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 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of extreme hypercalcaemia associated with a parathyroid adenoma in a young man. The patient presented with classical symptoms of a hypercalcaemic syndrome, and serum calcium and parathyroid hormone levels were 6.92 mmol L(-1) and 70.2 pmol L(-1) respectively. After stabilizing the patient and reducing the calcium level, a parathyroidectomy was performed. The postoperative course was uneventful with rapidly resolving clinical symptoms. Hypercalcaemic crisis is a rare but life-threatening complication of primary hyperparathyroidism. It should be suspected in acutely ill patients complaining of muscular weakness, gastrointestinal and cerebral symptoms. To reduce mortality, it is essential to correctly diagnose the condition without delay and provide appropriate emergency management correcting hypercalcaemia and dehydration. Successful parathyroidectomy quickly relieves symptoms and prevents recurrence.
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PMID:Surviving extreme hypercalcaemia--a case report and review of the literature. 1595 36

Myopathies encountered in uremic patients may have different pathogenetic mechanisms and treatment. Secondary hyperparathyroidism may cause uremic myopathy responding to specific treatment. This study aimed at presenting a case illustrative of the clinical features, diagnosis and management of uremic parathyroid myopathy. A 66-year old man with renal failure from membranous nephropathy developed sensory signs of uremic neuropathy and progressive painless weakness of the pelvic girdle muscles bilaterally. Motor nerve conduction velocity was normal, electromyogram was consistent with a myopathic pattern, while muscle biopsy showed a pattern of atrophy more consistent with a neuropathic pattern. Serological tests for collagen vascular diseases and hyperthyroidism were negative, while serum muscle enzymes were not elevated and serum phosphate levels were not low. Serum parathyroid hormone level was grossly elevated, while serum calcium was mildly elevated in a small fraction of the measurements, serum alkaline phosphatase showed a progressive rise and skeletal bone survey did not disclose osteopenia or signs of parathyroid bone disease. A course of calcitriol failed to improve the myopathy, which responded promptly and dramatically to parathyroidectomy. Uremic parathyroid myopathy, which has a characteristic clinical picture, must be differentiated from other neuropathic or myopathic conditions that require specific treatments. Progressive parathyroid myopathy is, by itself, an indication for parathyroidectomy, which is curative in this case.
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PMID:Severe proximal myopathy in advanced renal failure. Diagnosis and management. 1597 50

Vitamin-D deficiency is common in immobile elderly and non-Western immigrants and has been related to muscle weakness in these populations. When serum calcidiol concentrations are below 50 nmol/l, parathyroid hormone concentrations increase, causing bone resorption. Bone mineral density and proximal muscle strength increase as the serum concentration ofcalcidiol increases. Vitamin-D supplementation is reported to reduce the incidence of fractures in nursing home residents. Dutch guidelines recommend vitamin-D supplementation for nursing home residents and for those who are house-bound. Fortification of milk and other foods with vitamin D in the United States and Sweden has led to a better nutritional state with respect to vitamin D than in the Netherlands. Therefore the dairy industry should be allowed to add vitamin D to dairy products to prevent fractures.
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PMID:[Fortification of food with vitamin D is a reasonable approach to fracture prophylaxis]. 1676 82

Transient character of laboratory abnormalities is usually explained as a false result of estimation. Spontaneous disappearance of laboratory abnormalities could be recognized as non-important and contradicting serious disease. Presented case of multiple endocrine neoplasia type 1 (MEN 1) denies these assumptions. Sixty-nine-years old woma was admitted to the internal department because of weakness, fever, dehydration and hypotension--symptom accompanying an upper respiratory infection. Moderate hyponatremia (122.6 mmol/l) was found in a routine laborator examination. All clinical symptoms as well as hyponatremia disappeared during hospitalization. Transient hyponatremi was not ignored. Further laboratory and hormonal investigations were performed. Fasting, morning serum cortisol concentration and 24-hours urinary excretion of free corticosterids were decreased and Synacten stimulation test reveale incomplete cortisol stimulation. Pituitary tumour was found in the CT scan. Moreover blood ionized calcium an parathyroid hormone were elevated. These results revealed secondary adrenal insufficiency, non-functioning pituitary tumor and hyperparathyroidism. Removal of pituitary adenoma was done. Asymptomatic hypercalcemia persists. Presented MEN 1 was atypical because: 1. Usually hyperparathyroidism is the first and most frequent symptom while in our patient the first symptom was transient hyponatremia secondary to the pituitary tumor, 2. was diagnosed in the old age while the majority of MEN 1 patients are younger, 3. asymptomatic course of hypercalcemia indicates that in some of elder patients removal of the parathyroid glands might not be necessary.
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PMID:[Transient hyponatremia the first symptome of multiple endocrine neoplasia type 1 (MEN 1)--case report]. 1680 15

