Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

46-year-old male patient was born in Niigata Prefecture and thereafter lived in Tokyo. In late January 1985, he noticed swelling of the bilateral inguinal lymph-nodes followed by fever and lumbago. In February, he consulted a local doctor and hepatosplenomegaly, marked leukocytosis and renal dysfunction were pointed out and he was referred to our hospital on February 22nd. The clinical laboratory data on admission were as follows; WBC 23,200/microliter, serum-Ca 18.4 mg/dl, BUN 85.3 mg/dl, creatinine 5.4 mg/dl, antibody to ATLV x160. ATL was diagnosed by biopsy of lymph nodes and examinations of peripheral blood and bone marrow hemogram. Remission was achieved in March by the treatment with adriacin. Renal failure and hypercalcemia also improved. However his respiratory dysfunction gradually worsened. The chest radiographies++ showed pulmonary edema, although there was no clinical evidence of heart failure. When his condition became stable, TBLB was performed and revealed extensive deposition of calcium along alveolar septae, suggesting that pulmonary edema was induced by the metastatic calcification of the lung. After the second treatment for ATL, he died of pneumonia. The autopsy showed calcium deposition not only in the lung but in pyramids of the kidney and in sub-serous layer of the small intestine. There was no tumor cell invasion into the bone or parathyroid gland. High urinary c-AMP together with normal levels of PTH suggested that the hypercalcemia in this case was induced by PTH-related protein. It was concluded that careful treatment for hypercalcemia is important as regards the occurrence of pulmonary edema.
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PMID:[An autopsy case of adult T-cell leukemia complicated with metastatic calcification of the lung]. 204 Dec 50

A 57-year-old female was admitted to our hospital with general lassitude, loss of appetite, nausea, upper abdominal pain, thirst, polydipsia and polyuria. On admission, she had an asymmetrical pear-shaped tumor in the right supraclavicular region and severe hypercalcemia. Plasma C-PTH was elevated to 22.72ng/ml. Plasma calcitonin was also elevated to 336 pg/ml. She died of respiratory and cardiac failure of two weeks after admission without any positive response to the treatment, including hemodialysis. Pathohistologically, the tumor was a parathyroid adenoma. The concentrations of C-PTH, intact PTH and calcitonin in the tumor tissue were markedly high: 4.56 micrograms/g wet, 13.9 ng/g wet and 50.7 ng/g wet, respectively. Immunohistologically, the tumor cells and the fibrous stroma were stained strongly positive to rabbit anti-human calcitonin antibody and rabbit anti-human N-PTH antibody by indirect immunoperoxidase staining. Calcitonin-producing tumors, except for medullary thyroid carcinoma are rarely reported. To our knowledge, this is the first report of such a calcitonin-producing parathyroid adenoma associated with primary hyperparathyroidism.
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PMID:A case of calcitonin-producing parathyroid adenoma with primary hyperparathyroidism. 258 94

In senescence renal function is thought to decline markedly even in the absence of renal disease. It has also been proposed that the changes in renal function with age are not uniform and that confounding factors such as hypertension or atherosclerosis may play a role. We performed a comprehensive study to compare several aspects of renal function in four groups: (i) young healthy normotensive subjects (N = 24; 13 males; mean age 26 +/- 3 years); (ii) elderly healthy normotensive subjects (elderly NT; N = 29; 13 males; 68 +/- 7 years); (iii) elderly treated and untreated hypertensive patients (elderly HT; N = 25; 13 males; 70 +/- 6 years); and (iv) elderly patients with compensated mild to moderate heart failure (elderly HF; N = 14; 6 males; 69 +/- 6 years). Compared to young subjects mean GFR (C(In)) and ERPF (C(PAH)) were significantly lower in the elderly, despite similar mean plasma creatinine levels (young, 121 +/- 11, 650 +/- 85 ml/min/1.73 m2; elderly NT, 103 +/- 11, 486 +/- 102; elderly HT, 103 +/- 13, 427 +/- 55; elderly HF, 92 +/- 14, 377 +/- 103). Nevertheless, GFR was within the normal range in the majority of elderly NT and HT, but not in elderly HF. ERPF was significantly lower in elderly HT as compared with elderly NT, and still lower in elderly HF. Mean renovascular resistance and filtration fraction were significantly higher in the elderly, particularly in elderly HT and HF as compared with the young. Mean fractional excretion of Na+ was similar in all groups studied, but the lithium clearance was significantly lower in the elderly, suggesting a greater proximal and less distal sodium reabsorption in senescence. In the elderly, mean PTH concentration and urinary excretion of pyridoline cross-links were significantly higher and mean 25-(OH)D3, calcitriol and phosphate concentrations significantly lower; the correlation between PTH and GFR was significant (r = -0.432, P < 0.001). The results document that the decrease in renal hemodynamics with senescence is less marked than suggested by some studies using less stringent methodology and inclusion criteria. Comorbid conditions confound renal function in the elderly. Age-associated changes in renal hemodynamics are accompanied by significant alterations of renal hormones and of renal sodium handling.
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PMID:Renal function in the elderly: impact of hypertension and cardiac function. 908 86

