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)

A phase II study was conducted to evaluate the safety and efficacy of fludarabine, cytarabine (ara-C), cyclophosphamide, cisplatin and GM-CSF (FACPGM) treatment in patients with Richter's syndrome (RS), refractory prolymphocytic leukemia (PLL) or refractory non-Hodgkin's lymphoma (NHL). Twenty-two patients with RS, refractory PLL, or refractory NHL were entered into this trial between March 1997 and February 2001. Median age was 62 years (42-74); 77% were over 60 years of age. Histologic diagnosis was large cell NHL transformation in 15 patients with CLL, immunoblastic transformation of CLL in one, refractory PLL in three, and refractory NHL in three patients. Treatment consisted of fludarabine 30mg/m2 (days 1-3), ara-C 0.5g/m2 (days 3-4), cyclophosphamide 250 mg/m2 (days 2-4), cisplatin 15 mg/m2 IV CI (days 1-4) with GM-CSF 250 microg/m2 from day 5 to recovery of neutrophils and antibiotic prophylaxis. Patients with response were to receive a maximum of six cycles of therapy. Eighteen patients were evaluable for response; one patient achieved a complete remission (5%), 12 stable disease/no response (67%) and five patients had progressive disease (28%). The median survival was 2.2 months (range, 1-19); the median failure-free survival was 1.5 months (range, 0.5-18.6). Grade III/IV toxicities were as follows: anemia in 62% of cycles; leucopoenia in 66%; granulocytopenia in 90%; thrombocytopenia in 83%; hyperbilirubinemia in 14%; hyperuricemia in 17%; hyponatremia in 17%; hypokalemia in 14%; hypophosphatemia in 10%; hypoalbulinemia in 14%; hypocalcemia in 7%; and hypercalcemia in 3%. One (3%) patient developed cardiac failure. Forty-one percent of the cycles were complicated with fever, 34% with non-neutropenic fever, and 55% cycles with infections (fungal 31%; bacterial 57%; HSV 6%; VZV 6%). FACPGM had very limited activity and significant toxicity in a cohort of patients with heavily pretreated refractory lymphoproliferative disorders.
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PMID:Phase II study of fludarabine, cytarabine (Ara-C), cyclophosphamide, cisplatin and GM-CSF (FACPGM) in patients with Richter's syndrome or refractory lymphoproliferative disorders. 1215 63

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

The parathyroid hormone-related peptide (PTHrP) was initially identified in the early eighties, as the humoral mediator causing hypercalcaemia associated with malignancy. However, recently PTHrP was also shown to mediate a wide range of local paracrine/autocrine and intracrine functions in various tissues under physiological and pathological conditions. Indeed, PTHrP is a polyhormone, which can act through different receptors, including the type 1 parathyroid hormone (PTH) receptor 1 (PTH-1R). In the cardiovascular system, PTHrP appears to have potent effects on vascular smooth muscle cells and cardiomyocytes, where it participates in different pathological conditions, such as ischemia and heart failure. Therefore, it is conceivable that further studies on the regulation of PTHrP expression, characterization of its autocrine/paracrine/intracrine functions and definition of its intracellular signal transduction pathways in cardiomyocytes and cardiac vascular smooth muscle cells can elucidate the potential role of PTHrP in cardiovascular pathophysiology.
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PMID:Parathyroid hormone-related peptide and cardiovascular system. 1459 5

