Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Synthetic salmon calcitonin (sCT, doses of 0.7 Medical Research Council U per kg) was injected into nine normal subjects and three patients with hypergastrinemia (pemicious anemia). sCT depressed basal as well as food-stimulated serum gastrin concentrations without concomitant changes in total and ultrafiltrable concentrations of calcium in serum. Gel filtration of sera revealed that sCT reduced mainly the small components, III (gastrin-17 or "little" gastrin) and IV (gastrin-13 or "mini"-gastrin).
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PMID:Effect of calcitonin on serum gastrin concentration and component pattern in man. 117 Nov 12

This report deals with an unusual case of primary macroglobulinemia with hypercalcemia, chronic renal failure and systemic amyloidosis. In May 1990, a 63-year-old male was transferred to our hospital because of hypercalcemia (13.5 mg/dl) and renal failure. Clinical examinations showed anemia, macroglossia, lymph node swellings and hepatomegaly. Laboratory findings included Bence-Jones (kappa type) proteinuria (0.8 g/day), a monoclonal gammopathy of the IgM-kappa type (2.8 g/dl), a proliferation of lymphoid cells in the peripheral blood (5%) and the bone marrow (59.6%), and lymphomatous involvement of an inguinal lymph node. Serum creatinine concentration was 8.5 mg/dl. The serum levels of parathormone and vitamin D3 metabolites were normal. The roentgenogram of bones showed a compression fracture of the lumbar spine and systemic osteoporosis. The treatment included eel calcitonin, prednisolone and the CHOP regimen, followed by hemodialysis and plasmapheresis. The serum level of IgM increased to 4.6 g/dl. The patient died three months later and postmortem examination demonstrated marked systemic amyloidosis.
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PMID:[Primary macroglobulinemia with hypercalcemia, renal failure and systemic amyloidosis]. 146 88

Two patients with severe iron deficiency anemia and gastric antral vascular ectasia (GAVE) are reported. The anemia caused by the chronic blood loss from the abnormally dilated mucosal and submucosal capillary veins in the gastric antrum was unresponsive to oral iron supplementation. However, one of the patients was successfully treated with intramuscular injection of (Asu1,7) eel calcitonin. The other one was treated by oral prednisolone with resulting improvement iron deficiency anemia. The possible mechanisms of successful calcitonin and prednisolone treatments on chronic blood loss from GAVE is discussed.
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PMID:Two cases of gastric antral vascular ectasia--response to medical treatment. 176 49

We studied 57 tumors of the thymus seen at Vanderbilt University Medical Center between 1957 and 1982. By applying current diagnostic criteria, the classification of 13 tumors was changed. There were 45 epithelial tumors of thymus, including 32 thymomas, two thymic carcinomas, eight carcinoids, and three germinomas. The gross and microscopic features of these neoplasms overlap each other and several other tumors, but with knowledge of the variations it was usually possible to establish a diagnosis with light microscopy. In more difficult cases, electron microscopy was the most useful diagnostic method. New developments in immunologic staining were also of value. The diagnosis of thymoma was used for circumscribed and invasive neoplasms of thymic epithelium without anaplasia. Cytologically malignant thymic epithelial tumors were classified as thymic carcinoma. Thymic carcinomas were more aggressive than thymomas and were not associated with syndromes such as myasthenia gravis or anemia. Thymic carcinoids were frequently aggressive, and several of them produced corticotrophin or calcitonin. Thymic germinomas were histologically identical to testicular seminoma, but may be confused with thymoma because of their lymphocytic infiltrate. Invasive germinomas were radiosensitive.
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PMID:Thymic epithelial neoplasms. 299 53

Rhabdomyosarcoma and other small round-cell neoplasms of infancy and childhood frequently involve the bone marrow. An unusual clinical presentation of diffuse bone marrow involvement as the sole manifestation of the disease represents a difficult diagnostic challenge. We report the case of an 18-year-old boy presenting with lower back pain, sternum tenderness, anemia, thrombocytopenia, leukoerythroblastic blood film, hypercalcemia, and renal failure. No solid tumor was found. A diagnosis of rhabdomyoblastic bone marrow metastatic involvement was initially suggested by the morphological picture, and later confirmed by the ultrastructural findings. Hypercalcemia and renal failure were controlled, initially, with furosemide and calcitonin. The patient was treated with intensive chemotherapy, including vincristine, actinomycin D, cyclophosphamide, and doxorubicin. A remission was achieved, lasting 5 months until relapse.
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PMID:Rhabdomyosarcoma presenting with diffuse bone marrow involvement, hypercalcemia and renal failure. 335 35

Although in recent years experimental work on growth in uremia has clarified many issues, many key questions cannot be answered with available experimental data. In our own studies on subtotally nephrectomized rats, uremic animals consumed less food and grew less. However, although low energy intake diminishes growth, it has not been established that high protein energy intake will normalize growth. We showed that uremia reduced growth (and net protein synthesis) even under conditions of controlled food intake. In renal failure the optimal dietary protein level for growth or for efficiency of utilization has not been established, particularly since protein intake has an independent injurious effect on long-term renal function. Calcium and vitamin D supplements improved growth in uremic rats, but the data cannot easily be extrapolated to humans. The growth-promoting action of 1,25(OH)2D3 was not superior to that of equipotent doses of vitamin D3. Correction of anemia and physical exercise did not improve growth. Diminished stimulation of growth cartilage cyclic AMP with PTH and augmented stimulation with calcitonin was noted in uremic animals. Growth hormone in supraphysiological doses improved growth and raised IGF carrier protein in uremic animals. Spermine, a potential uremic toxin, inhibited growth cartilage 3H-thymidine incorporation, but only in concentrations higher than that encountered in uremia.
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PMID:Skeletal growth in experimental uremia. 636 50

