Tumor necrosis factor alpha (TNF-alpha) is a cytokine, implicated in the pathogenesis of many inflammatory diseases, as well as in the immune-mediated response to infection, especially against intracellular pathogens. TNF-alpha antagonists have represented a revolution in the management of connective tissue diseases, such as rheumatoid arthritis. However, the use of these agents has been implicated with the emergence of a growing number of opportunistic infections. Here we report the case of a visceral Leishmaniasis in a 77-year-old woman who had been previously treated for rheumatoid arthritis with infliximab. The atypical presentation of this patient, previously treated with an anti-TNF-alpha biologic agent, where no splenomegaly or hepatomegaly was identified, is emphasized.
We report the case of a 22-year-old patient who presented to the emergency department with epigastric pain and vomiting. Haematological studies showed a rapid decrease in haemoglobin levels from 13.6g/dl to 4.9g/dl. Abdominal ultrasonography revealed the presence of fluid around the spleen and the patient was immediately referred for surgery. An intra-abdominal desmoid tumour presenting as a hemorrhagic shock has not previously been described. Given the relatively benign course of the disease and the young age at presentation, this clinical entity should not be overlooked as it has the potential to invade vessels and therefore be fatal. KEywORdSDesmoid -Aggressive fibromatosis -Hemorrhagic shock Case historyA 22-year-old woman presented to the emergency department with epigastric pain of 12 hours' duration and vomiting. On examination, the patient was afebrile with mild epigastric tenderness. Upper and lower abdominal ultrasounography was unremarkable. Initial haematological and biochemical parameters were normal except for leucocytosis (white blood count: 14,000 cells/mm 3 ). At the time of admission, the patient looked acutely ill, was pale and pulseless with severe epigastric and left upper abdominal quadrant tenderness. Serial haematological studies showed a rapid decrease in haemoglobin level from 13.6g/dl at presentation to 4.9g/dl one hour later. New abdominal ultrasonography was performed, which revealed the presence of fluid around the spleen. The patient was referred for surgery immediately. An area of bleeding behind the body of the pancreas was located. A splenectomy was performed as a lifesaving manoeuvre to maximise access to the bleeding area. Palpation revealed the presence of a 1.5cm x 0.5cm tumour strangulating the splenic artery and branches of the artery to the pancreas. Resection of the mass en bloc with a portion of the splenic artery was undertaken. Nine units of packed red blood cells and seven units of fresh frozen plasma were administered.The patient was discharged a few days later completely well. Follow-up magnetic resonance imaging at three months did not show any recurrence. It is noteworthy that the patient had no history of familial adenomatous polyposis syndrome.Histological examination revealed proliferation of myofibroblasts with a fasciculate and storiform growth pattern in a background of a mainly collagenous and focally myxoid intercellular matrix. The benign tumour entrapped part of the pancreas and infiltrated medium-sized arteries, replacing their smooth muscle cells (Fig 1). Recent haemorrhage between myofibroblasts was found with absence of haemosiderin laden macrophages, suggestive of a chronic haemorrhage. No pleomorphic, atypical or hyperchromatic nuclei were seen. Immunohistochemical staining showed granular cytoplasmic positivity and focal nuclear positivity for β-catenin. Immunohistochemistry for desmin, smooth muscle actin, CD117 and CD34 was negative. The proliferation marker Ki-67 stained approximately 2% of cells. These features were suggestive of dee...
24 patients with preleukaemia were cytogenetically studied by the G-banding staining technique. All patients developed later frank acute non-lymphocytic leukaemia and died. 13 patients had a completely normal karyotype ("-patients) with a median survival time of 8 months. 6 patients had both normal and abnormal metaphases (AN-patients) with a median survival time of 18.5 months, while 5 patients had abnormal metaphases only (AA-patients) with a median survival time d 3 months.
This case report concerns the diagnosis of two independent chronic diseases in a patient hospitalized for stroke, myasthenia gravis (MG) and giant cell arteritis (GCA). MG has been found to be associated with several diseases, but there are very few cases documenting its coexistence with GCA. We report the case of a 79-year-old woman initially hospitalized for stroke. Patient's concurrent symptoms of blepharoptosis, dysphagia, and proximal muscle weakness were strongly suggestive of myasthenia gravis. The persistent low-grade fever and elevated inflammatory markers in combination with the visual deterioration that developed also raised the suspicion of GCA. Histological examination confirmed GCA, while muscle acetylcholine receptor antibodies were also present. Even though in medicine one strives to interpret a patient's symptoms with one diagnosis, when one entity cannot fully interpret the clinical and laboratory findings, clinicians must consider the possibility of a second coexisting illness.
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