Secondary hyperparathyroidism is highly prevalent in patients with end-stage renal disease. After successful kidney transplantation, however, parathyroid glands gradually involute to normal size with subsequent normalization of intact parathyroid hormone (PTH), serum calcium, and phosphorous concentrations. This report describes a 48-year-old diabetic end-stage renal disease patient who underwent a successful cadaveric kidney transplant. Serum calcium and phosphorous concentrations normalized within 6 months. Three years later, he presented with complaints of proximal muscle weakness that was progressively worsening. Physical examination revealed temporal wasting and proximal muscle weakness. Detailed neurologic examination was unremarkable except for decreased vibratory sensation in both feet. Laboratory data showed stable allograft function (serum creatinine, 1.3 mg/dL), hypocalcemia, and hypophosphatemia with markedly elevated alkaline phosphatase level (726 IU/L) and intact PTH level (947 pg/mL). Further laboratory evaluation revealed poor nutritional status and severe deficiency of 25(OH)D (4.0 ng/mL). Past medical history included remote episodes of acute pancreatitis due to prior alcohol abuse. Computed tomography of the abdomen showed calcific atrophic pancreas, and steatorrhea was confirmed on stool studies. Decreased bone mineral density was noted by computed tomography bone density scan. Secondary hyperparathyroidism and osteomalacia had developed due to severe vitamin D deficiency, occurring as a result of previously unrecognized, minimally symptomatic pancreatic exocrine insufficiency. Treatment with vitamin D, calcium, and pancreatic enzyme replacement led to remarkable resolution of clinical symptoms and secondary hyperparathyroidism (intact PTH, 65 pg/mL after therapy) and resulted in significant improvement in bone mineralization. Factors associated with vitamin D deficiency in the chronic kidney disease and post-transplant patient population are reviewed.
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PMID:Osteomalacia and secondary hyperparathyroidism after kidney transplantation: Relationship to vitamin D deficiency. 1722 Jun 96

We report a case of a 62-year-old postmenopausal hypertensive lady who was treated for osteoporosis with calcium and Vitamin D. She presented with progressive lower limb weakness and paresthesia with sensory level at T4. Investigations revealed high parathyroid hormone 1152 ng/dl, calcium 10.9 mg/dl, and low phosphorus of 2.4 mg/dl after stopping calcium supplement. Chest x-ray showed an expansile mass lesion of the right 6th rib confirmed by chest CT. Thoracic MRI showed a mass lesion extending from the T3 vertebral body and compressing the spinal cord. There were multiple lytic lesions of the scalp, ribs, femur, and pelvis suggesting metastatic lesions. A neck ultrasound and SESTA MIBI parathyroid scan confirmed a right lower parathyroid adenoma. Excision biopsy of the rib lesion confirmed a vascular lesion with features of brown tumor BT. Decompression surgery of the thoracic spine was performed, and the histopathology confirmed BT. Two weeks later the patient underwent right parathyroidectomy that proved to be a parathyroid adenoma. She showed a remarkable improvement in her clinical condition and there were some regression of the bony lesions observed 12 months post parathyroidectomy. This case should alert physicians to the association of multiple brown tumors in PHPT and that the presentation may be an aggressive one mimicking metastasis, patients with osteoporosis warrant at least calcium profile to rule out a secondary cause.
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PMID:Primary hyperparathyroidism. A rare cause of spinal cord compression. 1745 52

Primary hyperparathyroidism (PHPT) is classically thought of as the somatic manifestation of hypercalcemia in which patients suffer from a variety of complaints including abdominal pain, nephrolithiasis, osteopenia, and mental status changes. Contemporary PHPT patients are generally free of somatic manifestations and are most often diagnosed when routine biochemical testing shows an elevated serum calcium level. The modern day patient may present with much more subtle neurocognitive symptoms including fatigue, lethargy, muscle weakness, depression, and cognitive impairment. Advances in imaging technology, intraoperative parathyroid hormone measurement, and surgical technique now allow parathyroidectomy to be performed using a focused approach without the absolute need of a four-gland exploration. Minimally invasive techniques allow the procedure to be accomplished under local anesthesia on an outpatient basis. This brief review summarizes the presentation, biochemical evaluation, operative intervention, and follow-up care of the modern day PHPT patient.
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PMID:Primary hyperparathyroidism. 1760 56

