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)

We describe a case of inflammatory brachial plexopathy that occurred in the context of a mild, diffuse sensorimotor peripheral neuropathy associated with Hodgkin's disease. Clinical, electrophysiologic, and pathologic studies helped distinguish this disorder from other causes of brachial plexopathy in patients with cancer. Treatment with corticosteroids seemed beneficial in this patient. We suggest that this may be another type of paraneoplastic condition associated with Hodgkin's disease.
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PMID:Paraneoplastic brachial plexopathy in a patient with Hodgkin's disease. 184 35

Twelve patients who developed radiation-induced brachial plexopathy (RIBP) after receiving radiation therapy for breast carcinoma (7 patients) or Hodgkin's lymphoma (5 patients) were followed for 12 or more years, with a mean follow-up time of 20 years. Tingling and numbness of the fingers as well as weakness of the hand or arm were the most prominent presenting symptoms of RIBP. Whereas pain in most patients evolved only later in the course, it became a predominant feature in only 2. In 8 of the 12 patients, the plexopathy was surgically treated, either by neurolysis only or by neurolysis plus omental grafting in order to stop progression or paresis and/or pain. In 8 patients, including 6 of the operated group, there was slow and steady progression of RIBP over time, with the final outcome being almost complete paralysis of the arm (2 patients) or severe sensorimotor paresis rendering the hand useless (6 patients). In only 4 patients, including 2 of the non-operated group, was there absence of progression and stabilization of the paresis with only slight functional loss of the affected arm in 3 patients and severe palsy in 1. None of the 12 patients had any clear long-lasting improvement of their sensorimotor impairment. It is concluded from this study that RIBP, irrespective of surgery (neurolysis and/or omentum transplant), left two-thirds of the patients with severe or total paresis of the arm. However, the almost complete relief of severe pain (6 of 8 patients), both immediately and in follow-up patients treated with neurolysis and/or omental transplant, indicates that surgical treatment has a beneficial effect on pain relief.
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PMID:Natural history of radiation-induced brachial plexopathy compared with surgically treated patients. 239 47

Brachial plexus neuropathy is an unfortunate complication that sometimes follows radiotherapy to the axillary and supraclavicular regions. A patient is described who, 30 years after radiotherapy for Hodgkin's disease and more than 10 years after the development of radiation-induced bilateral brachial plexus neuropathy, presented with bilateral diaphragmatic weakness secondary to bilateral phrenic nerve weakness. Previous radiotherapy was the most probable cause of the condition.
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PMID:Bilateral diaphragmatic weakness: a late complication of radiotherapy. 937 Dec 19

A patient with painful peripheral neuropathy is presented, whose symptoms were thought to result from an infection with Borrelia burgdorferi sensu lato. Investigations of the cerebrospinal fluid for signs of inflammation and borrelial antibodies were negative, and the patient did not benefit from repeated antibiotic treatment. Electrophysiologic studies and sural nerve biopsy showed axonal neuropathy consistent with a paraneoplastic syndrome. Further workup revealed mediastinal Hodgkin's disease (HD; nodular sclerosing subtype) Ann Arbor stage II and non-small cell cancer of the lung (stage T1N0M0). Surgical resection of the lung cancer and combined chemo- and radiotherapy for HD resulted in complete remission of both malignancies. While the preexisting neurologic symptoms persisted during treatment, neurography showed some improvement of the distal nerves. During radiation therapy the patient developed transient left-sided brachial plexopathy. This case illustrates that the diagnosis of borreliosis in patients with isolated painful peripheral neuritis cannot be based solely upon positive IgG titers and supports the requirement for a thorough workup for an underlying--potentially curable--disease. In addition, singular pulmonary lesions in the setting of HD should be suspected to have a separate cause.
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PMID:Paraneoplastic polyneuropathy preceding the diagnosis of Hodgkin's disease and non-small cell lung cancer in a patient with concomitant Borrelia burgdorferi infection. 1140 Oct 90

Hodgkin's lymphoma is a hematolymphoid neoplasm, primarily of B cell lineage, that has unique histologic, immunophenotypic, and clinical features. Neurologic complications of Hodgkin's Lymphoma can be separated into those that result directly from the disease, indirectly from the disease, or from its treatment. Direct neurologic dysfunction from Hodgkin's Lymphoma results from metastatic intracranial spinal disease, epidural metastases causing spinal cord/cauda equina compression, leptomeningeal metastases, or intradural intramedullary spinal cord metastases. Indirect neurologic dysfunction may be caused by paraneoplastic disorders (such as paraneoplastic cerebellar degeneration or limbic encephalitis) and primary angiitis of the central nervous system. Hodgkin's lymphoma treatment typically includes chemotherapy or radiotherapy with potential treatment-related complications affecting the nervous system. Neurologic complications resulting from mantle-field radiotherapy include the "dropped head syndrome," acute brachial plexopathy, and transient ischemic attacks/cerebral infarcts. Chemotherapy for Hodgkin's lymphoma may cause cerebral infarction (due to emboli from anthracycline-induced cardiomyopathy) and peripheral neuropathy.
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PMID:Hodgkin's Lymphoma: A Review of Neurologic Complications. 2097 72

Radiation-induced peripheral neuropathy is a chronic handicap, frightening because progressive and usually irreversible, usually appearing several years after radiotherapy. Its occurrence is rare but increasing with improved long-term cancer survival. The pathophysiological mechanisms are not yet fully understood. Nerve compression by indirect extensive radiation-induced fibrosis plays a central role, in addition to direct injury to nerves through axonal damage and demyelination and injury to blood vessels by ischaemia following capillary network failure. There is great clinical heterogeneity in neurological presentation since various anatomic sites are irradiated. The well-known frequent form is radiation-induced brachial plexopathy (RIBP) following breast cancer irradiation, while tumour recurrence is easier to discount today with the help of magnetic resonance imaging and positron emission tomography. RIBP incidence is in accordance with the irradiation technique, and ranges from 66% RIBP with 60Gy in 5Gy fractions in the 1960s to less than 1% with 50Gy in 2Gy fractions today. Whereas a link with previous radiotherapy is forgotten or difficult to establish, this has recently been facilitated by a posteriori conformal radiotherapy with 3D-dosimetric reconstitution: lumbosacral radiculo-plexopathy following testicular seminoma or Hodgkin's disease misdiagnosed as amyotrophic lateral sclerosis. Promising treatments via the antioxidant pathway for radiation-induced fibrosis suggest a way to improve the everyday quality of life of these long-term cancer survivors.
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PMID:Radiation-induced neuropathy in cancer survivors. 2324 44