Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin-converting enzyme (ACE) inhibitor therapy has recently been shown to be effective in the treatment of post-renal transplant erythrocytosis (PTE). In an attempt to assess the effect of drug treatment on serum erythropoietin level, glomerular filtration rate, and urinary protein excretion, we prospectively evaluated 8 consecutive cadaveric renal transplant recipients with PTE treated with ACE inhibitor therapy for 3 months. In response to ACE inhibition, the mean hematocrit (HCT) value decreased from 53.7 +/- 0.6% before treatment to 42.7 +/- 2.2% at the conclusion of the study (p = 0.03). However, 1 patient failed to respond to ACE inhibition (HCT > 50%), and 2 patients with PTE developed anemia (HCT < 35%) while maintained on drug treatment. Although the mean serum erythropoietin level decreased during ACE inhibition (from 22.8 +/- 8.4 to 9.4 +/- 5.3 mU/ml; p = 0.06), a consistent change in individual erythropoietin levels was not identified. At the conclusion of the study, the serum erythropoietin levels were undetectable in 4 patients, decreased in 1, unchanged in 2, and increased in the only patient with PTE who failed to respond to drug treatment. All patients tolerated the ACE inhibitor therapy without developing cough or hyperkalemia. In addition, serum creatinine levels, 125I-iothalamate clearances, and mean arterial blood pressures were unchanged throughout the study. Microalbuminuria (spot urinary albumin/creatinine ratio between 30 and 200 mg/g) developed in 5 patients with PTE and coincided with the onset of erythrocytosis (25.2 +/- 7 mg/g before PTE and 76.3 +/- 36.7 mg/g at the time of PTE detection).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association of post-renal transplant erythrocytosis and microalbuminuria: response to angiotensin-converting enzyme inhibition. 757 90

Recent observations indicate that angiotensin-converting enzyme (ACE) inhibition corrects renal transplant erythrocytosis (RTE). The mechanism for this association is not known. We examined the effect of ACE inhibition on hematocrit, erythropoietin (EPO), and renin substrate. ACE inhibition has been reported to suppress renin substrate, which is known to stimulate EPO and erythropoiesis. In 15 patients with RTE, hematocrit dropped from 52.8 +/- 0.6 (SEM) to 45.8 +/- 1.4% after 8 weeks of treatment with Enalapril, 2.5-20 mg/day. Serum EPO (normal range: 9-30 mU/ml) was high in one, normal in seven, and low in seven patients. ACE inhibition reduced EPO in patients with initial high or normal levels but induced no change in patients with initial low levels. ACE inhibition had no significant effect on renin substrate. In one patient who rejected his first graft, erythrocytosis recurred following a second, successful transplant. Treatment was discontinued because of cough in two patients and symptomatic drop in blood pressure in one patient. We conclude RTE is not caused by hypererythropoietinemia. In patients with normal circulating EPO, erythrocytosis may result from an increase sensitivity to EPO, and ACE inhibition lowered hematocrit by further reduction of this hormone. However, the finding of erythrocytosis in half our patients with suppressed EPO, suggests the participation of non-EPO-mediated mechanism(s). The recurrence of RTE in a patient after a second transplant raises the additional possibility of patient-specific factors in the pathogenesis of this disorder. In contrast to other reports, we documented side-effects (cough, hypotension) in three (20%) of our patients. Our clinical experience, coupled with prior reports of spontaneous resolution of RTE in some patients, suggests that intermittent courses of ACE-inhibition may be the optimal strategy in the use of this form of therapy for RTE.
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PMID:Angiotensin-converting enzyme inhibition in the treatment of renal transplant erythrocytosis. Clinical experience and observation of mechanism. 762 54

Posttransplant erythrocytosis (PTE) represents a common complication in allograft recipients with normal renal function. Although the pathogenesis is not completely known, an alteration in the regulation of erythropoietin production by native kidneys or by renal allograft have been implicated as the main causes. Traditional therapies include repeated phlebotomies, bilateral native nephrectomies, and anticoagulant therapy. Recently, theophylline has been proposed as an effective therapy, although without general acceptance. Also, angiotensin-converting enzyme inhibitors have been involved in the development of anemia in chronic renal failure and dialysis patients. The aim of the present study was to demonstrate the efficacy of captopril on long-term treatment of PTE. Nineteen renal allograft recipients affected with severe PTE were included in the study. All patients had their native kidneys and none had a renal tumor or hydronephrosis. Restrictive criteria for PTE were applied to all patients and other causes of erythrocytosis were rationally excluded. Captopril was administered at a dose of 25 mg/24 hr (12.5 mg b.i.d.) during 12 months and no change on the initial dose was made during follow-up. After 3 months of captopril therapy and during the study period, significant reductions in hematocrit (P < 0.001), hemoglobin (P < 0.001), and RBC count (P < 0.001) were obtained in all patients. Erythropoietin levels decreased significantly during the study period, although the values were within the normal range of our laboratory. Captopril was well tolerated and only 1 patient had to be withdrawn from the drug because of dry cough. The present study has shown that captopril, at a low dose, represents a safe and effective therapy for PTE, without remarkable side effects or graft dysfunction. Long-term treatment with captopril in PTE did not induce anemia.
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PMID:Efficacy of captopril on posttransplant erythrocytosis. Long-term follow-up. 805 53

