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)

The brain of a patient with Hodgkin's disease and dementia showed numerous dystrophic axons in the thalamus. In absence of lymphomatous cellular infiltration, necrosis, hemorrhage, demyelination, neuronal loss, or infection by opportunistic organisms, the axonal dystrophy in this patient appeared to be directly related to the Hodgkin's disease itself. Moreover, dementia as a nonmetastatic complication of Hodgkin's disease may have been the result of the thalamic axonal dystrophy.
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PMID:Thalamic neuroaxonal dystrophy and dementia in Hodgkin's disease. 94 54

A 59-year-old Japanese woman with Hodgkin's disease developed progressive dementia and died of pneumonia. The autopsy revealed necrotizing ventriculo-encephalitis caused by cytomegalovirus (CMV) infection, which was confirmed by immunohistochemical and electron microscopic examinations. It is suggested that CMV ventriculo-encephalitis could occur not only in patients with acquired immunodeficiency syndrome, but also in other immunocompromised hosts.
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PMID:An autopsy case of necrotizing ventriculo-encephalitis caused by cytomegalovirus in Hodgkin's disease. 165 May 18

Alzheimer's disease is one of several brain disorders under the broad category of dementia. It is a gradually debilitating illness with no known cure. The first symptom is usually a slowly increasing memory loss, beginning between 40 and 65 years of age. As the disease progresses, the brain begins to deteriorate more rapidly, until it literally stops functioning. Of great concern is the projection that the number of people who will have Alzheimer's disease will double by the year 2030 because of the rising elderly population. Treating this population will escalate from the current estimate in excess of $2.5 billion to more than $6 billion. Speculation toward the increasing costs in money and workforce has led to an accelerated program in search of a cure or at least a symptomatic therapy for this condition. One of the most promising research leads is the striking connection between Alzheimer's disease and Down's syndrome and certain cancers: --Virtually 100% of patients with Down's syndrome who survive past age 35 show the same mental deterioration and identical brain changes seen in patients with Alzheimer's disease, including the presence of plaque and neurofibrillary tangles.--The presence of a high percentage of Down's syndrome among relatives of patients with Alzheimer's disease. --A high incidence of certain types of syndrome and among relatives of people who have Alzheimer's disease, such as leukemia, lymphomas, Hodgkin's disease, and immune system disorders. The key to the intercorrections between Alzheimer's disease and Down's syndrome seems to be a genetic component related to chromosome 21.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alzheimer's disease: an emerging affliction of the aging population. 293 67

A 62-year-old man with progressive cerebellar degeneration, corticospinal tract dysfunction, and mild dementia was found to have Hodgkin's disease. Serial computed tomographic studies revealed progressive cerebellar atrophy. The clinical features and neuroradiologic studies in nine previous cases are reviewed. A thorough search for lymphadenopathy should be made in patients with unexplained cerebellar degeneration.
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PMID:Cerebellar degeneration with Hodgkin's disease: computed tomographic correlation and literature review. 701 Dec 81

Epstein-Barr virus (EBV) has been associated with Hodgkin's disease (HD) in up to 50% of cases, but the subtype of EBV involved has only recently been studied. In this report, biopsy samples from 30 patients with HD were assessed for EBV sequences using both the polymerase chain reaction (PCR) and in situ hybridization (ISH). EBV sequences were localized to the malignant Reed-Sternberg cells and their mononuclear variants (Hodgkin's cells) in 9 of the 30 cases, with 7 demonstrating A-type and 2 B-type EBV sequences. Both of the patients with B-type EBV-associated HD had features to suggest pre-existing immune compromise: one was infected with human immunodeficiency virus (HIV) and had severe CD4+ T-lymphocyte depletion; the other was a debilitated elderly patient with dementia. A previous study suggested that A-type EBV alone is associated with HD and the finding of predominantly A-type EBV in the present series is in keeping with this report. The presence of B-type EBV in the HD of patients with pre-existing immunodeficiency, taken together with the recent report that B-type EBV occurs in HIV-associated non-Hodgkin's lymphoma, suggests that B-type EBV may be an important human pathogen in immunocompromised patients.
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PMID:Subtypes of Epstein-Barr virus (EBV) in Hodgkin's disease: association between B-type EBV and immunocompromise. 839 76

The paper presents a rare case of primary, non-Hodgkin brain lymphoma discovered in 64 years old woman. Non specific symptoms conducted to misdiagnoses of dementia and syderopenic anaemia. The proper identification has been made after 10 months by post-mortem histopathological analysis.
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PMID:[A case of primary non-Hodgkin brain lymphoma]. 1469 95

