Commonly encountered medical problems
Partha Ghosh, Shahid Anis Khan in Transcultural Geriatrics, 2018
Osteomalacia is a defect in bone mineralisation secondary to vitamin D deficiency or its metabolism. It is only encountered in adults when the epiphyseal plates have united. The two major causes of this disorder include a diet deficient in vitamin D and inadequate exposure to sunlight. As the Asian skin is more pigmented, ultraviolet rays in sunlight are less able to penetrate and this reduces production of vitamin D by the skin. The traditional clothing worn by elders from ethnic minorities further reduces their exposure to sunlight. Women are particularly affected as traditionally they are supposed to cover most of their bodies except for the face and hands. A home-bound lifestyle and less participation in outdoor activities may also contribute to this problem. Vegetarian diet is also a contributory factor for vitamin D deficiency. Chapatti flour contributes to the development of vitamin D deficiency. First-generation immigrants, especially the elderly, are more likely to adhere to their customs and hence be more prone to vitamin D deficiency, which seems to be most severe in the Hindu population.
Metabolic bone disease
Philip E. Harris, Pierre-Marc G. Bouloux in Endocrinology in Clinical Practice, 2014
It is important that patients with osteoporosis are vitamin D replete. Vitamin D deficiency is defined as 25(OH)D levels ≤20 ng/mL (50 nmol/L) and insufficiency as 25(OH)D levels of 21–29 ng/mL (52.5–72.5 nmol/L).23 Vitamin D deficiency may be associated with osteomalacia. Lesser degrees of deficiency/insufficiency may be associated with secondary hyperparathyroidism. The dose of vitamin D should be based on the clinical setting or severity of deficiency, to raise the serum level >75 nmol/L (30 ng/L).23 Calcium and vitamin D supplementation should be included in the treatment regimen of osteoporosis, unless there is evidence of adequate calcium intake and normal vitamin D level. The recommended daily dose of vitamin D is 800 IU. Due to the high risk of vitamin D deficiency in elderly patients who are house-bound, supplementation is recommended in these patients.
Other bone diseases in the elderly
Charles M Court-Brown, Margaret M McQueen, Marc F Swiontkowski, David Ring, Susan M Friedman, Andrew D Duckworth in Musculoskeletal Trauma in the Elderly, 2016
The causes of osteomalacia are summarized in Table 11.4. Osteomalacia can be caused by deficiency of vitamin D (cholecalciferol) as the result of poor diet, malabsorption or lack of sunlight exposure, genetic defects in vitamin D metabolism and genetic defects in renal phosphate handling. Osteomalacia may also be caused by certain drugs and by over production of the hormone FGF23 by tumours. There are various causes of osteomalacia as will be discussed below and traditionally vitamin D deficient osteomalacia has been considered the most common. The relative frequency of these different causes has been little studied, but in a recently published series of 28 osteomalacia patients referred to a teaching hospital in Barcelona over a 20-year period, about half had osteomalacia related to vitamin D deficiency and half had osteomalacia due to hypophosphataemia.42 Since the predominant cause of osteomalacia in the elderly is vitamin D deficiency, discussion of pathophysiology in this chapter will focus on mechanisms of vitamin D deficient rickets.
Serum Vitamin D Levels in Children with Vernal Keratoconjunctivitis
Published in Ocular Immunology and Inflammation, 2018
Banu Bozkurt, Hasibe Artac, Hulya Ozdemir, Ali Ünlü, Mete Kaan Bozkurt, Murat Irkec
Median serum total IgE levels in VKC patients was 45.40 IU/mL (range: 10.30–1090 IU/mL). Serum IgE levels were above 100 IU/mL in 12 VKC patients (41.4%). There were no differences in serum 25(OH)D3 levels between VKC children with and without increased serum IgE levels (10.30 ± 4.12 ng/mL and 11.53 ± 5.86 ng/mL, respectively, p = 0.54) and no significant correlation was found between serum 25(OH)D3 and IgE levels (Spearman’s rho 0.044, p>0.05). Serum 25(OH)D3 levels did not differ between VKC children with or without atopy or co-associated allergic diseases (p>0.05). Children who were diagnosed as vitamin D deficiency were referred to pediatricians for further clinical examination and treatment. None of the children with vitamin D deficiency had clinical signs of osteomalacia or decreased serum levels of calcium and phosphate. Vitamin D supplements were given to children with vitamin D levels <10 ng/mL.
Osteomyelitis and pyomyositis due to Staphylococcus aureus in an osteomalacic adult with multiple fractures
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Masumi Ogawa, Takatoshi Kitazawa, Yusuke Yoshino, Koji Morita, Toshio Ishikawa, Yasuo Ota
Tumor-induced osteomalacia (TIO) can be cured by complete resection of the responsible tumor. However, the tumor may be difficult to identify, because it is usually small and can arise anywhere in the body [17]. In TIO localization, a stepwise approach with functional imaging modality and anatomical imaging study had been advocated. Functional imaging includes gallium-68-DOTATATE positron emission tomography (PET), indium-111-pentetreotide single photon-emission computed tomography (SPECT) and fluorine-18-fluorodeoxyglucose PET, whereas anatomic imaging studies include CT and magnetic resonance imaging. Neither these imaging examinations nor pathological examinations were available in our case because the patient refused further examinations.
Endocrine complications of celiac disease: a case report and review of the literature
Published in Endocrine Research, 2019
Marcella D. Walker, Haley M. Zylberberg, Peter H. R. Green, Michael S. Katz
The pathogenesis of reduced BMD, microarchitectural deterioration, and increased skeletal fragility in CD remains incompletely investigated, but both local and systemic mechanisms have been implicated.15,39 The clinical features of CD-associated metabolic bone disease are shown in Table 3. While metabolic bone disease is one thought to be one of the most frequent complications of CD, few studies have directly investigated the mechanism and more research is needed in this area. Weight loss, general malnutrition, and hypogonadism may contribute to bone loss in some CD patients. A major mechanism, however, is thought to be villous atrophy in the small bowel, the major site of calcium and vitamin D absorption. In some cases, malabsorption of calcium and vitamin D may lead to compensatory secondary hyperparathyroidism and bone resorption to maintain normal serum calcium levels.15,21,39 Although there are limited data regarding the prevalence of secondary hyperparathyroidism in CD, one study indicates it is present in 28% of patients and that PTH level is negatively associated with BMD at the forearm.40 A second study suggested a prevalence of 25% in newly diagnosed patients as well as those refractory to treatment while the rate was 19% in those who were responsive to treatment.41 In some cases, prolonged secondary hyperparathyroidism can evolve into autonomous parathyroid function and primary hyperparathyroidism (PHPT). A recent study suggests that CD patients are at almost twice the risk for PHPT.42 Osteomalacia may be present in some patients due to prolonged vitamin D deficiency and calcium malabsorption, though it appears to be rare today.43