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)

A 40 year old woman with Hodgkin's disease twice developed signs of encephalitis while being treated with prednisone and cyclophosphamide for 10 months. Since on both occasions her Toxoplasma dye test titer was 1 : 8000 or higher, she was treated on suspicion of toxoplasmosis with sulfadizine and pyrimethamine. Her tumor therapy was changed to bleomycin with lower doses of prednisone for 12 months. After death from central pontine myelinolysis, Toxoplasma and cytomegalovirus could be isolated, but no lesions attributable to these infectious agents were present. Maintenance of the patient's immune competence suggested an inquiry into the effects of the chemotherapeutic agents and of tumor infiltration for their respective interference with immunity. Using hamsters with chronic latent toxoplasmosis, it was found that both cortisone and cyclophosphamide caused recrudescence of chronic inapparent infection, that vinblastine and bleomycin interfered only slightly with the development of immunity, whereas in infiltrating lymphoma permitted immunity to develop normally. It is concluded that greater attention should be directed to the immunosuppressive effects of tumor treatment. By choice of an effective tumor therapy which is least immunosuppressive, and if necessary under cover of antimicrobial therapy, a patient with Hodgkin's disease can be aided in developing immunities which he may subsequently be able to maintain.
Infection 1978
PMID:Immune competence in a patient with Hodgkin's disease and relapsing toxoplasmosis. 7 57

1. All essential attributes of the amyloidosis in aged persons ("senile amyloidosis") correspond to the condition which in younger individuals develops after infections, particularly following tuberculosis and lymphogranulomatosis, as so-called secondary amyloid degeneration, and also manifests many features of the so-called primary amyloidosis, not connected with infections. 2. Amyloid depositions in the brain, cardiac muscle, and in pancreatic islets (the "senile amyloidotic triad") dominate the morbid anatomic aspect. However, we know no organ or tissue which necessarily remains spared. The number of involved organs and tissues, in general, increases with the progressive aging of the patients. In those persons living long enough, amyloidosis affects every individual and probably all organs and tissues. 3. Contrary to the so-called secondary amyloidosis, in many cases of senile amyloidosis the spleen, liver and kidney remain intact. 4. In the so-called Alzheimers disease, in which both clinically and pathoanatomically a particularly destructive cerebral amyloidosis in relatively young persons prevails, just as in the common senile dementia of aged persons, the brain condition is associated with a systemic amyloid degeneration of many other organs. 5. Several cerebral and cardiac lesions due to amyloid accumulations can probably be diagnosed electrographically. Thus, through these already known morbid anatomical observations we have the promise of an essential enrichment of diagnostic perspectives. 6. In general, the etiologic manifoldness of amyloidosis presently seems to be incomparable. Infections, ionizing radiation, traumatic lesions in human pathology, the introduction of chemically definable substances, infections, and stress consequent to social burdening, proved effective in spontaneous and experimental amyloid degeneration of animals. 7. The demonstration of a tuberculous infection with the help of postmortem radiographs, as well as with the employment of histologic and microbiologic procedures to provide the evidence of acid fast bacilli in calcified remnants of pulmonary foci, proved to be eminently successful methods in the exploration of causes of senile tuberculosis and amyloidosis: Tuberculosis, after its invasion of the organism in early childhood, with its toxic and immunobiologic influences, holds it under its spell for an entire, even very long life and can be considered the most frequent cause of senile amyloidosis. 8. Chromosomal disturbances, with their hereditary manifestations, or, as in cases of mongoloid idiocy, associated with individual deformations, may present as amyloidoses. 9. Amyloid deposits in human pathology may develop by the transformation of normal structures, like cartilage, osteoid tissue, vascular elastic fibers, and also from scar hyalin and from fibrin. 10. We observed the disappearance of cerebral and cardiac amyloid accumulations producing typical defects. 11. Amyloidosis represents one of the most frequent spontaneous diseases of animals...
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PMID:[Amyloidosis as a manifestation and origin of presenile and senile degeneration]. 13 66

