal degeneration multiple system atrophy, Wilson disease, metachromatic leukodystrophy, adrenoleukodystrophy, hypoparathyroidism, sarcoidosis, and other CNS inflammatory disorders. Anatomic data suggest that the frontal signs result from a disconnection of the frontal cortex from the basal ganglia. However, most frontal-subcortical dementias show cortical atrophy in later stages, and cortical dementias have subcortical pathology at some point. In fact, the concept might be seen as a continuum, and only the 2 extremes would be represented by pure cortical or subcortical pathology. Anyway, subcortical disorders may still be more similar to one another than they are to AD. Possibly, frontal-subcortical and cortical dementias are the description of the prior main target of the disease process, ending up in both cases in a global dementia. Although the dichotomy cortical versus frontal-subcortical dementia is not strict, the 2 concepts still seem to have advantages.
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PMID:Frontal-subcortical dementias. 1833 39


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