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PubMed1960

Generalized cytomegalic inclusion-body disease associated with pneumocystis pneumonia in adults. A report of three cases. with Wegener's granulomatosis. thrombotic purpura, and Hodgkin's disease as predisposing conditions.

Three cases of generalized cytomegalic inclusion-body disease (salivary virus disease) in adults are reported, bringing the number of published cases up to 34. The infection is very rare in adults although well known in infants. As is often found in infants with this disease, pneumonia due to Pneumocystis carinii was also present in each case. The first patient had Wegener's granulomatosis, which presented with acute otitis media: a review of histological material obtained at mastoidectomy eight weeks before death showed that inclusion-body cytomegaly was already present then. Various antibiotics and prednisolone were given, and the lesions in the respiratory organs and the arteritis healed to a considerable extent. Renal failure, however, was progressive and led to death. The second patient had thrombotic purpura and died after a few weeks' illness, during which oxytetracycline and hydrocortisone were given. Congenital absence of the spleen was found at laparotomy, which was performed with the object of doing a splenectomy. Focal cryptococcal pneumonia was present post mortem: six years before death a solitary cryptococcal granuloma of one lung had been treated by lobectomy. The third patient had had Hodgkin's disease for 18 years. During the first 12 years the disease had the characteristics of the so-called indolent form ("Hodgkin's paragranuloma") and it then passed into the typical form. Deep x-ray therapy and cytotoxic drugs were used during the course of the disease at various times, and streptomycin and tuberculostatic drugs were given because of intercurrent tuberculous meningitis which developed three months before death. In all three cases it seems likely that the underlying disease, or the drugs used in its treatment, predisposed to cytomegalic inclusion-body disease and concomitant pneumocystis pneumonia by lowering the patients' resistance. Just as some unusual types of fungal and bacterial infections have become less rare since the introduction of certain drugs, including antibiotics and steroids, it is possible that cytomegalic inclusion-body disease and pneumocystis infection may also be met with oftener in adults, perhaps particularly as a complication of the use of these drugs in the treatment of diseases which are specially liable to interfere with the body's defences.

Adult↗

PubMed1996

Diffuse Lewy body disease: clinical features in nine cases without coexistent Alzheimer's disease.

OBJECTIVE: To further elucidate the relation between diffuse Lewy body disease and Parkinson's disease. METHODS AND RESULTS: The clinical features of nine cases of pure diffuse Lewy body disease without pathological evidence of coexisting Alzheimer's neuritic pathology were reported. All patients were aged less than 70 years at onset (mean 62 years). Five patients presented with clinical features, which included assymetric resting tremor had levodopa responsiveness, which were initially indistinguishable from idiopathic Parkinson's disease. All five patients later became demented (mean of three years after presentation). Two further patients presented with parkinsonism and dementia and two patients presented with dementia and developed parkinsonism at a later stage. Hallucinations appeared 2.5-9 years after the onset of symptoms in six patients and were a presenting feature in one patient. All patients met the pathological criteria of idiopathic Parkinson's disease, with respect to the midbrain changes, in addition to having diffuse cortical Lewy bodies. CONCLUSIONS: Diffuse Lewy body disease may present a parkinsonism, dementia, or both depending on whether the Lewy body pathology begins in the midbrain, the cortex, or both together. When it begins in the midbrain, diffuse Lewy body disease is indistinguishable initially from idiopathic Parkinson's disease. Diffuse Lewy body disease may be a common cause of dementia complicating Parkinson's disease.

Aged↗

PubMedDate not supplied

Genetics of inflammatory bowel disease. The candidate gene approach: susceptibility versus disease heterogeneity.

Ulcerative colitis and Crohn's disease are complex diseases of unknown etiology. Several genes are involved in the susceptibility. These genes are necessary to suffer from these diseases but not sufficient. Environmental factors trigger the inflammatory response. Evidence is accumulating that this response is abnormal in these patients. Therefore, the study of genes that are involved in the regulation of the inflammation may help to clarify the pathogenesis of the disease. The working hypothesis is that HLA and cytokine gene polymorphisms, of extreme importance in the regulation of inflammation, contribute to determining the heterogeneity of the disease and the prognosis. In this case, the candidate genes are those involved in the regulation of the immune response of the host. These studies may be of great importance in the tailoring of an appropriate treatment for particular subgroups of patients. A premise for the success of these studies is to use a solid classification, which should take into account the dynamic process and the natural evolution of the disease; to use a carefully selected and ethnically matched group of healthy controls, and to use the advanced molecular biological typing techniques. In the present article, this concept is explored by taking into account some of the recent findings obtained with the HLA and cytokine gene polymorphisms in inflammatory bowel diseases. The results support the concept that these gene polymorphisms are of greater importance in determining the severity of the disease than in determining the susceptibility to suffer from the disease. From this point of view, these studies are complementary and a necessary addition to studies using the whole genome approach in the effort to understand the genetics of these chronic multifactorial diseases.

