Infection among 210 patients with surgically staged Hodgkin's disease

Coker, Donald D.; Morris, Don M.; Coleman, John J.; Schimpff, Stephen C.; Wiernik, Peter H.; Elias, E. George

doi:10.1016/0002-9343(83)91173-7

Cited by 43 publications

(9 citation statements)

References 53 publications

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“…Individuals without a spleen run an increased risk of overwhelming infection with high case-fatality for several years after splenectomy (1,(3)(4)(5)(6)(7)(8)(9). More than half these severe infections are due to pneumococci.…”

Section: Discussionmentioning

confidence: 99%

“…Since the introduction of staging laparotomy with splenectomy in Hodgkin's disease patients in 1969, many reports have focused upon serious postsplenectomy infections (4)(5)(6)(7)(8)(9). When 145 reported postsplenectomy infections in 115 patients were reviewed (7), most cases presented as pneumonia, septicaemia, meningitis or combinations thereof, the most common offending organism being the pneumococcus.…”

Section: Foss Abrahamsen Et Almentioning

confidence: 99%

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Systemic pneumococcal disease after staging splenectomy for Hodgkin's disease 1969–1980 without pneumococcal vaccine protection: a follow‐up study 1994

Abrahamsen

Høiby

Hannisdal

et al. 1997

European J of Haematology

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We surveyed, during 1994, all 325 patients who underwent staging laparotomy with splenectomy for Hodgkin's disease in Norway 1969–80, before pneumococcal vaccine was available in this country. The patients were thus not immunized preoperatively. Of 162 patients (49.8%) who died before 1994, 8 (2.4% of the total study) died from pneumococcal septicaemia and 16 (6.2%) from infections totally. Of 163 patients (50.2%) who were alive in 1994, 158 cooperated and filled in a questionnaire: 22 had been hospitalized for serious infections; 2 with pneumococcal septicaemia, and 6 with pneumonia, although lacking a specified microbiological diagnosis. We observed 325 patients representing 4420 patient‐years, 3066 patient‐years among survivors and 1354 patient‐years among the dead. This resulted in an incidence rate of systemic pneumococcal disease of 226 per 100,000 patient‐years, which is a relative risk of 20.5 compared to the general Norwegian population during 1994. Septicaemia for these patients most often had an abrupt clinical start even for relapse‐free individuals and occurred from 2 to 17 yr after splenectomy (mean 10 yr). The risk of developing an overwhelming pneumococcal septicaemia with high case‐fatality in asplenic patients seems to persist for these patients at about the same level even 15–20 yr after splenectomy. Only 12.7% of the survivors had been given pneumococcal vaccine in the autumn of 1993. Despite the fact that medical journals and media in Norway focused upon the problem of pneumococcal disease in asplenic individuals in the autumn of 1993 and spring of 1994, a substantial proportion of these patients (55.3%) still remained unimmunized when interviewed in the autumn of 1994. None of our systemic pneumococcal disease patients was vaccinated. Our data underline the need for prophylactic immunization with effective vaccines against pneumococcal infection in splenectomized Hodgkin's disease patients.

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Section: Discussionmentioning

confidence: 99%

Section: Foss Abrahamsen Et Almentioning

confidence: 99%

Systemic pneumococcal disease after staging splenectomy for Hodgkin's disease 1969–1980 without pneumococcal vaccine protection: a follow‐up study 1994

Abrahamsen

Høiby

Hannisdal

et al. 1997

European J of Haematology

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“…2,3,7,11,12 In humans, the role of the spleen in sepsis has been well described. 13,14 Looareesuwan and others have studied the role of the spleen in another blood parasite infection (malaria). They suggested that the spleen may protect against human malaria by mediating humoral or cellular immune response or by clearing both rheologically and immunologically altered host erythrocytes.…”

Section: Discussionmentioning

confidence: 99%

Rhodesian trypanosomiasis in a splenectomized patient.

Malesker

Boken²,

Ruma³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

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Abstract. We report the first apparent case of a splenectomized individual who developed severe trypanosomiasis with central nervous system involvement. The patient was a 41-year-old man who participated in an east African safari. Upon his return to the United States, the patient presented with an infection with Trypanosoma brucei rhodesiense that was treated successfully with suramin and melarsoprol. The onset of symptoms, laboratory studies, and disease progression did not differ from previously reported cases in the literature. The role of the spleen in trypanosomiasis is not well understood and the few reports available describe only animal models. This report suggests that asplenia had no apparent effect on the onset of symptoms and overall severity of illness. Further studies are necessary to ultimately define the role of the spleen in trypanosomiasis.The acute form of African trypanosomiasis caused by Trypanosoma brucei rhodesiense occurs predominantly in east Africa, whereas the chronic form caused by T. b. gambiense occurs mainly in west and central Africa. Transmission is by the tsetse fly bite. 1,2 The incubation period for acute trypanosomiasis (T. brucei rhodesiense) ranges from 6 to 28 days. Infected travelers frequently become ill during their trips or shortly after returning. 3 Malaria also occurs commonly in Africa and the severity of presentation can be exacerbated by splenectomy. 4 We report a case of infection with T. b. rhodesiense with central nervous system involvement in a splenectomized American traveler and discuss the treatment of trypanosomiasis and the potential impact of asplenia. CASE REPORTThe case was a 41-year-old private investigator (height ϭ 198 cm, weight ϭ 92 kg) who recently returned from an African safari. His medical history included splenectomy in 1977 for Hodgkin's disease now in remission, as well as mild asthma, migraine headaches, hypothyroidism, and occasional sinusitis.He entered Africa on September 29, 1996 and hunted in Tanzania for cape buffalo where he sustained several painful tsetse fly bites. One bite on his left arm became moderately swollen several days later.He returned to the United States on October 5, 1996. Five days later, he developed weakness, headache, fever, chills, and sweats. Anorexia and weight loss of approximately 5 kg was noted. A trial of trimethoprim/sulfamethoxazole for presumed sinusitis failed. His temperature reached 104.4ЊF (40.2ЊC) and he became progressively lethargic and confused. On October 15, 1996, 10 days after his return to the United States, thick and thin blood smears revealed numerous trypanosomes.His admitting examination was remarkable for asthenia, fever, and a toxic appearance with moderate jaundice. On the left arm near the elbow there was a 3-cm, round, scaly, erythematous lesion with a small area of fluctuance in the center. Other healing insect bites were also noted. Regional lymphadenopathy was found in the left epitrochlear area.Other laboratory test abnormalities (normal ranges in parentheses) included a platele...

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“…The choice of therapy is also determined by the potential complications of laparotomy, namely, overwhelming sepsis (Coker et al, 1983), possible contribution towards the development of secondary leukaemia (Van Leeuwen et al, 1987), and delay in instituting radiation therapy. More data are becoming available to provide accurate predictions of the likely outcome of the operations in relation to presentation variables (Leibehaut et al, 1989;Tubiana et al, 1989), which may lessen the dilemma.…”

Section: Overallmentioning

confidence: 99%