One family (3 cases) with the Kenny syndrome and a second family (3 cases) with features of Kenny syndrome but lacking medullary stenosis are reported. The main symptoms in both families are proportionate dwarfism, cortical thickening of tubular bones, variable anomalies of the calvaria, anemia, transient hypoparathyroidism and variable ocular anomalies. The latter include microphthalmia, and moderate-to-severe myopia or hyperopia. In the first family there was medullary stenosis of most tubular bones. In the second family two cases exhibited mild-to-moderate cortical thickening of tubular bones, but absent or mild medullary stenosis. Possible variability of the Kenny syndrome is discussed. Endocrine studies failed to demonstrate any permanent disturbance of parathormone or calcitonin metabolism, or GH deficiency. Pathogenesis remains unclear. Autosomal dominant inheritance seems to be likely.
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PMID:The Kenny syndrome, a rare type of growth deficiency with tubular stenosis, transient hypoparathyroidism and anomalies of refraction. 721 88

After a near total small bowel resection for an acute thrombosis of the mesenterial artery, a 61 year-old man was treated with total parenteral nutrition at home for five years. The treatment was complicated by episodes of sepsis, anaemia and uremia. After four years he developed pain in long bones and the back and grave hypercalcuria. Roentgenogram showed demineralisation. There was no hyperparathyroidism and serum phosphate and serum calcium were normal. His chronic metabolic acidosis was treated continuously with enteral acetate. He received basal amounts of vitamin D and amino acids. By administering calcitonin we were able to cure his progressive bone pains and normalize his calcium urinary output. No side effects were observed. Therefore, calcitonin may contribute to the treatment of bone disease associated with total parenteral nutrition.
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PMID:[Calcitonin treatment of metabolic bone disease induced by parenteral nutrition]. 832 48

Parathyroid hormone and calcitonin, both endocrine modulators of calcium homeostasis, may influence blood rheology. Parathyroid hormone is known to reduce erythrocyte survival, leading to anemia. Calcitonin has been found to have some vascular effects. We have analyzed the Influence of parathyroid hormone (10(-7) to 10(-10) mol/L), calcitonin (10(-6) to 10(-12) mol/L), 1,25(OH)2 cholecalciferol (10(-7) to 10(-10) mol/L), additional calcium in plasma (+1 and 2 mmol/L), and the calcium lonophore A23187 (50 micromol/L) on erythrocyte morphology and blood viscosity at high shear rate (94 s(-1)) and low shear rate (0.1 s(-1)) in vitro. The loading of erythrocytes with calcium by the ionophore A23187 produced a marked echinocytic shape transformation, an increased blood viscosity at high shear rate caused by decreased deformability of these cells, and a decreased viscosity at low shear rate caused by decreased aggregation of echinocytes. In contrast, increasing plasma calcium concentrations, parathyroid hormone, calcitonin, and 1,25(OH)2 vitamin D3 had no effect on erythrocyte morphology and blood viscosity. We conclude that an increase in intraerythrocytic calcium leads to severe echinocytosis and altered blood viscosity. The endocrine modulators of calcium homeostasis--namely, parathyroid hormone, calcitonin, and 1,25(OH)2 vitamin D3--apparently do not influence intraerythrocytic calcium to a significant degree and have, therefore, no influence on cell morphology and blood viscosity.
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PMID:Influence of parathyroid hormone, calcitonin, 1,25(OH)2 cholecalciferol, calcium, and the calcium ionophore A23187 on erythrocyte morphology and blood viscosity. 1077 51

An intestinal carcinoid with multiple metastases was identified in a 5-year-old male Shih Tzu with a clinical history of anemia, fatigue, anorexia, vomiting, intermittent diarrhea, intestinal bleeding, and progressive emaciation. There was a yellowish-white mass 15 mm in diameter in the anterior jejunum and white nodules consistent with metastases in many organs. Histopathologically, the mass consisted of neoplastic cells arranged in lobules, trabeculae, or closely interdigitating islands of cells. Neoplastic cells were generally polygonal with round hyperchromatic nuclei, modest amounts of eosinophilic cytoplasm, and eosinophilic cytoplasmic granules. Mitoses were common. Rosette formations of tumor cells were apparent in metastatic tumors. Immunohistochemically, tumor cells stained positive for cytokeratin 13, synaptophysin, protein gene product 9.5, neuron-specific enolase, chromogranin A, calcitonin gene-related peptide, serotonin (5-HT), and Leu-7. Serum 5-HT concentrations for this dog were increased 10-fold compared with those of normal dogs. All findings were consistent with a diagnosis of a malignant intestinal carcinoid.
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PMID:Immunohistochemical evaluation of a malignant intestinal carcinoid in a dog. 1263 63


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