Central nervous system manifestations of hyperparathyroidism

Cogan, Martin G.; Covey, Catherine M.; Arieff, Allen I.; Wisniewski, Amy; Clark, Orlo H.

doi:10.1016/0002-9343(78)90748-9

Cited by 163 publications

(62 citation statements)

References 20 publications

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“…(37) reported that small amounts of PTH stimulated mitotic activity and RNA and heme synthesis by erythroid precursors, while large amounts of the hormone inhibited these processes. Finally, it should be mentioned that the prolonged exposure of other tissues such as the brain or the peripheral nerves to excess PTH significantly increased their calcium content and was associated with disturbances in their function (55)(56)(57)(58)(59)(60).…”

Section: Discussionmentioning

confidence: 99%

Effect of parathyroid hormone on erythropoiesis.

Meytes¹,

Bogin²,

Ma³

et al. 1981

J. Clin. Invest.

224

112

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A B S T R A C T Inhibitors of erythropoiesis have been found in the blood of uremic patients but their nature has not been identified. These patients have excess blood levels of parathyroid hormone (PTH) and it is possible that PTH inhibits erythropoiesis. The present study was undertaken to examine the effect of intact PTH molecules and some of its fragments on human peripheral blood and mouse bone marrow burst-forming units-erythroid (BFU-E), on mouse bone marrow erythroid colony-forming unit (CFU-E), and granulocyte macrophage progenitors (CFU-GM), and evaluate the interaction between PTH and erythropoietin (Ep) on human BFU-E. Intact PTH (1-84 bPTH) in concentrations (7.5-30 U/ml) comparable to those found in blood of uremic patients produced marked and significant (P < 0.01) inhibition of BFU-E and mouse marrow GFU-GM, but not of mouse marrow CFU-E. Inactivation of 1-84 bPTH abolished its action on erythropoiesis. Increasing the concentration of Ep in the media from 0.67 to 1.9 U/ml overcame the inhibitory effect of 1-84 bPTH on BFU-E. The N-terminal fragment of PTH (1-34 bPTH) and 53-84 hPTH had no effect on BFU-E.The results deomonstrate that (a) either the intact PTH molecule or a C-terminal fragment(s) bigger than 53-84 moiety exerts the inhibitory effect on erythropoiesis, and (b) adequate amounts of Ep can overcome this action of PTH. The data provide one possible pathway for the participation of excess PTH in the genesis of the anemia of uremia.

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Section: Discussionmentioning

confidence: 99%

Effect of parathyroid hormone on erythropoiesis.

Meytes¹,

Bogin²,

Ma³

et al. 1981

J. Clin. Invest.

224

112

View full text Add to dashboard Cite

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“…In addition, increased levels of aluminum in the brain may be related to some forms of uremic encephalopathy (9). However, removal of certain potential "uremic neurotoxins," such as aluminum or PTH, does not reverse uremic encephalopathy, although parathyroidectomy in uremic subjects does result in improvement both in physiologic testing and the electroencephalogram (10). Thus, other biochemical alterations are most likely present.…”

mentioning

confidence: 99%

Abnormal sodium transport in synaptosomes from brain of uremic rats.

Fraser¹,

Sarnacki²,

Arieff³

1985

J. Clin. Invest.

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The causes of central nervous system (CNS) dysfunction in uremia are not well known and are not completely reversed by dialysis. This problem was investigated in synaptosomes, which are membrane vesicles from synaptic junctions in the brain. We measured Na uptake under conditions of control, veratridine stimulation, and tetrodotoxin inhibition, in synaptosomes from normal and acutely uremic (blood urea nitrogen, 250 mg/dl) rats. In the control state, maximal Na uptake was 2.2±0.2 and 1.9±03 nmol/mg of protein in normal and uremic synaptosomes, respectively. With veratridine stimulation, Na uptake was increased by 1.9 and 3.6 nmol/mg of protein in normal vs. uremic rats (P < 0.001). The increased veratridine-stimulated Na uptake observed in uremia could be due either to increased membrane permeability to Na or decrease in the Na-K ATPase pump activity. To investigate this, we studied the Na-K ATPase pump function by evaluating uptake of K (using rubidium as a tracer), uptake of Na during ATP stimulation, and inhibition of Rb and Na uptake by ouabain. In uremic rats both Rb uptake and ATP-stimulated Na uptake were significantly less than in normals (P < 0.005). This suggests a defect in the Na-K ATPase pump. Membrane permeability for Na was then evaluated both by measuring initial Na uptake, and with addition of valinomycin. No change in Na uptake pattern was observed with valinomycin, and initial Na uptake was not significantly different in normal versus uremic synaptosomes. These data show that (a) in uremic rats veratridine-stimulated Na accumulation is significantly greater than normal; (b) the increased Na accumulation observed in uremia appears to be due to alterations in Na-K ATPase pump activity, and (c) the

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“…Although the precise mechanism which caused par kinsonism in our patient is somewhat unclear, hyper calcemia or a parathormone neurotoxicity independent calcium toxic effect (16,17) may have contributed to the symptoms. It seems likely that there may be some kind of transitory functional influence of calcium or para thormone on the dopamine turnover or post-synaptic dopamine receptor site (18,19), since her parkinsonian features improved after parathyroidectomy.…”

Section: Introductionmentioning

confidence: 83%

Hyperparathyroidism Associated with Parkinsonism.

et al. 1992

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A 70-year-old woman with hyperparathyroidism associated with parkinsonism is reported. Her primary initial symptom was parkinsonism, but it was levodopa-resistant. Chemical and hormonal findings revealed that she had hyperparathyroidism. The symptoms were relieved after the surgical removal of a parathyroid adenoma. Although this type of case has been reported only rarely, it suggests that hypercalcemia might be an aggravating factor in levodopa resistant parkinsonism. (Internal Medicine 31: 904-907, 1992)

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Central nervous system manifestations of hyperparathyroidism

Cited by 163 publications

References 20 publications

Effect of parathyroid hormone on erythropoiesis.

Effect of parathyroid hormone on erythropoiesis.

Abnormal sodium transport in synaptosomes from brain of uremic rats.

Hyperparathyroidism Associated with Parkinsonism.

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