Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Genetic disease often predisposes to neoplastic processes because of either alterations in both oncogenes and tumor suppressor genes or imbalances in the cell cycle. The authors present the case of a 15-year-old boy with Hodgkin's disease associated with Becker muscular dystrophy. Becker muscular dystrophy is an X-linked neuromuscular disease due to in-frame mutations in the dystrophin gene, and it is considered a milder variant of Duchenne muscular dystrophy. In most patients with Becker muscular dystrophy, the myopathic process affects the myocardium, leading to cardiomyopathy.
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PMID:Becker muscular dystrophy in a patient with Hodgkin's disease. 1470 20

The N terminus of skeletal myosin light chain 1 and the cardiomyopathy loop of human cardiac myosin have been shown previously to bind to actin in the presence and absence of tropomyosin (Patchell, V. B., Gallon, C. E., Hodgkin, M. A., Fattoum, A., Perry, S. V., and Levine, B. A. (2002) Eur. J. Biochem. 269, 5088-5100). We have extended this work and have shown that segments corresponding to other regions of human cardiac beta-myosin, presumed to be sites of interaction with F-actin (residues 554-584, 622-646, and 633-660), likewise bind independently to actin under similar conditions. The binding to F-actin of a peptide spanning the minimal inhibitory segment of human cardiac troponin I (residues 134-147) resulted in the dissociation from F-actin of all the myosin peptides bound to it either individually or in combination. Troponin C neutralized the effect of the inhibitory peptide on the binding of the myosin peptides to F-actin. We conclude that the binding of the inhibitory region of troponin I to actin, which occurs during relaxation in muscle when the calcium concentration is low, imposes conformational changes that are propagated to different locations on the surface of actin. We suggest that the role of tropomyosin is to facilitate the transmission of structural changes along the F-actin filament so that the monomers within a structural unit are able to interact with myosin.
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PMID:The regulatory effects of tropomyosin and troponin-I on the interaction of myosin loop regions with F-actin. 1569 27

We report the case of a 15-year-old male developing progressive myocardiopathy secondary to late anthracycline cardiotoxicity. At 2 years of age, the patient received chemotherapy with anthracyclines (adriamycin) at an accumulated dose of 510 mg/m2 due to the presence of non-Hodgkin lymphoma which subsided completely and he has been asymptomatic since then. A number of recurrent respiratory infections occurred as triggering factors of the condition, and the laboratory tests evidenced positive serology for Mycoplasma pneumoniae suggesting a recent contact.
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PMID:Late anthracyclines cardiotoxicity associated with infection by Mycoplasma pneumoniae. A case report. 1574 4

In the last 10 years, interesting results have been reported concerning the impact of highly active antiretroviral therapy (HAART) on the changing pattern of organ-specific manifestations of HIV-1 infection. There has been a clear step-wise reduction in the incidence of several opportunistic infections (OIs), particularly Pneumocystis carinii pneumonia, whereas a nonsignificant reduction in incidence has been observed for other organ-specific diseases, including invasive cervical cancer and Hodgkin disease. In addition, several organ-specific manifestations, including HIV-associated nephropathy, wasting syndrome and cardiomyopathy, are a direct consequence of damage by HIV-1, and so HAART may have a therapeutic effect in improving or preventing these manifestations. Finally, the introduction of HAART has seen the emergence of several complications, termed immune reconstitution inflammatory syndrome, which includes OIs such as cytomegalovirus vitritis, Mycobacterium avium complex lymphadenitis, paradoxical responses to treatment for tuberculosis, and exacerbation of cryptococcosis. Because not all HIV-1 organ-specific manifestations are decreasing in the HAART era, this review will analyse the influence of HAART on several organ-specific manifestations, and in particular OIs related to several organs, cerebral disorders and HIV-1-related neoplasia.
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PMID:Impact of highly active antiretroviral therapy on organ-specific manifestations of HIV-1 infection. 1580 12

