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Plasma adenine concentration was measured in five units of citrate-phosphate-dextrose-adenine (0.25 mmol/l adenine) whole blood during storage at +4 degrees C. The adenine levels decreased to 50% in 9-10 days and to approximately 15% in 3 weeks. In spite of this rapid consumption of adenine, the adenosine triphosphate levels were well maintained: almost 100% after 3 weeks and 60% after 6 weeks of storage.
OBJECTIVE: To determine the cause and extent of hypocalcemia observed in children after severe burns. DESIGN: We studied 10 children with burns covering 57% +/- 17% (SD) body surface area, ages 9.6 +/- 4.7 years, who were admitted consecutively during a 6-month period. Diet supplied a minimum of 2.7 gm/m2 of calcium, 0.3 gm/m2 of magnesium, and 2.2 gm/m2 phosphate. Blood specimens were obtained daily for 10 +/- 5 days for the following tests: (1) simultaneous analysis for ionized calcium, magnesium, and intact parathyroid hormone (group A); (2) two of these children, randomly selected, had serial 2-hour determinations on a single day (group B); (3) a modified Ellsworth-Howard test, consisting of a 10-minute infusion of synthetic parathyroid hormone 18 +/- 10 days post-burn and associated changes in urinary cyclic adenosine monophosphate excretion and renal threshold phosphate concentration (group C). Three of these children, when normomagnesemic, also received a standard magnesium infusion to determine magnesium retention (group D). Data were analyzed with chi-square, regression analysis, and non-parametric testing as appropriate. RESULTS: All patients showed sustained hypocalcemia and hypomagnesemia; intact parathyroid hormone response was inappropriately low and response to synthetic parathyroid hormone infusion was blunted. Lowest ionized calcium levels were associated with hypomagnesemia. CONCLUSION: Hypoparathyroidism and blunted renal response to parathyroid hormone suggest that magnesium depletion may contribute to their pathogenesis. Magnesium repletion and monitoring are recommended.
The effects of Salmonella typhimurium lipopolysaccharide (LPS) on the physiology of 3-wk-old broiler chickens were studied at 12, 24, and 48 h after a single intravenous injection of saline or LPS. Lipopolysaccharide elevated cloacal temperature by 3 h after injection, induced a diuretic response, and decreased BW gain. An increase in the relative liver weight was evident in LPS-treated birds at all time intervals, whereas a decrease in the relative weight of bursa of Fabricius was observed only at the 48-h time point. The plasma interleukin (IL)-6 and the blood heterophil concentrations were elevated at 12 and 24 h following LPS administration. These changes were not observed in control chickens or in LPS-treated chickens at 48 h. A decrease in the blood glucose concentration in LPS-treated birds at 12 h was accompanied by an elevation in the blood phosphate level. An increase in total plasma protein concentration was observed only at 24 and 48 h after LPS treatment. Comparative SDS-PAGE analysis of plasma proteins from these birds under nonreducing conditions showed some quantitative differences in four bands of proteins between saline and LPS-treated chickens. A protein corresponding to an approximate molecular weight (MW) of 65 kDa increased in LPS-treated chickens, and three other proteins with MW of approximately 39, 49, and 56 kDa showed reductions in concentration compared with saline-treated controls. These results show that LPS induces a number of physiological changes that may be responsible for the regulation of the acute phase response in chickens.
Our objective was to monitor serum and urine biochemical changes after oral sodium phosphate cleansing in a prospectively designed study. The study subjects were seven healthy, asymptomatic adults. Sodium phosphate 45 ml diluted in 45 ml water was given orally at baseline and 12 hr later. Calcium, ionized calcium, phosphorus, sodium, potassium, creatinine, and PTH were analyzed at 2, 4, 6, 9, 12, 14, 16, 18, 21 and 24 hr after the first challenge. Urinary calcium, phosphorus, sodium, potassium, and cyclic AMP were analyzed at baseline and every 2 hr after oral sodium phosphate. Blood pressure, pulse, and respiratory rate were recorded every 2 hr and symptom questionnaires using visual analog scales were completed. A marked rise in phosphorus (peak range 3.6-12.4 mg/dl, P < 0.001) and falls in calcium (P < 0.001) and ionized calcium (P < 0.001) were seen. Rises seen in PTH and urinary cAMP confirmed the physiologic significance of the biochemical effect. There were no significant changes in other serum and urine laboratory or clinical assessments. Reported significant symptoms included bloating, cramps, abdominal pain, and nausea. Significant hypocalcemia and hyperphosphatemia after oral sodium phosphate raises concern about its use in normal individuals. Oral sodium phosphate should not be administered in patients with cardiopulmonary, renal, or hepatic disease.
