The practice of travel medicine: guidelines by the Infectious Diseases Society of America.
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Biomedical subjects
Publications and source records attributed to Philip R Fischer.
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OBJECTIVE: To assess the effect of vitamin D(2) administration on serum vitamin D metabolite concentrations in calcium deficiency rickets. STUDY DESIGN: We administered vitamin D(2), 50,000 IU orally to 16 Nigerian children 15 to 48 months of age with radiographically active rickets. We measured calcium and vitamin D metabolites at baseline and at 1, 3, 7, and 14 days. RESULTS: At baseline, ranges of serum 25-hydroxyvitamin D (25(OH)D) concentrations were 18 to 40 nmol/L (7-16 ng/mL), and 1,25-dihydroxyvitamin D (1,25-(OH)(2)D) concentrations were 290 to 790 pmol/L (120-330 pg/mL). After vitamin D administration, serum 25(OH)D and 1,25(OH)(2)D concentrations rapidly rose and peaked at 2.8 and 1.9 times the baseline values (P < .001), respectively, at 3 days. Positive correlations between 1,25(OH)(2)D and 25(OH)D were strongest at day 3 (r = 0.84, P < .001) and weakest at day 14 (r = 0.41, P = .11). The relationship of 1,25(OH)(2)D with 25(OH)D at baseline and the increase in 1,25(OH)(2)D in response to vitamin D were similar to those described in children with vitamin D deficiency. However, unlike the pattern in vitamin D deficiency, 1,25(OH)(2)D remained positively correlated with 25(OH)D after administration of vitamin D. CONCLUSION: Dietary calcium deficiency increases the demand for 25(OH)D above that required in vitamin D deficiency to optimize 1,25(OH)(2)D concentrations. Assessment of vitamin D sufficiency in persons or communities may need to be adjusted for habitual dietary calcium intake.
AIM: Despite similarly low calcium intakes and normal vitamin D status, only some Nigerian children develop nutritional rickets. We hypothesized that mothers with children who had developed rickets might have lower breast-milk calcium concentration than mothers with normal children and compared the breast-milk calcium concentration of mothers who had had children with rickets with those who had not (controls). METHODS: We collected breast milk from 35 Nigerian mothers who had previously had children with nutritional rickets. For each case mother, we collected breast milk from three matched control mothers at the same stage of lactation (+/-4 weeks) who had had no children with rickets. Data were collected about parity, stage of lactation, and the infant's intake. The mother's bone density was measured. RESULTS: The mean breast milk calcium concentration of mothers of children with rickets (4.30+/-1.24 mmol/L) was less than that of control mothers (4.65+/-1.03 mmol/L; P=0.034 in multivariate regression controlling for duration of lactation and resumption of menses). Forearm bone mineral content was significantly related to breast milk calcium concentration (r=0.20) after adjusting for height, weight, and bone area (P=0.028). CONCLUSION: Reduced breast-milk calcium concentration may contribute to a reduced calcium intake in infancy and predispose children to nutritional rickets.
INTRODUCTION: Nutritional rickets has been described from at least 59 countries in the last 20 years. Its spectrum of causes differs in different regions of the world. METHODS: We conducted a systematic review of articles on nutritional rickets from various geographical regions published in the last 20 years. We extracted information about the prevalence and causes of rickets. RESULTS: Calcium deficiency is the major cause of rickets in Africa and some parts of tropical Asia, but is being recognised increasingly in other parts of the world. A resurgence of vitamin D deficiency has been observed in North America and Europe. Vitamin D-deficiency rickets usually presents in the 1st 18 months of life, whereas calcium deficiency typically presents after weaning and often after the 2nd year. Few studies of rickets in developing countries report values of 25(OH)D to permit distinguishing vitamin D from calcium deficiency. CONCLUSIONS: Rickets exists along a spectrum ranging from isolated vitamin D deficiency to isolated calcium deficiency. Along the spectrum, it is likely that relative deficiencies of calcium and vitamin D interact with genetic and/or environmental factors to stimulate the development of rickets. Vitamin D supplementation alone might not prevent or treat rickets in populations with limited calcium intake.
Accidents and injury contribute greatly to the morbidity and mortality of travellers worldwide, with road traffic accidents being a major contributer. Those travelers with serious illness and injury may need specialised medical evacuation services, which may involve an air ambulance and a specialised medical team. Such aeromedical repatriations require considerable organisation and liaison between the sending and receiving medical services and other interested parties. However, the majority of travellers requiring emergency assistance are stable patients requiring referral for medical or dental attention or special requirements for carriage on scheduled aircraft.