Anthracyclines are widely used chemotherapeutic agents in the treatment of lymphomas known to induce cardiomyopathy in more than 20% of patients. There is increasing experimental evidence that cardiac endothelial cells regulate cardiac performance and that endothelin-1 (ET-1) is a central substance in this regulatory mechanism. Twenty (seven male, aged 20-68 years) patients with Hodgkin's or non-Hodgkin's lymphoma treated with anthracycline were followed-up for 1 year. At baseline, after cessation of anthracycline treatment and at 1 year, the plasma ET-1 level was measured by enzyme-linked immunosorbent assay and cardiac function was estimated by echocardiographic measurement of the ejection fraction, the E/A ratio and the deceleration time. The ET-1 level decreased significantly after therapy (5.47 +/- 3.34 pg/mL versus 3.44 +/- 0.69 pg/mL, P < 0.02), and remained significant at 1 year (3.43 +/- 0.57 pg/mL, P < 0.008). The ejection fraction (57.80 +/- 4.73% versus 48.05 +/- 5.65%, P < 0.0001) and the E/A ratio (1.35 +/- 0.40 versus 1.15 +/- 0.40, P < 0.01) decreased, and the deceleration time (177.00 +/- 44.96 ms versus 209.50 +/- 66.25 ms, P < 0.04) increased significantly after therapy, showing that both systolic and diastolic left ventricular performance were deteriorated. Compared with the baseline, the same significant changes were found at 1 year (ejection fraction, 50.65 +/- 8.87%, P < 0.0007; E/A ratio, 1.10 +/- 0.34, P < 0.003; deceleration time, 223.25 +/- 46.85 ms, P < 0.002). The decrease of the ET-1 concentration might be a result of anthracyclines' direct cytotoxic effect and the decreasing level of ET-1 may play a role in the ejection fraction reduction. The results of 1-year follow-up suggest that, although anthracycline toxicity occurs shortly after treatment, the undesirable effect remains.
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PMID:Endothelin-1 and cardiac function in anthracycline-treated patients: a 1-year follow-up. 1583 23

Irradiation of the heart begets different complications in which pericardial disease is the most common manifestation. Thoracic irradiation of lymphoma, Hodgkin's disease, lung and breast cancer could be complicated by adverse effects to every structure of the heart. Potential injury of mediastinal irradiation can include acute and late pericarditis, cardiomyopathy, valvular disease and conduction abnormalities. The pathophysiology of these various syndromes is probably similar, starting by prior microvascular injury that leads to subsequent myocardium ischemia, all of which cause late fibrous scars. Acute pericarditis is often asymptomatic and clear spontaneously. Late pericarditis affects approximately 5% of the patients when the irradiation dose exceeds 40 Gy. At this dose, the mortality rate is below than 1%. Cardiomyopathy is rare and often asymptomatic. A long time unrecognized, coronary artery disease, diagnosed in 5 to 10% of the patients, begets multifarious sequelae like myocardial infarction, valvular abnormalities and cardiac rhythm changes. This coronary artery disease is more likely to occur if the patient was young at the time of the irradiation (< or = 21 years) and/or if other cardiovascular risk factors are associated. Incidence and mortality rates of valvular defects are about 20 and 0.5%, respectively. Conduction dysfunctions can also be seen in 5% of the patients. Radiation-induced heart complications seem to be related to total dose (> 30 Gy), irradiated tissue volume and fraction size. Since cardiac complications appear months to years following incidental irradiation of the heart, appropriate screening and long-term cardiac follow-up of these patients is essential.
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PMID:[Radiation toxicity to the heart: physiopathology and clinical data]. 1589 21

Hodgkin Lymphoma (HL), follicular lymphoma (FL), and diffuse large B cell lymphoma (DLBCL) are three of the commonest subtypes of malignant lymphomas. Optimal treatments for these lymphomas should be chosen based upon prognostic indexes defined internationally and current available best therapeutic strategies. For patients with newly diagnosed HL, ABVD as standard chemotherapy is chosen in order to cure the disease and to reduce late toxicities such as cardiomyopathy and second cancers. Chemotherapy with or without radiotherapy is unlikely to cure patients with FL except early or limited disease, although their clinical courses are indolent. However, rituximab (RIT), an anti-CD20 monoclonal antibody, will improve the outcome of FL since the results of several phase II and III trials of RIT alone and in combination with chemotherapy are promising. In treatment for newly diagnosed DLBCL, RIT combined with CHOP (R-CHOP) has become a current standard initial therapy based upon the superior results of R-CHOP from phase III studies comparing CHOP to R-CHOP. RCHOP has overcome several poor prognostic biomarkers such as BCL-2 and BCL-6 in DLBCL. In addition, novel treatment strategies combining RIT and intensive chemotherapy such as EPOCH for patients younger than 60 years of age will improve the outcome of these patients with poor prognosis of international prognostic index (IPI).
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PMID:[Current treatment for malignant lymphomas]. 1807 19

