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BACKGROUND & AIMS: Undernutrition in home care and care home settings is an unrecognized problem with significant consequences. The present work was edited after a forum concerning nutrition in these settings was held in Brussels in order to tackle the problem. METHODS: Various aspects of the question were addressed with the participation of scientific experts. The proceedings of the forum were edited and completed by a review of previously published material. RESULTS: Prevalence of undernutrition in home care and care home settings varies between 15% and 65%. Causes of undernutrition are various: medical, social, environmental, organizational and financial. Lack of alertness of individuals, their relatives and health-care professionals play an important role. Undernutrition enhances the risk of infection, hospitalization, mortality and alter the quality of life. Moreover, undernutrition related-disease is an economic burden in most countries. Nutritional assessment should be part of routine global management. Nutritional support combined with physical training and an improved ambiance during meals is mandatory. Awareness, information and collaboration with all the stakeholders should facilitate implementation of nutritional strategies. CONCLUSIONS: Undernutrition in home care and care home settings is a considerable problem and measures should be taken to prevent and treat it.

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A 73-year-old obese woman underwent coronary artery-bypass operation in 11/1995 because of a coronary two vessel disease. The left coronary artery was bypassed by the left mammarial internal artery. In 2 and 3/2002, balloon-dilatation of stenoses of the right coronary artery and the circumflex was performed. Angina pectoris relapsed and in 9/2002 the patient was admitted to our hospital with tentative diagnosis of restenosis. Physical investigation showed a blood pressure of the right arm of 160/80 and of the left arm of 120/ 80 mmHg. Coronarography showed the three vessel disease known since 2/2002 with a restenosis of the right coronary artery which was immediately treated by balloon-dilatation and stent-implantation. Colour duplex-sonography of the carotid and subclavian arteries revealed extraordinary plaques and a reduced flow of the left vertebral artery. The left subclavian artery could only be seen distal to the discharge of the vertebral artery and showed a poststenotic flow. The patient had angina pectoris when carrying out personal hygiene already 2 days after balloon-dilatation and stent-implantation. ECG showed new aspects. Coronarography showed no relapse of stenosis, but 70% stenosis of the left subclavian artery with a marked coronary-steal-syndrome. In 10/ 2002, the patient underwent balloon-dilatation and stent-implantation of the subclavian stenosis and became free of complaints. Coronary-steal-syndrome can be the reason for persistent angina pectoris in spite of successful coronary artery-bypass operation with a mammarial internal bypass. It is absolutely necessary to take blood pressure from both arms to recognise a possible stenosis of the subclavian artery which can be the key to all.

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HISTORY: A 65-year-old woman had suffered from relapsing ventricular tachycardias (VT) since 1996. FINDINGS: Physical examination was normal. An arrhythmogenic substrate was found in the right ventricular outflow tract by electrophysiological examination. Nuclear magnetic resonance imaging (MRI) showed an infiltration of the right heart. Myocardial biopsy revealed a high-grade centroblastic non Hodgkin lymphoma. The patient was now transferred to our hospital for further treatment. Lactate dehydrogenase was elevated (2,030 U/l). Echocardiography showed a thickened and more reflecting right ventricular myocardium. Bone marrow aspiration and MRI/computed tomography of abdomen and thorax excluded a generalized stage. Ventricular tachycardias were caused by a primary cardiac lymphoma. TREATMENT AND COURSE: Combined radio-chemotherapy succeeded in complete remission. High-frequency ablation and amiodarone failed. Although MRI showed no more vital lymphoma after the combined radio-chemotherapy the patient suffered from spontaneous and symptomatic relapses of VT. Therefore this patient with primary cardiac lymphoma was the first in literature to get a defibrillator (ICD). The incidence of VT decreased and up to now the patient showed no relapse of the non Hodgkin lymphoma (follow-up 23 months).

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A 53-year-old female patient from the Philippines was admitted with intermittent complete heart block and assumed coronary artery disease. Physical examination was normal except for moist pulmonary sounds. ECG and monitoring showed bifascicular block and polymorphic ventricular tachycardia. A markedly reduced left ventricular function was seen in the echocardiogram. Coronary angiography showed two vessel disease. Endomyocardial biopsy revealed florid giant cell myocarditis. Heart failure and ventricular arrhythmias were ameliorated under immunosuppressive triple-therapy (corticosteroid, cyclosporin A, and azathioprine). Four weeks later, the patient received a cardiac transplant without complications. Two months later, a clinically inapparent cardiac rejection was diagnosed by endomyocardial biopsy, which was treated by corticoid pulse therapy and antithymocyteglobulin. Four weeks later, pneumocystis carinii pneumonia and cytomegaly virus exacerbation were diagnosed and successfully treated. Idiopathic giant cell myocarditis is a rare disease with progressive congestive heart failure and ventricular arrhythmias or complete heart block often accompanied by syncope or sudden death. Associations with autoimmune diseases have been reported. Giant cell myocarditis is diagnosed by endomyocardial biopsy or at autopsy. Treatment is difficult and comprises immunosuppressive agents (triple-therapy) and cardiac transplantation. Recurrence of giant cell myocarditis in cardiac transplants has been described. Without immunosuppressive treatment the median survival is three months.

