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• W2017164048 abstract "No reports exist that specifically address hypocalcemia in HIV-infected pediatric populations. Hypocalcemia, in the context of HIV infection, has been attributed to drugs such as foscarnet, ketoconazole, aminoglycosides, pentamidine, and didanosine [1–5], as well as hypoparathyroidism, hypoalbuminemia, renal failure, pancreatitis, malabsorption, and sepsis [6,7]. Vitamin D deficiency has been found to be a relatively common cause of hypocalcemia in HIV-positive adults [7–9]. One study revealed significantly lower mean serum calcium levels and a higher incidence of hypocalcemia in an HIV-infected adult population [7]. A recent abstract reported an increased incidence of osteopenia and osteoporosis in an HIV-infected pediatric population [10]. Their results highlighted the possibility of an association of HIV disease with calcium homeostasis, resulting in decreased bone density in children, an effect that may be compounded by protease inhibitor therapy. We report two cases of hypocalcemia recently seen in our HIV-positive urban pediatric patients. Patient 1 is a 14-year-old perinatally-infected HIV-positive African-American boy (CDC classification N3), who presented to our clinic for routine follow-up and was found to be hypocalcemic. He reported good adherence to antiretroviral medications, which included ritonavir, indinavir, didanosine, stavudine, hydroxyurea, and Bactrim. Apart from intermittent abdominal pain at school for a few days, he was feeling well. His appetite was ‘good’ although dairy intake was difficult to quantify. Physical examination was normal and showed a well-appearing boy with a body mass index above the 95th centile for his age. His blood tests are summarized in Table 1. All other routine laboratory tests were normal. His calcium level had varied between 7.5 and 8.7 mg/dl in the previous year.Table 1: Laboratory serum values for patients 1 and 2 on day of diagnosis (day 1) and days subsequent to the initiation of treatment.Vitamin D (ergocalciferol) 2000 U per day was commenced by mouth on day 21. On day 69, a bone density scan (dual energy X-ray absorptiometer, model Delphi A; Hologic, Inc., Waltham, MA, USA) showed low–normal bone density for his age at −0.78 SD. On day 69, after a dramatic improvement in his serum calcium level, vitamin D was decreased to 800 U a day administered by mouth. On day 85, calcium carbonate 600 mg a day was added. On day 160, in view of his improvement, calcium carbonate was decreased to 200 mg a day. His calcium level has since remained between 9.0 and 9.3 mg/dl. One year later, a repeat bone density scan showed an improvement at −0.4 SD. Patient 2 is a 13-year-old perinatally HIV-infected African-American boy (CDC classification C3), who presented to our clinic for routine follow-up and was found to be hypocalcemic. His viral load had been undetectable and his CD4 cell count had been above 25% for 4 years. His previous serum calcium levels were normal. His history revealed that although he felt well, he had not received his nutritional supplementation (Suplena) for the previous 2 weeks, which accounted for 76% of his daily recommended intake of calcium and 30% of his daily recommended intake of vitamin D. His medications included stavudine, nevirapine, ritonavir, and saquinavir mesylate, intravenous immunoglobulin and penicillin. Upon presentation, he was found to have lost 3.3% of his body weight over the course of one month, but appeared otherwise to be healthy. He was 93% of his ideal body weight. His neurological examination was significant for a positive Chvostek's sign, lower extremity clonus bilaterally, and hyperreflexia in all extremeties. In addition to the laboratory results presented in Table 1, he was found to have normal renal, pancreatic and hepatic function. A bone density scan showed reduced bone mineral density for his age at −2.5 SD. On day 1, he began treatment with vitamin D 800 U a day by mouth, calcium carbonate 600 mg a day by mouth and a multivitamin. On day 29, his total calcium, vitamin D 25OH, and alkaline phosphatase levels normalized to values shown above, and his intact parathyroid hormone levels showed a marked improvement. In these cases, hypocalcemia was probably secondary to nutritional vitamin D deficiency. A combination of oral vitamin D and calcium supplementation was sufficient to improve their total calcium levels. Other factors possibly contributing to the low levels of 25OH vitamin D in both patients included their race and minimal sunlight exposure [11,12]. We found this disorder to be a relatively rare phenomenon in our HIV-positive pediatric population. Despite screening for electrolyte abnormalities at every routine office visit, only the two patients described here out of 130 under our care were found to be hypocalcemic over a 12-month period. These cases, especially in light of recent evidence of an increased risk of osteopenia and osteoporosis in HIV-infected pediatric patients, illustrate the importance of monitoring calcium levels regularly in HIV-infected pediatric patients, and maintaining vigilance for signs and symptoms of hypocalcemia during routine office visits. Attention to these disturbances may help to prevent the neurological, cardiovascular, and musculoskeletal consequences associated with low calcium levels." @default.
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• W2017164048 title "Two cases of hypocalcemia secondary to vitamin D deficiency in an urban HIV-positive pediatric population" @default.
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• W2017164048 doi "https://doi.org/10.1097/00002030-200311070-00020" @default.
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