Retrospective study was performed to measure the results of parathyroidectomy in patients with secondary hyperparathyroidism. From 1987 to 2000, 48 patients underwent surgery for secondary hyperparathyroidism. There were 30 of 48 patients on haemodialysis treatment, and 11 patients were in pre-dialysis stage. Parathyroidectomy was performed after successful kidney transplantation in 4 cases. Indication of the surgery was extremely elevated serum level of parathyroid hormone (at least 10 fold elevation), which was resistant for the conservative medical therapy. Subtotal parathyroidectomy (3 1/2) was performed in 30 patients. Five patients underwent total parathyroidectomy and autotransplantation. Only 2 or 3 parathyroid glands have been removed in 13 patients. Haematoma occurred in 3 cases after parathyroidectomy. Recurrent nerve injury or septic complication did not occur. Two patients died in the early postoperative period due to cardiac failure. Tetania was noted in 2 patients after surgery. Permanent postoperative hypocalcaemia (over 6 months) occurred in 3 cases. Persistent hyperparathyroidism was diagnosed in 5 patients. In these patients 2 parathyroid glands were removed during the primary operation. Recurrent hyperparathyroidism was detected in 2 patients. Subtotal parathyroidectomy was carried out in these cases previously. At the reoperation for persistent and recurrent hyperparathyroidism, total parathyroidectomy and autotransplantation was performed. Serum alkaline phosphatase level and serum parathyroid hormone value decreased after surgery, except those patients with persistent hyperparathyroidism. Bone pain decreased in 96% of the cases and pruritus decreased in 92% of the patients after parathyroidectomy. Soft tissue calcification showed improvement in 45% of cases. In conclusion, the subtotal parathyroidectomy or total parathyroidectomy with autotransplantation cause a rapid decrease of PTH level and the improvement of the clinical symptoms in patients with medical treatment resistant secondary hyperparathyroidism. Persistent hyperparathyroidism occurs in those cases when inadequate parathyroidectomy was performed.
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PMID:[Results and complications of parathyroidectomy in secondary hyperparathyroidism]. 1181 32

Autosomal dominant hypocalcemia (ADH) caused by activating mutations of calcium-sensing receptor (CaSR) is characterized by hypocalcemia with inappropriately low concentration of PTH and relative hypercalciuria. Active vitamin D treatment often leads to nephrolithiasis and renal impairment in patients with ADH. However, differential diagnosis between ADH and idiopathic hypoparathyroidism is sometimes very difficult. Here, we report a mutation of CaSR and its functional property found in three generations of a Japanese family. The proband developed seizures at 7 days of age. His mother and elder sister were discovered to have hypoparathyroidism by family survey, but his father was normocalcemic. His grandfather developed heart failure and was found to have hypoparathyroidism. All affected members had been treated with active vitamin D3 and bilateral nephrolithiasis were detected in three of them. DNA sequencing revealed that all affected patients had a heterozygous mutation in CaSR gene that causes proline to leucine substitution at codon 221 (P221L). In vitro functional analysis of the mutant CaSR by measuring inositol 1,4,5-trisphosphate production in response to changes of extracellular Ca indicated that this mutation is an activating one and responsible for ADH in this family. Therefore, careful monitoring of urinary Ca excretion before and during treatment of PTH-deficient hypoparathyroidism is very important, and screening of CaSR mutation should be considered in patients with relative hypercalciuria or with a family history of hypocalcemia.
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PMID:A family of autosomal dominant hypocalcemia with an activating mutation of calcium-sensing receptor gene. 1273 14

