Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interferon-alpha-n1 (lymphoblastoid interferon-alpha) is a nonrecombinant 'natural' interferon derived from lymphoblastoid cells exposed to Sendai virus. In common with endogenous and recombinant interferon-alpha molecules, interferon-alpha-n1 has antiviral, immunomodulatory and antiproliferative properties. Interferon-alpha-n1 shows some efficacy in immunocompetent adults with well-compensated chronic viral hepatitis B. Rates of complete virological response (defined as an absence of detectable hepatitis B virus-DNA in the serum) ranged from 5 to 79% of adults who received various dosage regimens of interferon-alpha-n1 in monotherapy trials. Clearance of hepatitis B 'e' antigen was reported in 5 to 70% of patients treated with the drug. Spontaneous virological responses occurred in 0 to 48% of untreated patients. The clinical efficacy of interferon-alpha-n1 in patients with chronic hepatitis B is not improved by concomitantly administered deflazacort, zidovudine or levamisole, but may be increased by a course of corticosteroid pretreatment in some patients. Interferon-alpha-n1 also shows therapeutic benefit in adults with chronic hepatitis C. Complete biochemical responses (defined as normalisation of serum ALT levels) were achieved in 27 to 60% of adult patients treated with the drug, whereas spontaneous normalisation of serum ALT levels occurred in up to 11% of untreated patients. Responses to interferon-alpha-n1 were temporary in 27 to 78% of treatment responders but were sustained in 6 to 40% of patients. Emerging data delineating baseline factors predictive of a positive response to interferon-alpha-n1 treatment may aid in the selection of patients with hepatitis B or C most likely to benefit from treatment with this drug. Most patients receiving interferon-alpha-n1 experience a transient 'influenza-like' syndrome during the first week of treatment. The syndrome, which is dose related and alleviated by paracetamol (acetaminophen), is characterised by fever, chills, and arthralgia. Dose-limiting adverse effects occurring during longer term interferon-alpha-n1 therapy include fatigue, myalgia, headache, depression, pruritus and seizures. Neutropenia and thrombocytopenia may also occur during interferon-alpha-n1 treatment. Autoimmune thyroid disease may develop in up to 9% of patients treated with interferon-alpha-n1 for >or=6 months. At present, interferon-alpha-n1 and the recombinant forms of interferon-alpha are the only drugs available for the treatment of adults with well-compensated hepatitis B or C. Interferon-alpha-n1 produces moderate response rates in adults with well-compensated chronic hepatitis B or C. Thus, it is positioned alongside recombinant interferon-alpha products as a useful first-line treatment option for patients with chronic hepatitis B or C.
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PMID:Interferon-alpha-n1: a review of its pharmacological properties and therapeutic efficacy in the management of chronic viral hepatitis. 1802 May 50

Pegylated (PEG)-IFN-alpha-2a is a modified form of recombinant human IFN-alpha-2a with sustained absorption and prolonged half-life. Our aim was to evaluate its safety profile in adjuvant treatment of high-risk melanoma patients in a single centre setting and to compare this safety profile with data obtained from the literature for a) low dose IFN-alpha and b) high dose IFN. Eighteen consecutive melanoma patients (AJCC 2002 stages IIa-IIIc) were retrospectively analyzed for toxicities associated with adjuvant PEG-IFN-alpha-2a (180 microg/week s.c.). The most frequently reported adverse events were constitutional side effects (78%), myelosuppression (83%) and hepatotoxicity (78%). The proportion of patients receiving PEG-IFN-alpha-2a and suffering from myelosuppression and liver toxicity was significantly higher than for patients reported in the literature undergoing low-dose IFN-alpha treatment (P = 0.008, P = 0.001 respectively), while fatigue and depression were seen less frequently with PEG-IFN-alpha-2a. By contrast, compared to patients treated with high-dose IFN-alpha, PEG-IFN-alpha-2a treated patients less frequently experienced fatigue (P < 0.001), neutropenia (P < 0.068) and neuropsychiatric (statistically not significant) adverse events. In conclusion, subcutaneously delivered PEG-IFN-alpha-2a is well tolerated in a once-weekly dose of 180 mug by most patients with high risk malignant melanoma. The frequency of side effects is increased compared to low dose, but reduced compared to high dose standard IFN-alpha. Due to its pharmacokinetic properties, pegylated IFN-alpha has, as in the treatment of hepatitis C, potential for increased efficacy in adjuvant therapy of melanoma.
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PMID:Safety of pegylated interferon-alpha-2a in adjuvant therapy of intermediate and high-risk melanomas. 1808 86

