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)

An 8-year-old boy had nausea and vomiting associated with nystagmus, ataxia, and dysarthria of acute onset. Three years later he had a mass in the anterior mediastinum as a result of Hodgkin disease of mixed cellularity. This association of paraneoplastic cerebellar degeneration with Hodgkin disease has been described in adults.
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PMID:Paraneoplastic syndrome manifesting as chronic cerebellar ataxia in a child with Hodgkin disease. 173 28

One of 4 siblings affected by hereditary spinocerebellar ataxia (HSCA) of Marie's type developed Hodgkin's disease (HD): the stage was IV B, the patient was submitted to conventional chemo- and radiotherapy and achieved complete remission. An accurate clinical, genetic and immunological study was carried out on all his family, including a complete HLA typing, a chromosome study, the immunophenotyping of peripheral blood mononuclear cells (PBMC), the PBMC response to polyclonal mitogens, to interleukin 2 (IL-2), to the association of PHA + IL-2 and the evaluation of the IL-2 receptor expression. No association was clearly demonstrable between an HLA haplotype and HSCA, while the patient with HSCA and HD was HLA-B18- and DQw3-positive (the last at homozygous level), two antigens known to be strongly associated with HD, mainly among the Sardinian ethnic group. The mode of inheritance of HD susceptibility is however completely different from that of Marie's HSCA. The chromosome study did not show any characteristic pattern of the karyotype, neither of the HSCA affected nor of the unaffected members. The immunological investigations did not elucidate any characteristic behavior of the family members, apart from the typical findings of HD seen on patients with HSCA and HD. Our study could not demonstrate any genetic and/or immunologic common background shared by the two diseases, HSCA and HD. Their coexistence in our patient, although the statistic probability is very low, seems to be a fortuitous coincidence more than the result of a common genetic and pathogenetic mechanism.
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PMID:Hodgkin's disease presenting in 1 of 4 siblings affected by hereditary spinocerebellar ataxia: clinical, immunological and genetic study. 278 67

T-cell lymphoma may involve the CNS as either a primary or secondary neoplasm. This report describes 8 patients with either primary or secondary T-cell malignancies in the CNS. Five patients presented with symptoms and signs of CNS disease that included seizures, visual impairment, cranial nerve palsies, sensory and motor deficits, gait ataxia, and paraparesis. Three of them had primary parenchymal CNS lymphoma, and 2 had epidural lymphoma that originated in adjacent bone marrow. Three patients were neurologically asymptomatic, but had leptomeningeal tumor and focal parenchymal infiltration at postmortem examination. Histologically, 4 lymphomas were large cell, 3 were mixed large and small cell, and 1 could not be classified by the working formulation for non-Hodgkin's lymphomas. The clinical and pathologic manifestations of T-cell lymphoma in the CNS may be diverse. This report demonstrates that neurologic abnormalities may be the presenting signs of either primary CNS or systemic T-cell lymphoma.
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PMID:T-cell lymphoma in the CNS: clinical and pathologic features. 278 32

The case of a child presenting with Hodgkin's disease (stage I A, mixed cellular type) at the age of 23 months is reported. Chemotherapy (six treatments with MOPP) enabled a clinical remission, but an in situ relapse with the same histological pattern was observed at the age of 3 years and 9 months. After local irradiation, a second complete remission was observed. At the age of 6, a clinical picture of intraskull hypertension with ataxia, lead to the diagnosis of posterior cavity tumor. Complete excision was performed and the pathological examination showed a typical medulloblastoma. Adjuvant radiotherapy was carried out. Eight months later, a fatal plurifocal medullar relapse was observed. Second tumors in Hodgkin's disease are well known. However, this new case appeared to be the first report of a medulloblastoma after Hodgkin's disease.
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PMID:[Medulloblastoma of the posterior cranial fossa. A second tumor after Hodgkin's disease]. 361 42

The importance of humoral immune defects and of the antibody deficiency syndrome, respectively, at adult age was examined on 69 patients. As immunological methods the estimation of the immunoglobulins G, A, M, D with Mancini's technique, of IgA-antibodies with Ouchterlony's technique, of T-lymphocytes with the sheep erythrocyte rosette test, of B-lymphocytes with direct immunofluorescence and mouse erythrocyte rosette test were used. The enzyme adenosine deaminase was determined in the plasma, the erythrocytes and the lymphocytes. 31 patients with primary antibody deficiency syndrome, of them 22 patients with selective IgA-deficiency could be diagnosed. 38 patients with secondary antibody deficiency syndrome came from groups of patients with lymphoproliferative diseases (non-Hodgkin-lymphoma and plasmocytoma), chronic dialysis and other haematological diseases. In 80% of the patients clinical symptoms of an immune defect could be proved. Chronically relapsing infections of the respiratory tract are in the first place. Familial accumulation, allergic reactions, antibodies against IgA, statistically significant accumulation of gastric and duodenal ulcers set off the anyway large group of patients with selective IgA-deficiency. An antibody deficiency syndrome with IgA-deficiency could be proved in 5 of 16 patients undergoing the dialysis programme, but clinically it is perhaps insignificant. Disturbances of the cell-mediated immune reaction occurred in a child with teleangiectatic ataxia and lymphoproliferative diseases. A deficiency of adenosine deaminase, which is of importance in combined immune defects syndrome at adult age, but it is to be proved in the plasmocytoma and the non-Hodgkin-lymphoma. The necessity of the knowledge of forms of the antibody deficiency syndrome at adult age results from the increasingly immunosuppressively acting therapeutic measures, correct and well-timed diagnosing as well as the necessity of aimed consultation of the physician in institutions specialised in immunology.
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PMID:[Humoral immune defects in adults]. 711 11

