Renal carcinoma: bilateral breast metastases in a child

Malignant metastasis to the breast, rare in adults, has occurred in children from hematologic malignancies and from neuroblastoma and rhabdomyosarcoma. We report a case of bilateral breast metastases in a 14-year-old girl with a prior nephrectomy for renal cell carcinoma; the breast masses were the first sign of recurrence. Received: 25 March 1996 Accepted: 3 July 1996     

Congenital rickets caused by maternal vitamin D deficiency

The cases of four newborn infants with congenital rickets are reported. All infants were native Canadian: three were Cree and one was Inuit. One had a narrow chest and pulmonary hypoplasia, two had clinical and radiological signs of rickets with craniotabes, thickened wrists, and prominent costochondral junctions, and one had perinatal asphyxia and hydrops. All had hypocalcemia, hypophosphatemia and secondary hyperparathyroidism. Serum 25-hydroxyvitamin D levels were low in three of the infants. The four mothers had evidence of vitamin D deficiency. All infants recovered following treatment with 5000 IU oral vitamin D daily.     

Severe acute hypercalcemia in a child caused by accidental vitamin D poisoning

The authors report a case of acute severe hypercalcemia (5.20 mmol/l) in a 9-month-old boy. Vitamin D poisoning is confirmed by high serum level of 25 OHD (287 mcg/l; N = 10-60) while the source of intoxication is unknown. Individual idiopathic vitamin D hypersensitivity is eliminated because of a negative diagnosis test. Management with prednisone, high intravenous fluid saline intake, furosemide and calcitonin results in a favourable outcome. Vitamin D intoxication has always to be evoked when acute severe hypercalcemia occurs in infants.     

Hypocalcemic seizures and secondary bilateral femoral fractures in an adolescent with primary vitamin D deficiency

Nutritional rickets and osteomalacia are reemerging in Western societies, particularly in young children and in adolescents of African or Asian descent. Hypocalcemic seizures resulting from vitamin D deficiency are rare in adolescents, whereas fractures caused by seizures without evidence of direct trauma have not yet been reported in this population. We present an unusual case of secondary bilateral femoral fractures caused by hypocalcemic seizures in a 17-year-old boy with primary vitamin D deficiency. We examine the epidemiology and the clinical presentation of rickets and osteomalacia in the adolescent population, the risk of secondary injuries in patients with seizures, and the evaluation and management of hypocalcemic seizures and primary vitamin D deficiency.     

Congestive heart failure caused by vitamin D deficiency?

We describe a child, 3.5 months old, with severe vitamin D deficiency, profound hypocalcaemia, hyperphosphataemia, dilated left ventricle, severely reduced myocardial contractility and congestive heart failure. She also had depressed thyroid function with subnormal thyroxine and non-detectable serum thyrotropin (TSH) levels. The child promptly responded to calcium infusions, conventional anticongestive therapy and calcitriol. She is now 3 years old and received no medication. Myocardial function is normal but she has motor delay. We believe that her transitory congestive heart failure was caused by severe vitamin D deficiency with profound hypocalcaemia.     

Congestive heart failure in rickets caused by vitamin D deficiency

We describe a case of a three and half month old infant presenting with a congestive heart failure due to hypocalcemic cardiomyopathy. Vitamin D deficiency rickets was found to be the cause for the hypocalcemia. The heart failure responded promptly to adequate Calcium therapy accompanied by usual anticongestive therapy.     

Renal cell carcinoma presented with hypocalcemia in an adolescent

Renal cell carcinoma is very rare in childhood. It is a different entity from its adult counterpart. We report a case of renal cell carcinoma presented with hypocalcemia in a 16-year-old girl that is, to the best of our knowledge, the first such published incident. The patient was treated by radical nephrectomy with regional lymphadenectomy. Hypocalcemia amended after surgery. Neither chemotherapy nor radiotherapy was given. She has remained disease free for 34 months.     

Brown tumour as a complication of secondary hyperparathyroidism in severe long-lasting vitamin D deficiency rickets

Brown tumour is a localised form of fibrous-cystic osteitis associated with primary or secondary hyperparathyroidism. Despite the fact that secondary hyperparathyroidism occurs in vitamin D deficiency rickets, no cases of rickets with brown tumour have so far been described. We present a 2.9-year-old girl who had brown tumour of the mandible due to severe vitamin D deficiency rickets. Treatment with vitamin D₃ corrected the hyperparathyroidism rapidly which was followed by gradual regression in tumour size. Conclusion Brown tumour can develop in severe, long-standing vitamin D deficiency rickets and responds to vitamin D treatment. Received: 10 March 1999 and in revised forms: 20 June 1999 and 27 June 1999 / Accepted: 27 July 1999     

High prevalence of moderately severe vitamin D deficiency in preterm infants

Background: The recommended dose of vitamin D supplementation of preterm infants is based on data from populations in which severe vitamin D deficiency is uncommon and may be inadequate for infants in high risk population. However, data on vitamin D status of preterm infants in high‐risk populations, such as Middle Eastern countries is scarce. Methods: This study investigates the vitamin D status of Arab mothers and their preterm infants. Maternal serum and cord blood 25(OH)D, calcium (Ca), phosphorus (P) and alkaline phosphate (ALP) were measured at delivery. Serum 25(OH)D was measured by HPLC while the other biochemical parameters were measured by standard autoanalyzer. Results: Thirty‐four preterm infants were studied. The mean gestational age was 31.4 weeks and birth weight was 1667 g. The median serum 25(OH)D of 17.0 nmol/L in 28 mothers and 14.5 nmol/L in 34 cord blood samples were low. The median maternal and cord blood Ca, P and ALP levels were within normal range. Fifteen (44%) of the infants had moderately severe vitamin D deficiency (serum 25 (OH)D levels <12.5 nmol/L). The median serum 25(OH)D levels of mothers who had reportedly taken prenatal vitamin D supplementation and those who had not were similar (17.3 vs 16.3) nmol/L. The mean serum 25(OH)D levels among preterm infants in this study were low when compared to levels in Caucasians preterm infants on which the current vitamin D recommendations are based. Conclusion: The high prevalence of moderately severe vitamin D deficiency in Arab preterm infants provides a justification to investigate vitamin D requirement of preterm infants in this and other high‐risk populations.     