Cytokines↗

PubMedDate not supplied

Prion diseases in humans and their relevance to other neurodegenerative diseases.

Molecular genetics has led to considerable advances in our understanding of the transmissible spongiform encephalopathies. The identification of pathogenic mutations in the prion protein gene has enabled a molecular reclassification of the familial forms of these diseases, which may now be referred to as inherited prion diseases. Prion diseases of both humans and animals are associated with deposition of an abnormal isoform of a host-encoded protein, the prion protein (PrP). Human prion diseases have inherited, sporadic and acquired forms. A considerable body of evidence now supports the idea that the transmissible agent in these diseases may be an abnormal isoform of the prion protein. The identification of pathogenic mutations in the PrP gene has enabled the identification of cases of inherited prion disease that would not have been recognised using existing clinical and pathological diagnostic criteria. Since marked clinical and neuropathological overlap between the different neurodegenerative disorders is well recognised, PrP gene analysis is of increasing importance in differential diagnosis. Frontal lobe dementia of non-Alzheimer type and Pick's disease share a number of important clinical and pathological features with prion diseases, and could be considered as candidate prion diseases. However, we have not been able to demonstrate either PrP mutations or the presence of the disease-associated isoform of prion protein in several well-characterised families with these disorders.

Humans↗

PubMed2004

Preventing cancer, cardiovascular disease, and diabetes: a common agenda for the American Cancer Society, the American Diabetes Association, and the American Heart Association.

Collectively, cardiovascular disease (including stroke), cancer, and diabetes account for approximately two thirds of all deaths in the United States and about 700 billion dollars in direct and indirect economic costs each year. Current approaches to health promotion and prevention of cardiovascular disease, cancer, and diabetes do not approach the potential of the existing state of knowledge. A concerted effort to increase application of public health and clinical interventions of known efficacy to reduce prevalence of tobacco use, poor diet, and insufficient physical activity-the major risk factors for these diseases-and to increase utilization of screening tests for their early detection could substantially reduce the human and economic cost of these diseases. In this article, the ACS, ADA, and AHA review strategies for the prevention and early detection of cancer, cardiovascular disease, and diabetes, as the beginning of a new collaboration among the three organizations. The goal of this joint venture is to stimulate substantial improvements in primary prevention and early detection through collaboration between key organizations, greater public awareness about healthy lifestyles, legislative action that results in more funding for and access to primary prevention programs and research, and reconsideration of the concept of the periodic medical checkup as an effective platform for prevention, early detection, and treatment.

Cardiovascular Diseases↗

PubMed1998

Neuropsychiatric correlates and treatment of lenticulostriatal diseases: a review of the literature and overview of research opportunities in Huntington's, Wilson's, and Fahr's diseases. A report of the ANPA Committee on Research. American Neuropsychiatric Association.

This report reviews clinical neuropsychiatric findings and opportunities for research in Huntington's, Wilson's, and Fahr's diseases. Consistent, systematic methodology is lacking among neuropsychiatric studies in these lenticulostriatal diseases. Systematic cross-sectional and longitudinal assessments are needed to ascertain the prevalence of psychiatric disorders as a function of disease course. Preliminary synthesis of existing data suggests the following heuristic relationships in these diseases: depression with parkinsonian states; personality changes with caudate or putamen disease; psychosis, impulsivity, and sexual disorders with caudate disease; dementia and mania with caudate and pallidal diseases; and compulsions with pallidal disease. Correlation of neuropsychiatric findings with disease stage, clinical signs, and radiologic, metabolic, physiologic, and pathologic markers of disease will add to our understanding of these conditions.

Basal Ganglia Diseases↗

PubMed2003

Metabolic changes in the knockout mouse for Canavan's disease: implications for patients with Canavan's disease.

