Early biochemical alterations in manganese toxicity: ameliorating effects of magnesium nitrate and vitamins

Manganese-induced early biochemical changes and effects of supplementation of magnesium nitrate (Mg(NO3)2) and antioxidant vitamins (A, C, D and E) were studied in rats intoxicated with manganese. Significant elevation in the level of chlorides in plasma, erythrocytes, liver and cerebellum, and a decrease in plasma inorganic phosphate (pi) with an increase in liver pi were observed in animals exposed to manganese as compared to controls. The level of erythrocyte-acid labile phosphate (ALP), nicotinamide adeninedinucleotide (NAD+) and plasma sialic acid (N-acetylneuraminic acid, NANA) also increased significantly. Elevated levels of chlorides in plasma, erythrocytes and cerebellum reversed to normal control values whereas liver chlorides restored partially by the supplementation of Mg(NO3)2. Vitamins supplementation was effective to reverse chlorides level in erythrocytes, liver and cerebellum. Decreased level of pi in plasma and the highly elevated level of erythrocyte ALP were also recovered in animals received Mg(NO3)2 in addition to MnSO4. However, such effect of Mg(NO3)2 was not seen in lowering the elevated level of NANA that restored by the administration of vitamins. Thus, the early alterations in plasma levels of chlorides, pi, and NANA and erythrocyte-ALP seem to be an indicative of early manganese toxicity while Mg(NO3)2 and vitamins supplementation appear to provide, at least in part, protection against manganese toxicity.     

Myocardial Calcification Caused by Secondary Hyperparathyroidism Due to Dietary Deficiency of Calcium and Vitamin D

A 6-year-old girl presented with respiratory distress. Chest radiographs exhibited calcifications in the mediastinum. Further imaging revealed extensive cardiac calcifications on computed tomography of the chest. The laboratory parameters were consistent with findings of secondary hyperparathyroidism. Detailed review of her dietary history revealed a prolonged history of dietary deficiency of calcium and vitamin D. Treatment consisted of adequate daily replacement of calcium and ergocalciferol. On follow-up, her parathyroid hormone level was significantly reduced and substantially reduced cardiac calcifications were seen on echocardiogram. Pediatric cardiologists must be aware of this potentially fatal but treatable disease in children with cardiac calcifications unexplained by other causes.     

Use of pupil size and reaction to detect orbital trauma during and after surgery

We describe how pupillary reactions, used as an index of optic nerve function, can be elicited using only one working pupil. This is to challenge the conclusion of a study that did not appreciate this physiological phenomenon and thus gave rise to erroneous conclusions that might otherwise limit the scope of pupil measurements during and after surgery. For suitable cases, non-opioid anaesthesia and further clinical development of pupillometry are suggested by us as measures to monitor optic nerve function.