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Vitamins
Published in Stanley R. Resor, Henn Kutt, The Medical Treatment of Epilepsy, 2020
Prophylactic treatment may be beneficial for patients who are inactive, lack sufficient vitamin D in the daily usual diet, and are deprived of sunlight. After 6 months on AEDs such as PHT, PB, or CBZ, determination of calcium, phosphorus, and alkaline phosphatase levels is helpful. If there is suspicion of vitamin D deficiency, then a vitamin D level can also be measured. The average patient with epilepsy who is otherwise well on a normal diet probably does not need prophylactic vitamin D supplements. The symptoms of hypercalcemia from hypervitaminosis D or excessive calcium intake include weakness, nausea, vomiting, diarrhea, and obtundation. Nephrocalcinosis, nephrolithiasis, and metastatic calcification can ensue (29). If vitamin D or calcium is prescribed, then monitoring of the calcium, phosphorus, alkaline phosphatase, and creatinine should be done after a month, then every 3 months. Vitamin D and circulating 25-hydroxyvitamin D levels should be checked 1 month after starting such therapy, and then every 6 months (30).
The Injured Cell
Published in Jeremy R. Jass, Understanding Pathology, 2020
Metastatic calcification occurs in normal tissues in subjects with hypercalcaemia. Common causes of hypercalcaemia include overproduction of parathyroid hormone (for example by a parathyroid adenoma), vitamin D intoxication and excessive consumption of alkali. Metastatic calcification is most common in sites of ion exchange: alveoli of lung, gastric mucosa and renal tubules.
Noninfectious Pulmonary Manifestations of Renal Disease In Children
Published in Lourdes R. Laraya-Cuasay, Walter T. Hughes, Interstitial Lung Diseases in Children, 2019
Stephen T. Lawless, H. Jorge Baluarte
This picture of metastatic calcification is related partly but not entirely to secondary hyperparathyroidism. All the etiologic factors are not completely understood as serum calcium, phosphate, the Ca x P04 solubility product, and parathyroid hormone in those patients with histologic calcification are only slightly altered.4 The diagnosis of metastatic lung calcification can be made by Technetium 99 (Tc99) diphosphate lung scan. Technetium seeks bone and calcium, so the lungs show enhancement on bone scan if calcifications are present. The calcifications may reverse somewhat with more frequent and efficient dialysis. Surprisingly, the incidence of pulmonary embolus among patients with renal insufficiency appears less than in the general population. In one series of adult patients, the incidence of embolus on autopsy was 32%, while in those with a serum creatinine > 5 mg% the incidence was 9.5%,5 in spite of the usually high risk factors present in adults. It is possible that there are nonspecific platelet abnormalities inherent in the uremic condition which help decrease the incidence of emboli. Pulmonary hemosiderosis with fibrosis can occur as a result of multiple blood transfusions and iron overload.
Therapeutic effect of intravenous sodium thiosulfate for uremic pruritus in hemodialysis patients
Published in Renal Failure, 2020
Yu-Huan Song, Si-Yang Wang, Jia-Hui Lang, Yue-Fei Xiao, Guang-Yan Cai, Xiang-Mei Chen
Sodium thiosulfate (STS) has been used to treat calcific uremic arteriolopathy (CUA) in HD patients [6]. CUA, also referred to as calciphylaxis, is a thrombotic disorder of the skin and subcutaneous tissue [7,8]. Reported patient symptoms included pain, skin lesions, and pruritus [9]. STS is one of the cornerstones of calciphylaxis therapy and has been used for over 10 years for this indication, although this use remains off-label [9]. It also decreases metastatic calcification in patients with chronic kidney disease (CKD) [10]. The recommended dosage for the treatment of CUA is 12.5 g to 25 g, three times per week at the end of each HD session for 6 weeks to 34 months [11–13]. Several Chinese studies reported that STS had a nonspecific antiallergic and antipruritic effect, which can be helpful with regard to relieving asthma and atopic dermatitis [14,15]. It acts as a potent antioxidant by regenerating glutathione and prompting endothelial nitric oxide production through the action of hydrogen sulfide, thereby increasing tissue blood flow and oxygenation [16,17]. This multifactorial activity is perhaps responsible for the response in pruritus patients.
An unusual case of idiopathic calcinosis of the eyelid
Published in Orbit, 2019
Ashlie A. Bernhisel, Brian E. Zaugg, Nick Mamalis, Jonathan J. Dutton, Bhupendra C. K. Patel
Soft tissue calcium deposits are a common clinical finding, which have been classified as dystrophic, metastatic, calciphylaxis, iatrogenic, and idiopathic in nature. There is also calcification that occurs in several dermal diseases of the eyelid including calcifying epithelioma of Malherbe (pilomatrixoma), chalazia, and pilar cysts.1,2 Dystrophic calcification refers to tissue calcification caused by trauma or an underlying medical condition such as CREST syndrome, which causes chronic inflammation and alterations within connective tissue resulting in calcium deposits.3 Metastatic calcification is associated with metabolic disorders that cause elevated blood calcium, phosphorus, or vitamin D levels. Calciphylaxis is small vessel calcification that occurs in end stage renal disease and iatrogenic calcification occurs with use of calcium gluconate or calcium chloride therapy.3