Acute vitamin D intoxication in a child

We present the unique case of a previously healthy, 2-year-old boy with resistant hypercalcemia and hypertension resulting from an unintentional overdose with an imported vitamin D supplement. The patient presented initially to the emergency department with colic and constipation and was discharged after a benign physical examination. The symptoms persisted and, on the second visit, the patient was found to have a serum calcium level of 14.4 mg/dL. Despite therapy with intravenously administered 5% dextrose solution at one-half normal strength, furosemide, calcitonin, and hydrocortisone, the calcium concentration increased to 15.0 mg/dL on the second hospital day and did not decrease until the fourth hospital day, when it fell to 13.9 mg/dL. The vitamin D concentration peaked at 470 ng/mL on hospital day 3. With additional questioning, the mother revealed that she had been giving her son a daily dose of 1 ampule of Raquiferol, an imported vitamin D supplement, instead of the recommended 2 drops per day. Each ampule contained 600,000 IU of vitamin D; therefore, the boy received a total of 2,400,000 IU over 4 days. The patient's hypercalcemia persisted for 14 days and was complicated by persistent hypertension. No renal, cardiac, or neurologic complications were noted. At discharge, the vitamin D concentration was still elevated at 389 ng/mL and the total calcium level had decreased to 11 mg/dL. The boy made a complete clinical recovery. This case highlights the need for caution when using imported and/or unregulated medicines, as well as the dangers of parental dosing errors.     

Two cases of fractures in neonates associated with maternofetal vitamin D deficiency

Vitamin D supplementation is essential for the entire population, especially during pregnancy and in the pediatric period. We report two case studies of full-term newborns who presented long-bone fractures associated with severe vitamin D deficiency transmitted to them by their mothers, even though maternal supplementation had been implemented according to the existing recommendations. These observations encourage the investigation of neonatal vitamin D deficiency in the presence of long-bone fractures in the absence of traumatic birth and the necessity of reenforcing the means of prevention and the selection of risk groups in order to adjust vitamin D supplementation during pregnancy individually.     

Coma and respiratory failure in a child with severe vitamin B(12) deficiency.

OBJECTIVE: Psychofunctional follow-up of severe vitamin B(12) deficit. DESIGN: Case report. SETTING: Pediatric intensive care unit. Patient: Ten-month-old boy. INTERVENTION: Follow-up at 3 yrs. MEASUREMENTS AND MAIN RESULTS: A 10-month-old boy was admitted to the pediatric intensive care unit with respiratory failure, muscular hypotonia, and involuntary movements. Although a central nervous system infection was excluded, computed tomography scan showed a diffuse cortical-subcortical atrophy. Vitamin B(12) deficiency was suspected because of a red-cell count of 1,350,000/mm(3) and a hemoglobin value 5.9 g/dL (MCV 116). The baby had been exclusively breast-fed, but his mother had been a strict vegan for 10 yrs. Chronic dietary vitamin B(12) deprivation was confirmed by blood and urinary samples. Treatment with vitamin B(12) led in 2 wks to rapid and complete hematological improvement and to partial regression of neurologic symptoms. During the following 3 yrs the boy had normal vitamin intake and underwent intensive rehabilitative treatment. The brain atrophy regressed, but linguistic and psychomotor delay persisted. CONCLUSIONS: Rapid clinical improvement after vitamin supply does not correlate with a complete recovery.     

Idiopathic Fanconi's syndrome with nephrogenic diabetes insipidus in a child who presented as vitamin D resistant rickets--a case report and review of literature

Fanconi's syndrome is a complex of multiple tubular dysfunctions of proximal tubular cells occurring alone or in association with a variety of inherited (primary) or acquired (secondary) disorders. It is characterized by aminoaciduria, normoglycemic glycosuria, tubular proteinuria without hematuria, metabolic acidosis without anion gap and excessive urinary excretion of phosphorous, calcium, uric acid, bicarbonate, sodium, potassium and magnesium. Diabetes insipidus is a disease of collecting tubules and a child mainly presents with dehydration and hypernatremia. We report the first case of idiopathic Fanconi's syndrome along with nephrogenic diabetes insipidus (NDI) in a child who presented to us as resistant rickets. Medline search did not reveal any case of nephrogenic diabetes insipidus associated with idiopathic Fanconi's syndrome. We hypothesized that the NDI may be due to severe hypokalemia induced tubular dysfunction. The child was treated for hypophosphatemic rickets with severe metabolic acidosis and the treatment for NDI was also given. Now he has healed rickets and normal blood pH, sodium and osmolarity.     

Malignant osteopetrosis obscured by maternal vitamin D deficiency in a neonate

A neonate presented with clinical, biochemical, endocrine and radiographic features consistent with vitamin D deficiency rickets of maternal origin. Persistent hypocalcemia and subsequent development of pancytopenia, hemolysis and hepatosplenomegaly prompted further studies that led to the diagnosis of infantile osteopetrosis. Conclusion Osteopetrosis is an important differential diagnosis of neonatal rickets and is not excluded by low vitamin D levels. Received: 19 May 1999 / Accepted: 15 September 1999