Dietary factors and hyperuricaemia

The connection of gout and hyperuricaemia with gluttony, overindulgence in food and alcohol and obesity dates from ancient times. Studies from different parts of the world suggest that the incidence and severity of hyperuricaemia and gout may be increasing. Uric acid (urate) is the end product of purine degradation. Although most uric acid is derived from the metabolism of endogenous purine, eating foods rich in purines contributes to the total pool of uric acid. Sustained hyperuricaemia is a risk factor for acute gouty arthritis, chronic tophaceous gout, renal stones and possibly cardiovascular events and mortality. Before starting lifelong urate-lowering drug therapy, it is important to identify and treat underlying disorders that may be contributing to hyperuricaemia. It is relevant to recognize the strong association of the insulin resistance syndrome (IRS) (abdominal obesity, dyslipidaemia, hypertension, raised serum insulin levels and glucose intolerance) with hyperuricaemia. Consumption of meat, seafood and alcoholic beverages in moderation and attention to food portion size is important. Moderation in the consumption of not only beer but also other forms of alcohol is essential. In the obese, controlled weight management has the potential to lower serum urate in a quantitatively similar way to relatively unpalatable "low purine" diets. Non-fat milk and low-fat yogurt have a variety of health benefits and dairy products may have clinically meaningful antihyperuricaemic effects. In addition, fruits, such as cherries and high intakes of vegetable protein diet may reduce serum urate levels.     

Autonomic hyperreflexia during cystoscopy in patients with high spinal cord injuries

Cystoscopic procedures were performed on 102 patients with histories of traumatic spinal cord lesion; 57 patients had sensorimotor levels above T7, and the remaining 45 patients had levels below T7. In 40 of the 57 patients (70 per cent) with levels above T7, signs and symptoms of autonomic hyperreflexia were seen during bladder distension and cystoscopy; the remaining 17 of these patients (30 per cent) did not have this response. No autonomic hyperreflexia was seen during cystoscopy in any of the 45 patients with sensorimotor levels below T7.     

Thoracoscopic repair of congenital diaphragmatic hernia by inflation-assisted bowel reduction, in a resuscitated neonate: a better access?

Elective endoscopic diaphragmatic hernia repairs have been reported. But endoscopic surgery was regarded unsuitable for emergency repair of diaphragmatic hernia in ventilated newborn children in bad general condition. We report a new method for inflation-assisted reduction and thoracoscopic repair of congenital diaphragmatic hernia diaphragmatic in a vitally endangered neonate. From three 2.7 mm to 5 mm accesses warmed low-pressure, low-volume CO₂ was inflated into the thorax at 100 ml/min and 2 mm mercury. This allowed spontaneous reduction of the thoracic viscera into the abdomen and diaphragmatic suture with minimal handling. The 65-min procedure was tolerated well without perioperative deterioration. The baby was weaned off the respirator and breast-fed within 2 days, mediastinal shift normalized in 6 days. In suitable infants thoracoscopic repair and inflation-assisted reduction of thoracic contents is a more physiological access to congenital diaphragmatic hernia than laparoscopy or laparotomy.     

Complement protein C3 binding to Mycobacterium tuberculosis is initiated by the classical pathway in human bronchoalveolar lavage fluid

In high concentrations of fresh nonimmune human serum, Mycobacterium tuberculosis activates the alternative pathway of complement and binds C3 protein, resulting in enhanced phagocytosis by complement receptors on human alveolar macrophages. Yet in the lung, the alternative pathway of complement is relatively inactive compared to the classical pathway. To begin to determine whether C3 opsonophagocytosis of M. tuberculosis by alveolar macrophages can occur in the lung of the immunologically naive host, we characterized the binding of C3 to M. tuberculosis in different concentrations of fresh nonimmune human serum and concentrated human bronchoalveolar lavage fluid. Here we show that in human serum, C3 binding to M. tuberculosis is rapid, initiated by either the alternative pathway or the classical pathway, depending on the concentration of serum, and occurs by covalent linkages between the bacterial surface and the C3 cleavage products, C3b or C3bi. Human bronchoalveolar lavage fluid contains C3 protein and functional classical pathway activity that mediates the binding of C3 to the surface of M. tuberculosis. These studies provide evidence that when M. tuberculosis is first inhaled into the lungs of the human host, the bacterium is opsonized by C3 cleavage via classical pathway activation within the alveolus, providing a C3-dependent entry pathway into resident alveolar macrophages.