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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atrial fibrillation is the most common arrhythmia, however, the mechanism of atrial fibrillation is not well explained. It has been considered that inflammation plays a role in atrial fibrillation, recently. Patients undergoing coronary artery bypass graft are at high risk for developing postoperative atrial fibrillation. The peak levels of C-reactive protein (CRP) were paralleled to the incidence of postoperative atrial fibrillation. In general population, CRP was also higher in patients with atrial fibrillation than in control people. Persistent atrial fibrillation patients had a higher CRP level than paroxysmal atrial fibrillation patients. CRP was not only associated with the presence of atrial fibrillation but may also predict patients at increased risk for future development of atrial fibrillation. Why inflammation markers in atrial fibrillation are high is a puzzling problem. We hypothesized that Chlamydia pneumoniae infection is a possible cause of atrial fibrillation by initiating inflammation response. It was demonstrated that infection of endothelial cells with C. pneumoniae elicited the production of Monocyte Chemoattractant Protein-1, interleukin-1, interleukin-8, interleukin-18, tumor necrosis factor, interferon and soluble intercellular adhesion molecule. Most of these cytokines play a crucial role in inflammation response that associate with the initiating and maintenance of atrial fibrillation. There are so many pathogens that can trigger inflammation. Some evidences showed that C. pneumoniae was the most likely pathogen of atrial fibrillation. In epidemic study, the incidence of atrial fibrillation increased from younger to elder and atrial fibrillation was more common in men than in women. C. pneumoniae has the same epidemic trend as the incidence of atrial fibrillation. Hypertension, myocardial infarction and reduced lung function are predictors of atrial fibrillation. C. pneumoniae infection is high in the patients with the above diseases. C. pneumoniae was found in endomyocardial biopsy samples, which supported C. pneumoniae was the candidate pathogen, too. Chlamydia infection can cause myocardial interstitial fibrosis and inflammation cells infiltration. The pathology characters of C. pneumoniae infection are similar to that found in atrial fibrillation. Seroepidemic study should be carried out to evaluate if there is relationship between C. pneumoniae and atrial fibrillation. If the hypothesis is confirmed, macrocyclic lactone antibiotics may be used to eliminate the pathogen. It will be a new target point to treat atrial fibrillation.
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PMID:Inflammation and atrial fibrillation: is Chlamydia pneumoniae a candidate pathogen of atrial fibrillation? 1679 13

Peripartum cardiomyopathy creates complications for 1 in 3000 to 4000 pregnant women in the US. As this rare condition is associated with a high mortality rate (50% to 85%), it has been investigated to define the possible associated causes. Several factors including hypertension, nutritional and dietary discrepancies, and, recently, myocarditis are being implicated, but the mechanism of cardiac injury is yet to be discovered. Here we present an interesting case of possible interferon-induced reversible peripartum cardiomyopathy. The patient, with a diagnosis of chronic myelogenous leukemia, had been given interferon for 6 years. The therapy was discontinued when she became pregnant, and later she presented with symptoms of heart failure 6 weeks after her c-section. Interferon is an immunomodulating agent and used as an antiviral and an anticancer agent. Interferon-related dilated cardiomyopathy has been described as a rare side effect of the drug, the mechanism of which is unknown. There is compelling data supporting the fact that both peripartum cardiomyopathy and interferon-related cardiomyopathy are autoimmune disorders; so it is suggested that interferon therapy given in the past can have an additive effect in causing dilated cardiomyopathy. It is therefore advisable to follow closely those pregnant patients; who received interferon therapy in the past, for symptoms of cardiac failure, as there can be synergistic action between interferon and pregnancy causing dilated cardiomyopathy.
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PMID:Reversible peripartum cardiomyopathy in a patient with prior exposure to interferon. 1685 74

We present a case of deep venous thrombosis (DVT) during pegylated interferon (peg-IFN)-alpha2b plus ribavirin treatment of chronic hepatitis C (CHC). A 67-year-old man, who had been under treatment for hypertension and diabetes mellitus, was admitted to our hospital for peg-IFN-alpha2b plus ribavirin treatment for CHC. His serum hepatitis C virus (HCV) RNA level became undetectable 1 week after the initiation of peg-IFN-alpha2b plus ribavirin treatment. He suffered from severe pain, flare, and edema in both of his lower legs 6 weeks after the initiation of peg-IFN-alpha2b plus ribavirin treatment. He was diagnosed as having DVT because of the presence of a thrombus in the right soleus vein by ultrasonography. Peg-IFN-alpha2b plus ribavirin treatment was discontinued because a causal relationship between DVT and peg-IFN-alpha2b plus ribavirin treatment was suspected. DVT was not observed and the symptoms in both of his legs were improved after the administration of warfarin potassium. Subsequently, DVT has not recurred, and he has remained HCV-RNA negative.
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PMID:A case of deep venous thrombosis associated with pegylated interferon alpha2b plus ribavirin treatment of chronic hepatitis C. 1728 4

