1.
Hypocalcaemia of malignancy.
Schattner, A, Dubin, I, Huber, R, Gelber, M
The Netherlands journal of medicine. 2016;(6):231-9
Abstract
BACKGROUND Hypercalcaemia of malignancy is well recognised, but hypocalcaemia in cancer patients is not, although it is increasingly encountered. METHODS Analysis of an exemplary case and a narrative review of the literature based on the search terms cancer and hypocalcaemia. RESULTS Hypocalcaemia may affect as many as 10% of hospitalised cancer patients. We identified 12 different potential mechanisms of hypocalcaemia of malignancy. Identifying the pathogenesis is essential for the correct treatment and can usually be performed at the bedside, based on serum parathyroid hormone (PTH) levels, creatinine, phosphate, magnesium, creatine kinase, liver enzymes and 25(OH)D. Essentially, decreased or normal PTH hypocalcaemia is seen after removal or destruction of its source, hypomagnesaemia, or cinacalcet treatment. In all other cancer-associated hypocalcaemia, PTH is elevated, including significant renal impairment, critically ill patients, extensive cell destruction (rhabdomyolysis, tumour lysis, haemolysis), acute pancreatitis, adverse drug reactions, cancer or cancer treatment-related malabsorption syndromes, vitamin D deficiency, or osteoblastic metastases. Different mechanisms may often operate in tandem. Pathogenesis determines treatment and affects prognosis. However, hypocalcaemia of malignancy as such did not imply a worse prognosis, in contrast with hypercalcaemia. CONCLUSION Hypocalcaemia in cancer patients is commonly encountered, particularly in hospitalised patients, may be mediated by diverse mechanisms and should be better recognised.
2.
[Calcific uremic arteriolopathy. a case report and review of the literature].
Vassallo, M, Bello, I, Hamana, L, Ferrer, A, Rojas, F, Cantele, H
Revista clinica espanola. 2011;(7):e37-41
Abstract
BACKGROUND Calcific uremic arteriolopathy is defined as a syndrome consisting of ischemic skin ulceration due to calcification of the wall of the arterioles of the subcutaneous tissue as a result of hyperparathyroidism in uremic patients. CASE REPORT A 55-year old female patient, hypertense, with heart failure and kidney failure treated with hemodialysis, who presented lower limb pain and hypercalcemia. On physical examination, skin lesions with symmetrical peripheral pulses present in the limbs. Laboratory tests revealed hypercalcemia, hyperphosphatemia, and very high parathyroid hormone levels. Parathyroidectomy was performed and biopsy of skin lesions, the patient having a torpid course causing exitus. Autopsy was performed, with histologic features characteristic of calcific uremic arteriolopathy. CONCLUSIONS Calcific calcium uremic arteriolopathy or calciphylaxis is a complex and variable disease that is difficult to diagnose and whose treatment is complicated. Despite the efforts of the investigators, there are still many questions regarding its pathogenesis. This acts as an incentive for further research to establish the most appropriate actions to take to maintain an adequate quality of life for the patients and avoid complications that trigger death in some cases.
3.
Calciphylaxis: what nurses need to know.
Bliss, DE
Nephrology nursing journal : journal of the American Nephrology Nurses' Association. 2002;(5):433-8, 443-4; quiz 445-6
Abstract
Calciphylaxis is a rare and potentially fatal complication of end stage renal disease (ESRD) and secondary hyperparathyroidism associated with abnormal calcium metabolism. Painful purple skin lesions are often the presenting sign with digital ischemia, ulcerations, and necrosis being the characteristic features of the disease. Skin or incisional biopsy showing widespread calcifications and fibrinous thrombi without inflammation will confirm the diagnosis. Early recognition and prompt treatment of calciphylaxis is vital for symptom relief, ulcer healing, and prevention of sepsis and death. This article will educate nurses to recognize this disease in hope of early treatment. The article includes information about disease history, pathogenesis, etiology, clinical manifestations, diagnosis, prevention, and current treatment, and, in addition, presents case study of a patient with calciphylaxis.
4.
Treatable lower motor neuron disease due to vitamin D deficiency and secondary hyperparathyroidism.
Whitaker, CH, Malchoff, CD, Felice, KJ
Amyotrophic lateral sclerosis and other motor neuron disorders : official publication of the World Federation of Neurology, Research Group on Motor Neuron Diseases. 2000;(4):283-6
Abstract
Vitamin D deficiency and osteomalacia are frequently associated with muscle weakness and atrophy. We present a 78-year-old man with complaints of progressive painless weakness who was referred to us with a diagnosis of suspected motor neuron disease. Results of the neurological examination were remarkable, showing diffuse limb weakness and atrophy, rare fasciculations, normal sensory examination, no bulbar weakness, and no upper motor neuron signs. Electromyography revealed mild chronic changes, denervation and re-innervation, without fibrillations or positive waves. Serum laboratory studies showed an elevated serum parathyroid hormone and markedly reduced vitamin D level. Although the etiology of the vitamin D deficiency was not determined, the patient made a substantial clinical improvement following vitamin D therapy. Vitamin D deficiency and secondary hyperparathyroidism need to be included in the differential diagnosis of patients presenting with a progressive lower motor neuron disease.