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)

During 59 periods of hospitalisation, 39 patients with either acute myeloid leukemia (22), acute lymphatic leukemia (9), acute undifferentiated leukemia (1), blastic crisis of chronic myeloid leukemia (6) or high-grade malignant non-Hodgkin lymphoma (1) were subjected to aggressive polychemotherapy after selective decontamination of the gut. The patients were given an amphotericin B suspension in a dosage of 1.2 g/day for two days, after which one tablet of trimethoprim/sulphamethoxazole (TMP/SMZ) (160 mg TMP and 800 mg SMZ) t.i.d. was added to prevent endogenous infections by gram-negative aerobic bacteria or moulds and to maintain the "colonisation resistance" endowed by the anaerobes. During 16 of the 59 periods of hospitalisation, no potentially pathogenic aerobic bacteria were isolated. TMP/SMZ-resistant Escherichia coli were the etiological agent of septicemia in two patients, and resistant Klebsiella pneumoniae and Pseudomonas aeruginosa in two other patients. These bacteria were cultured from the patients' fecal samples prior to the development of septicemia. We observed that long-term prophylaxis with TMP/SMZ modified the normal aspect of the fecal biotop culture, not only by suppressing the aerobic gram-negative bacteria, but also by allowing certain clostridia to appear. We differentiated 207 clostridia from the fecal samples of 29 patients and observed a predominance of TMP/SMZ-resistant Clostridium difficile, Clostridium innocuum and Clostridium clostridiiforme. C. difficile was also isolated from the blood culture of a neutropenic patient treated with TMP/SMZ and proved to be very toxic in the Verocell culture.
Infection
PMID:The "clostridial effect" of selective decontamination of the human gut with trimethoprim/sulphamethoxazole in neutropenic patients. 635 9

Forty-two cases of Toxoplasma gondii infection were analyzed, 25 in patients with neoplastic disease and 17 in apparently normal patients. Infection in normal hosts was usually manifested by adenopathy and ran a benign course. Infection in patients with neoplastic diseases was usually manifested by fever and/or neurologic symptoms. Patients with leukemias and lymphomas, particularly Hodgkin's Disease, were at highest risk for infection. Most, but not all, patients developed serologic titers indicative of infection. T. gondii infections were fatal in all eight cases with central nervous system involvement despite treatment in five cases. Leukopenia was a significant complication of treatment with sulfadiazine and pyrimethamine despite the use of folinic acid.
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PMID:Toxoplasmosis. Problems in diagnosis and treatment. 661 13

An autopsy study of 218 cases of lymphoproliferative disease was performed to establish the cause of death. It covered 144 cases of malignant nonHodgkin's lymphoma, 23 cases of Hodgkin's disease and 51 cases of myeloma. It was established that infection is by far the most frequent cause (34% of cases) followed by tumor invasion (11.5% of cases), hemorrhage (9% of cases) and other pathologies linked to the basic process (10% of cases). The proportion of patients who die from intercurrent illness is still considerable (62 cases, 28%). Infection is most often pulmonary or systemic; gram-negative bacteria play a predominant role. Toxicity of treatment is obvious in causing neutropenia and thrombocytopenia among other side effects with fatal consequences.
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PMID:[Causes of death in cases of lymphoma, myeloma and Hodgkin disease. Study of 218 cases]. 686 58

The autopsies of 80 patients with Hodgkin's disease (HD) were reviewed. Nearly one-third of the patients died without evidence of HD at autopsy. Four patients died with clinically unsuspected HD. Infection was the most common cause of death but a significant number of patients died of complications of therapy, both benign and malignant, including five patients with hematologic or de novo lymphoid malignancies. There was wide histologic variation of HD at autopsy and many cases had a pleomorphic appearance with few of the typical features of Hodgkin's disease. Fibrous nodules interpreted as sites of eradicated HD were found in many organs, most commonly lymphoreticular. Nonfatal histopathologic effects of therapy were common and specifically assessed thyroid and gonads.
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PMID:Hodgkin's disease at autopsy: 1972-1977. 722 80