The use of angiotensin-converting enzyme inhibitors can be accompanied by a number of adverse events, including cough, angioedema, and hyperkalemia, as well as a peculiar form of functional renal insufficiency. Other, less obvious side effects accompany ACE inhibitor use, such as a reduction in red blood cell production. This feature of ACE inhibitor use may be employed to good effect, as in the management of post-transplant erythrocytosis. Alternatively, the suppressive effect of ACE inhibitors on red blood cell production may intensify the anemia of chronic renal failure and/or congestive heart failure. The untreated congestive heart failure patient typically has an increased red blood cell mass as a consequence of increased erythropoietin levels, with the latter governed by congestive heart failure-related renal hypoxia. This is not expressed as an increase in hemoglobin concentration because of the increase in plasma volume that marks advanced congestive heart failure. ACE inhibitor therapy can be expected to both reduce plasma volume and decrease red blood cell production. As a result, the hemoglobin concentration changes very little in the ACE inhibitor-treated congestive heart failure patient and usually falls in the low normal range. Recently, erythropoietin has been employed to good effect in congestive heart failure patients with borderline anemia. (c)2000 by CHF, Inc.
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PMID:Pharmacotherapy in congestive heart failure: ACE inhibitors and anemia in congestive heart failure. 1218 39

A male patient aged 67 years with chronic renal failure (CRF), who had undergone hemodialysis since June 3, complained of dyspnea while walking on June 23, 1998. Rapidly progressive anemia and severe reticulocytopenia were noted. Serological tests showed that parvovirus B19- (B19) specific IgM antibody, but not IgG antibody, was present in the patient's serum. B19 DNA was detected in the patient's serum by the polymerase chain reaction (PCR). Therefore, a definite diagnosis of transient aplastic crisis induced by B19 was made. On June 10, prior to the appearance of this case, a female nurse aged 27 years working in our hemodialysis center, complained of cough, fever and arthralgia. Another female nurse, aged 35 years, developed similar symptoms on July 3. Both nurses had a positive IgM titer against B19, but were negative for IgG, indicating an acute B19 infection. These findings led us to suspect that this series of B19 infection was spread by nosocomial transmission. Although some cases of B19 infection have been reported to occur in laboratory staffs, the B19 nosocomial infection has not been described in the literature. We also suggest that a transient aplastic crisis due to B19 infection could lead to severe anemia in cases of CRF whose erythropoiesis is maintained by a recombinant human erythropoietin.
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PMID:A nosocomial parvovirus B19 infection-induced transient aplastic crisis in a patient with chronic renal failure. 1650 66

The Drug Safety Information Section of the Division of Safety Information on Drug, Food and Chemicals has been providing bulletins titled "Overseas Drug Safety Information" in Japanese since 2003. These bulletins comprise summarized and translated reports of important post-marketing drug safety information that are published by foreign regulatory agencies such as the US Food and Drug Administration (FDA) and the European Medical Agency. A new issue of the bulletin is posted every two weeks on the website of the National Institute of Health Sciences, Japan; to date (May 2013), a total of 280 issues have been posted, covering approximately 2400 foreign news items and articles since its inception. Recently, visits to the bulletin website have been increasing: the number of hits for each issue totaled 570,000 in fiscal 2012. Among the "Overseas Drug Safety Information" issued in the past five years, I briefly describe here several topics which interested me: erythropoietin-stimulating agents in chronic kidney disease and their cardiovascular risk; bisphosphonates and atypical femur fracture; effectiveness of oral liquid cough medicines containing codeine in children; bevacizumab for metastatic breast cancer; and congenital abnormality associated with the use of antiepileptic drugs by pregnant women. I also describe the potential safety signals identified by FDA using its Adverse Event Reporting System, and their importance in ensuring the safe use of drugs in the post-marketing phase.
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PMID:[Topics from "Overseas Drug Safety Information" in the past five years]. 2434 Jun 68

Lung transplantation is a life-saving alternative for patients with end-stage lung disease. The procedure itself has a high risk of bleeding. Jehovah's Witness patients refuse to accept blood products due to religious beliefs. A 48-year-old Jehovah's Witness woman presented with an 8-year history of cough, dyspnea along with progressive worsening of her functional class and quality of life. A diagnosis of autoimmune interstitial lung disease was made, for which cyclophosphamide was administered without improvement of symptoms, and the patient was accepted as a transplant candidate. Transplantation was performed without complications, nor blood products requirement, intraoperative cell salvage was performed, and pharmacological agents were used preoperatively for bleeding prevention. The patient only developed anemia after administration of immunosuppressor therapy, which was treated with erythropoietin in the outpatient setting.
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PMID:First Lung Transplantation in Jehovah's Witness Patient in Latin America. 3273 26