Canavan's disease is an autosomal recessive disorder caused by aspartoacylase deficiency, which leads to accumulation of N-acetylaspartic acid in the brain and blood and an elevated level of N-acetylaspartic acid in the urine. The brain of patients with Canavan's disease shows spongy degeneration. How the enzyme deficiency and elevated N-acetylaspartic acid cause the pathophysiology observed in Canavan's disease is not obvious. The creation of a knockout mouse for Canavan's disease is being used as a tool to investigate metabolic pathways in the mouse and correlate them with the patients with Canavan's disease. The level of glutamate is lower in the knockout mouse brain than in the wild-type mouse brain, similar to what we have found in children with Canavan's disease, and so are the levels of gamma-aminobutyric acid (GABA). The level of aspartate is higher in the Canavan's disease mouse brain. The activity of aspartate aminotransferase, an enzyme involved in the malate-aspartate shuttle, is lower in the Canavan's disease mouse brain. The lower weight of the Canavan's disease mouse was in direct proportion to low total-body fat and bone mineral density. These changes might be similar to what is seen in patients with Canavan's disease and could have therapeutic implications.

Animals↗

PubMed2003

Early-onset peripheral arterial occlusive disease: clinical features and determinants of disease severity and location.

UNLABELLED: Early-onset peripheral lower extremity arterial occlusive disease (PAD) is an uncommon, poorly characterized manifestation of atherosclerotic vascular disease. We studied the clinical presentation and correlates of disease severity and location in patients with early-onset PAD identified at non-invasive arterial evaluation. We identified a series of 159 patients who were younger than 50 years and had an abnormal resting or postexercise ankle brachial index (ABI) (< 0.9) or, if arteries were noncompressible, monophasic arterial Doppler signals. Disease severity and location were determined based on results of noninvasive vascular laboratory testing. Presence of coexisting atherosclerosis in other arterial beds was ascertained by review of patient records. Multivariable logistic regression analyses were used to identify risk factors associated with disease severity and location. Mean age of the patients was 42.7 +/- 4.2 years and 55% were women. Prevalence of risk factors was 76% for current or past smoking; 71%, dyslipidemia; 53%, hypertension; 35%, diabetes; and 53%, family history. Claudication was present in 50%, rest pain in 3%, ulceration in 31% and the remaining 16% did not have symptoms from PAD. Low high-density lipoprotein (HDL)-cholesterol and female sex were associated with severity. Of 102 patients in whom disease location could be determined noninvasively, 65% had aortoiliac disease. Female sex, low HDL-cholesterol, and absence of diabetes were associated with aortoiliac disease. Atherosclerosis in other arterial beds was identified in 53% of the patients. CONCLUSION: In this study population of early-onset atherosclerotic PAD, men and women were equally represented. The disease involved predominantly the aortoiliac location. Low HDL-cholesterol and female sex were associated with disease severity. An aggressive approach to diagnosis and treatment may be warranted as atherosclerosis in other arterial beds was prevalent in half of the patients.

Adult↗

PubMed1993

Cardiac disease following treatment of Hodgkin's disease in children and adolescents.

PURPOSE: Cardiac disease is second only to neoplastic disease as a cause of death after treatment for Hodgkin's disease. This study evaluates the risks of cardiac disease following treatment of Hodgkin's disease during childhood and adolescence. PATIENTS AND METHODS: We reviewed records of 635 patients treated for Hodgkin's disease before 21 years of age at Stanford University between 1961 and 1991. Mean age was 15.4 years; mean follow-up duration was 10.3 years, representing 6,564 person-years of observation. Relative risks (RRs) of death from cardiac diseases were calculated by comparison with age-, sex-, and race-matched general population rates from United States decennial life-tables. RESULTS: Twelve patients have died of cardiac disease (RR, 29.6; 95% confidence interval [CI], 16.0 to 49.3), including seven deaths from acute myocardial infarction ([AMI] RR, 41.5; 95% CI, 18.1 to 82.1), three from valvular heart disease, and two from radiation pericarditis/pancarditis. Thus far, the risk of AMI death was comparable after radiation alone (RO) or after chemotherapy and radiation (CM) (RO-AMI RR, 52.2; 95% CI, 21.1 to 108.7; CM-AMI RR, 21.1; 95% CI, 0.0 to 104.4; P = .6). The risk for other cardiac death (CD) tended to be higher after combined treatment (RO-non-AMI RR, 7.4; 95% CI, 0.0 to 36.5; CM-non-AMI RR, 45.8; 95% CI, 14.4 to 110.6; P = .1). Deaths occurred 3 to 22 years after patients received 42 to 45 Gy to the mediastinum between 9 and 20 years of age. There have been no deaths among patients treated to lower mediastinal radiation doses or without mediastinal radiation. There are no clear trends in the latency of risk. One hundred six nonfatal abnormalities have also been diagnosed. CONCLUSION: Mediastinal radiation of 40 to 45 Gy increases the risk of death from coronary artery and other cardiac diseases. The risk increases within 5 years of irradiation. These observations support combined-modality, low-dose irradiation regimens in children and adolescents and suggest the need for careful cardiac screening of treated patients.