Vitamin D is a hormone that controls phosphorus, calcium, and bone metabolism and neuromuscular function. Vitamin D synthesis is a process in which the skin, liver, and kidney are sequentially involved. The vitamin D pool is completed by the amount taken with food and supplements. Vitamin D deficiency causes osteopenia, precipitates and exacerbates osteoporosis, causes a painful disease, osteomalacia, and increases muscle weakness, which worsens the risk of falls and fractures. A high prevalence of vitamin D insufficiency exists in the apparently healthy population, osteoporotic patients, and patients with prior fractures. Factors contributing to low vitamin D levels include low sunlight exposure, decreased skin synthesis and intestinal absorption, and inadequate diet. The simplest way to correct hypovitaminosis is adequate nutrition and supplements. However, few patients with osteoporosis and/or fractures, receive adequate supplements. Vitamin D insufficiency may alter the regulatory mechanisms of parathyroid hormone and may induce a secondary hyperparathyroidism that increases the risk of osteoporosis and fractures, although the necessary degree of this is not established. Monitoring of serum 25-hydroxyvitamin D levels is the only way to assess vitamin D status. The ideal healthy blood levels of 25-hydroxyvitamin D are controversial, although a range from 30 to 60ng/mL is widely accepted. The role of vitamin D supplementation is to provide humans with the nutrient in an amount closer to the biological norm for our species. This amount of vitamin D results in optimal function of many aspects of health, including balance and muscle strength, thus reducing the risk of fracture beyond what is possible via the quality and quantity of bone itself.
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PMID:Vitamin D and its implications for musculoskeletal health in women: an update. 1760 80

Clonal assessment suggests that most parathyroid adenomas and a subset of uremic parathyroid hyperplasia are monoclonal. A weakness that remains in the prior clonal studies is assessing the clonal status of the tissue fragments containing multiple nodules rather than a single nodule emerging in the uremic parathyroid hyperplasia. We applied the X chromosome-linked phosphoglycerate kinase (PGK) gene inactivation assay method for clonality to study individual nodules. Materials were obtained from 31 cases with parathyroid adenoma and 16 with uremic parathyroid hyperplasia. 17 cases were heterozygous in the PGK-1 locus. We were able to assess the clonality of 10 parathyroid adenomas and 7 hyperplastic glands. Monoclonality was demonstrable in 9 of the 10 parathyroid adenomas and in 4 of the 7 hyperplastic glands. Further analysis of 11 individual nodules microdissected from 3 monoclonal and 1 polyclonal hyperplastic glands revealed that 6 nodules were monoclonal and 5 were polyclonal. Nodules arising in a hyperplastic gland could be of monoclonal or polyclonal origin. Polyclonal and monoclonal nodules coexisted within single glands. Our findings indicate a progression from generalized hyperplasia to a monoclonal tumor in uremic parathyroid hyperplasia. Comparing clonality with the parathyroid hormone (PTH) immunoreactivity and histological features, we found that monoclonal nodules showed a homogeneous immunoreactivity against PTH antibody, whereas most of the polyclonal nodules showed a heterogeneous staining. Classic morphological criteria alone was inadequate to distinguish a monoclonal from a polyclonal nodule.
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PMID:Clonality of the parathyroid nodules with uremic parathyroid hyperplasia. 1847 Jul 30

Nephrogenic systemic fibrosis (NSF) is a rare disorder in patients with chronic kidney disease characterized by an increased tissue deposition of collagen. Its pathogenesis remains unclear. Prior studies indirectly suggested a possible impact of chronic inflammation and accelerated atherosclerosis--a common feature in kidney diseased patients--whereas recent data focused almost exclusively on gadolinium (Gd)-based MR contrast agents. Usually NSF develops a maximum of 2-3 months after Gd. Longer intervals have not yet been described. Therefore, we present the first case with an extraordinary long time course in terms of chronic inflammation. A 52-year-old Caucasian woman with end-stage renal disease was admitted to our hospital with progressive muscle weakness and skin induration resulting in growing immobility. Her past medical history revealed a secondary HPT, multiple vascular complications, a seronegative rheumatoid arthritis, and a pituitary gland adenoma. The latter conditions led to multiple MR examinations with Gd-based contrast agents, the last one more than 4 years ago. Numerous laboratory tests were performed including ESR, CRP, intact parathyroid hormone (iPTH), serum ferritin, cyclic-citrullinated peptide antibodies (CCP), ANA, ANCA, immunoelectrophoresis, and serology for hepatitis as well as human immunodeficiency virus. Eventually a skin biopsy of her left thigh was obtained. The laboratory investigation showed persistently elevated levels of CRP, ESR, serum ferritin, and iPTH, whereas all other parameters were inconspicuous. The hisology displayed typical signs of nephrogenic systemic fibrosis. NSF can occur at any time after Gd exposure in the long term. Gd is a necessary, but not the sole cause of NSF. Certain other cofactors such as chronic inflammation and accelerated atherosclerosis seem to be involved.
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PMID:Chronic inflammation and accelerated atherosclerosis as important cofactors in nephrogenic systemic fibrosis following intravenous gadolinium exposure. 1855 Dec 45


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