Cases reported "Sepsis"

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1/75. parathyroid hormone-related protein (PTH-rP)-associated hypercalcemia in a patient with an atypical chronic lymphocytic leukemia.

    We describe a patient with an atypical chronic lymphocytic leukemia (CLL) of the mixed cell type with a hypercalcemia due to parathyroid hormone-related protein production by the malignant B cells. On regard of the elevated serum calcium level without overt lytic bone lesions we found elevated serum levels of PTH-rP and demonstrated the presence of PTH-rP on the malignant lymphocytes. PTH-rP-related hypercalcemia in CLL is very rare. The role in PTH-rP in humoral hypercalcemia of malignancy is discussed.
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2/75. Autoimmune enteropathy with distinct mucosal features in T-cell activation deficiency: the contribution of T cells to the mucosal lesion.

    BACKGROUND: Autoimmune enteropathy is normally characterised by crypt hyperplastic villous atrophy with enterocyte autoantibodies, activation of mucosal lymphocytes and increased epithelial HLA-DR. This case involved a severely affected Portuguese infant who was found to have lymphocyte activation deficiency and demonstrated correspondingly distinct mucosal features. methods: A female infant of nonconsanguineous parents was treated for vomiting and diarrhoea, first with milk exclusion and then with parenteral nutrition. lymphocyte subsets and immunoglobulin concentrations were normal, but in vitro testing showed no activation in response to phytohaemagglutinin, candida, or purified protein derivative, although the response to interleukin (IL)-2 was intact. interleukin-2 deficiency was excluded. Analysis of jejunal biopsy specimens revealed only mild villous blunting with absent goblet cells, normal epithelial proliferation, and no crypt hyperplasia. The dense infiltrate of CD8 and CD4 T lymphocytes showed normal CD2 and CD3 expression but no activation or proliferation markers. HLA-DR was not increased on epithelium or lymphocytes. Thus, in addition to in vitro evidence for lymphocyte activation deficiency, the mucosal specimens showed no evidence of in situ T-cell activation. RESULTS: After development of overwhelming septicaemia, the patient died at 18 months, just before a planned bone marrow transplant. CONCLUSIONS: These findings confirm significant heterogeneity within autoimmune enteropathy. Formal immune function testing should be performed in all affected infants to identify T-cell activation deficiencies. The distinct mucosal findings suggest that activated T cells usually induce the crypt hyperplastic villous atrophy characteristic of classic autoimmune enteropathy.
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3/75. Staged operative treatment in a septic patient with an infected, unstable pelvis, and a missed bladder rupture.

    This case demonstrates once again the potential and serious complications of pelvic fractures, especially when associated urogenital injuries are missed. Missing the bladder rupture proved almost fatal to our patient. Second, it was confirmed that in very unstable pelvic fractures, external fixation alone does not provide enough stability. Local stability is the cornerstone in the treatment of (bone) infection, and in these cases, maximal stability is only obtainable with internal fixation. The advantages of metal implants in infected areas outweigh the disadvantages by far. For the bladder-rupture, we chose a two-stage approach. First, we performed a urinary diversion, to avoid surgical closure of the infiltrated bladder wall. All cavities, including the open bladder, were packed with omentum to fill the dead space with highly vital tissue to offer stout resistance to infection. Two years later, with the patient in excellent physical condition, urinary undiversion was carried out. Ultimately physical and social recovery was complete.
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4/75. mycobacterium tuberculosis infection in allogeneic bone marrow transplantation patients.

    Bone marrow transplant (BMT) recipients are prone to bacterial, viral and fungal infections. mycobacterium tuberculosis infection can occur in these patients, but the incidence is lower than that of other infections. This report describes four patients with mycobacterium tuberculosis infection identified from 641 adult patients who received a BMT over a 12-year period (prevalence 0.6%). The pre-transplant diagnosis was AML in two patients and CML in the other two. Pre-transplant conditioning consisted of BU/CY in three patients and CY/TBI in one. Graft-versus-host disease (GVHD) prophylaxis was MTX/CsA in three patients and T cell depletion of the graft in one patient. Sites of infection were lung (two), spine (one) and central nervous system (one). Onset of infection ranged from 120 days to 20 months post BMT. Two patients had co-existing CMV infection. One patient had graft failure. The two patients who received anti-tuberculous (TB) therapy recovered from the infection. Although the incidence of tuberculosis in BMT patients is not as high as in patients with solid organ transplants, late diagnosis due to the slow growth of the bacterium can lead to delay in instituting anti-TB therapy. A high index of suspicion should be maintained, particularly in endemic areas.
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5/75. Marked histiocytosis in the portal tract in a patient with reactive hemophagocytic syndrome: An autopsy case.

    We report an autopsy case of reactive hemophagocytic syndrome with peculiar liver histology. A 71-year-old female was diagnosed as having acute myelogenous leukemia and treated with chemotherapy. During her course, methicillin-resistant staphylococcus aureus (MRSA) was noted in blood culture and she was diagnosed as having MRSA sepsis. She died of respiratory failure 5 months after the onset of leukemia and 10 days after the MRSA sepsis. Ante-mortem liver function tests were within normal ranges. At autopsy, myeloblastic leukemia cells positive for CD13 were present in the bone marrow and, to a much lesser extent, in the spleen and liver. Numerous histiocytes of a bland appearance with erythrophagocytosis were noted in the bone marrow and spleen. The histiocytes were positive for CD68, but negative for S-100 and lysozymes. In the liver, many histiocytes of bland appearance with erythrophagocytosis and CD68 positivity were present in the portal tracts with no Kupffer cell hyperplasia. There were no hepatocellular degeneration, fatty changes or sinusoidal dilations. We consider that this histiocytosis was associated with MRSA infection and diagnosed this as infection-associated hemophagocytic syndrome. In previously reported cases, hemophagocytosis in hyperplastic kupffer cells was the main liver change of reactive hemophagocytic syndrome. The present case suggests that marked histiocytosis in portal tracts only may be a main feature of liver changes in reactive hemophagocytic syndrome and that such cases may not show abnormal liver function tests.
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6/75. Congenital neutropenia. Report of a case and a biorationale for dental management.