The concentrations of pyridoxal phosphate have been estimated in cord blood and capillary blood samples taken at 3 hours, 2 days, 4 days, 7 days and 6 weeks of age, from eleven full-term infants. Pyridoxal phosphate concentrations were also determined in venous blood samples taken from the mothers at delivery. A highly significant correlation between pyridoxal phosphate in cord whole blood and venous whole blood taken from the mothers at delivery was found. Infants whose mothers had taken extra pyridoxol during pregnancy had a higher concentration of pyridoxal phosphate at 3 hours of age compared with infants whose mothers had not taken extra pyridoxol. During the first week of life the concentrations of pyridoxal phosphate in capillary blood decreases strikingly. At 6 weeks of age the concentration of pyridoxal phosphate is in the same range as that of normal adults. Findings are also discussed which indicates that: 1) Vitamin B6 is transported in breast milk; 2) The giving of supplemental pyridoxol during pregnancy in ordinary doses (2-6 mg/day) does not have an antilactogenic effect. No correlation between the erythrocyte aspartate aminotransferase activation with pyridoxal phosphate in vitro and pyridoxal phosphate concentration in plasma was found during the first 6 weeks of life.
Whole blood oxygen affinity, erythrocyte pH and organic phosphates were studied in five anaemic untransfused patients with end stage renal disease undergoing continuous ambulatory peritoneal dialysis. Decreased whole blood oxygen affinity with increased adenosine triphosphate and normal 2.3 diphosphoglycerate (DPG) values were observed. Normal and stable serum phosphate and permanent mild metabolic acidosis may be important factors contributing to maintain DPG levels within the normal range despite anaemia. Continuous dialysis avoids cyclic fluctuation of blood oxygen affinity as described during and after dialysis sessions in patients on maintenance haemodialysis.
The August 2003 COM. A 47-year-old woman presented with a long history of muscle pain, weakness, and visual disturbances. Over the last year, she developed diplopia and left sixth nerve palsy. No other neuro-ophthalmologic abnormalities were found. Past medical and family history was unremarkable. Laboratory investigation disclosed hypophosphatemia, phosphaturia, elevated serum alkaline phosphatase activity, and normal serum calcium levels. CT scans showed a lobulated mass arising on the meningeal surface of the cavernous sinus, measuring 3x 2 x 2 cm. The lesion was partially resected and microscopic examination revealed a highly vascularized tumor composed of primitive mesenchymal cells arranged whether in a patternless-pattern or surrounding thin-walled, branching vascular spaces and thick-walled hyalinized vessels. Other eye-catching features were microcystic areas, multinucleated osteoclastic-like giant cells, scattered islands of mature adipocytes, foci of hemorrhage, thrombosed medium-sized-to-large vessels, and hemosiderin-laden macrophages. After surgery, the patient recovered from the muscle pain and weakness, with a significant improvement of serum calcium and alkaline phosphatase levels and phosphate blood levels. Taken together, the clinical and pathologic features were consistent with a diagnosis of phosphaturic mesenchymal tumor (mixed connective tissue variant) of the cavernous sinus in a setting of oncogenic osteomalacia. No further treatment was carried out. The patient has been followed for the last 4 years with no evidence of recurrent disease. Oncogenic osteomalacia is a rare clinical entity characterized by hypophosphatemia, phosphaturia, and a low concentration of 1,25-dihydroxyvitamin D(3) caused by a neoplasm. Pathologists should be aware of this entity, because surgical excision of the tumor is usually curative.
