Effects of hypomagnesemia on reactivity of bovine and ovine platelets: possible relevance to infantile apnea and sudden infant death syndrome.

Abstract

Blood platelet function and possible involvement in death of hypomagnesemic ruminants was investigated with 26 Angus cows, 15 mature Hampshire wethers, eight Finnish-Hampshire ewes, and 36 growing Dorset lambs. Hypomagnesemia was induced by feeding vegetative spring tall fescue to 13 cows and semipurified diets low in Mg to nine wethers, four ewes, and 18 lambs. In comparison with controls, dietary treatments reduced plasma Mg concentrations 55% in cows, 36% in wethers, 66% in ewes, and 78% in lambs. Hypomagnesemia reduced in vitro reactivity of cow and lamb platelets to thrombin, ADP, and platelet active collagen, but in vitro tests may not accurately reflect in vivo platelet reactivity. Microscopic examination of platelet-rich plasma revealed a threefold increase in clumped platelets from four hypomagnesemic ewes compared to four normomagnesemic ewes. This suggests that in vivo activation and exhaustion of platelets may have contributed to reduced in vitro platelet reactivity. Six of 18 hypomagnesemic lambs died spontaneously in tetany after 2-12 months on low-Mg diets. Heart and lung lesions were markedly similar to pathological changes induced in other lambs by intravascular activation of platelets with 500 micrograms of vascular collagen fibrils per kg body weight injected intravenously. These results suggest the possibility of abnormal blood platelet activation as a significant mortality risk factor in severe hypomagnesemia.

Consequences of magnesium deficiency on the enhancement of stress reactions; preventive and therapeutic implications (a review).

“…Pregnant Mg deficient cows and ewes exhibited 3-fold more clumping of platelets than did controls, and 6 of 18 lambs that died in tetany after being fed low Mg diet for 2-12 months had heart and lung lesions very similar to those produced by collagen-activation of platelets [120]. Miller et al [120] suggest that abnormal blood platelet activation may be a significant mortality risk factor in severe gestational and infantile Mg deficit and draw a parallel between the pathologic findings in Mg deficient lambs with those in the sudden infant death syndrome (SIDS). Caddell proposes that neonatal and postneonatal apnea and respiratory distress syndrome (RDS) are pre monitory findings in infants who are later victims of SIDS, and advises Mg treatment in doses low enough not to constitute a risk (0.4-1 mEq/kg/d for about 2 weeks) in RDS infants with immature kidneys [121][122][123].…”

“…Rats born to Mg deficient dams are less tolerant of stress, even after infancy [119]. Pregnant Mg deficient cows and ewes exhibited 3-fold more clumping of platelets than did controls, and 6 of 18 lambs that died in tetany after being fed low Mg diet for 2-12 months had heart and lung lesions very similar to those produced by collagen-activation of platelets [120]. Miller et al [120] suggest that abnormal blood platelet activation may be a significant mortality risk factor in severe gestational and infantile Mg deficit and draw a parallel between the pathologic findings in Mg deficient lambs with those in the sudden infant death syndrome (SIDS).…”

A 26-Day-Old Neonate Presenting with Familial Hypomagnesemia with Secondary Hypocalcemia Associated with the Novel Homozygous TRPM6 Gene Variant c.5281C>G p. (Arg1761Gly) chr9: 77354845 – A Case Report

“…Infants have presented with carpopedal spasms, hemiparesis, and aphasia [ 21 , 22 ]; basal ganglia calcification [ 23 ]; arrhythmia [ 24 ]; misdiagnosis as nutritional rickets [ 25 ]; repeated self-terminating Torsades de pointes [ 26 ]; and hypertensive urgency with unknown mechanisms [ 27 ]. The potential relevance of infantile apnea and sudden infant death syndrome (SIDS) caused by severe hypomagnesemia has also been considered [ 28 ]. To the best of our knowledge, no case reports of bleeding diathesis or near-miss SIDS have been reported in association with the TRPM6 gene mutation.…”

Σχέση Των Επιπέδων Μαγνησίου Ορού Και Ερυθρών Ασθενών Στη Διαβητική Θρομβοπάθεια

“…Δίαιτα τριών εβδομάδων, πολύ πτωχή σε μαγνήσιο, προκάλεσε υπομαγνησιαιμία σε φυσιολογικά άτομα. Διαπιστώθηκε αυξημένη απαντητικότητα συγκόλληση των αιμοπεταλίων μετά το τέλος της περιόδου της ειδικής διατροφής (351).…”

“…Μειωμένα επίπεδα μαγνησίου του ορού σε διαβητικούς ασθενείς διαπιστώθηκε ότι αυξάνουν την ενεργοποίηση των αιμοπεταλίων (206,351). Θεραπεία με μαγνήσιο για οκτώ εβδομάδες αύξησε σημαντικά τα επίπεδα του μαγνησίου, όμως δεν μείωσε την προθρομβωτική κατάσταση (206).…”