An archive autopsy case of a 50-year-old man who died of Hodgkin's lymphoma had a 4-year, 4-month history of dementia. After radiochemotherapy, the lymphoma subsided except for involvement of the spleen, but the dementia remained. Neuropathological examination revealed that the pathology was confined to the hippocampus, both hippocampi showing sclerosis without inflammation. Neurons of sector cornu ammonis (CA) 1 were completely lost whereas moderate neuron loss was also observed in sectors CA3 and 4, and the dentate gyrus. Neurons of sector CA2 were relatively well preserved and the subiculum was intact. There was no evidence of global hypoxia, or of neurodegenerative disorders with pathological changes affecting the hippocampus. Although there was a long preneoplastic history, and no inflammatory changes were found at autopsy, the present case of hippocampal sclerosis could be included in the category of paraneoplastic limbic encephalitis associated with Hodgkin's lymphoma or the Ophelia syndrome.
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PMID:Pathology of pure hippocampal sclerosis in a patient with dementia and Hodgkin's disease: the Ophelia syndrome. 1638 85

In many neurodegenerative disorders that lead to memory loss and dementia, the brain pathology responsible for neuronal loss is marked by accumulations of proteins in the form of extracellular plaques and intracellular filamentous tangles, containing hyperphosphorylated cytoskeletal proteins. These are assumed to arise as a consequence of deregulation of a normal pattern of topographic phosphorylation-that is, an abnormal shift of cytoskeletal protein phosphorylation from the normal axonal compartment to cell bodies. Although decades of studies have been directed to this problem, biochemical approaches in mammalian systems are limited: neurons are too small to permit separation of cell body and axon compartments. Since the pioneering studies of Hodgkin and Huxley on the giant fiber system of the squid, however, the stellate ganglion and its giant axons have been the focus of a large literature on the physiology and biochemistry of neuron function. This review concentrates on a host of studies in our laboratory and others on the factors regulating compartment-specific patterns of cytoskeletal protein phosphorylation (primarily neurofilaments) in an effort to establish a normal baseline of information for further studies on neurodegeneration. On the basis of these data, a model of topographic regulation is proposed that offers several possibilities for further studies on potential sites of deregulation that may lead to pathologies resembling those seen in mammalian and human brains showing neurodegeneration, dementia, and neuronal cell death.
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PMID:Squid (Loligo pealei) giant fiber system: a model for studying neurodegeneration and dementia? 1680 5

Anaplastic large cell lymphoma (ALCL) is a type of non-Hodgkin lymphoma composed of CD30-positive cells. Anaplastic lymphoma kinase (ALK) -1 positive ALCL frequently involves both lymph nodes and extranodal sites. While primary extranodal involvement of ALK-1 negative ALCL is rare, this case is unique in that it is a case of primary ALK-1 negative ALCL of the brain. A 79-year-old man presented with dementia-like symptoms. Neuroimaging revealed a well-enhanced mass in the left parieto-occipital region. The tumor was excised and histological diagnosis of primary ALK-1-negative ALCL was made. Primary ALK-1-negative ALCL in this case showed aggressive clinical behavior and fatal outcome. It is of great importance to avoid any delay in reaching an accurate diagnosis, as even primary ALCL of the brain is too seldom suspected clinically.
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PMID:Primary ALK-1-negative anaplastic large cell lymphoma of the brain: case report and review of the literature. 1856

We report a case of a 39-year-old man with Hodgkin lymphoma who developed depressive symptoms after starting adriamycin, bleomycin, vinblastine and dacarbazine chemotherapy and later exhibited sexual disinhibition in addition to cognitive dysfunction (mainly executive dysfunction). Seven months after the start of adriamycin, bleomycin, vinblastine and dacarbazine chemotherapy, he was finally diagnosed as having fronto-temporal lobular degeneration-like dementia facilitated by adriamycin, bleomycin, vinblastine and dacarbazine chemotherapy. At the time of writing, the patient's condition has persisted for more than 6 months after the discontinuation of adriamycin, bleomycin, vinblastine and dacarbazine chemotherapy, and the changes in brain function brought on by the adriamycin, bleomycin, vinblastine and dacarbazine chemotherapy may now be irreversible. This case points to the importance of being attentive to the appearance of neuropsychiatric symptoms and evaluating brain functions properly when performing anti-cancer chemotherapy.
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PMID:A case with Hodgkin lymphoma and fronto-temporal lobular degeneration (FTLD)-like dementia facilitated by chemotherapy. 2002 58


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