Chemotherapy-related toxicities are common and often undertreated in routine cancer care. Initiatives to improve toxicity management in practices may not always be effective. Quality improvement programs must engage multiple disciplines of the healthcare team and sustain efforts to institute and maintain procedures that address practice needs. The Assessment, Information, and Management (AIM) Higher Initiative, a quality improvement program undertaken at 15 community oncology practices, was initiated to improve the AIM of chemotherapy-related toxicities in patients with cancer. AIM Higher focuses on improving five chemotherapy-related toxicities: neutropenia, anemia, depression and anxiety, diarrhea and constipation, and nausea and vomiting. Led by a nurse champion at each of the clinics, a variety of new procedures, processes, and tools were implemented to improve quality of care. Nurses and practice administrators can use the quality improvement processes to generate changes in procedures and practices.
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PMID:The AIM Higher Initiative: new procedures implemented for assessment, information, and management of chemotherapy toxicities in community oncology clinics. 1839 Apr 59

Valganciclovir is an l-valyl ester pro-drug of ganciclovir that was initially used to treat cytomegalovirus (CMV)-associated retinitis in patients with human immunodeficiency virus. Currently, it is also indicated for the prevention of CMV disease in solid-organ transplantation. It is primarily eliminated via the kidneys through glomerular filtration and tubular secretion. Decreased renal function results in decreased drug clearance. Valganciclovir has been reported to cause usually mild to moderate hematologic adverse effects such as leukopenia, neutropenia, anemia, thrombocytopenia, and pancytopenia. Severe and fatal bone marrow depression has been described in 1 adult patient. Herein, we describe the cases of 4 patients with end-stage renal disease who underwent cadaveric renal transplantation and received valganciclovir prophylaxis for CMV at a standard dose of 900 mg/d despite persistant renal failure. This therapy resulted in severe bone marrow failure after 18 to 20 days in all 4 patients, with fatal infections in 2 patients. This report demonstrates the in vivo pharmacodynamics of valganciclovir overdose in terms of hematotoxicity in the setting of renal impairment. Valganciclovir, as its derivative ganciclovir, should be used cautiously in patients with renal impairment.
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PMID:Severe bone marrow failure due to valganciclovir overdose after renal transplantation from cadaveric donors: four consecutive cases. 1954

The immune reconstitution inflammatory syndrome is a heterogeneous collection of pathological manifestations attributed to an excessive and deregulated immune response to various infectious and non-infectious pathogens consecutive to the modification of immune status. Mycobacteria and mycoses in the context of an HIV infection are the main causes of IRIS but this syndrome is also observed with many infectious pathogens in the context of auto-immune or inflammatory diseases. An excessive specific CD4 Th1 response leading to delayed hypersensitivity with imbalanced effector and regulatory cellular immune responses is suggested. The role played by host polymorphisms remains to be investigated. The emergence of a unique syndrome gathering multiple immune-depression/reconstitution such as HIV infection and antiretroviral therapy, decrease of immune depression in transplant, recovery from neutropenia after chemotherapy for cancer, and even post-partum period, could link various specialties and help to better understand physiopathology which is crucial to elaborate preventive therapies.
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PMID:[Immune reconstitution inflammatory syndrome or IRIS]. 2034 78

The combination of pegylated-interferon (PEG-IFN)/ribavirin is currently the standard of care antiviral treatment for chronic hepatitis C (CHC), but optimal results require an individual approach. Key issues are to deliver doses that confer optimal antiviral efficacy against hepatitis C virus (HCV) for a time sufficient to minimise relapse. Viral monitoring during therapy guides the subsequent treatment course, particularly HCV RNA results at 4 weeks (rapid viral response [RVR]) and 12 weeks (complete early viral response [cEVR]). There is strong evidence that for most patients with genotypes 2 or 3 HCV infection, RVR allows truncation of treatment to 16 weeks, provided ribavirin dose is weight-based. However, those patients with cirrhosis, insulin resistance/diabetes or older than 50 years need 6-12 months treatment. For "difficult-to-treat" CHC (genotypes 1 and 4), RVR is infrequent (approximately 15% in European studies), but allows treatment to be truncated from 48 to 24 weeks. Without RVR, there is some evidence that longer treatment (72 weeks) improves sustained viral response (SVR). However, "induction dosing" first 12 weeks of PEG-IFN clearly does not improve SVR. To prevent dose reductions and complete therapy, it is critical to detect and treat depression and other disabling side-effects, including judicious use of growth factors for severe anemia or neutropenia and possibly, thrombocytopenia. Another potentially important aspect may be attempts to counter central obesity and insulin resistance, which confer suboptimal antiviral response with any HCV genotype. Treatment partnerships with specialist nurses, psychological therapists and other healthcare workers are also essential for optimal individual management of patients with CHC.
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PMID:Individualisation of antiviral therapy for chronic hepatitis C. 2059 46

