新生儿颅内出血与低钙低镁血症

为了探讨新生儿颅内出血与低钙低镁血症的关系，本文作者对３６例新生儿颅内出血患者进行了血清钙、镁的检测。结果低血钙２２例，低镁６例，钙镁均低者５例。说明新和儿因可导致低钙低镁血症．     

先天性厚性幽门狭窄围手术期低钙低镁血症

３２例肥厚性幽门狭窄患儿，因长期大量哎吐、摄入中足及吸收障碍等原因，均有不同程度的低钙、低镁血症，其中低鲈４例，低镁１８例，钙、镁均低者１６例。临床表现为易惊、睡眠不安、夜器、四肢震颤、头向后仰、背肌紧张、面部抽搐，严重者出现喉痉挛。经使用钙／镁制剂后得到控制。     

新生儿低镁血症(附17例临床报告)

本文报道了17例新生儿低镁血症，以早产儿、早期新生儿、牛乳喂养儿多见。低镁时往往同时存在低钙或新生儿时期的其他疾病，其临床症状难以与低钙血症鉴别或被原发病掩盖。应及早进行血清镁测定，以提高诊断率。治疗时单纯低镁者仅补镁即可，对同时低钙者也强调先补镁盐。     

新生儿低镁并低钙血症14例临床分析

对14例新生儿低镁并低钙血症进行了临床分析。年龄<3天8例,～15天3例,～28天3例,牛乳喂养11例,母乳喂养1例,混合喂养2例,有原发疾病12例。所有病例均表现为程度不同的惊厥。血清镁均低于0.6mmol/L,血清钙均低于1.75mmol/L。除积极治疗原发病外,同时补充钙镁。有2例死于原发病,余12例均治愈。并对新生儿低镁并低钙血症的病因、临床表现、预防及治疗进行了讨论。     

窒息后脑损伤并新生儿低钙,低镁血症21例

窒息后脑损伤并新生儿低钙、低镁血症２１例江苏盐城市妇幼保健院（２２４００２）魏建芳本文对２１例窒息后脑损伤并低钙、低镁血症，就其病因、临床表现、预防、治疗进行分析。临床资料性别及年龄２１例为我科１９９３年以来收治的病人。经头颅ＣＴ确诊为ＩＣＨ８例，Ｈ...     

新生儿低镁惊厥

本文报导我院1981年9月至1983年1月收治的新生儿低镁惊厥17例。仅2例为母乳喂养。如不测定血镁,低镁血症与低钙血症的症状和体征无法鉴别。我们测定了50例正常儿童的血清镁浓度,其平均值——2个标准差=2.17-2×0.34=1.49毫当量/升。我们暂定血镁<1.48毫当量/升为低镁血症。17例患者血清镁浓度为0.65-1.46毫当量/升。10例血清钙浓度<7毫克/100ml。测定血清磷浓度8例,其中5例76毫克/100ml。一般静脉滴注2.5％硫酸镁2—4毫升/公斤体重,每天两次。惊厥停止后,改用肌肉注射25％硫酸镁0.4毫升/公斤体重,每天两次。往往在应用硫酸镁1—4次后,惊厥得到控制,而血清镁浓度要在用硫酸镁2—6天后才升至正常。5例患者同时有低钙血症和低镁血症。反复应用葡萄糖酸钙,惊厥未得到控制,仅在应用硫酸镁后,血清钙浓度才升至正常水平,惊厥停止。有7例患儿检查过心电图,除1例正常外,6例均异常。因此,镁对心脏的影响应予重视。     

新生儿惊厥伴有原发性钙、磷、镁代谢障碍

作者在两年内观察了75例新生儿惊厥伴有原发性钙、磷及镁的代谢障碍。第一次惊厥多发生于生后第6天,在生后48小时内及第10天以后则少见。血生化检查:75例惊厥患儿中,低血钙者69例占92%,低血镁者40例占53%,高血磷者48例占64%。约80%的惊厥患儿出现多种的血生化改变,常见的有低钙、低镁、高磷,共24例占32%;低钙、高磷20例占27%;低钙、低镁11例占15%。又14例仅表现有低钙,2例单独有低镁,1例单独有高磷。(注:婴儿血钙正常值10.1±1.8毫克%,血磷正常值7.5±2.5毫克%,血镁正常值1.9±0.7毫克%)。     

