A CHILD WITH VITAMIN D DEFICIENCY RICKETS AND SUPPURATIVE ARTHRITIS

Nutritional rickets most commonly presents between 6 and 24 months with skeletal findings, growth failure, developmental delay, tetany or seizures. Unusual presentations can occur. I report the case of a black child with nutritional rickets who presented with septic arthritis, an association not previously described and that may be related to the immunologic effects of vitamin D deficiency. The incidence of nutritional rickets in developed countries is increasing. Vitamin D is recognized as an immunoregulatory hormone, and a deficiency of vitamin D is associated with an increased incidence and complications from infectious diseases. This report describes a child with florid rickets who presented with suppurative arthritis that may have been related to vitamin D deficiency. Case presentation. A 20-month-old black boy was brought to hospital because of left hip swelling and refusal to walk. He had been well until 3 weeks before admission when a tactile fever was noted. One week before admission the child refused to bear weight on his lower extremity, and discomfort was appreciated during diaper changes. The parents noted swelling of the proximal left leg on the day of admission, and he was taken to the hospital. On physical examination he was irritable and cachectic but not acutely unwell. He was afebrile. Weight was 8.6 kg (less than the 3rd percentile), height 76 cm (less than the 3rd percentile) and head circumference 48 cm (50th percentile). Frontal bossing, a rachitic rosary, widening of the wrists and ankles and bowing of the legs were present. The left leg was maintained in a flexed and externally rotated position, and there was soft tissue swelling of the anteromedial aspect of the hip with pain on minimal passive movement. The patient was born after an uncomplicated term pregnancy during which the mother did not take a vitamin supplement. He was breast-fed exclusively without vitamin D supplementation until the age of 1 year when a soy-based health food beverage, which was not fortified with vitamin D, was added. The remainder of his diet consisted of fruits and vegetables, juices, lentils, chickpeas, kidney beans, millet and rice. Both parents were educated and had sought nutritional advice from a health food store. He had been born and resided in Toronto and spent most of his time indoors. There was no history of vomiting, diarrhea or family history of bone diseases, and his development was normal. Laboratory investigations revealed a white blood cell count of 8.9 × 109/l with a normal differential count, hemoglobin 99 g/l, and platelet count 569 × 109/l. Hemoglobin electrophoresis was normal. The erythrocyte sedimentation rate was 109 mm/h, total serum calcium 2.24 mmol/l (normal, 2.25 to 2.62 mmol/l), albumin 33 g/l, phosphate 0.5 mmol/l (normal, 1.16 to 2.10 mmol/l), alkaline phosphatase 700 units/l (normal, 175 to 400 units/l), parathyroid hormone 350 ng/l (normal, 10 to 65 ng/l), 25-hydroxyvitamin D 13 nmol/l (normal, 30 to 150 nmol/l) and 1,25-hydroxyvitamin D 323 nmol/l (normal, 40 to 140 nmol/l). The serum ferritin value was 21 μg/l (normal, 22 to 400 μg/l). Red blood cell folate and serum B12 concentrations and the liver and renal function tests were normal. Serologic tests for celiac disease were negative. Ultrasonography of the hip showed a large hyperechoic, heterogeneous collection within the joint; radiographs showed severe osteopenia and cupping and fraying of the metaphyses. The child underwent arthrotomy of the hip. The white blood cell count in the joint fluid was 110 000/μl with 90% polymorphonuclear leukocytes, and the joint aspirate grew Staphylococcus aureus. A spica cast was applied, and intravenous cefazolin was administered for 6 weeks. The dietary history, physical examination, laboratory and radiographic evidence were diagnostic of nutritional rickets. He was given 4000 units of ergocalciferol daily, calcium and iron supplementation and a commercial infant soy formula to be used as a milk substitute. Five weeks after institution of therapy, he was ambulating and had a weight gain of 500 g. The parathyroid hormone, alkaline phosphatase and 25-hydroxyvitamin D values were normal, and a radiograph of the wrist showed healing of the rachitic changes. Discussion. There have been numerous reports highlighting a resurgence of vitamin D deficiency rickets in developed countries. The increase in rickets during the last two decades is likely a result of a combination of factors including prolonged breast-feeding without a dietary or supplemental source of vitamin D, maternal vitamin D deficiency and cultural factors that limit sun exposure. Dark skinned infants are especially at risk because melanin acts as a sun barrier. The child reported is typical of those described in the recent reports of nutritional rickets, i.e. a dark skinned infant with limited sun exposure because of climate and social custom and unsupplemented, prolonged breast-feeding. The child presented with the characteristic skeletal, radiographic and laboratory evidence of rickets. Rickets can, however, present with protean manifestations including seizures, tetany, delayed gross motor development and cardiomyopathy. Our patient had a coincident septic arthritis, an association that has not been previously reported. The lack of a prior report of a suppurative arthritis associated with nutritional rickets suggests that there may not be a causal relationship, but there is a theoretical basis for reasoning that vitamin D deficiency might have contributed to the development of septic arthritis. Rickets is associated with a higher incidence of infectious diseases, and vitamin D is recognized as an important immunoregulatory hormone. 1 Descriptions from the preantibiotic era cite the beneficial use of vitamin D in infants with pneumonia and the increased frequency and severity of pertussis in children with vitamin D deficiency. 2 There is a well-established epidemiologic link between the incidence of tuberculosis and vitamin D deficiency, with the observations that patients with tuberculosis have lower serum vitamin D concentrations than healthy subjects and that, in temperate climates, the reactivation of tuberculosis tends to occur more commonly at the end of winter when synthesis of vitamin D from sun exposure is reduced. 3 In experimental studies calcitriol inhibits mycobacterial growth in infected macrophages, and it is necessary for the regulation of lymphocyte proliferation, immunoglobulin production and cytokine synthesis. 4 In a study addressing the relationship between rickets and pneumonia in >1000 Ethiopian children, there was a 13-fold higher incidence of rickets among children with pneumonia than among controls after correcting for confounding factors such as malnutrition and poverty. 5 Of special relevance to our patient, a study involving a group of infants with nutritional rickets demonstrated decreased phagocytic function of neutrophils of affected patients compared with healthy controls after in vitro exposure to common bacterial pathogens. 6 Animal studies have also shown impaired phagocytosis and antibody production in rats with experimentally induced rickets. 2 Impairment of phagocytosis associated with rickets could be a mechanism for the development of a pyogenic joint infection. This case highlights several issues. The incidence of nutritional rickets is increasing even in sun-abundant climates, demonstrating that recommending vitamin D supplementation only for infants without adequate sun exposure may not be wise, especially in view of the dangers of excessive sun exposure. Rickets can be associated with significant morbidity and even mortality, and its prevention is inexpensive and simple. The development of septic arthritis in the setting of rickets is intriguing and may be related to vitamin D deficiency.

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