Amongst the principal metabolic situations that can require emergency attention in the oncology patient we find: hypercalcaemia, hyponatraemia, tumoural lysis syndrome, lactic acidosis, hyperuricaemia, renal failure, hyperammonaemia, hypermpotasaemia, etc. Hypercalcaemia is the most frequent metabolic complication in oncology, appearing in 10-30% of these patients. It has two main mechanisms, tumoural lysis and humoural hypercalcaemia mediated by PTHrP (a protein related to parathormone). The principal factor for its diagnosis is suspicion, since some symptoms are non-specific and can be attributed to other causes such as somnolence, constipation, etc. Treatment will be based on intensity and is started with calciuretic measures with an intense hydration with physiological serum and on some occasions with furosemide. Anti-reabsorptive measures include calcitonin, bisphosphonates, mithramycin, gallium nitrate and on occasions corticoids. Bisphosphonates such as pamidronate and zoledronate seem to be highly useful in these cases. Hyponatraemia is classified depending on plasmatic osmorality; when this is low we find ourselves facing an authentic hyponatraemia that can develop with an extra-cellular volume that is high (cardiac insufficiency, cirrhosis, nephrotic syndrome and renal insufficiency), low (renal and extra-renal sodium losses) and normal (principally SIADH, related to a high elimination of sodium in the urine with high urinary osmolarity in spite of this being low in blood). Several types of tumour and different chemotherapy drugs can produce this SIADH. Treatment will vary according to the type and intensity, but in general this is based on hydric restriction and the replacement of the sodium deficit, either through physiological serum or through hypertonic saline serums depending on the case, and on occasions furosemide for the elimination of excess water.
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PMID:[Metabolic emergencies in the oncology patient]. 1572 5

The increasing knowledge on bone calcification processes has revealed some similarities with vascular tissue, where calcifications of arteries and cardiac valves contribute to several cardiovascular problems, such as heart failure, systolic hypertension, and myocardial and peripheral ischemic disease. Bisphosphonates have been used extensively for over two decades for the treatment of diseases associated with excessive bone resorption, i.e., osteoporosis, osteolytic bone metastasis, hypercalcemia and Paget's disease, by blocking osteoclastic function. Etidronate, pamidronate and clodronate has been shown to inhibit the development of experimental atherosclerosis, and proposed mechanisms for this action include inhibition of arterial calcification and lipid accumulation, degradation of atherogenic LDL-cholesterol and reduced foam cell formation. Bisphosphonates inhibit various enzymes involved in cholesterol biosynthesis and suppress macrophages in atheromatous lesions. The possibility of pharmacological agents that effectively treat both osteoporosis and atherosclerosis is attractive, however, current evidence is not conclusive and further research is necessary to confirm these actions in the clinical setting.
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PMID:Bisphosphonates and atherosclerosis: why? 1721 1

We report a 61-year-old woman who was admitted to our hospital in August 2004 with severe hypercalcemia and osteoporosis. Although she was found to have hypercalcemia five years earlier, she has never been treated. The patient was transferred to our hospital for further management of a recently-identified left neck mass. Serum calcium level was 15.0 mg/dL and intact parathyroid hormone (PTH) 3,321 pg/mL. (99m)Tc-methoxyisobutylisonitrile (MIBI) scintigraphy showed marked accumulation in the left neck. We diagnosed the tumor as parathyroid gland tumor and it was enucleated surgically. Although serum Ca level returned to normal after surgery, the patient suffered multiple rib fractures, complicated with marked paradoxical breathing. Internal fixation of the thorax was necessary due to deterioration of the heart failure. Progression of severe osteoporosis was associated with multiple fractures of the ribs and other serious complications including congestive heart failure occurred after surgery, reflecting the extreme difficulty in treating this patient.
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PMID:[Primary hyperparathyroidism complicated with flail chest due to severe osteoporosis]. 1658 22

A 71-year-old man presented with acute pulmonary edema related to new onset of severe left ventricular dysfunction (ejection fraction, 30%). His symptoms did not improve with emergency therapy with diuretics and dobutamine. He was noted to be severely hypocalcemic (5.5 mg/dL) and subsequently showed dramatic improvement in symptoms and ejection fraction (58%) with correction of hypocalcemia with intravenous calcium and calcitriol replacement. Hypocalcemia was related to surgically induced hypoparathyroidism. The patient had been instructed to decrease calcium supplements and to discontinue calcitriol 3 months previously due to hypercalcemia. Additional factors that may have contributed to hypocalcemia included vitamin D deficiency, alendronate therapy for osteoporosis, and chronic kidney disease. We concluded that the patient's congestive heart failure was precipitated by severe hypocalcemia and resolved with correction of hypocalcemia. Hypocalcemia is a rare cause of reversible congestive heart failure that should be in the differential diagnosis in any patient presenting with heart failure and not responding to traditional therapy.
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PMID:Reversible congestive heart failure related to profound hypocalcemia secondary to hypoparathyroidism. 1743 16