Barth syndrome is an X-linked genetic disorder caused by mutations in the tafazzin (taz) gene and characterized by dilated cardiomyopathy, exercise intolerance, chronic fatigue, delayed growth, and neutropenia. Tafazzin is a mitochondrial transacylase required for cardiolipin remodeling. Although tafazzin function has been studied in non-mammalian model organisms, mammalian genetic loss of function approaches have not been used. We examined the consequences of tafazzin knockdown on sarcomeric mitochondria and cardiac function in mice. Tafazzin knockdown resulted in a dramatic decrease of tetralinoleoyl cardiolipin in cardiac and skeletal muscles and accumulation of monolysocardiolipins and cardiolipin molecular species with aberrant acyl groups. Electron microscopy revealed pathological changes in mitochondria, myofibrils, and mitochondrion-associated membranes in skeletal and cardiac muscles. Echocardiography and magnetic resonance imaging revealed severe cardiac abnormalities, including left ventricular dilation, left ventricular mass reduction, and depression of fractional shortening and ejection fraction in tafazzin-deficient mice. Tafazzin knockdown mice provide the first mammalian model system for Barth syndrome in which the pathophysiological relationships between altered content of mitochondrial phospholipids, ultrastructural abnormalities, myocardial and mitochondrial dysfunction, and clinical outcome can be completely investigated.
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PMID:Cardiac and skeletal muscle defects in a mouse model of human Barth syndrome. 2106 80

The natural history of hairy cell leukemia (HCL) includes frequent and potentially life-threatening infections. Prior to the development of effective therapy, the incidence in patients followed for several years was as high as 60%, with infection as a prime cause of death in patients. Studies of the immune system of patients with HCL identified several potential reasons, including profound neutropenia and monocytopenia. In addition, treatment including chemotherapy and splenectomy further compromised the immune system. The success of new therapies has changed the frequency and severity of infections in patients with HCL. During the initial phase of treatment, however, infection risk remains high, with incidence ranging from 30 to 50%. Attempts to ameliorate the risk with growth factors in conjunction with treatment have not been successful, but lower doses of drugs and/or combination therapy have been tried with reported success. In the majority of patients, successful therapy results in normalization of the neutrophil count and marked reduction in the severity and frequency of infections. Interestingly, after purine nucleoside treatment, there is profound depression of CD4+ cells without development of the opportunistic infections seen with patients with human immunodeficiency virus (HIV). Studies to reduce morbidity and mortality should focus on initial induction regimens, as well as confirming the long-term benefit of treatment on risk of infection.
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PMID:Infectious complications in hairy cell leukemia. 2150 85

The addition of direct-acting antivirals (DAAs) to hepatitis C virus (HCV) treatment regimens has made treatment more effective and patient management more complex. Shepherding patients through a full course of HCV therapy requires motivation and involvement on the part of the patient and the physician. Indeed, physician inexperience and lack of confidence in guiding patients through the challenges of treatment appears to be a primary reason for early discontinuation of therapy. Among the many complications of HCV treatment that must be managed efficiently and effectively are depression and other psychiatric disorders; hematologic abnormalities including DAA- and ribavirin-associated anemia and peginterferon alfa-associated neutropenia and thrombocytopenia; rash and drug eruptions, including telaprevir-associated rash; and weight loss. Practical considerations in management of these common complications are offered. This article summarizes a presentation by Kenneth E. Sherman, MD, PhD, at the IAS-USA live continuing medical education course held in New York in June 2012.
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PMID:Managing adverse effects and complications in completing treatment for hepatitis C virus infection. 2315 51

We evaluated the roles of sociocultural status, distress and cognitive functions in rheumatoid arthritis (RA) patients who developed methotrexate (MTX)-related neutropenia. The data of 37 RA patients with MTX-related neutropenia who were being followed up at 3 centers were evaluated. The control group included 74 RA patients. The clinical features, biochemical tests and treatment modalities of the patients were obtained from hospital files. The mini-mental state examination (MMSE) test and the Hospital Anxiety and Depression Scale (HADS) were administered for all RA patients with neutropenia as well as the control group. The frequencies of male patients, illiterate patients, patients living alone, patients with serious visual impairment, those with low income, and patients with high creatinine were significantly higher among RA patients with MTX-related neutropenia than in controls (p values <0.05). The RA patients with MTX-related neutropenia had significantly lower MMSE scores, and significantly higher HADS-A and HADS-D scores than controls (p values <0.05). In addition, the proportion of patients with probable dementia was significantly higher in RA patients with MTX-related neutropenia than in controls (p < 0.001). Twenty-six of the 37 patients (70.3 %) developed neutropenia with daily dosing. Patients who used MTX daily were more likely to be living alone than those using weekly dosing (p = 0.011). Multivariate analysis showed that having probable dementia on the MMSE test (OR 52.6), low income level (OR 56.8) and age (OR 1.12) were independent risk factors for the development of MTX-related neutropenia. The presence of probable dementia on MMSE, low socioeconomical status and older age are associated with serious toxicity in RA patients using MTX. Measures should be taken to prevent wrong MTX dosing by the patients. Compliance and patient education is of major importance, in particular, in the patients presented in this study.
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PMID:Do impaired memory, cognitive dysfunction and distress play a role in methotrexate-related neutropenia in rheumatoid arthritis patients? A comparative study. 2374 24


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