With focused pretravel counseling and intervention, travelers can be prepared to avoid many risks of in-flight problems. Travel medicine practitioners can include appropriate guidance for in-flight health and safety in discussions during pretravel visits.
Hundreds of millions of people suffer from malaria, and more than a million children die of malaria each year. Malaria typically presents with fever and headache, but the presentation often is nonspecific. The diagnosis should be based on blood tests, and thick and thin smears are the standard means of identifying parasites. In some areas, chloroquine still is effective as treatment, but other medications are needed in most parts of the world. Patients with severe disease (altered consciousness, marked anemia, and/or respiratory distress) should begin therapy parenterally. Control measures depend on the use of insecticide-treated bednets, early identification and treatment of symptomatic individuals, and intermittent preventive therapy. Progress continues toward the development of a useful vaccine.
While resistance to older antimalarials is increasingly common, newer antimalarials are still not widely available or affordable in much of Africa. Older antimalarials used in combination might be adequately effective in treating uncomplicated malaria. The objective of this study was to determine whether the combination of sulfadoxine-pyrimethamine (SP) and chloroquine (CQ) is superior to SP alone in the treatment of uncomplicated Plasmodium falciparum malaria in Nigerian patients. We recruited subjects with malaria, defined as the presence of fever and parasitemia > 2,000/microL, from the outpatient department of a Nigerian teaching hospital. We alternately assigned 280 subjects to receive SP with or without CQ. We assessed clinical and parasitologic responses on days 1, 2, 3, 7, and 14. A total of 114 in the SP + CQ group and 116 in the SP group completed the study. By day 3, 97 (75%) in the SP + CQ group and 52 (42%) in the SP group had cleared their parasitemia (P < 0.001); by day 14, 112 (98%) and 67 (58%), respectively, had cleared their parasitemia (P < 0.001). By day 3, 82 (63%) in the SP + CQ group and 20 (16%) in the SP group were symptom free (P < 0.001). When a modified World Health Organization clinical classification system was used, adequate clinical response occurred in 99 (87%) and 61 (53%) of those in the SP + CQ and SP groups, respectively. RI, RII, and RIII resistance to SP + CQ was 7.9%, 3.5%, and 1.8%, respectively, whereas resistance to SP was 23%, 17%, and 5%, respectively. Combined SP + CQ is superior to SP alone for treatment of uncomplicated malaria in Nigerian patients and may prolong the usefulness of these readily available and affordable drugs.
BACKGROUND: Nutritional rickets is common in Nigerian children and responds to calcium supplementation. Low dietary calcium intakes are also common in Nigerian children with and without rickets. OBJECTIVE: The objective was to assess intestinal calcium absorption in Nigerian children with rickets. DESIGN: Calcium absorption was assessed in 15 children with active rickets (2-8 y of age) and in 15 age- and sex-matched children without rickets by using a dual-tracer stable-isotope method. The children with rickets were supplemented with calcium for 6 mo; calcium absorption was reevaluated 12 mo after the baseline study. Fractional calcium absorption could be determined in 10 children with rickets and in 10 children without rickets. RESULTS: The children with and without rickets had dietary calcium intakes of approximately 200 mg/d. Compared with the control children, the children with rickets had lower serum 25-hydroxyvitamin D and calcium concentrations and greater 1,25-dihydroxyvitamin D and parathyroid hormone concentrations. In fact, there were 15 rachitic and 15 control children in the study. Mean (+/-SD) fractional calcium absorption did not differ between those with (61 +/- 20%) and without (63 +/- 13%) rickets (P = 0.47). Calcium absorption was not associated with serum concentrations of calcium, alkaline phosphatase, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, or parathyroid hormone. Mean fractional calcium absorption was significantly greater after (81 +/- 10%) than before (61 +/- 20%) calcium supplementation for the treatment of rickets (P = 0.035). CONCLUSIONS: In Nigerian children with rickets, the capacity to absorb calcium is not impaired; however, fractional calcium absorption increases after the resolution of active disease. Calcium absorption may be inadequate to meet the skeletal demands of children with rickets during the active phase of the disease, despite being similar to that of control children.