Primary hyperparathyroidism and malignancy are responsible for greater than 90% of all cases of hypercalcemia. Compared with the hypercalcemia of malignancy, hyperparathyroidism tends to be associated with lower serum calcium levels (< 12 mg/dL) and a longer duration of hypercalcemia (more than 6 months). The hypercalcemic symptoms are usually fewer and subtle. Hyperparathyroidism tends to cause kidney calculi, hyperchloremic metabolic acidosis, and the characteristics of metabolic bone disease osteitis fibrosa cystica, but no anemia. In contrast, hypercalcemia of malignancy is typically rapid in onset, with higher serum calcium levels, and more severe symptoms. Patients so affected show marked anemia, but they never have kidney calculi or metabolic acidosis. Parathyroid hormone assay is the most useful test for differentiating hyperparathyroidism from malignancy and other causes of hypercalcemia. In hyperparathyroidism, serum parathyroid hormone levels will be elevated. In other cases, the high serum calcium concentration usually results in suppression of parathyroid hormone. Treatment of hypercalcemia should be started with hydration. Loop diuretics may be required in individuals with renal insufficiency or heart failure to prevent fluid overload. Calcitonin is administered for the immediate short-term management of severe symptomatic hypercalcemia. For long-term control of severe or symptomatic hypercalcemia, the addition of biphosphonate is typically required. Among intravenous bisphosphonates, zoledronic acid or pamidronate are the agents of choice. Glucocorticoids are effective in hypercalcemia due to lymphoma or granulomatous diseases. Dialysis is generally reserved for those with severe hypercalcemia complicated with kidney failure.
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PMID:Hypercalcemia: an evidence-based approach to clinical cases. 1939 81

Primary systemic amyloidosis is a relatively uncommon disease characterized by the production and deposition of pathological insoluble fibrillar proteins in organs and tissues. It has been estimated that between one-third and one-half of all patients with primary amyloidosis experience clinically significant cardiac involvement. The present study reports a case involving a 77-year-old woman with ischemic heart disease who presented to the cardiology department because of syncope due to slow atrial fibrillation. Laboratory tests revealed a monoclonal spike in the gamma fraction and impairment of renal function, normocytic anemia, mild hypercalcemia, hypoalbuminemia and increased levels of beta-2 microglobulin. Suspicion of cardiac involvement was supported by the echocardiographic pattern and increased levels of troponin I and brain natriuretic peptide, along with clinical signs of heart failure and systemic amyloidosis diagnosis, confirmed by abdominal fat aspiration.
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PMID:Syncope in cardiac amyloidosis and chronic ischemic heart disease: A case report. 2174 65

A 77-year-old man previously treated with maintenance hemodialysis was admitted due to appetite loss, nausea and shortness of breath. He showed progressive heart failure and eosinophilia without any basal disorders and was diagnosed with idiopathic hypereosinophilic syndrome (HES) accompanied by eosinophilic myocarditis. Laboratory data revealed hypercalcemia, a low serum parathyroid hormone level and a high 1,25(OH)(2)D concentration in spite of renal failure and no causal medications. Steroid therapy resulted in the patient's rapid recovery from heart failure, hypereosinophilia and hypercalcemia. Since the serum 1,25(OH)(2)D level promptly and markedly decreased, the hypercalcemia complicated with HES was most likely caused by extrarenal production of 1,25(OH)(2)D.
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PMID:Hypercalcemia associated with eosinophilic myocarditis in a patient undergoing maintenance hemodialysis. 2306 67


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