Hyperparathyroidism (HPT) is common in patients on dialysis, and parathyroidectomy (PTx) is often required. We present a retrospective, descriptive analysis of data corresponding to 148 patients on dialysis undergoing PTx due to severe refractory HPT (PTH 1401 +/- 497 pg/mL, Ca 10.6 +/- 0.8 mg/dL, P 6.9 +/- 1.7 mg/dL). Demographic data were compared with those recorded in 309 patients on dialysis not subjected to PTx who were managed at the same hospital. In the PTx group, the factors age (49.3 +/- 14 years), male gender (48.6%), and diabetes (0.7%) were significantly lower than in the non-PTx group (61.5 +/- 14.9 years, male gender 59%, diabetes 19.4%), while time on dialysis was longer (8.6 +/- 5.8 vs. 5.5 +/- 5.4 years). In 129 of the study patients (87.4%), four or more glands were identified, and total PTx plus autotransplantation (AT) in the forearm was performed. In the remaining 19 patients, two to three glands were identified, and AT was not undertaken. Four of the 19 patients were successfully operated on again for persistent HPT, seven showed PTH levels <250 pg/mL, and eight maintained severe HPT. Perioperative complications included one death due to cardiac insufficiency, two repeat operations due to bleeding, and one patient with chronic hoarseness. Hospital stay was prolonged in 20% of patients due to a hungry bone syndrome. Among those patients with PTx and AT, HPT recurred in 21 patients (16.2%) at 3.1 +/- 2.3 years. In 13 of these patients, autograft was removed at 7.5 +/- 2.9 years. Serum calcium and phosphate levels improved after PTx, and these results were maintained for 5 years (9.6 +/- 0.8 and 4.2 +/- 1.2 mg/dL, respectively). In conclusion, PTx with AT is a safe option for the treatment of severe HPT that is accompanied by low morbidity and mortality and a good outcome. Medical treatment should not be prolonged at the expense of long repeated bouts of hypercalcemia and/or hyperphosphatemia with their irreversible consequences.
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PMID:Parathyroidectomy: whom and when? 1275 76

Inflammation in vascular (mostly arterial) walls and heart valves triggered by the trans-endothelial influx of LDL particles and the action of subsequently modified (e.g., by oxidation) LDL particles can trigger true bone formation by valvar fibroblasts, by a subpopulation of re-differentiation-competent VSMCs (vascular smooth muscle cells) or by vascular pericytes. Vascular ossification can lead to heart failure and death. Elderly osteoporotic women who need osteogenic drugs to restore their lost skeletal bone are paradoxically prone to vascular ossification-the "calcification paradox." The recent introduction into the clinic of a potently osteogenic parathyroid hormone peptide, Lilly's rhPTH-(1-34)OH (Forteotrade mark), to reverse skeletal bone loss raises the question of whether this and other potently osteogenic PTHs still in clinical trial might also stimulate vascular ossification in such osteoporotic women. Indeed the VSMCs in human and rat atherosclerotic lesions hyperexpress PTHrP and the PTHR1 (or PTH1R) receptor as do maturing osteoblasts. And the evidence indicates that endogenous PTHrP with its NLS (nuclear/nucleolar localization sequence) does stimulate VSMC proliferation (a prime prerequisite for atheroma formation and ossification) via intranuclear targets that inactivate pRb, the inhibitory G1/S checkpoint regulator, by stimulating its hyperphosphorylation. But neither externally added full-length PTHrP nor the NLS-lacking PTHrP-(1-34)OH gets into the VSMC nucleus and instead they inhibit proliferation and calcification by only activating the cell's PTHR1 receptors. No PTH has an NLS and, as expected from the observations on the externally added PTHrPs, hPTH-(1-34)OH inhibits calcification by VSMCs and cannot stimulate vascular ossification in a diabetic mouse model. Encouraging though this may be for osteoporotics with their "calcification paradox," more work is needed to be sure that the skeletally osteogenic PTHs do not promote vascular ossification with its cardiovascular consequences.
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PMID:Osteogenic PTHs and vascular ossification-Is there a danger for osteoporotics? 1578 90