Infection of cells of the Epstein-Barr virus (EBV)-negative human B-lymphoma lines BJAB and Ramos with EBV preparations from P3HR-1 or B 95-8 cells converted these cells to EBV genome carriers expressing Epstein-Barr nuclear antigen (EBNA) in almost 100% of these cells. Induction of these cells as well as of clones from P3HR-1 EBV-converted BJAB cells with iododeoxyuridine, aminopterin, and hypoxanthine resulted in the appearance of a nuclear antigen in about 1-6% of the cells 1-4 days after induction. The antigen is different from known EBV-induced antigens like EBNA, viral capsid antigen (VCA) or the D- and R-subspecificities of the early antigen (EA) complex. It is demonstrated by indirect immunofluorescence and inactivated after acetone fixation. The antigen was not detectable after induction of uninfected BJAB and Ramos cells nor has it been found in noninduced or induced P3HR-1 and Raji cells. Thus, it appears that EBV-infection mediates the expression of this antigen, for which the name TINA (transiently induced nuclear antigen) is suggested. Sera reacting against TINA generally contained high antibody titers against EBV-induced EA. Only a limited number of highly EA-reactive sera, however, were also positive for TINA. Among 200 sera tested thus far, TINA reactivity was most frequently observed in sera of patients with nasopharyngeal carcinoma (7 out of 28), in sera of the only two patients with immunoblastoma tested and occasionally in sera from patients with Hodgkin's disease and chronic lymphatic leukemia. Among 70 sera from nontumor patients, TINA reactivity was observed three times: two patients suffered from "chronic" infectious mononucleosis, the other revealed persistent splenomegaly.
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PMID:Transient induction of a nuclear antigen unrelated to Epstein-Barr nuclear antigen in cells of two human B-lymphoma lines converted by Epstein-Barr virus. 18 13

Infection with Histoplasma capsulatum in 58 patients whose immune responses were suppressed (Immunosuppressed patients) (16 from the present series and 42 described previously) was analyzed. The most common underlying diseases were Hodgkin's disease (29 per cent), chronic lymphocytic leukemia (19 per cent) and acute lymphocytic leukemia (17 per cent). Sixty-three per cent of the patients had received cytotoxic drugs, and 57 per cent had taken corticosteroids. Widely disseminated infection occurred in 88 per cent of the patients, with predominant involvement of lungs and organs of the reticuloendothelial system. Localized pulmonary infection was present in the remaining patients. The most useful diagnostic method was bone marrow biopsy with microscopic examination for the intracellular yeast form of H. capsulatum. Biopsy of oral lesions, lung, liver and lymph node also proved diagnostically helpful. Growth of H. capsulatum in culture was frequently too slow to be beneficial in diagnosing histoplasmosis in ill patients. Serologic methods were of little diagnostic help in this population of immunosuppressed patients. The response to amphotericin B therapy was excellent (6.7 per cent mortality rate) in those patients in whom the diagnosis was established early and in whom a full course of antifungal therapy could be given. In contrast, the mortality rate in patients who received no antifungal therapy or less than 1 g of amphotericin B was 100 per cent.
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PMID:Histoplasmosis in immunosuppressed patients. 35 45

Retrospective evaluation of the occurrence of septicemia and meningitis in 200 children who had staging laparotomy iwth splenectomy for Hodgkin's disease revealed 20 episodes occurring in 18 children. Symptoms were usually fulminant; only 10 of these patients survived their episode. Infections occurred eight days to three years after splenectomy. Adolescents, as well as younger children, were affected; half were older than 10 years of age. Leukopenia was not a major factor in onset or survival since the average white-cell count was 12,000 in both survivors and children who died. Pneumonococcus accounted for 50 per cent, and streptococcus for 15 per cent of infections; there was one episode each of Haemophilus influenzae and meningococcus; in 25 per cent, no organism was isolated. Predominance of penicillin-sensitive organisms and high mortality suggest that penicillin prophylaxis and the protection offered by bacterial vaccines should be evaluated in children with Hodgkin's disease whose staging laparotomy includes splenectomy.
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PMID:Septicemia and meningitis in children splenectomized for hodgkin's disease. 95 75

Infections that occurrred in 92 previously untreated patients with Hodgkin's disease were reviewed from the time of laprotomy and splenectomy. Pneumonias occurred in nine patients with urinary tract infections in twelve during the immediate postoperative period. Severe bacterial infections did not occur in any patients during initial radiation therapy, adjuvant chemotherapy (stages I through IIIA), initial intensive chemotherapy (stages IIIB and IV) or during remission. Severe infections occurred in eight profoundly granulocytopenic patients with recurrent Hodgkin's disease. Streptococcus (Diplococcus) pneumoniae and Hemophilus spp infections were distinctly uncommon during the remission period. Herpes zoster, however, was very common developing in 22 of 92 (24 per cent) patients. Predisposing factors to herpes zoster included sex (female more than male), therapy (radiation plus chemotherapy more than chemotherapy alone), and age (less than 30 years of age more often than 30 to 50 years of age). Severe infection was uncommon in these patients except in ascociation with specific predisposing factors such as the immediate postoperative state of prolonged granulocytopenia associated with recurrent Hodgkin's disease or its therapy. Splenectomy per se did not affect either the incidence or the severity of infection during this period of 12+ months of observations per patient.
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PMID:Infections in 92 splenectomized patients with Hodgkin's disease. A clinical review. 120 37