Central pontine myelinolysis was found histologically in a young man who died with Hodgkin's lymphoma. Clinically he had developed a progressive peripheral sensory deficit, ataxia, quadriparesis, dysarthria, incontinence and drowsiness. This is the fifth case reported in the British literature. The pathogenesis and aetiology of this primary demyelinating disease are considered.
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PMID:Central pontine myelinolysis in association with Hodgkin's lymphoma. 730 76

Ten of 18 children in a highly inbred Arab kindred suffered from either ataxia telangiectasia (AT) or a variant syndrome consisting of ataxia, microcephaly, and congenital cataract (AMC). Four of the nine afflicted children were treated in our unit when they developed lymphomas (both Hodgkin's and non-Hodgkin's including Burkitt's). They were given chemotherapy (either standard COMP or low-dose ABV/CVPP). The children with non-Hodgkin's lymphomas died of sepsis after receiving full-dose COMP. Low-dose ABV/CVPP brought about a 20-month remission in one child with nodular sclerosing Hodgkin's lymphoma and both AT and AMC, but she developed a preleukemic syndrome and her parents refused further treatment; she too died. A fourth child, also with nodular sclerosing Hodgkin's lymphoma, is currently in complete remission after ABV/CVPP. Treatment of lymphomas in patients with AT is extraordinarily difficult and has potential side effects so grave as to necessitate careful monitoring and individualized protocols.
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PMID:Ataxia telangiectasia and lymphoma: an indication for individualized chemotherapy dosing--report of treatment in a highly inbred Arab family. 762 85

We describe a 12-year-old black male who presented with cervical lymphadenopathy, hepatosplenomegaly of 3 months duration, and ataxia and incoordination of recent onset. Hodgkin's disease, stage IVB, was diagnosed. An MRI of the head demonstrated a nonenhancing, well-defined pontine lesion. The pontine lesion and the associated neurologic symptoms were consistent with central pontine myelinolysis. Treatment of Hodgkin's disease resulted in complete remission and complete disappearance of the pontine abnormality.
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PMID:Hodgkin's disease associated with central pontine myelinolysis. 768 85

We describe two patients who developed paraneoplastic neurological syndromes and have reviewed the literature. One patient with Hodgkin's disease developed brachial neuritis. The other with a non Hodgkin's lymphoma of thyroid suffered from ataxia owing to cerebellar degeneration. Both neurological syndromes developed following marked nodal shrinkage following chemotherapy. Although both patients are in complete remission there has been no recovery of the neurological deficit. The patient with brachial neuritis developed L'hermitte's sign after a modest dose radiation (35Gy in 20 fractions) to the cervical cord and a vincristine sensory neuropathy. Vincristine may also have increased the degree of ataxia in the second patient. We suggest that potentially neurotoxic treatment should be given with extra care to patients with paraneoplastic neurological disorders.
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PMID:Paraneoplastic neurological syndromes associated with lymphomas. 787 6

Low-grade non-Hodgkin B-cell lymphoma was found during the evaluation of 3 aged patients with predominantly sensory neuropathy of mild to moderate severity. Presenting manifestations were sensory ataxia and right ulnar mononeuropathy in a 75-year-old man, and painful dysesthesias of the legs in two 78-year-old women. A neurophysiological study showed mainly axonopathic alterations. M-protein was present in all cases (Ig-kappa in two, triclonal gammopathy IgG(kappa)/IgM(kappa)/IgM-gamma in one). The male patient had IgM antisulfatide antibody in high titer, whereas the other 2 patients had cryoglobulinemia (type II and type III, respectively). Our report emphasizes the occurrence of mild polyneuropathy as presenting manifestation of low-grade non-Hodgkin lymphoma, different from the clinicopathological entity of neurolymphomatosis, in which severe nerve damage occurs in association with manifest lymphoma, related to nerve infiltration by lymphomatous cells. Alternative pathogenetic mechanisms, such as antibody-mediated nerve damage, or vasa nervorum changes caused by cryoglobulin, may be implicated in our cases. Non-Hodgkin lymphoma should be considered in the diagnostic evaluation of polyneuropathy of unknown cause, especially in patients with paraproteinemia and/or cryoglobulinemia.
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PMID:Low-grade non-Hodgkin B-cell lymphoma presenting as sensory neuropathy. 873 42


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