Thrombotic thrombocytopenic purpura (TTP) is a rare disorder characterized by microangiopathic haemolytic anemia, consumption thrombocytopenia, renal impairment, neurological dysfunction, and fever, but all these features are not present in every patient. Although the prognosis of TTP has improved since it was demonstrated that large volumes of fresh frozen plasma (FFP) lead to a remission in most patients, the disease remains fatal in many instances. Therefore, other therapies are often used in TTP, but there is skepticism about their value, since such treatments are often used in combination, making evaluation difficult. This report describes three patients with TTP and a consistent therapeutic response occurring 5 days after vincristine in each of four instances.

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SummaryA 29-year-old man with asthma presenting as right sided congestive cardiac failure is reported. There was rapid resolution of the heart failure with standard bronchodilator therapy and corticosteroid therapy.KEY WORDS: asthma, cor pulmonale.Cor pulmonale is a well recognized and common sequela ofchronic airflow obstruction. It must be rare as a presenting symptom in asthma and has not to our knowledge been previously reported. Case reportA 29-year-old male, non-smoking farmer was admitted with a 5-week history of progressive swelling of the legs. On direct questioning, he admitted to a productive cough, mild dyspnoea and wheezing since his early teens. He gave no history of chest pain or haemoptysis and denied any recent deterioration in his breathing, although his family noticed that he was frequently incapacitated by breathlessness. He was taking no medication and had visited his general practitioner only once before with 'bronchitis' at the age of 12 years.On examination he was breathless, plethoric and cyanosed but had no finger clubbing. The pulse rate was 140/min, jugular venous pressure elevated and there was pitting oedema to his upper thighs. Bilateral expiratory rhonchi were heard and the liver was palpable 4 cm below the costal margin.On admission the forced expiratory volume in the first second (FEV,) was 10 litre and forced vital capacity (FVC) was 3-1 litre, improving to 16 and 3-8 litre respectively 15 min after 5 mg nebulized salbutamol. An electrocardiogram (ECG) showed right axis deviation and evidence of right ventricular hypertrophy. The chest X-ray showed cardiomegaly and hyperinflation of the lung fields.Arterial blood gases showed pH of 7-3 1, Po2 of 4-3 kPa and a Pco2 of 6-7 kPa. Haemoglobin was 20-2 g/dl with a haematocrit of 60%o. The sputum was purulent, growing Streptococcus pneumoniae and Haemophilus influenzae. Further investigations including farmers' lung and aspergillus precipitins were negative and an isotope lung scan showed no evidence of pulmonary embolus.He was treated with continuous 24% oxygen, prednisolone, nebulized salbutamol, diuretics and an antibiotic. He was venesected 1500 ml of blood.He rapidly improved and, on discharge 10 days later, he was oedema free and taking salbutamol 200 Ag and beclomethasone dipropionate 100 ,ug by inhaler four times a day and a reducing regime of prednisolone.Three weeks later, he was reviewed when he was asymptomatic, had stopped the prednisolone and his FEV,/FVC had increased to 3-65/4 65. His haemoglobin had fallen to 16 g/dl with a haematocrit of 51%. The chest X-ray had returned to normal.Since then his symptoms have been controlled by regular use of salbutamol and beclomethasone dipropionate by inhaler and a salbutamol spandet at night. When seen 3 months after admission he was well, at work and had a normal ECG, haemoglobin and chest X-ray. DiscussionCor pulmonale is common in severe chronic airflow obstruction after prolonged hypoxia. It is often accompanied by polycythaemia (Crofton and Douglas, 1975). These changes a...

Objectives In type 2 diabetes (T2DM), low dose Aspirin has been established for secondary cardiovascular prevention, but as yet there is no definitive data showing primary cardiovascular prevention. We hypothesized that a double dose of ASA would further reduce platelet reactivity and, given the increased platelet turnover, may be most effective when given in divided doses twice-daily. Methods This 3-period, 3-treatment, crossover study randomized 24 adults (51 ± 7 years old, BMI 31.4 ± 7.2 kg/m2, HbA1c 47 ± 7 mmol/mol) with T2DM and no prior cardiovascular disease to 2-week treatment periods with single (100 mg once-daily), double (200 mg once-daily) or split (100 mg twice-daily) ASA doses, with intervening 2 week washout periods. A generalized linear mixed model with random subject effect was used to estimate the dose response of platelet reactivity using Verify Now ASA™ as the primary outcome. Results ASA at all doses significantly reduced platelet reactivity measured by all platelet function tests except PFA-100 CADP. Verify Now ASA™ was decreased significantly from baseline 650.0 ± 19.4 aspirin reaction units (ARU) to 447.6 ± 68.1 ARU with single dose (p<0.0001), 430.1 ± 64.6 ARU with double dose (p<0.0001), and 416.4 ± 38.5 ARU with split dose (p<0.0001) aspirin. After fitting the model, Verify Now ASA™ was reduced to a greater extent with split dose compared with single dose ASA (p = 0.043), but did not differ significantly for single versus double dose (p = 0.20) or double versus split dose (p = 0.44). Split dose was also more effective compared to single dose, as measured by PFA-100™ CEPI (p = 0.031) and urinary thromboxane (p = 0.048) with a trend toward reduced reactivity measured by serum thromboxane (p = 0.055). Both high (p = 0.0043) and split (p<0.0001) doses were more effective than low dose ASA at reducing AA-induced Multiplate™ aggregation. No significant differences between ASA doses were seen for LTA (AA and ADP) or PFA-100™ CADP. Conclusions ASA 100 mg given twice-daily was numerically the most effective regimen for reducing platelet reactivity as measured by platelet function tests, but future clinical outcome trials are required to confirm whether ASA 100 mg twice-daily will reduce the risk of primary cardiovascular events in patients with T2DM. Clinical Trial Registration: 2011-003123-35 (need to list URL for EUDRACT website)