Adolescent↗

PubMed1994

[111In-DTPA-D-Phe1] octreotide scintigraphy in thyroidal and orbital Graves' disease: a parameter for disease activity?

Visualization of malignant lymphomas and granulomatous disease is possible by [111In-DTPA-D-Phe1]octreotide scintigraphy through binding of the radioligand to somatostatin receptors on activated leukocytes. Because thyroidal and orbital tissues are infiltrated by activated leukocytes in Graves' disease, a cross-sectional study to visualize disease activity with [111In-DTPA-D-Phe1]octreotide scintigraphy was performed. A correlation between thyroidal [111In-DTPA-D-Phe1]octreotide accumulation and free T4 (disease expression) and thyroid binding-inhibiting immunoglobulins (disease activity) is present in untreated hyperthyroid Graves' disease. There is also a correlation between orbital [111In-DTPA-D-Phe1]octreotide uptake and the clinical activity score (disease activity) and total eye score (disease expression), respectively, in Graves' orbitopathy. Visualization of thyroidal and orbital Graves' disease is feasible, but further investigation is necessary to establish the role of [111In-DTPA-D-Phe1]octreotide scintigraphy in representing disease activity and expression and in predicting therapeutical outcome.

Eye↗

PubMed1998

Cardiac sequelae in recurrent cases of Kawasaki disease: a comparison between the initial episode of the disease and a recurrence in the same patients.

OBJECTIVE: Cardiac sequelae develop more frequently after recurrent Kawasaki disease than from the initial onset of the disease. The purpose of this study was to observe the existence of the sequelae at the initial and second onsets of the disease simultaneously with a large cohort. MATERIALS AND METHODS: From the database of patients with Kawasaki disease prepared by the Japanese Kawasaki Disease Research Committee, 559 cases with recurrences recorded between 1989 through 1994 and their initial occurrence listed in the database were selected. Their proportions of cardiac sequelae after the initial and second onsets of Kawasaki disease were compared. RESULTS: Of the 68 patients with cardiac sequelae after the initial onset, 32 (47%) suffered the sequelae after the second onset, whereas 78 (16%) of the 491 who were without cardiac sequelae after the initial onset developed the sequelae after the recurrence. Both proportions were higher than proportions in all patients with Kawasaki disease. In addition to the sex (male) and the existence of the sequelae after the initial onset, age at the second onset (older age) and the interval between the two episodes (longer period) were suspected to be risk factors for sequelae attributable to recurrent Kawasaki disease. CONCLUSION: Linked data of the initial and second episodes of Kawasaki disease showed that the risk of developing cardiac sequelae attributable to recurrent Kawasaki disease is high among both those with and without the sequelae at the initial episode. mucocutaneous lymph node syndrome, recurrence, cardiac sequelae, risk factors.

Age of Onset↗

PubMed2004

Cigarette smoking, periodontal disease: and chronic obstructive pulmonary disease.

BACKGROUND: Cigarette smoking is a significant risk factor for both chronic obstructive pulmonary disease (COPD) and periodontal disease. The goal of this study was to better understand the role of smoking in a possible relationship between periodontal disease and COPD. METHODS: The study population consisted of 7,625 participants in the Third National Health and Nutrition Examination Survey (NHANES III) during 1988-1994 who were aged 30 years or older when examined and who received a spirometric examination. The data analysis employed logistic regression models and accounted for the complex sampling design used in NHANES III. RESULTS: After adjustment for potential confounders, there was no statistically significant association between periodontal disease and COPD among former or non-smokers. Current smokers with > or = 4 mm mean loss of attachment had an odds ratio of 3.71 (95% confidence interval: 1.74, 7.89). CONCLUSIONS: These results suggest that cigarette smoking may be a cofactor in the relationship between periodontal disease and chronic obstructive pulmonary disease. The key role played by smoking in the etiology of both periodontal disease and chronic obstructive pulmonary disease suggests that much of the observed increase in risk may actually reflect the exposure to smoking. Additional research into smoking-related effect modification is needed to clarify the role of periodontal disease in the etiology of smoking-related systemic diseases.

