Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diagnosis of multiple myeloma is based on the triad paraproteinemia, osteolytic bone lesions and bone marrow plasma cell infiltration. Clinically, rheumatoid-like pain induced by osteolytic skeletal lesions often prevails. Occasionally, foudroyant bacterial infections - the most frequent cause of death in myelomatosis - or acute/subacute renal failure or rarely, acute hemi- or paraparesis precede diagnosis. Establishment of diagnosis early in the course of the disease and improved cytostatic and symptomatic treatment has led to a decrease in episodes of hyperviscosity-syndromes. Severe renal insufficiency due to Bence-Jones proteinuria prevails in 20% of patients already at time of diagnosis. With increasing duration of the disease, frequency of renal insufficiency further increases. Hypercalcemia with consecutive dehydration and renal insufficiency usually is a complication of long-standing disease. Anemia, leukopenia and thrombo-cytopenia are not only side effects of cytostatic treatment, but also consequences of tumor-induced suppression of hematopoiesis. Polyneuropathies are common in myelomatosis. They probably are the result of specific and/or unspecific binding of paraproteins to myelin sheaths. Effective treatment for this complication is not available at present. Thrombohemorrhagic complications are more frequent in patients with myeloma than in the control group of other hospitalized patients. Non-secretory myeloma, osteoblastic myeloma and Takatsuki syndrome are variants of myelomatosis. Solitary and extramedullary plasmocytoma are different, potentially curable entities. Prognosis is especially poor in patients with plasma cell leukemia and poor in primary amyloidosis.
 ...
PMID:[The clinical picture of multiple myeloma]. 353 47

Controlled studies in 1990-1992 with Danish, Sardinian, and Hongkong-Chinese patients consistently revealed a prevalence of goiter of about 50% in lithium treated patients. This is far beyond the frequency generally assumed for Germany, the whole country still known to be an endemic goiter area. Hypothyroidism as a side effect of lithium occurs in a clearly different group of patients and is much less frequent, the overall incidence being not substantially different from the incidence in the general population. But the risk of becoming hypothyroid as well as hyperparathyroid during lithium prophylaxis is markedly higher in women over 45 years of age, who in the general population are also prone to both endocrine dysfunctions. Lithium is considered to have a provoking role. Lithium is known to be accumulated in the bone and an impact on bone metabolism was shown in animal studies. The data reviewed prohibit the use of lithium during lactation and enforce strict indication in children. In adults the effect of lithium on bone should be considered only in osteomalacia and severe osteoporosis. This review is illustrated by the case of a 60-year-old woman, who after 4 years of successful treatment with lithiumcarbonate because of schizoaffective psychosis, developed a syndrome of hypercalcemia. Exstirpation of a parathyroid adenoma rendered her normocalcemic. Moreover, a pre-existing diffuse goiter had grown to a large nodular goiter within the course of her 5-year treatment. As she finally became paraparetic, she was admitted to our rehabilitation center for the diseases of the spinal cord. Her paraparesis may have been caused not only by the lithium-induced primary HPT, but in part by lithium itself. There are a few reports on lithium causing peripheral neuropathy at toxic levels. A transient deterioration of a pre-existing neuropathy, as in our case study, may have happened at lithium serum levels not far beyond the upper limit of 0.8 mmol/l.
 ...
PMID:[Lithium and its effects on the endocrine system, bones and peripheral nerves--a current review]. 775 53

