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| Year : 1998 | Volume
: 46
| Issue : 4 | Page : 261--267 |
Digoxin : a model for hypothalamic regulation of neuronal transmission, endocrine function, immunity and cytodifferentiation.
RA Kurup, J Augustine, PA Kurup, Kurup A RavikuJan-Mar
Department of Medicine, Medical College, Trivandrum, Kerala, India
Correspondence Address:
RA Kurup
Department of Medicine, Medical College, Trivandrum, Kerala
India
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 29508817 
The case report of a family with coexistence of schizophrenia, systemic malignancy, Parkinson's disease, rheumatoid arthritis and syndrome X is described. The coexistence of malignant transformation, neuronal degeneration, immune dysfunction and psychiatric manifestation have been extensively documented in literature. It is possible that a central dysfunction in neuroendocrine and immune integration may play a role in the pathophysiology of these diseases. Elevated levels of an endogenous sodium-potassium ATPase inhibitor, digoxin, a steroidal glycoside, has been reported in syndrome X. The human hypothalamus is the principal source of digoxin. Serum digoxin level and RBC sodium-potassium ATPase were measured in the members of the index family and8 groups of patients with CNS gliomas, Parkinson's disease, motor neuron disease, CNS vasculitis, multiple sclerosis, primary generalised epilepsy, schizophrenia and the acquired immunodeficiency syndrome. Digoxin, being a isoprenoidal compound, its synthesis was assessed by HMG CoA reductase activity. The levels of serum digoxin and HMG CoA reductase activity were found to be increased in the members of the index family and all the 8 groups studied with a corresponding reduction in RBC sodium-potassium ATPase activity. The role of hypothalamic digoxin in the pathogenesis of these diseases is discussed. A digoxin model for hypothalamic regulation of neuronal transmission, endocrine function, immunity and cytodifferentiation is proposed.
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