Adult↗

PubMed1997

Urinary excretion of iohexol as a marker of disease activity in patients with inflammatory bowel disease.

BACKGROUND: Increased intestinal permeability of water-soluble contrast medium during an intestinal follow-through is found in patients with active Crohn's disease in the small bowel. METHODS: Urinary excretion of the water-soluble X-ray contrast medium iohexol was measured after oral administration in patients with inflammatory bowel disease and in healthy controls. The patients were grouped on the basis of disease activity and location and extent of intestinal involvement. RESULTS: Urinary excretion of iohexol was significantly higher in patients with active disease than in patients with quiescent disease or in healthy controls (P = 0.005), and it correlated positively with activity indices and with the extent of the disease. CONCLUSION: The intestinal permeability of iohexol is significantly increased in patients with active inflammatory bowel disease in the small bowel and in the colon, whereas the permeability of patients with inactive disease is similar to that in healthy controls. We suggest that urinary excretion of iohexol can be used as a marker of disease activity in patients with inflammatory bowel disease.

Administration, Oral↗

PubMedDate not supplied

Serum thrombopoietin in chronic liver disease: relation to severity of the disease and spleen size.

BACKGROUND/AIMS: Thrombopoietin is a thrombopoietic factor mainly synthesized in the liver. Its production is regulated by the mass of megakaryocytes and platelets. Impaired production of thrombopoietin may be responsible for thrombocytopenia in chronic liver disease. METHODOLOGY: We studied thrombopoietin serum concentration in 68 patients with chronic liver disease of various degrees (39 with thrombocytopenia), in 5 patients with thrombocytopenia due to hematological disease, and in 27 healthy controls. RESULTS: Thrombopoietin concentration was higher in patients with liver disease than in controls. Patients with hematological disease had much higher thrombopoietin concentration than patients with liver disease. Among patients with liver disease and thrombocytopenia, thrombopoietin concentration was higher in cirrhosis than in chronic hepatitis. A negative correlation was found between platelet counts and spleen size and between thrombopoietin concentration and spleen size. No correlation was found between thrombopoietin concentration and liver disease severity. CONCLUSIONS: Patients with liver disease and thrombocytopenia have serum thrombopoietin concentration higher than normal controls. It seems therefore that the liver, even seriously diseased, maintains the ability to produce thrombopoietin. In the liver patients the number of circulating platelets and the serum levels of thrombopoietin are inversely correlated with the size of the spleen suggesting that thrombopoietin, although normally produced, might be turned over in platelets sequestrated in the spleen.

Aged↗

PubMedDate not supplied

Chronic sinonasal disease in patients with inflammatory bowel disease.

BACKGROUND: The objective of this study was to explore the possible relationship between inflammatory bowel disease (IBD) and chronic sinonasal disease. METHODS: A cross-sectional study was undertaken of 241 patients with Crohn's disease (CD) or ulcerative colitis from a tertiary medical center IBD clinic. Patient demographic data and information regarding IBD diagnosis and management, sinonasal disease diagnosis and management, and complications related to these diagnoses were gathered by retrospective chart review and a standardized patient survey. RESULTS: One hundred sixty surveys (67%) were returned and analyzed. Overall 48% of patients with IBD reported chronic sinonasal disease symptoms. Patients with CD had a higher prevalence of sinonasal disease than patients with ulcerative colitis (53% versus 32%; p < 0.02). The subgroup of CD patients with obstructive bowel complications had the highest prevalence of sinonasal disease (68% versus 27%; p = < 0.001), with 23% reporting chronic rhinosinusitis, 13% reporting chronic rhinitis, and an additional 32% reporting chronic nasal or sinus symptoms. CONCLUSION: The prevalence of chronic sinonasal disease is elevated in patients with IBD, occurring in approximately one-half of patients followed at a tertiary IBD center. Patients with CD experiencing obstructive complications had significantly increased rates of sinonasal disease. The relationship between chronic sinonasal disease and obstructive CD is not defined, but several hypotheses are generated.

Adrenal Cortex Hormones↗

PubMed1989

[Clinical significance of serum acid soluble glycoproteins (ASP) and immunosuppressive acidic protein (IAP) in inflammatory diseases and liver diseases].