We report on an in vivo model of human myeloma producing bone disease in irradiated severe combined immunodeficiency disease mice using the human myeloma cell line JJN-3 and its subline JJN-3 T1. The cell lines are not Epstein-Barr virus transformed and produce large amounts of hepatocyte growth factor (HGF). Mice had radiological signs of osteolysis and mild hypercalcemia. Xenografted cells were predominantly found in bone marrow and brown adipose tissue, but also in meninges and liver. Take was documented by histopathological examination, immunophenotyping of cultured bone marrow, and radiography. HGF was detected in serum and bone marrow plasma. Disease generally occurred within 45 days of intravenous inoculation and was signaled by paraparesis or signs of intracranial neoplasia. More than 90% of the mice had take of xenografts. The subline JJN-3 T1 gave more reproducible bone marrow take than the native cell line. Bone histomorphometric examination revealed a 99% reduction in osteoblast counts and a 33% reduction in osteoclast counts in areas of tumor growth. Bone formation rates were reduced by 53%. The results suggest that osteoblastopenia and reduced bone formation is of importance for the occurrence of osteolytic lesions in this model.
 ...
PMID:Marked osteoblastopenia and reduced bone formation in a model of multiple myeloma bone disease in severe combined immunodeficiency mice. 993 80

The case is presented of a 65 year old lady with recent onset of neuromuscular manifestations, comprising paraparesis, areflexia and unsteady gait, along with episodes of slurring of speech and diplopia, later confirmed to be due to severe hypercalcaemia--which itself was caused by primary hyperparathyroidism. Restoration of normocalcaemia, by means of rehydration and bisphosphonate therapy, resulted in clinical improvement--whilst subsequent parathyroidectomy was followed by complete resolution of all symptoms. In order to make prompt differentiation between the neurological sequelae of hyperparathyroidism and a primary neurological disorder, a high index of suspicion is required. An urgent serum calcium assay, as part of a bone profile, is mandatory in patients who present with neurological symptoms--especially the elderly, amongst whom hyperparathyroidism is especially common.
 ...
PMID:Lessons to be learned: a case study approach. Primary hyperparathyroidism simulating an acute severe polyneuritis. 1007 44

An unusual clinical presentation of lymphoma with vertebral involvement in a dog is reported. A 20-month-old intact female Golden Retriever presented with progressive paraparesis and anorexia. Complete blood count and serum biochemistry profile demonstrated pancytopenia and hypercalcemia. Ventral fusion of the lumbar vertebrae by new bony tissue deposition was evident on X-ray and CT scan. Fine needle aspiration revealed neoplastic lymphoid cells in lymph nodes and bone marrow. Histologically, vertebral bone and osteophytes, liver, bone marrow, kidney, and lymph nodes were diffusely infiltrated by neoplastic, lymphoid cells, with scant cytoplasm and round hyperchromatic nuclei. Polyostotic and medullary T-cell lymphoma with spondylosis was diagnosed. Lymphoma mainly affecting bone is uncommon in the dog. The present case differs from previously described polyostotic lymphomas in clinical signs of the disease, mainly attributable to spondylarthrosis. In addition, lymphomatous proliferation was associated with osteoproductive lesions of the vertebrae.
 ...
PMID:Vertebral polyostotic lymphoma in a young dog. 1740 20

Brown tumors also called as osteoclastomas, are rare nonneoplastic lesions that arise in the setting of primary or secondary hyperparathyroidism. Parathyroid adenomas or hyperplasia constitute the major Brown tumor source in primary hyperparathyroidism while chronic renal failure is the leading cause in secondary hyperparathyroidism. Most of the patients with the diagnosis of primary hyperparathyroidism present with kidney stones or isolated hypercalcemia. However, nearly one third of patients are asymptomatic and hypercalcemia is found incidentally. Skeletal involvement such as generalized osteopenia, bone resorption, bone cysts and Brown tumors are seen on the late phase of hyperparathyroidism. The symptoms include axial pain, radiculopathy, myelopathy and myeloradiculopathy according to their locations. Plasmocytoma, lymphoma, giant cell tumors and metastates should be ruled out in the differential diagnosis of Brown tumors. Treatment of Brown tumors involve both the management of hyperparathyroidism and neural decompression. The authors report a very rare spinal Brown tumor case, arisen as the initial manifestation of primary hyperparathyroidism that leads to acute paraparesis.
...
PMID:Brown Tumor of the Thoracic Spine: First Manifestation of Primary Hyperparathyroidism. 2658 96