It is still controversial whether intrinsic interferon (IFN)-gamma promotes or attenuates vascular remodeling in hyperproliferative vascular disorders, such as neointima formation after balloon injury. Thus, we investigated whether inhibition of intrinsic IFN-gamma function prevents neointima formation. For this purpose, naked DNA plasmid encoding a soluble mutant of IFN-gamma receptor alpha-subunit (sIFNgammaR; an IFN-gamma inhibitory protein) or mock plasmid was injected into the thigh muscle of male Wistar rats 2 days before balloon injury (day -2). sIFNgammaR gene transfer significantly elevated serum levels of sIFNgammaR protein for 2 weeks. In mock-treated rats, balloon injury induced smooth muscle cell proliferation in the neointima with a peak at day 7 and produced thick neointima at day 14. sIFNgammaR treatment reduced the number of proliferating intimal smooth muscle cells by 50% at day 7 and attenuated neointima formation with a 45% reduction of the intima/media area ratio at day 14. In mock-treated rats, at day 7, balloon injury induced phosphorylation of signal transducer and activator of transcription-1 and upregulations of IFN regulatory factor-1 (a transcription factor mediating IFN-gamma signal). Balloon injury also upregulated the key molecules of neointima formation, such as intercellular adhesion molecule-1 and platelet-derived growth factor beta-receptor. These changes were suppressed by sIFNgammaR treatment. In conclusion, it is suggested that intrinsic IFN-gamma promotes neointima formation probably through IFN regulatory factor-1/intercellular adhesion molecule-1-mediated and platelet-derived growth factor-mediated mechanisms. Thus, inhibition of IFN-gamma signaling may be a new therapeutic target for prevention of neointima formation of hyperproliferative vascular disorders.
Hypertension 2007 Apr
PMID:Inhibition of intrinsic interferon-gamma function prevents neointima formation after balloon injury. 1730 51

A 38-year-old pregnant woman (19th week of pregnancy) complained of fatigue, cold inducible paresthesias, generalized edema and mild arterial hypertension. Her past medical history was notable for frequent episodes of polyarthralgia and positivity for rheumatoid factor. On admission, acanthocyturia and unselective glomerular-tubular proteinuria with 19 g/d were detected with a slight decrease in creatinine clearance. Rheumatoid factor was robustly elevated and a cryocrit of 1.5 vol%, caused by a so far unknown replicative hepatitis C, was detected. Renal biopsy yielded membrano-proliferative glomerulonephritis. During pregnancy, high-dose corticosteroid therapy was administered. Edema disappeared and blood pressure normalized under albumin substitution and low-dose furosemide application. However, Cesarian section became necessary due to placental insufficiency at 27 weeks of gestation. Thereafter, neither virus load, cryocrit nor proteinuria decreased significantly under a combined therapy with pegylated interferon-a and ribavirin. Thus, cryoprecipitate apheresis was initiated resulting in robust decreases of clinical complaints, viral load, cryocrit and proteinuria. Cryoglobulinemia with renal involvement caused by hepatitis C is difficult to treat due to limitations of immunosuppressive and anti-viral therapy. In our patient, cryoprecipitate apheresis was a safe and effective therapeutic addition to standard therapy.
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PMID:Effective treatment of hepatitis C-associated immune-complex nephritis with cryoprecipitate apheresis and antiviral therapy. 1747 61

Renal cell cancer (RCC) is a relatively uncommon malignancy, with 51,190 cases expected to be diagnosed in 2007. Localized disease is curable by surgery; however, locally advanced or metastatic disease is not curable in most cases and, until recently, had a limited response to drug treatment. Historically, biologic response modifiers or immunomodulating agents were tested in clinical trials based on observations that some cases of RCC can spontaneously regress. High-dose aldesleukin is approved by the United States Food and Drug Administration as a treatment for advanced RCC; however, the drug is associated with a high frequency of severe adverse effects. Responses have been observed with low-dose aldesleukin and interferon alfa, but with little effect on overall survival. Sorafenib and sunitinib are novel therapies that target growth factor receptors known to be activated by the hypoxia-inducible factor and the Ras-Raf/MEK/ERK pathways. These pathways are important in the pathophysiology of RCC. Sorafenib and sunitinib have shown antitumor activity as first- and second-line therapy in patients with cytokine-refractory metastatic RCC who have clear-cell histology. Although complete responses are not common, both drugs promote disease stabilization and increase progression-free survival. This information suggests that disease stabilization may be an important determinant for response in RCC and possibly other cancers. Sorafenib and sunitinib are generally well tolerated and are considered first- and second-line treatment options for patients with advanced clear cell RCC. In addition, sorafenib and sunitinib have shown promising results in initial clinical trials evaluating antitumor activity in patients who are refractory to other antiangiogenic therapy. The most common toxicities with both sorafenib and sunitinib are hand-foot syndrome, rash, fatigue, hypertension, and diarrhea. Research is directed toward defining the optimal use of these new agents.
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PMID:Sorafenib and sunitinib: novel targeted therapies for renal cell cancer. 1765 13

