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Mannose binding protein deficiency is not associated with malaria, hepatitis B carriage nor tuberculosis in Africans.

Year 1998
Bellamy R. Ruwende C. McAdam KP. Thursz M. Sumiya M. Summerfield J. Gilbert SC. Corrah T. Kwiatkowski D. Whittle HC. Hill AV.
Wellcome Trust Centre for Human Genetics, Oxford University, UK.
We retrospectively studied MBP genotypes in patients with malaria, tuberculosis (TB), and persistent hepatitis B virus (HBV) carriage, in clinics and hospitals in The Gambia. Children under 10 years with cerebral malaria and/or severe malarial anaemia, were compared with children with symptomatic, mild malaria, and controls of the same age and ethnicity. Adult TB cases with smear-positive pulmonary TB were compared with healthy blood donors from the same ethnic groups. Malaria cases and controls were tested for hepatitis B core antibody (anti-HBc) and surface antigen (HBsAg). TB patients were tested for HIV antibodies. Genotyping used sequence-specific oligonucleotide analysis to identify MBP variant alleles. Overall, 46% (944/2041) of patients and controls were homozygous for the wild-type MBP allele, 45% (922/2041) were carriers of a single variant allele and 8.6% (175/2041) had two variant alleles. Neither homozygotes nor heterozygotes for MBP variants were at increased risk of clinical malaria, persistent HBV carriage or TB. The most common mutation in Africans, the codon 57 variant allele, was weakly associated with resistance to TB (221/794 in TB cases and 276/844 in controls, p = 0.037). MBP deficiency is not a significant risk factor for persistent HBV, severe malaria nor pulmonary TB in West Africa.

Haemodynamic parameters predicting variceal haemorrhage and survival in alcoholic cirrhosis.

Year 1998
Stanley AJ. Robinson I. Forrest EH. Jones AL. Hayes PC.
Department of Medicine, Royal Infirmary of Edinburgh, UK.
The relationship between the various haemodynamic abnormalities observed in cirrhosis and their prognostic value remains unclear. We report haemodynamic measurements on 96 patients with alcoholic cirrhosis (mean Childs-Pugh Score, CPS, 9.0 +/- 0.2, mean age 55.6 +/- 1.0 years) and assess their value in predicting variceal bleeding and death during a mean follow-up of 19.3 +/- 1.5 months. Baseline CPS correlated with hepatic venous pressure gradient (HVPG) (p = 0.001), azygos blood flow (p < 0.05), cardiac index (p < 0.05), and inversely with mean arterial pressure (p < 0.01) and systemic vascular resistance index (p < 0.05). Renal blood flow was not related to any haemodynamic parameter or CPS. Thirty-eight patients died during follow-up, and 16 had a variceal bleed. Death (p = 0.001) and variceal bleeding (p < 0.05) were more likely in patients with HVPG > 16 mmHg than in those with HVPG < 16 mmHg, and variceal bleeding was more likely in patients with HVPG > 12 mmHg (vs. HVPG < 12 mmHg, p < 0.05). HVPG also predicted death and variceal haemorrhage on univariate and multivariate analyses. No other haemodynamic parameter predicted death or bleeding. In alcoholic cirrhosis, severity of liver disease is related to HVPG, collateral blood flow and degree of systemic circulatory abnormalities. HVPG is a useful predictor of survival and variceal bleeding in these patients.

The outcome of bleeding duodenal ulcer in the era of H2 receptor antagonist therapy.

Year 1998
Bardhan KD. Nayyar AK. Royston C.
Rotherham General Hospitals NHS Trust, UK.
We studied 2119 patients presenting with duodenal ulcer as sole lesion, in the period 1976-1993, the era of H2 receptor antagonist (H2RA) therapy, prior to the introduction of Helicobacter pylori eradication. We used clinical assessment and serial check endoscopy to investigate the incidence of bleeding at presentation (group I, n = 286, 13.5%), the long-term outcome in this group and in that presenting with pain alone (group II, n = 1833, 87%) with respect to ulcer recurrence and bleeding, and the effect of H2RA maintenance therapy. Most patients were treated with H2RA, principally cimetidine. In group I, seven patients died early on; 38 had urgent surgery, of whom six died post-operatively. The remainder were treated; five immediately re-bled, of whom three were operated on. On follow-up, 98/227 group I patients relapsed, 21 (21%) of whom rebled. Relapse in group II was 1017/1668, with only 42 (4%) bleeding (p < 0.001). In patients without maintenance treatment, relapse was markedly higher (50/78 group I, 529/742 group II), but group II still bled significantly less (20% group I vs. 3% group II). Relapse on maintenance was: 48/149 with five (10%) rebleeding in group I, and 488/926 with five (1%) bleeding in group II (p < 0.001). Despite the introduction of H2RA therapy, patients presenting with haemorrhage still have a risk of bleeding at ulcer relapse about 7-fold higher than that for those presenting with pain alone.

Atypical chest pain: looking beyond the heart.

Year 1998
Chambers J. Bass C.
Department of Cardiology, Guy's Hospital, London, UK.
Chest pain is common, and tends to be overinvestigated. Patients with normal coronary anatomy have a low mortality, but remain significantly incapacitated. We discuss ways of improving the management of such patients. An early diagnosis of a non-cardiac cause of pain should be made, ideally by the general practitioner, taking account of risk factors for cardiac as well as psychological disorders, the quality of the pain, the patient's concerns and worries and the presence of stressful life events. The minimum of investigation should be performed. Cardiological referral should be considered for patients with a high a priori risk of ischaemic heart disease. Otherwise referral, if necessary, should be to a gastroenterologist, psychiatrist or clinical psychologist, as appropriate. Treatment options are medications with musculoskeletal or oesophageal activity, simple or repeated reassurance, cognitive therapy, psychiatric drugs, and respiratory retraining. We suggest that a multidisciplinary chest-pain clinic may improve the care of such patients.

Источник: https://gastroportal.ru/science-articles-of-world-periodical-eng/qjm.html
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