Hodgkin's disease, nodular sclerosing, developed in a 16-year-old man with the Wiskott-Aldrich syndrome. Two brothers and two nephews had documented Wiskott-Aldrich syndrome and had died of infectious complications in childhood. While the patient reported here had lifelong thrombocytopenia and recurrent upper respiratory infections, he had no severe infection prior to the development of Hodgkin's disease. Skin test sensitization with dinitrochlorobenzene was unsuccessful. No antibodies were found after immunization with pneumococcal polysaccharides. Platelet aggregation studies were abnormal in the patient, his mother, and one of his nephews. A complete response of short duration occurred after treatment with nitrogen mustard, vincristine, procarbazine, and prednisone. On recurrence, he proved unresponsive to further chemotherapy or radiation therapy. Infection with four different fungi was found at autopsy. This patient is the third recorded case of Hodgkin's disease associated with the Wiskott-Aldrich syndrome.
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PMID:Hodgkin's disease occurring in a patient with the Wiskott-Aldrich syndrome. 735 Oct 18

Incidence of HD varies from about 0.5 per 100,000 person-years in parts of Asia to over 3 in parts of North America. In recent decades, many registries have reported slightly declining age adjusted incidence among men and women. Some lymphomas previously diagnosed as HD now would be classified as NHL, but this shift does not explain all of the decline. When analysed by age group, incidence has decreased substantially at older ages, whereas increases have been reported among young adults in some industrial countries. Less developed countries continue to show high rates in childhood. Hodgkin's disease of the nodular sclerosis subtype has increased over time, whereas HD of mixed cellularity has declined. Improved therapy for HD has led to sharply declining mortality rates, but further understanding of the role of EBV and other possible causal agents should afford opportunities for prevention. Non-Hodgkin's lymphoma stands out from most other malignancies because incidence and mortality rates have risen dramatically, steadily and almost universally during the past few decades. Incidence overall has been rising 3-4% per year. No sudden rise has occurred in specific birth cohorts or calendar year of diagnosis, although incidence rates have increased more steeply at older ages. Diagnosis of NHL has improved with time, perhaps beyond the ways considered herein, but has it improved so much more than diagnosis of other malignancies, and roughly simultaneously around the world? Although it appears that diagnostic improvements are partly responsible for the upward trend, it is likely that aetiological factors are playing an important part. Infections with HIV have started to inflate NHL incidence rates further but cannot account for the striking trend already under way for several decades. Clues should be vigorously pursued to determine the role of other known viruses, immunosuppressive states, herbicides and other chemicals in the environment, and commercial products such as hair dyes. To clarify reasons for the upward trends and to take preventive action will require a better understanding of the origins of the lymphomas through epidemiological research, including interdisciplinary approaches that can identify new viruses, host-environmental interactions and lifestyle and other exposures that alter susceptibility.
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PMID:Hodgkin's and non-Hodgkin's lymphomas. 753 35

Infection with the human immunodeficiency virus-type 1 (HIV-1) may produce a variety of central nervous system (CNS) symptoms and signs. CNS involvement in patients with the acquired immunodeficiency syndrome (AIDS) includes AIDS dementia complex or HIV-1 associated cognitive/motor complex (widely known as HIV encephalopathy), progressive multifocal leucoencephalopathy (PML), opportunistic infections such as Toxoplasma gondii, TB, Cryptococcus and infiltration by non-Hodgkin's B cell lymphoma. High resolution structural imaging investigations, either X-ray Computed Tomography (CT scan) or Magnetic Resonance Imaging (MRI) have contributed to the understanding and definition of cerebral damage caused by HIV encephalopathy. Atrophy and mainly high signal scattered white matter abnormalities are commonly seen with MRI. PML produces focal white matter high signal abnormalities due to multiple foci of demyelination. However, using structural imaging techniques there are no reliable parameters to distinguish focal lesions due to opportunistic infection (Toxoplasma gondii abscess) from neoplasm (lymphoma infiltration). In this manuscript we review the use of radionuclide brain imaging techniques in the investigation of HIV infected patients. Brain perfusion single photon emission tomography (SPET), neuroreceptor and positron emission tomography (PET) studies are reviewed. Greater emphasis is put on the potential of some radiopharmaceuticals, considered to be brain tumor markers, to distinguish intracerebral lymphoma infiltration from Toxoplasma infection. SPET with 201Tl using quantification (tumour to nontumour radioactivity ratios) appears a very promising technique to identify intracerebral lymphoma.
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PMID:Radionuclide brain imaging in acquired immunodeficiency syndrome (AIDS). 755 47