Cardiovacular disease is the main cause of morbidity and mortality in hemodialysis (HD) patients. However, there are no reliable data neither on the prevalence of cardiovacular disease nor its risk factors in Spain. The Morbidity and mortality Anemia Renal study (MAR) is a two-year multicenter, open-label, prospective cohorts study. Its main objective is to assess the general morbidity and mortality, particularly of a cardiovascular cause, and its relationship with the degree of anemia. Secondary objectives are: a/ the description of current clinical practices in anemia, dialysis, vascular access, and CV risk factor management; and b/ the description of hospitalization and mortality causes. This paper describes the prevalence of cardiovascular disease and risk factors of the HD population in Spain. A total of 1.710 patients were included (60% male, aged 64.4 years, 16.2 months on HD). The mean co-morbidity Charlson index was 6.5 +/- 2.3. Cardiovascular disease was the most prevalent comorbidity, 16.7% had a coronary disease, and 13.9% had different degrees of heart failure, while 11.6% had arrhythmia, 1.7% stroke and 5.5% peripheral artery disease. The prevalence of hypertension was 75.8%, 74.4% of patients received antihypertensive drugs, and still 40% of patients had an inadequate blood pressure control. The investigators considered as dyslipidemic 34.1% of patients, and prescribed treatment to 69.5% of them, while the remaining 30.5% (10.4% of the total) had hyperlipidemia with no drug therapy. Eleven percent was active smoker, and 26.6% former smoker. There was 47.4% of patients with a corporal mass index above 25. Secondary hyperparathyroidism with PTH above of 300 pg/ml was present in 22.2% of patients. Despite the EBPG and K-DOQI recommendations, only 68.8% of prevalent hemodialysis patients attained a hemoglobin (Hb) above 11 g/dl, 89.4% ferritin levels above 100 ng/ml, 66.5 degrees/a a transferrin saturation index (TSI) above 20%, and 61.1% met all three objectives. In summary, this first cross-sectional analysis has allowed us to know in detail the standard practice in multiple aspects of management of HD population in Spain. It has also established clear differences in the prevalence of cardiovascular disease and risk factors from the US registries. Last but not least we have identified therapeutic opportunities to improve the course and prognosis of our patients.
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PMID:[Cardiovascular risk in hemodialysis in Spain: prevalence, management and target results (MAR study)]. 1605 11

Myocardial hypertrophy is associated with specific histological changes, which are representative of the cardiomyocytes cellular response to overload. Evidently, transcriptional modulation of specific genes is implicated in myocardial hypertrophy. Recently, the parathyroid hormone-related protein (PTHrP)/PTH-1 receptor (PTH-1.R) bioregulation system was shown to participate in specific regulatory processes of the cardiomyocyte function and proliferation, which can be related to cardiac hypertrophy and heart failure. We review the literature on the pathophysiology of cardiac hypertrophy vis-a-vis the role of PTHrP/PTH-1.R system as a good therapeutic target.
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PMID:The PTHrP/PTH.1-R bioregulation system in cardiac hypertrophy: possible therapeutic implications. 1720 76

The aim of the study was to identify factors related to heart valve calcification (HVC) and effect of HVC on intracardiac hemodynamics in patients with chronic kidney disease (CKD). 377 CKD patients of the control group and 132 ones treated by hemodialysis (HD) were examined using echocardiography, cardiomonitoring, measurement of the carotid intima-media thickness and mineral bone density, X-ray imaging of calcified abdominal aorta. HVC was diagnosed in 38.9 and 27.3% of the CKD patients on hemodialysis and without it respectively. In both groups, patients with HVC were older than HVC-free ones, more of them had coronary heart disease, cardiac insufficiency, aortic calcinosis, and biochemically identifiable inflammation. In the absence of hemodialysis, patients with HVC had thicker intima-media compex, lower glomerular filtration rate, higher arterial pressure, and increased occurrence of diabetes mellitus. In HVC patients receiving hemodialysis, its duration was longer, blood PTH and calcium levels higher, forearm MOC lower. HVC associated with stenosis of mitral and aortic valves, aortic regurgitation, enlarged left and right atrium, thickened left and right ventricular wall. Multifactor analysis showed that HVC in patients receiving hemodialysis was related to the age, disbalance of phosporus and sodium, and duration of hemodialysis; in its absence, it was related to intima-media thickness and diabetes mellitus. Thus, in patients of the latter group, HVC was in the first place associated with atherosclerosis aggravated by a decrease of glomerular filtration rate and with the presence of diabetes. In patients receiving hemodialysis, HVC correlated with phosporus/sodium disbalance and atherosclerosis. The study revealed negative effect of HVC on intracardiac hemodynamics and for the first time demonstrated decreased MOC in patients with HYC.
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PMID:[Heart valve calcification in patients with chronic kidney disease]. 1967 Jul 13


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