    Congenital neutropenia is characterized by a marked decrease in or lack of circulating PMN's in children with no prior history of drug intake. The neutropenia is persistent and the clinical course is one of early onset of severe, recurrent, and eventually fatal infections. Bone marrow studies show a maturation arrest of neutrophilic precursors. Because of their greatly increased susceptibility to infection, patients with congenital neutropenia present a difficult dental management problem. A case of congenital neutropenia has been presented, as well as a biorationale for dental treatment. On the basis of reports in the literature, the following recommendations for the management of patients with congenital neutropenia are made: 1. The prevention and control of infection and the interception of dental disease before surgical intervention becomes necessary should be the overriding considerations in the management of patients with congenital neutropenia. 2. The carious breakdown of teeth should be prevented by the daily application of a 0.4 per cent stannous fluoride gel in addition to oral hygiene and limitation of sucrose intake. 3. Periodontal therapy should be palliative only, since alveolar bone loss is progressive despite frequent oral hygiene instruction and prophylaxis. The goal of periodontal therapy for patients with congenital neutropenia should therefore be a decrease in gingival inflammation to make the patient's mouth more comfortable and to slow down alveolar bone loss. Periodontal surgery is contraindicated. 4. bacteremia and subsequent septicemia should be prevented since a minor infection can become life threatening in patients with congenital neutropenia. The patient should rinse for 30 seconds and the gingival sulci should be irrigated with a phenolated antiseptic mouthwash prior to all dental manipulations of the soft tissue. This will significantly reduce the incidence of bacteremia. 5. Surgery should be avoided if at all possible because of the high risk of post-operative infection. All surgery sholld be performed in the hospital, and the patient should be given antibiotics as determined by his physician. Primary closure should be done with fine polyglycolic acid sutures to reduce the chance of infection. If postoperative infection can be prevented, wound healing will progress normally despite the complete absence of PMN's.
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7/75. Splenic lymphoma presenting as warm autoimmune hemolytic anemia associated with pure red cell aplasia.

    BACKGROUND AND OBJECTIVE: Warm autoimmune hemolytic anemia (AIHA) is a condition in which peripheral red blood cell (RBC) destruction is induced by the presence of an autoantibody. Pure red cell aplasia (PRCA) represents an isolated process of decreased erythropoiesis. The combination of both is quite rare, with a very poor prognosis. We describe a patient with isolated splenic lymphoma whose presentation was a combination of AIHA and PRCA. The patient was resistant to all treatment. MATERIALS AND methods: Erythroid colony assays were performed, in order to compare the effect of the patient's serum on colonies with that of a normal control. RESULTS: The patient's serum significantly suppressed normal erythroid colony growth. A red cell eluate revealed the presence of a warm autoantibody. CONCLUSIONS: The patient's serum contained warm autoantibody responsible for peripheral RBC destruction and a humoral factor, perhaps the warm autoantibody, which suppressed bone marrow erythropoiesis. Establishing an early diagnosis, and treatment of the underlying disease might result in a better prognosis.
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8/75. Severe disseminated BCG infection in an 8-year-old girl.

    An 8-year-old girl died of sepsis due to staphylococcal infection one year and 8 months after Bacille Calmette-Guerin (BCG) revaccination. Two months after the vaccination in accordance with the school health program, she was hospitalized with a high fever, skin rash over the face and lower limbs, and leukopenia. Her clinical and laboratory pictures were not compatible with those of any established type of immunodeficiency. The polymerase chain reaction (PCR) test for M. tuberculosis complex was positive for bone marrow, pleural fluid, and peripheral blood. The strain recovered from a mycobacterial culture of the blood was identical to the BCG strains with which the patient was vaccinated, based on restriction fragment length polymorphism (RFLP) and a pulse-field gel electrophoresis (PFGE) analyses of dna. She developed finally a lung abscess due to staphylococcal septicemia, which was the direct cause of her death.
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9/75. The Ilizarov method for failed knee arthrodesis following septic TKR.

    knee arthrodesis is a well-recognized salvage procedure in patients with infected total knee arthroplasties. If a fusion is achieved, it offers the opportunity for a stable lower limb and eradication of infection, but at the expense of knee motion. However, knee arthrodesis in this setting may be difficult to achieve because of poor bone stock, persistent infection, soft tissue compromise, and often the poor general health of the patient. We report two cases of failed knee arthrodesis following periprosthetic infection where a fusion was successfully achieved with open debridement and a hybrid advanced Ilizarov fixator.
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10/75. listeria monocytogenes tricuspid valve endocarditis with septic pulmonary emboli in a liver transplant recipient.

    listeria monocytogenes has long been known as a pathogen of immunocompromised hosts, including solid organ and bone marrow transplant recipients. Its principal manifestations include bacteremia and meningitis. endocarditis due to Listeria is far less common and in general affects the left side of the heart. We here report an unusual case of Listeria tricuspid valve endocarditis and septic pulmonary emboli in a sulfa-intolerant liver transplant recipient with a history of relapsing cytomegalovirus (CMV) hepatitis and an indwelling Hickman catheter. The literature on Listeria endocarditis and infections in transplant recipients is reviewed. The possible relationship between susceptibility to Listeria infection and the discontinuation of trimethoprim-sulfamethoxazole prophylaxis is of interest.
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