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HISTORY AND ADMISSION FINDINGS: A 71-year old heavy smoker was admitted because of chest pain unrelated to physical activity, radiating into the left arm and neck as well as exertional dyspnoea and dizziness. Physical examination was unremarkable except for mild venous congestion over the upper part of the body. Myocardial infarction was excluded. A haemodynamically significant pericardial effusion developed a few days later and required emergency pericardiocentesis. INVESTIGATIONS: Laboratory tests indicated marked inflammatory disease. Echocardiography demonstrated the pericardial effusion. Needle aspiration revealed coagulase-negative staphylococcus and plant cells. Chest X-ray showed a pneumopericardium. Computed thoracic tomography suggested malignant tumour of the oesophagus with spread to the surrounding lymph nodes and pericardial fistula. Proximal endoscopy showed a highly malignant looking ulcer, 30 cm in diameter, in the anterior wall of the oesophagus with a central fistula. The endoscopic biopsy indicated a poorly differentiated non-cornified squamous cell carcinoma. TREATMENT AND COURSE: An uncovered self-expanding metal stent was placed into the fistula, whereupon the perimyocarditis quickly healed. When the patient was discharged he was able to take food by mouth and the signs of inflammation subsided. He died at home 6 weeks later. CONCLUSION: An oesophageal carcinoma with fistula should be included in the differential diagnosis of purulent pericardial effusion even in the absence of dysphagia. Implantation of a self-expanding metal stent into the fistula is the treatment of choice for palliation.

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BACKGROUND: Fibrin deposition and thrombosis have been implicated in both allograft rejection and vasculopathy after cardiac transplantation. Because monocytes play a pivotal role in the pathophysiology of intravascular coagulation activation through their ability to synthesize tissue factor (TF), we asked (1) whether monocyte TF activation occurs in cardiac transplant recipients and (2) whether monocyte TF expression is affected by treatment with cyclosporin A (CsA). METHODS AND RESULTS: We measured levels of TF activity in peripheral blood mononuclear cells and highly purified monocytes/macrophages from 10 consecutive cardiac transplant recipients and 10 healthy control subjects. TF activity generated by both unstimulated and endotoxin-stimulated cells was significantly higher in transplant recipients than in control subjects (P<.05). Increased monocyte TF expression in transplant recipients was shown to be adversely affected by treatment with CsA: TF induction was markedly reduced by CsA serum concentrations reaching peak CsA drug levels. Inhibition of TF induction in the presence of high CsA blood concentrations was also observed when stimulation of cells was performed with interferon-gamma or interleukin-1beta. As shown by reverse transcription-polymerase chain reaction and electrophoretic mobility shift assay, respectively, treatment with CsA leads to decreased TF mRNA expression and reduced activation of the NF-kappaB transcription factor, which is known to contribute to the induction of the TF promotor in human monocytes. CONCLUSIONS: This study demonstrates that TF activation, occurring in mononuclear cells of cardiac transplant recipients, is inhibited by treatment with CsA. Inhibition of monocyte TF induction by CsA may contribute to its successful use in cardiac transplant medicine and might be useful in managing further settings of vascular pathology also known to involve TF expression and NF-kappaB activation.

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BACKGROUND AND DESIGN: Since patients with cutaneous T-cell lymphoma (CTCL) demonstrate several immunologic abnormalities such as elevated serum immunoglobulin levels or reduced natural killer cell activity, we analyzed functional properties of the peripheral blood mononuclear cells in patients with nonleukemic CTCL and healthy donors. RESULTS: After priming with phytohemagglutinin for 3 days, a reduced proliferation in the presence of interleukin 2 and interleukin 4 was found. Limiting dilution technique revealed a diminished number of peripheral blood mononuclear cells from patients with CTCL that were capable of proliferating on interleukin 2 but not on interleukin 4 stimulation. Phytohemagglutinin induced a significantly higher release of interleukin 4 (mean +/- SD, 196 +/- 149.8 pg/mL [n = 19] vs 76.4 +/- 16.4 pg/mL [n = 248]) and a significantly lower secretion of interferon-gamma (24.9 +/- 30.7 U/mL [n = 17] vs 47.5 +/- 43.5 U/mL [n = 18]) in the peripheral blood mononuclear cells of patients with CTCL compared with the peripheral blood mononuclear cells of healthy donors (P < or = .02, U test). CONCLUSION: These functional characteristics can be explained by an imbalanced T helper-1/T helper-2 system and allow speculations concerning clinical features such as elevated immunoglobulin serum levels and reduced cytotoxic activity in patients with CTCL.

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