It has been established that in conditions of intraoperative blood and plasma loss base deficiency is determined not only by hypocarbonatemia, but also by hypoproteinemia, hypophosphatemia and HCO3 metabolism disturbances caused by anemia. Correction of metabolic acidosis in such patients should include infusions of NaHCO3, protein preparations, blood, phosphates. Mellemgaard and Astrup's technique presupposes correction of the deficiency of all buffer bases only with NaHCO3, which dramatically increases its dosage. Thus, it is evident that the technique should be revised. The comparison of the results of metabolic acidosis correction using a conventional and adapted techniques (hydrocarbonate dose in mmol or ml of a 8.4% solution is 24-SB.body weight.0.2%) in statistically homogeneous groups has shown that differentiated "polybuffer" correction of metabolic acidosis with adapted NaHCO3 dose 1.7 times more frequently normalized acid-base balance parameters, reducing the risk of the onset of post-correction metabolic alkalosis to minimum.
In 25 women with ovariectomy made before the menopause and in a control group of 11 women after the menopause the authors examined laboratory values of the calcium phosphate metabolism and bone density. They repeated the examinations 6 and 12 months after treatment with a combined sequence oestrogen and gestagen preparation--Presomen 0.6 comb. of KaliChemie (Solvay), FRG. After one year of treatment the calcium and phosphate blood levels did not change substantially nor the alkaline phosphatase activity or its bone isoenzyme (although an insignificant increase occurred after six months). On the other hand, the originally elevated calciuria suggesting enhanced resorption of bone mineral, declined in the group of ovariectomized women on average by 3.02 mmol/d, i.e. the women lost by 120 mg less Ca, and the density increased by 6.80%! In a group of postmenopausal women the calciuria declined on average by 2.80 mmol (urinary Ca losses were by 113 mg lower) and the density increased by 4.18%. The results of this investigation support unequivocally not only the benefit but also the necessity of combined hormonal treatment after ovariectomy made before the menopause and provide also evidence of its importance in the prevention of osteoporosis in postmenopausal women.
Blood storage in CPD-adenine supplemented with 25 mM inosine and 10 mM phosphate gave 2,3-DPG levels as high as 140 per cent of normal for six weeks of blood storage at 4 C. Lower but normal 2,3-DPG levels were maintained throughout six weeks with inosine or inosine plus ribose. Ribose alone provided marginally increased DPG maintenance over the control, but ribose with phosphate maintained 2,3-DPG levels above 70 per cent of normal for five weeks of storage and two weeks longer than the control preservative. ATP levels were maintained at normal or above for six weeks with phosphate plus ribose or inosine. 2,3-DPG maintenance has previously been shown to be impaired by phosphate, unless inosine is also present. The ribose and inosine effects on 2,3-DPG maintenance are not additive. Phosphate also has an enhancement effect on ATP maintenance in the presence of either ribose or inosine.
Two cases of rhabdomyolysis with renal failure followed by hypercalcaemia are reported. Both had major hyperphosphataemia and hypocalcaemia, requiring haemodialysis. Hypercalcaemia developed during the diuretic phase, when renal function was still abnormal, and before phosphate blood levels had returned to normal. Soft tissue calcifications occurred in one of the patients. The pathogenesis and treatment of this condition are discussed. Increased levels of serum calcitriol may play an important role in the genesis of hypercalcaemia, which may last for several months. Giving calcium salts and or vitamin D to these patients during the hypocalcaemic phase is dangerous, and should be avoided. The usual treatment for hypercalcaemia my remain ineffective. Mithramycin can lower the serum calcium concentration but the new diphosphonates (sodium etidronate) are very effective in the treatment of this hypercalcaemia. However, in serious or urgent cases, hypocalcaemic haemodialysis may be required, with the simultaneous administration of calcitonin and diphosphonates.