We evaluated the efficacy and safety of piperacillin-pefloxacin potentially associated to vancomycin as a non nephrotoxic antimicrobial therapy in febrile neutropenic cancer patients, treated with nephrotoxic chemotherapy. Fifty-seven patients: 49 with solid tumors and 8 non-Hodgkin lymphomas, were treated during 85 episodes with: piperacillin 4 g IV every 8 h pefloxacin 400 mg IV every 12 h. If the patient remained febrile after 72 h, 1 g of vancomycin IV was added every 12 h. The mean duration of neutropenia was 7 days (3-14 days). In 44 episodes, the granulocyte nadir was < 100/mm3. Infection was microbiologically documented in 17 episodes (20%) with ten Gram-positive cocci and 11 Gram-negative bacilli. There were 64 apyrexia with piperacillin-pefloxacin (75%) and further 14 were resolved by the addition of vancomycin (total success = 92%); three early changes because of clinical deterioration (two episodes) or germ resistance (one episode); three protocol violations, and one apyrexia by addition of amphotericin. Neither septic death nor toxicity were observed. We conclude that this empirical treatment is active and safe and avoids nephrotoxicity in cancer patients heavily treated with nephrotoxic chemotherapy.
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PMID:[Value of the combination of piperacillin and pefloxacin possibly followed by vancomycin in the treatment of febrile neutropenia in nephrotoxic chemotherapy]. 146 96

To define the incidence and spectrum of pulmonary complications following autologous bone marrow transplantation (BMT), we retrospectively reviewed the course of 77 consecutive patients with Hodgkin's disease (HD) and non-Hodgkin's lymphoma (NHL) who failed conventional therapy and underwent autologous BMT. Forty-five percent of the 77 patients developed respiratory complications with a mortality from pulmonary causes of 26%. A total of 38 episodes of respiratory compromise occurred in 35 patients. Infections accounted for 15 episodes (39%) and included bacterial (16%), Aspergillus (8%) cytomegalovirus (8%), Herpes simplex (3%), and other (5%) pneumonias. The spectrum of infections was similar to that reported following allogeneic BMT, but cytomegalovirus pneumonia was not as frequent a problem in those with autologous transplant. Mortality from pulmonary infections was 33%. Noninfectious disorders accounted for 23 episodes (61%) and included recurrent HD (18%), radiation/drug toxicity (16%), and acute respiratory failure thought secondary to pulmonary alveolar hemorrhage (26%). This latter entity developed acutely within 2 wk following BMT and was associated with use of thoracic radiation for treatment of malignant disease in the chest just prior to BMT (p < 0.05). It was not associated with the age of the patient or presence of thrombocytopenia, coagulopathy, renal insufficiency or neutropenia (p NS). Mortality from noninfectious causes was 65%, but in those with pulmonary hemorrhage it was 100%. In conclusion, pulmonary complications are a major source of morbidity and mortality in patients with HD and NHL undergoing autologous BMT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary complications in lymphoma patients treated with high-dose therapy autologous bone marrow transplantation. 148 45

We evaluated the efficacy of piperacillin-pefloxacin as a non-nephrotoxic antibiotic combination in febrile neutropenic cancer patients treated with nephrotoxic chemotherapy. 40 patients: 34 with solid tumours and 6 with non-Hodgkin lymphoma, were treated during 55 episodes with: piperacillin 4 g intravenously every 8 h and pefloxacin 400 mg intravenously every 12 h. If the patient remained febrile after 72 h, 1 g vancomycin intravenously was added every 12 h. The mean duration of neutropenia was 7 days (range 3-13). Infection was microbiologically documented in 13 episodes (8 gram-positive cocci and 7 gram-negative bacilli). Temperature became normal in 38 patients with piperacillin-pefloxacin and 12 further episodes were resolved by the addition of vancomycin. 2 patients had an early change of antibiotics because of clinical deterioration, there were 2 protocol violations and 1 patient's temperature became normal after the addition of amphotericin. Neither septic death nor toxicity were observed. We conclude that this empirical treatment is active and safe and warrants further comparative trials.
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PMID:Non-nephrotoxic empiric antimicrobial therapy in febrile neutropenic cancer patients. 152 11

Infection by human immunodeficiency viruses (HIV) is associated with an increased incidence of non-Hodgkin's lymphomas (NHL) of B cell origin and of intermediate grade (diffuse large cell lymphomas according to the Working Formulation) or high grade (Kiel classification and Working Formulation). They may be either primary central nervous system lymphomas or systemic lymphomas and are considered as AIDS-defining events. Systemic lymphomas are usually disseminated with a high frequency of extranodal sites. Their overall prognosis is much worse than for NHL in the general population. Pathogenesis is still a matter of debate. An increased incidence of Hodgkin's diseases (HD) in HIV infection is being suspected but has not been proved yet. However, HIV-associated HD differ from usual HD by clinical presentation, histological type repartition, and evolution. Finally, low grade lymphomas have been described in HIV infection, the only peculiarity being the unusual age of occurrence.
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PMID:[Human immunodeficiency virus infection and malignant lymphoma]. 156 99


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