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Nutritional rickets has occasionally been described in children with lamellar ichthyosis, but their vitamin D endocrine status has not been described. We report 3 cases of vitamin D-deficiency rickets associated with ichthyosis in African children. A 13-month-old Nigerian boy with lamellar ichthyosis had rib beading, elevated alkaline phosphatase, and rachitic changes on radiographs. His rickets did not resolve with calcium therapy, and his 25-hydroxyvitamin D level was low. His rickets resolved with parenteral vitamin D treatment, but his skin did not improve. Topical 0.005% calcipotriene (an analog of 1,25-dihydroxyvitamin D that has been useful in treating adults with psoriasis) was similarly ineffective in improving the child's skin condition. An 8-year-old Nigerian boy with life-long skin findings consistent with lamellar ichthyosis had windswept deformity of the legs with rib beading and enlargement of the wrists and ankles. Radiographs showed active rickets, and the boy had an elevated alkaline phosphatase level and a decreased calcium level. Before knowing that his 25-hydroxyvitamin D level was low, he was treated with calcium and showed radiologic improvement. The skin did not improve with resolution of the rickets but did improve with unilateral topical application of 0.005% calcipotriene. A 7-year-old South African girl presented with progressive windswept deformities of the legs and a 4-year history of skin disease (and a skin biopsy consistent with X-linked ichthyosis). Radiographs and biochemical data confirmed active rickets. Her rickets improved dramatically with vitamin D treatment. Thus, 3 African children with ichthyosis developed vitamin D-deficiency rickets, probably because of a combination of impaired skin production and sunlight avoidance. This is consistent with previous findings of hypovitaminosis D in adults with ichthyosis and other disorders of keratinization. Measurement of 25-hydroxyvitamin D may be indicated in children with ichthyosis to identify those at risk for vitamin D-deficiency rickets, because it is possible that the cutaneous synthesis of vitamin D in such children is impaired. Although the ichthyosis did not improve with resolution of vitamin D deficiency and rickets, 1 of 2 children treated with topical calcipotriene showed improvement in the treated areas of skin. Calcipotriene does not seem to be effective in reversing systemic vitamin D deficiency but can be effective in improving the severity of skin disease in children with ichthyosis.
Malaria continues to be a problem for children returning or immigrating to industrialized countries from tropical regions. Proper diagnosis begins with clinical suspicion. In nonimmune children, malaria typically presents with high fever that might be accompanied by chills and headache. Symptoms and signs may be more subtle in partially immune children, and anemia and hepatosplenomegaly may also be present. Children may present with respiratory distress and/or rapidly progressing cerebral malaria that manifests as altered sensorium and, sometimes, seizures. Thick blood smears help to determine when infection is present, but a single smear without parasites is not sufficient to rule out malaria. Thin blood smears aid in identifying the species of parasite. Treatment must include careful supportive care, and intensive care measures should be available for treating children with complicated Plasmodium falciparum malaria. Medical regimens can include mefloquine, atovaquone-proguanil, sulfadoxine-pyrimethamine, quinine or quinidine, clindamycin, doxycycline, chloroquine, and primaquine.
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Although malaria kills approximately 1 million children each year, preventive measures can be effective in limiting the mortality and morbidity associated with malaria. Mosquito bites can be avoided by use of appropriate environmental control and use of protective clothing, bed nets, repellents, and insecticide. Chemoprophylaxis is a mainstay of malaria prevention, and new, effective agents are increasingly available. Rapid, accurate diagnosis and effective medical treatment can help people who become ill with malaria despite their preventive efforts. With careful attention to preventive efforts, malaria should be extremely rare in travelers; similarly, broader implementation of preventive measures could decrease the burden of malaria on residents in areas where it is endemic.
Diarrhea in the returned traveler is common, but it is generally self-limited. Although the concern is often directed at the presence of an ongoing infection, postinfectious and noninfectious etiologies must be considered [table: see text] also. Answers to the clinical questions posed in this article will guide the clinician toward an appropriate diagnostic and management strategy.
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To develop a clinical prediction rule that could accurately identify children with active rickets in countries where nutritional rickets is common, we prospectively recorded clinical features in 736 Nigerian children aged 18 months and older presenting with leg deformities or inability to walk. We scored radiographs of the wrists and knees for active rickets of the growth plates. Sensitivities and specificities of clinical variables for radiographically active rickets were calculated and, using logistic regression, we derived a clinical prediction rule. The prediction rule was tested in a validation set of 89 children. Wrists and costochondral enlargement were the clinical signs with the best combination of sensitivity (72% and 76%, respectively) and specificity (81% and 64%, respectively) for active rickets. Age < 5 years, height-for-age Z-score < -2, leg pain during walking, wrist enlargement and costochondral enlargement were independently predictive of active rickets (p < 0.01 for each in multivariate model). In the validation set, any three of these clinical features accurately identified 87% of children with active rickets, whereas only 24% of those without active rickets had three or more features. We conclude that clinical features can be used to identify children with active rickets.