High-resolution 31P nuclear magnetic resonance spectra at 73.83 MHz are reported for rat heart in vivo. In live rats, it was possible to observe the cardiac content of ATP, phosphocreatine, and Pi. Only a small amount of whole-blood 2,3-diphosphoglycerate was observed in the spectra, precluding the possibility that blood phosphate compounds were masking the spectra of cardiac phosphate compounds. The 31P nuclear magnetic resonance spectra of in vivo and perfused rat hearts were similar and support the utilization of the perfused rat heart as a model system for studying high-energy phosphate metabolism of the heart in vivo. The dynamic flux of high-energy phosphate compounds was investigated by subjecting the rat to respiratory arrest. In this experiment, the heart followed the classic metabolic pattern known to occur during cardiac arrest; phosphocreatine and then ATP decreased in concentration while Pi increased in concentration. The 31P nuclear magnetic resonance analysis of rat heart in vivo is demonstrated to be a practical and feasible method for studying cardiac high-energy phosphate metabolism.
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There are several reports regarding the efficacy of vitamin B6 in the treatment of tardive dyskinesia (TD). Vitamin B6 plays a key role in the synthesis of several neurotransmitters, including serotonin, dopamine, norepinephrine, and gamma-aminobutyric acid, all of which have been proposed to be involved in the development of TD. The purpose of this study was to examine whether there are special markers to distinguish long-term neuroleptic exposure patients who have TD from those patients who do not develop this side effect. In view of the pivotal role of vitamin B6 in the synthesis of all neurotransmitters believed to take part in the pathogenesis of TD, we decided to examine whether basal levels of vitamin B6 might explain the difference between these two groups. Such a finding could provide a predictive marker for vulnerable patients. The active metabolite of vitamin B6 is pyridoxal phosphate (PP). Pyridoxal phosphate blood levels were measured in 15 schizophrenic and schizoaffective patients with TD and compared with 15 patients without evidence of TD (matched by sex, age, smoking, and diagnosis). We found that, although patients in the TD group were exposed to neuroleptic drugs for significantly longer periods of time, there were no differences in serum PP levels between the groups. The reports of the effectiveness of vitamin B6 supplementation in the treatment of TD could therefore be explained by the assumption that central nervous system or intracellular vitamin B6 levels, which are involved in the pathogenesis of TD, are not the same as vitamin B6 peripheral serum levels. There is need for further studies, which will clarify the relationship between vitamin B6 and TD.
BACKGROUND: Atrial fibrillation is a frequent arrhythmia in patients undergoing hemodialysis. The consequences of hemodialysis on P wave durations and P wave dispersion have not been fully understood. The objective of this study was to study the effect of dialysis on P wave maximum (Pmax), P wave minimum (Pmin), and P wave dispersion (Pd). METHODS: We studied Pmax, Pmin, and Pd in 32 patients (17 men and 15 women, mean age 54 +/- 18 years) with chronic renal failure undergoing hemodialysis. The difference between maximum and minimum P wave duration was calculated and defined as P wave dispersion (Pd= Pmax- Pmin). RESULTS: There was a significant increase in Pmax at the end of dialysis compared to the beginning (98 +/- 13 ms vs. 125 +/- 12 ms, P < 0.001). Pmin did not show any significant change (71 +/- 11 ms vs. 73 +/- 10 ms, P = 0.42). Pd was significantly increased at the end of dialysis (27 +/- 9 ms vs. 52 +/- 11 ms, P < 0.001). There was a negative correlation between serum potassium, magnesium, phosphate, blood urea nitrogen, and creatinin at the end of dialysis and Pmax and Pd, respectively (P < 0.05). A weak positive correlation was found between serum calcium, bicarbonate at the end of dialysis and Pmax and Pd (P < 0.05). CONCLUSION: Hemodialysis ends with significant increase in P wave maximum duration and P wave dispersion, which might be responsible for the increased occurrence of atrial fibrillation in these groups of patients.
A case of primary hyperparathyroidism in a patient with myotonic dystrophy is reported. A 56-year old female with myotonic dystrophy, admitted to hospital with a urinary tract infection, had widespread muscle atrophy and myotonia with bilateral cataracts. Biochemical findings of normal renal function but raised blood calcium, depressed blood phosphate and increased parathyroid hormone, were consistent with a diagnosis of primary hyperparathyroidism. Thallium scanning of the parathyroids showed an area of discordant thallium suggesting a parathyroid adenoma. When the left lower parathyroid was later excised, histology was consistent with the diagnosis of parathyroid adenoma. As far as the authors are aware this is the first report of myotonic dystrophy and primary hyperparathyroidism in the same patient.
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