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A 77-year-old man with dyspnoea was suspected to have a decompensatio cordis by the general practitioner. A diuretic was prescribed. Additional radiological and laboratory investigation (e.g. natriuretic peptides and D-dimers) showed pulmonary embolism instead of heart failure. A second patient, a woman aged 79 years, with a history of leukaemic mantle cell lymphoma, was treated with poly-chemotherapy (R-CHOP), after which remission was achieved. Four years later the lymphoma recurred and R-CHOP treatment was started. However this was without success, after which R-CHOP treatment was repeated. Subsequently the patient developed dyspnoea and pneumonia. Following additional radiological and laboratory investigation (e.g. natriuretic peptides) the patient was finally diagnosed with doxorubicin-induced heart failure. Based upon these case studies, the role of brain-natriuretic peptides in the differential diagnostic work-up of dyspnoea is highlighted. Test performance, correlation with disease, monitoring, prognostics, differential diagnostic power, reference values and pitfalls of brain natriuretic peptides are discussed.

A 71-year-old man with deep venous thrombosis treated with fenprocoumon presented after a trauma with a haematoma due to an INR > 8.0, and later with haemorrhagic bullae, due to venous obstruction.

A woman aged 35 years presented with a haemarthros of the left elbow 6 months after her first parturition due to acquired haemophilia A. The bleeding episodes were mild and treated with recombinant activated factor VII. Because of the mild bleeding tendency and the chance of spontaneous remission it was decided to withhold immunosuppressive treatment. During the course of one year, the factor VIII level and the activated partial thromboplastin time (APTT) normalized and the autoantibodies disappeared. Four years after her first parturition, she had an uncomplicated pregnancy and the postpartum period was uneventful. Up to fourteen months postpartum, there are no signs of recurrence of the acquired haemophilia A. Acquired haemophilia A post partum usually presents in the first 3 months post partum. Frequently presenting symptoms are haemorrhages post partum, menorrhagia, soft-tissue haemorrhages and haemorrhages during surgical procedures. As a rule, the haemorrhages are slight. The titers of blocking antibodies are low in comparison with the titers in congenital haemophilia A.

In a 64-year-old white male with abdominal pain, fever, diarrhoea and weight loss there were radiological signs of mesenteric panniculitis: thickening of the small bowel loops, an infiltrate above the bladder and in the lower right abdomen an ileum loop with a spiculated border, and streaky strands emanating from the mesenteric fat in the lower abdomen. The clinical signs resolved spontaneously with conservative treatment in 3 weeks and after 3 months the radiological abnormalities had disappeared completely. The pathogenesis of mesenteric panniculitis is unknown. The prognosis is favourable. In advanced cases of the disease, anti-inflammatory or immunosuppressive medication may be beneficial.

Elevated levels of serum cobalamin may be a sign of a serious, even life-threatening, disease. Diseases such as chronic myeloid leukaemia, promyelocytic leukaemia, polycythaemia vera and hypereosinophilic syndrome are often accompanied by markedly elevated levels of cobalamin in the blood. A rise in the serum cobalamin concentration is one of the diagnostic criteria for polycythaemia vera and hypereosinophilic syndrome. In haematological disorders, the increase in circulating cobalamin levels is predominantly caused by enhanced production of haptocorrin. Several liver diseases such as acute hepatitis, cirrhosis of the liver, hepatocellular carcinoma and metastatic liver disease can also be accompanied by an increase in circulating cobalamin. In liver diseases, the increase in cobalamin is predominantly caused by cobalamin release during hepatic cytolysis and/or through decreased clearance of circulating cobalamin by the affected liver. Liver disorders are not an indication for determining the serum cobalamin concentration. However, a coincidentally observed elevated serum cobalamin concentration is reason for further investigation.

A 65-year-old woman developed haemorrhagic diathesis due to a profound thrombocytopenia (thrombocyte count: 1 x 10(9)/l) within one week after a 10-day course of norfloxacin (2 x 400 mg/day), prescribed for cystitis. On account of increased megakaryopoiesis in the bone marrow and absence of other causes of thrombocytopenia norfloxacin-induced immune thrombocytopenia was diagnosed. No norfloxacin-dependent antibodies against platelets were detected. Treatment with prednisone (1.5 mg/kg/day) resulted in the normalization of the platelet count within 5 days.

A 40-year-old man developed cortical blindness during cyclosporin treatment shortly after an allogeneic bone marrow transplantation for chronic myeloid leukaemia. At that time the patient had a therapeutic cyclosporin blood level (226 ng/ml), but a low serum magnesium level and a marginally decreased serum cholesterol level. In addition the patient had hypertension, headache and paraesthesia in the oral, palmar and plantar areas. Vision was fully recovered after discontinuation of the cyclosporin treatment and correction of the hypomagnesaemia. Eighteen cases of cortical blindness during cyclosporin treatment are now known in the literature. Hypomagnesaemia appears to be implicated in the pathogenesis.

Peripheral blood stem cells can reconstitute bone marrow function after high-dose chemo-/radiotherapy. We describe 17 patients treated with a three-day course of chemotherapy consisting of cyclophosphamide or ifosfamide and etoposide (malignant lymphoma and germ cell tumor) or a one-day course of 5-fluorouracil, epidoxorubicin and cyclophosphamide (breast cancer), followed by the administration of recombinant human granulocyte colony-stimulating factor (G-CSF). Maximum numbers of peripheral blood stem cells were recruited on day 9-10 of the G-CSF administration with 0.1 x 10(9)/l CD34+ cells (median; range 0-0.36). The total number of peripheral stem cells harvested with two-three leukaphereses was 40 x 10(4)/kg CFU-GM (4-257) or 8 x 10(6)/kg CD34+ cells (1-39). Ten patients with malignant lymphoma or solid tumours received high-dose chemotherapy followed by bone marrow and peripheral stem cell infusion (n = 7) or peripheral stem cell infusion alone (n = 3). The recovery of granulocytes, platelets and reticulocytes after peripheral stem cell infusion, in addition to or instead of bone marrow, was markedly accelerated compared with the infusion of BM alone. The accelerated haemopoietic recovery was associated with a reduction in platelet and red blood cell transfusion, reduction in fever periods and earlier discharge from hospital. Peripheral stem cell transplantation may become an important alternative to autologous bone marrow transplantation. This transplantation technique may also allow application of multiple-cycle intensive chemotherapy.