The serum levels of soluble interleukin 2 receptors (sIL-2R) were determined in 19 patients who received high-dose chemotherapy and an autologous or syngeneic bone marrow transplant (BMT) for treatment of Hodgkin's disease (n = 18) or non-Hodgkin's lymphoma (n = 1). Twelve patients received granulocyte colony-stimulating factor (G-CSF) from day 0 or day +1 after autologous BMT until the white blood cell count had been stable for 9 d above 1 x 10(9)/l, the remaining seven patients did not receive growth factors. In all G-CSF-treated patients the sIL-2R levels increased steadily in the early post-transplant course, even in the absence of infection. This increase was statistically significant 2-4 d prior to the appearance of leucocytes in the peripheral blood (median 340 pM versus median 256 pM immediately after BMT, P < 0.025) and peaked with the appearance of first peripheral blood leucocytes (median 536 pM, P < 0.001). Cessation of G-CSF administration resulted in a decline of sIL-2R levels. In contrast, five of seven patients without G-CSF treatment did not exhibit an sIL-2R increase before or at the time of engraftment. Infection was associated with a rise of sIL-2R levels. A correlation between sIL-2R levels and total leucocyte count, lymphocyte count, or CD25+ lymphocyte count was not evident. These data suggest that after autologous BMT G-CSF induces increased sIL-2R levels, which occur independent of lymphocyte activation. This may be compatible with involvement of immature bone marrow cells in G-CSF-induced sIL-2R release.
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PMID:Granulocyte-colony-stimulating factor induces increased serum levels of soluble interleukin 2 receptors preceding engraftment in autologous bone marrow transplantation. 767 89

Dysphagia or odynophagia occurs in an estimated 21% of patients with human immunodeficiency virus infection. A causal agent can be identified in 60-90% of the cases and generally can be successfully eradicated. Oesophageal candidosis, the predominant disorder, usually responds to nitrate derivatives and amphotericine B after a 10 to 15 day cure. Ulcerations of the oesophagus is the second major cause of dysphagia in these patients and result from cytomegalovirus and herpes simplex infections or unknown causes. Epstein-Barr virus infection has been suggested but is rarely demonstrated in clinical situations. Similar to other localizations in HIV-infected patients, Kaposi sarcoma and non-Hodgkin malignant lymphomas are the predominant tumours in the bowel. Infections are essentially revealed by sometimes very severe diarrhoea. Infective agents include Cryptosporidium parvum, microsporidiosae, cytomegalovirus, adenovirus, Isospora belli, Clostridium difficile, Salmonellae and non-tuberculous mycobacteria among others. When the search for an infective agent is negative, the diarrhoea is usually considered to be the expression of HIV infection itself. The clinical approach to HIV-related diarrhoea can be based on decision making management scheme according to the results of stool cultures or on complete exploration protocols. Whatever the diagnostic procedure, symptomatic treatment is of major importance because of the severe nutritional impact of HIV-related diarrhoea.
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PMID:[Digestive involvements in human immunodeficiency virus infection]. 789 94

The wide clinicopathologic heterogeneity of non-Hodgkin's lymphoma is reflected by the various molecular pathways underlying non-Hodgkin's lymphoma pathogenesis, including activation of dominantly acting oncogenes, deletion and inactivation of tumor-suppressor genes, viral infection, deregulation of cytokine networks, and chronic antigenic stimulation. Molecular lesions involving protooncogenes include activation of bcl-2 and bcl-1 in specific subsets of low-grade non-Hodgkin's lymphomas and c-myc in a proportion of intermediate- and high-grade non-Hodgkin's lymphomas. The deregulation of these genes promotes cell growth or protects the tumor population from programmed cell death, or both. Additional genetic abnormalities representing putative sites of novel oncogenes contributing to lymphomagenesis include chromosomal breaks at 3q27 in intermediate-grade non-Hodgkin's lymphoma and at 9p13 in small lymphocytic lymphoma. The role of inactivation of tumor-suppressor loci is best exemplified by the frequent inactivation of p53 in Burkitt's lymphoma and by the recurrent deletion of 6q25-q27 and 6q21-q23 in intermediate- and high-grade non-Hodgkin's lymphoma, respectively. Infection by Epstein-Barr virus occurs in a variable fraction of high-grade non-Hodgkin's lymphomas, whereas it is usually absent in other types of non-Hodgkin's lymphoma. Other mechanisms supporting non-Hodgkin's lymphoma growth and development include autocrine or paracrine cytokine loops, or both, and clonal expansion through antigen receptor stimulation. The heterogeneity of non-Hodgkin's lymphoma pathogenesis provides a framework for the development of novel classification methods of potential clinical relevance.
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PMID:Biologic and molecular characterization of non-Hodgkin's lymphoma. 821 89


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