In order to study the clinical significance of ASP and IAP, we have measured serum concentration of ASP and IAP in 259 patients with inflammatory diseases, non-inflammatory diseases, autoimmune diseases and liver diseases. Significantly higher correlation (coefficient of correlation = 0.922) was found between ASP and IAP. There were good correlation between ASP, IAP levels and erythrocyte sedimentation rate (ESR), C-reactive protein (CRP). Coefficient of correlation were 0.705 and 0.673 between ESR and ASP, IAP; 0.621 and 0.623 between CRP and ASP,IAP, respectively. There were food correlations between ASP levels and thrombo test (TT) and hepaplastin test (HPT). The positive rate and mean concentration of ASP, IAP in patients with inflammatory diseases were significantly higher than noninflammatory diseases. It is suggested that serum ASP, IAP could be one of the useful indicator for evaluating the clinical course of patients with inflammatory diseases. Serum concentration of ASP, IAP in patients with chronic liver diseases were lower than normal subjects, especially serum levels in patients with decompensated liver cirrhosis and chronic hepatitis (active) were significantly lower than normal subjects. In patients with hepatoma with cirrhosis, serum levels of ASP, IAP were significantly lower than the hepatoma patients without cirrhosis. The determination of ASP, IAP in liver diseases seems to be useful for evaluating the severity of diseases, the effects of therapy and the forecast of prognosis.

Autoimmune Diseases↗

PubMed1994

Blindness in different types of eye disease. A study based on the records of the Department of Eye Diseases in the Medical University, Plovdiv for the period 1982-1991.

Between 1982 and 1991, inclusive, a total of 13718 patients were treated in the Department of Eye Diseases in Plovdiv University of Medicine. Cataract patients formed the most numerous group (19.71%), followed by those with diseases of the retina (9.53%), glaucoma (7.95%), uveitis (4.9%), diseases of the cornea (3.86%), malignant tumors of the eyelids and the eyeball (2.29%) and diseases of the optic nerve (1.54%). Of these 13718 patients, 1727 (12.58%) had monocular and binocular vision below 0.08. The patients with visual acuity from 0 to 0.03 were 1330 (9.69%). Nosologically, they were distributed as follows: glacoma-422 (3.07%), eye traumas-281 (2.04%), diseases of the retina-270 (1.96%), diseases of the cornea-89 (0.64%), cataract-80 (0.58%), uveitis-77 (0.56%), malignant tumors of the eyelids and the eyeball-66 (0.48%), and diseases of the optic nerve-45 (0.32%). Glaucoma was found to be the most common cause of blindness among the patients treated in the Department of Eye Diseases, followed by eye traumas and disease of the retina. The importance of the vascular factor in inducing blindness is undeniably great. It is the underlying cause of the open-angle glaucoma, the diseases of the retina and the optic nerve.

Blindness↗

PubMed1993

Factors affecting late mortality from heart disease after treatment of Hodgkin's disease.

OBJECTIVE: To assess the risk of death from heart disease after Hodgkin's disease therapy. DESIGN: Retrospective study comparing treated patients with a matched general population. SETTING: Referral center. PATIENTS: A total of 2232 consecutive Hodgkin's disease patients treated from 1960 through 1991. Follow-up averaged 9.5 years. MAIN OUTCOME MEASURES: Relative risks (RRs), the ratio of the observed to the expected cases with 95% confidence intervals (CIs), chi tests for trends, and Kaplan-Meier actuarial risks. RESULTS: Of the 2232 patients, 88 (3.9%) died of heart disease, 55 from acute myocardial infarction and 33 from other cardiac diseases, including congestive heart failure, radiation pericarditis or pancarditis, cardiomyopathy, or valvular heart disease. The RR for cardiac death was 3.1 (CI, 2.4 to 3.7). Mediastinal radiation of 30 Gy or less (n = 385 patients) did not increase risk; above 30 Gy (n = 1830), RR was 3.5 (CI, 2.7 to 4.3). Blocking to limit cardiac exposure reduced the RR for other cardiac diseases from 5.3 (CI, 3.1 to 7.5) to 1.4 (CI, 0.6 to 2.9), but not acute myocardial infarction (RR, 3.7 vs 3.4). The RRs increased with duration after treatment (trend in acute myocardial infarction, P = .02; in other cardiac diseases, P = .004). The RR for acute myocardial infarction was highest after irradiation before 20 years of age and decreased with increasing age at treatment (P < .0001 for trend). CONCLUSIONS: Mediastinal irradiation for Hodgkin's disease increases the risk of subsequent death from heart disease. Risk increased with high mediastinal doses, minimal protective cardiac blocking, young age at irradiation, and increasing duration of follow-up.

Adolescent↗