危重新生儿低钙血症原因探讨

测定２３例足月危重新生儿危重期及恢复期双份血样中与钙代谢有关的生化指标，结果显示危重期血总钙、游离钙、镁、甲状旁腺激素及红细胞膜钙泵活性低于对照组及恢复期（Ｐ〈０．０１），而血磷、降钙素、红细胞总钙浓度高于对照组恢复期（Ｐ〈０．０１），恢复期与对照组各指标差异无显著性（Ｐ〉０．０５）。说明危重新生儿常伴有低钙血症，其原因为甲状旁腺受损功能低下、降钙素分泌增多、钙泵活性下降钙内流及低血镁、高血磷等。     

遗传相关性低镁血症

镁离子在体内参与多种生化代谢反应,对各器官系统发挥正常生理功能起重要作用.体内镁离子的平衡主要依赖于肠道镁吸收和肾脏镁排泄的精密调节.遗传性低镁血症包括家族性低镁血症合并高尿钙和肾钙质沉着、常染色体显性遗传低镁血症合并低尿钙、家族性低镁血症继发低钙血症、常染色体显性遗传低钙血症等.近年来,对于这些遗传性低镁血症的基因研究及相关蛋白质功能研究使人们对体内镁离子转运机制有了更深一步的认识.     

遗传相关性低镁血症

镁离子在体内参与多种生化代谢反应,对各器官系统发挥正常生理功能起重要作用.体内镁离子的平衡主要依赖于肠道镁吸收和肾脏镁排泄的精密调节.遗传性低镁血症包括家族性低镁血症合并高尿钙和肾钙质沉着、常染色体显性遗传低镁血症合并低尿钙、家族性低镁血症继发低钙血症、常染色体显性遗传低钙血症等.近年来,对于这些遗传性低镁血症的基因研究及相关蛋白质功能研究使人们对体内镁离子转运机制有了更深一步的认识.     

Autosomal dominant hypoparathyroidism with severe hypomagnesemia and hypocalcemia, successfully treated with recombinant PTH and continuous subcutaneous magnesium infusion

Activating calcium sensor receptor (CaSR) mutations often present with hypocalcemia and hypomagnesemia. Severe hypocalcemia with this mutation has been reported but severe hypomagnesemia has not been well described. AIM: To identify the cause of severe hypocalcemia and hypomagnesemia in a young child, and explore the efficacy of continuous subcutaneous magnesium therapy as a safer alternative to intravenous magnesium. PATIENT: A 2-8/12 year-old female with severe hypocalcemia and hypomagnesemia of unknown etiology. METHODS: Genetic analysis was performed on the proband and both parents. The proband was treated with human parathyroid hormone (teriparatide) and a continuous infusion of subcutaneous magnesium sulfate initially using a Deltec insulin pump and subsequently a Curlin infusion pump. RESULTS: The patient has a known de novo mutation in the CASR gene (A843E). She could not be adequately managed with enteral and intravenous electrolyte replacement even after adding teriparatide. She responded well to adjunctive therapy with continuous subcutaneous magnesium. CONCLUSIONS: Severe hypomagnesemia can be part of the phenotype of activating CaSR mutations. Subcutaneous magnesium should be considered in patients with difficult to control hypomagnesemia.     

Polycythemia, hypomagnesemia, and hypocalcemia in infants of diabetic mothers

Hypomagnesemia (serum magnesium concentration, less than 1.5 mg/dL [0.62 mmol/L]) and hypocalcemia (serum calcium concentration, less than 8 mg/dL [2.00 mmol/L]) have been reported in polycythemic infants, as well as in infants of diabetic mothers (IDMs). These latter infants are at risk for neonatal polycythemia (venous hematocrit, greater than or equal to 65% [0.65]). We tested the hypothesis that neonatal polycythemia in IDMs is associated with increased serum calcitonin concentration, hypomagnesemia, and hypocalcemia. Serum magnesium and calcium concentrations were measured at 24 and 72 hours of age in 76 IDMs; serum calcitonin concentration was measured at 24 hours of age. Peripheral venous spun hematocrit was measured between 2 and 4 hours of age. The rates of hypomagnesemia and hypocalcemia were similar in polycythemic and nonpolycythemic IDMs (0% vs 9% and 56% vs 49%, respectively). The serum calcitonin concentration was similar in both groups. There was no correlation between hematocrit and the serum magnesium or calcium concentration; a significant association existed between hypocalcemia and hypomagnesemia.     

Myocardial dysfunction due to hypocalcemia

Hypocalcemia is a curable cause of myocardial dysfunction and clinical congestive cardiac failure, with only stray reports available in literature. We describe 15 infants presenting with severe left ventricular dysfunction, who were found to have hypocalcemia with or without hypomagnesemia. Vitamin D deficiency was identified as the main cause of hypocalcemia. These children improved on supplementation of vitamin D and calcium.     