Mutations in the p63 gene have been identified in five types of syndromic ectodermal dysplasias (EDs) with overlapping phenotypes: Ectrodactyly-Ectodermal dysplasia-Clefting (EEC syndrome, MIM 604292), Ankyloblepharon-Ectodermal dysplasia-Clefting (AEC syndrome, MIM 106260) [3], Acro-Dermato-Ungueal-Lacrimal-Tooth (ADULT syndrome, MIM 103285), Rapp-Hodgkin (RHS syndrome, MIM 129400) and Limb-Mammary (LMS syndrome, MIM 603543) [2]. In all those conditions congenital heart defects have been only occasionally found and to date, arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVC) has never been observed in patients affected by p63-related ectodermal dysplasia [9]. Here we describe for the first time this association.
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PMID:R298Q mutation of p63 gene in autosomal dominant ectodermal dysplasia associated with arrhythmogenic right ventricular cardiomyopathy. 1945 Apr 41

Aim of the study was to investigate LV structural and functional parameters in doxorubicin chemotherapy and idiopathic dilated cardiomyopathy as well as to study dynamics of LV systolic-diastolic dysfunction in relation to the increasing doxorubicin dosage. Patients with malignant blood diseases (with non-Hodgkin's, Hodgkin's lymphoma and chronic lymphatic leukaemia) and patients with idiopathic dilated cardiomyopathy were investigated. Patients were divided into 2 groups. The first group included 49 patients (25 men and 24 women, average age was 41.2+/-2.1) with malignant blood diseases. The second group consisted of 50 patients with idiopathic dilated cardiomyopathy (39 men and 11 women, average age was 38.8+/-9.36). Patients were divided into three subgroups according to the dose of administration of doxorubicin: I subgroup--232.2+/-5.8 mg/m(2), II subgroup--388+/-15.3 mg/m(2) and III subgroup--533.1+/-13.6 mg/m(2). The LV systolic-diastolic function was evaluated twice using echo CG. Consistent dose-dependent evolution of doxorubicin cardio toxicity was observed, which eventually resulted in development of anthracycline myocardiopathy. Doxorubicin cardio toxicity is evident as early as at low total doses (232 mg/m(2)); at a "critical dose" (356-388 mg/m(2)) LV diastolic dysfunction with clinical signs of HF develops; at a total dose of 533 mg/m(2) anthracycline dilated myocardiopathy with LV systolic-diastolic dysfunction and clinical signs of HF develops in 100% of cases. In anthracycline myocardiopathy, LV undergoes the same structural and functional mass index >120 g/m(2) and idiopathic dilated myocardiopathy: LV eccentric hypertrophy (II type LV remodelling with myocardial mass index >120 g/m(2) and relative thickness of LV posterior wall <0.44); decreased LV systolic-diastolic dimensions/volumes; LV diastolic dysfunction of the restrictive type. Etiologic factor is not so important for remodelling of left ventricle, which is the basis of clinically manifested dilated cardiomyopathy.
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PMID:Left ventricular function in patients with toxic cardiomyopathy and with idiopathic dilated cardiomyopathy treated with Doxorubicin. 1920 17

Mediastinal irradiation for cancers, mainly breast cancer and Hodgkin's disease, has numerous potential adverse effects, including coronary artery disease, pericarditis, cardiomyopathy, valvular disease, and conduction abnormalities. The prevalence of valvular dysfunction is relatively low, and regurgitation is more common. We report the case of a 58-year-old woman with severe radiation-induced mitral stenosis and discuss the potential additional value of three-dimensional transesophageal echocardiography.
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PMID:Radiotherapy-induced mitral stenosis: a three-dimensional perspective. 1976 51


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