Toxic megacolon and perforation caused by Salmonella.
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Biomedical subjects
Publications and source records attributed to J Davson.
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A retrospective and comparative study of 127 case reports of Meleney's postoperative progressive synergistic gangrene and of 62 examples of postoperative amoebic skin gangrene, showed that these two entities were clinically indistinguishable and that therefore a purely clinical diagnosis of Meleney's gangrene could not be made. Furthermore, a critical appraisal of the bacteriological data indicated that a certain diagnosis of Meleney's gangrene cannot be provided by the clinical bacteriologist. Finally, the histological features were entirely non-specific thus precluding a definitive diagnosis by the histopathologist. If Meleney's entity cannot be diagnosed its existence becomes debatable. The alternative diagnosis of cutaneous amoebiasis is advanced for consideration. Several of the outstanding features of Meleney's progressive gangrene, hitherto unexplained, are better understood if Entamoeba histolytica is accepted as the prime cause rather than bacteria.
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A 15-year-old male developed features of Still's disease. He was treated, with incomplete response, with aspirin and corticosteroids. Some 10 months after the onset he contracted chickenpox and became gravely ill. A diagnosis of histiocytic medullary reticulosis was made because erythrophagocytic histiocytes were detected in marrow aspirate films. Necropsy studies showed systemic infiltration by benign-appearing histiocytes and led to the final diagnosis of the virus-associated haemophagocytic syndrome due to varicella-zoster infection in an immunocompromised patient.
On the basis of the trephine marrow histology at presentation, 52 Ph1 positive cases of chronic myeloid leukaemia were divided into two subgroups, classical chronic granulocytic leukaemia (CGL) and chronic megakaryocytic granulocytic myelosis (CMGM). In 24 cases in which conventional therapy had preceded trephine biopsy, the distribution of cases between the two groups was found to have been significantly altered. Subsequent analysis was therefore confined to the remaining 28 untreated cases; of these 15 were classified as CGL and 13 as CMGM; no statistically significant difference was found between the two groups in respect of patient's age, leucocyte counts, platelet counts, NAP scores or of occurrence of 'blast' crisis. The differential diagnosis between idiopathic myelofibrosis (IMF) and CMGM subgroup is discussed. It was concluded that classification of chronic myeloid leukaemia on the basis of marrow histology should be restricted to Ph1 positive cases in order to obviate the possible inclusion of cases of IMF within the CMGM subgroup.
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A survey of the Western literature of histiocytic medullary reticulosis (malignant histiocytosis) provided 104 case reports with sufficient data from which the presence or absence of an absolute lymphopenia could be ascertained. Of these, 46 (44%) were lymphopenic at presentation or within the subsequent 10 days. A survey of a series of publications containing detailed peripheral leucocyte counts recorded in patients with diseases that, like HMR, may present with, or develop, pancytopenia showed that the incidence of lymphopenia ranged from 14% (Hodgkin's: stages I & II) to 46% (acute myelofibrosis; systemic lupus erythematosus; angio-immunoblastic lymphadenopathy). It was concluded a that HMR should be added to the list of accepted causes of lymphopenia, b that lymphopenia, as an aid to the diagnosis of HMR, will be of limited value, c that when the peripheral leucocyte count of a patient is recorded in a case report, it should be accompanied by a full differential count.
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A case of systemic mastocytosis is described in which the finding on initial presentation was hepatosplenomegaly. No dermatological abnormality was present, and the bone marrow histology originally caused some confusion with primary myelofibrosis. The clinical course and the importance of distinguishing between these two diseases is discussed. The dermatological manifestation of systemic mastocytosis, in the form of urticaria pigmentosa, is well recognised, and alerts the physician to the underlying disease. In the absence of cutaneous signs, however, the diagnosis is less obvious. The case reported had predominantly marrow and splenic involvement by the disease process, giving rise to portal hypertension, and illustrates the problems of diagnosis which can arise.
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Serial trephine biopsies were performed in 45 cases of chronic granulocytic leukaemia (CGL) in order to determine the frequency and significance of secondary myelofibrosis in the evolution of the disease. Histological changes were graded 1-5b, ranging from no increase in reticulin to dense osteomyelosclerosis. Many cases showed a progressive increase from Grade 1 to Grade 3, and accelerated disease, or blast crisis, often supervened when Grade 3 changes were present. However, a significant number of cases showed Grade 4 and 5 changes, which were indistinguishable histologically from those found in agnogenic myeloid metaplasia (AMM) (idiopathic myelofibrosis), at the time of diagnosis. These patients did not always show a rapidly fatal course and may be considered as an example of 'transitional myeloproliferative disorder', with features intermediate between CGL and AMM.
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