Severe renal osteodystrophy without elevated serum immunoreactive parathyroid hormone concentrations in hypomagnesemia due to renal magnesium wasting

An 8 1/2-year-old girl presented with a long history of seizures, growth retardation, muscle weakness, gait disturbance, and hearing loss. Her evaluation revealed chronic moderate renal failure (serum creatinine 2.2 mg/dL), severe hypocalcemia (5 mg/dL), hyperphosphatemia (8.1 mg/dL), hypomagnesemia (1.5 mg/dL), increased urinary magnesium excretion (2 mg/kg/d), high fractional excretion of magnesium (21.7%), hypokalemia (3.2 mEq/L), and hyperkaliuria (26 mEq/L). Low circulating immunoreactive parathyroid hormone levels for the degree of the hypocalcemia (serum N-parathyroid hormone 212 pg/mL) and severe rickets without evidence of osteitis fibrosa cystica were found. The patient probably has primary renal leak hypomagnesemia (magnesuric hypomagnesemia) which caused impaired secretion of immunoreactive parathyroid hormone leading to severe hypocalcemia and calcium deficiency rickets. Treatment with magnesium and calcium supplements, calcitriol, and aluminum hydroxide resulted in marked clinical, biochemical, and radiologic improvement. Calcium deficiency rickets due to primary or secondary renal magnesium wasting in conjunction with moderate renal failure represents a largely unrecognized metabolic bone disease.     

Prevalence of Hypocalcemia in Seizures in Infancy

A one-year prospective study on developmentally normal children between 1-mo to 2-y with seizures was done to study the prevalence of hypocalcemia. The contribution of hypovitaminosis-D to hypocalcemia was also studied. Of 78 infants (51 boys) enrolled, 18 (23.1%) had hypocalcemia. Fifteen (19.2%) had hypocalcemia secondary to hypovitaminosis-D and 3 (3.8%) had hypomagnesemia. In infants aged less than 6 mo who were exclusively breastfed, 15 (41.67%) had hypocalcemia in comparison to other two age groups [2 (10.53%) in 6–12 mo age-group and 1 (4.35%) in 1–2 y age-group]. This association was statistically significant (p?=?0.001).     

Cis-platinum-induced renal sodium wasting

A 10-year-old girl with a malignant ovarian germ cell tumor was treated with cis-platinum-based chemotherapy. During the third and fourth courses of therapy, the patient developed hyponatremia, hypomagnesemia, and hypocalcemia. Renal sodium wasting was documented to be the cause of the hyponatremia. Despite normalization of serum electrolytes, hyponatremia again occurred during a period of stress following cessation of cis-platinum. Prior work has documented that cis-platinum-induced hypomagnesemia is related to renal tubular dysfunction with resulting magnesium wasting. A similar etiology for cis-platinum-induced hyponatremia and renal sodium wasting is proposed.     

Transient neutral fat steatorrhea, elevated sweat chloride concentration, and hypoparathyroidism in a child with celiac disease

A patient with celiac disease and the unusual features of transiently elevated sweat chlorides, reversible exocrine pancreatic insufficiency, symptomatic hypocalcemia/hypomagnesemia, and transient secondary hypoparathyroidism is presented along with a brief discussion of the physiologic mechanisms thought to underlie their development.     

Primary idiopathic hypomagnesemia in two female siblings

Two female siblings with primary idiopathic hypomagnesemia, born to consanguineous parents, are described. Both presented at 6 weeks of age, with convulsions and persistent hypocalcemia (calcium 1.5 and 1.6 mmol/1; normal range (NR) 2.2-2.6 mmol/1), which could not be controlled with anticonvulsants and/or calcium gluconate. On further investigation they were also found to have hypomagnesemia (magnesium 0.17 mmol/1 and 0.22 mmol/l; NR 0.65-1.05 mmol/l). Convulsions and the low serum calcium and magnesium levels were first managed by im and then by oral administration of magnesium supplements. A burst in circulating parathyroid hormone levels to well above the physiological range was observed at the start of therapy. Serum magnesium values of the mother and father were just below the normal range, with normal serum calcium. This type of infantile primary hypomagnesemia appears to be a hereditary disease with autosomal recessive characteristics, although a partially penetrant X-linked or autosomal dominant trait cannot be excluded.
Convulsions,primary hypomagnesemia