(1) Sunitinib, a tyrosine kinase inhibitor, is marketed for the treatment of advanced-stage and metastatic renal carcinoma, and for second-line treatment of gastrointestinal stromal tumours. Sorafenib arrived on the market almost simultaneously for second-line treatment of kidney cancer. (2) In second-line treatment of kidney cancer, two non comparative trials showed an unusually high rate of at least partial tumour regression with sunitinib (25%, compared to only 2% with sorafenib). Head-to-head trials of the two drugs are lacking. Although indirect comparisons are notoriously unreliable, sunitinib appears to provide longer progression-free survival than sorafenib (about 9 months versus 5.5 months), although overall survival times are similar. (3) Preliminary results of a trial comparing sunitinib with interferon alfa as first-line treatments in 750 patients with kidney cancer show a 6-month event-free survival advantage in the sunitinib arm. The precise overall survival time has not yet been calculated. (4) In 312 patients with gastrointestinal stromal tumours in whom imatinib has failed, a double-blind placebo-controlled trial showed that sunitinib prolonged overall survival time, but potential biases undermine these results. (5) The adverse effect profile of sunitinib appears to be similar to those of imatinib and sorafenib, apart from more thyroid disorders. The principal adverse effects are cutaneous, gastrointestinal, cardiovascular and haematological disorders. Arterial hypertension, sometimes severe, occurred in 16% of patients treated with sunitinib. Other serious adverse events included tumour haemorrhage and pulmonary embolism. A risk of cardiac toxicity leading to heart failure cannot currently be ruled out. (6) Sunitinib is metabolised by cytochrome P450 isoenzyme CYP 3A4, increasing the likelihood of drug interactions. (7) These results support the use of sunitinib as second-line therapy for patients with gastrointestinal stromal tumours. Additional clinical evaluation is needed, however. In first-line treatment of kidney cancer, it is preferable to wait for detailed results of the ongoing trial, especially effects on survival time, before judging the possible advantages and disadvantages of sunitinib compared to interferon alfa. In second-line treatment, sorafenib is better-assessed than sunitinib and should therefore be preferred, pending a direct comparison of the two drugs.
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PMID:Sunitinib: new drug. For some gastrointestinal stromal tumours. 1772 33

HCV infection may be related to many extrahepatic manifestations including mixed cryoglobulinemia (MC). Clinical manifestations commonly associated to MC include arthralgia, purpura, vasculitis, peripheral neuropathy and renal function abnormalities. Treatment with interferon often leads to remission, especially in virological responders, or to disappearance of MC-related clinical manifestations. We report on a patient with chronic hepatitis C, deficit of G6P-DH, type II MC, who developed a cryoglobulinemic vasculitis with purpura, renal impairment and arterial hypertension, during treatment with PEG-interferon a-2b plus amantadine. The occurrence of purpuric lesions and MC-related nephropathy with increased cryocrit despite negative viremia, in a patient previously asymptomatic, during interferon treatment, is unusual.
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PMID:Cryoglobulinemia-related vasculitis during effective anti-HCV treatment with PEG-interferon alfa-2b. 1796 5

The coexistence of systemic sclerosis (SSc) and multiple sclerosis (MS) in the same patient has been described in few cases. We refer here a further case of association between these diseases, which highlight the difficulty of treating such patients. A 57-year-old male with relapsing-remitting MS since 20 years, shortly after having received high-dose corticosteroids for a relapse of MS, suddenly developed SSc, with onset of Raynaud phenomenon simultaneous to that of scleroderma skin involvement, new appearance of accelerated arterial hypertension, and rapidly progressive oliguric renal failure, indicative of scleroderma renal crisis, that was controlled with ramipril, irbesartan and amlodipin. A further disabling relapse of MS was treated with interferon-beta, but 19 months later he developed multiple severe digital necrotic ulcers, that resolved with interferon discontinuation and therapy with iloprost. This case report shows that some form of treatment useful for MS might enhance the manifestations of SSc.
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PMID:Onset and enhancement of systemic sclerosis after treatments for multiple sclerosis. 1806 51

Interferon-alpha is a biological response modifier with antiviral and tumoral effect that is used in the treatment of chronic viral hepatitis. Cardiovascular complications occurred in clinical trials of interferon. The most common presentations of cardio toxicity were cardiac arrhythmia, dilated cardiomyopathy, atrial extrasystole and symptoms of ischemic heart disease, including myocardial infarction and other effects less common and dangerous: low-level conduction impairment or reversible hypertension. The physiopathology of this cardiotoxicity remains unknown, but rigorous cardiological monitoring of all patients receiving this treatment seems necessary.
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PMID:[Cardiovascular complications of alpha interferon]. 1817 61


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