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Biomedical subjects

P Crook

Publications and source records attributed to P Crook.

14 recordsLinked to original sources
PubMed2004

Burden and cost of imported infections admitted to infectious diseases units in England and Wales in 1998 and 1999.

BACKGROUND: International travel from the UK has been rising, and the number of imported infections has increased. This study aimed to describe the number, nature, origin, clinical burden and cost of imported infections treated in infectious disease units (IDU) in England and Wales. METHOD: Information about all admissions in 1998 and 1999 with illnesses considered to have been acquired during their most recent travel abroad was collected retrospectively by IDUs using a pre-piloted questionnaire. RESULTS AND ANALYSIS: Four of the 23 IDUs in England and Wales were able to complete the questionnaires. They reported a total of 421 travel related admissions during the 2-year period. Three hundred and ninety-two of these cases were attributed to infectious causes, and of these a discharge diagnosis was made for 340 cases. The total number of bed days used to treat cases of imported infection was 2918. The most common diagnosis was malaria. The odds ratio that cases of imported infection were malaria was highest following visits to Africa. The average cost per bed day on the IDUs was around pound sterling 100, and on this basis, the total cost of treating imported infections on the four IDUs in 2 years was around pound sterling 289,000. The relative risk of acquiring an imported infection requiring treatment on an IDU was greatest for travellers to Africa. CONCLUSIONS: From this study, the estimate of the total annual cost of IDU treatment for imported infections in England and Wales is in excess of pound sterling 800,000. Many cases may be preventable with prophylactic medication and vaccination and travel advice on risk reduction. Further information about imported infections would be useful to inform travel medicine services, other clinicians and travellers about the health risks associated with travel to specific areas, and help to target and assess the cost effectiveness of preventative measures.

Adult↗
PubMed2004

Ethnic differences in patient perceptions of heart failure and treatment: the West Birmingham heart failure project.

OBJECTIVE: To investigate further the hypothesis that ethnic groups would have different levels of knowledge and perceptions of congestive heart failure (CHF) and treatments for this condition, a cross sectional survey was conducted of patients who were attending the heart failure clinics in two teaching hospitals of Birmingham, UK, that serve a multiethnic population. METHODS: 103 patients with CHF (66 men, 37 women) were surveyed by standard questionnaire: 42 were white, 34 Indo-Asian, 22 Afro-Caribbean, and 5 Oriental. RESULTS: When asked about their beliefs about control of one's health, 22 (64.7%) of Indo-Asians felt that God/fate controlled their health. The majority of white patients tended to believe that the greatest factor influencing their health was the doctor (15 (35.7%)). Of the total study cohort, only 68 (66%) of patients were aware of their primary diagnosis of heart failure; the majority of Indo-Asians (21 (61.8%)) were not aware of their diagnosis. Half of Indo-Asians (17 (50%)) felt that heart failure was not severe, in contrast to 40.9% (n = 9) of Afro-Caribbeans and only 19.1% (n = 8) of white patients. Of the study cohort, 38 (36.9%) were taking their drugs because their doctor told them to, a response most common among the Indo-Asians. The majority of Indo-Asians (22 (64.7%)) and Afro-Caribbeans (14 (63.6%)) stated that they did not have, or did not know whether they had enough, information about their drug. The corresponding figure for white patients was 21.4% (n = 9). When asked whether they took their medication regularly as prescribed, 7 (31.8%) of Afro-Caribbeans reported that they did not take their drugs regularly. CONCLUSIONS: Our study has highlighted deficiencies in the knowledge of CHF among patients from ethnic minority groups, as well as deficiencies in the information being given to these patients. There is a clear need to invest more in patient education for CHF, with special emphasis on certain high risk subgroups.

Aged↗
PubMed2002

Enhancing surveillance of cryptosporidiosis: test all faecal specimens from children.

The heightened risk of waterborne cryptosporidiosis, associated with heavy rainfall in autumn 2000, prompted us to survey laboratory practice in the South East Region of England in testing faecal specimens for Cryptosporidium spp. oocysts and reporting to the Public Health Laboratory Service Communicable Disease Surveillance Centre (PHLS CDSC). Varied practices were found. Ideally, all faecal specimens should be tested, but where laboratories are unable to do so, screening all faecal specimens from children age 15 years or younger would improve surveillance and could probably be accomplished with minimal additional resources.

Adolescent↗
PubMed2000

Early predictors of mortality in pneumococcal bacteraemia.

OBJECTIVES: Pneumococcal bacteraemia carries a mortality of about 20%. Approximately 50% of deaths from pneumococcal bacteraemia occur within the first 48 h of admission. In order to influence outcome, critically ill patients should be identified at the time of presentation. This study enables the clinician to rapidly make an evidence-based assessment of a patient's prognosis, allowing the identification of patients who should be placed in a high-risk category at an early stage, when appropriate management is most likely to be effective. METHODS: Data were collected from the medical record of history, physical examination, radiological examination and laboratory investigations done on initial presentation using a standardized proforma. The data were first examined by Pearson's Chi-squared test, with Yates' correction if needed. Variables found to be significantly associated with case fatality ( P < 0.05) by these methods were examined by stepwise logistic regression analysis in order to identify those factors which were independent predictors of case fatality. RESULTS: The overall case fatality was 21%. Older age, apyrexia, tachypnoea, bilateral consolidation, hypoalbuminaemia, elevated aminotransferases, renal impairment, acidosis and leucopaenia were significantly associated with higher case fatality. Older age, acidosis and elevated serum alanine aminotransferase (ALT) were independent predictors of case fatality. Fifty-five percent of isolates belonged to serotypes 4, 6B, 9V, 14, 19F and 23F, to which good antibody levels have been documented in both young and elderly patients post-vaccination. Serotype 14 was most common, and was significantly associated with higher case fatality. Colder weather was associated with a higher incidence of both infection and case fatality. The case fatality amongst patients receiving ITU management was 44%. Less than 50% of patients who died received ITU management. CONCLUSIONS: Despite the increased availability of new antibiotics and vaccines, the mortality of patients with pneumococcal bacteraemia remains unchanged. The parameters above allow early identification of patients with a higher case fatality; these patients may benefit from being placed in a "high-risk" category early on in their management. Vaccination of the elderly may reduce the incidence and/or mortality from pneumococcal bacteraemia. Further studies are required to understand the reasons for referral for intensive therapy in acute pneumococcal bacteraemia and whether ITU management affects outcome.

Acidosis↗
PubMed1993

Altered platelet function associated with the bronchial hyperresponsiveness accompanying nocturnal asthma.

BACKGROUND: Nocturnal awakening is a common feature of bronchial asthma, and yet the mechanisms underlying this phenomenon are poorly understood. We investigated whether nocturnal awakening is associated with changes in platelet function with the use of a variety of markers of platelet activation. METHODS: Ten patients with a history of nocturnal asthma and 10 age- and sex-matched healthy control subjects were studied at 10:00 PM, 4:00 AM, and 10:00 AM on 2 consecutive days. The following parameters were tested: forced expiratory volume in 1 second (FEV1), log dose of methacholine inducing a 20% fall in FEV1, platelet count and volume, platelet aggregation induced by collagen or activating factor, and plasma and intraplatelet levels of beta-thromboglobulin and platelet factor 4. RESULTS: We have demonstrated that altered platelet function and platelet activation occurs at 4:00 AM in patients with nocturnal asthma and is associated with the maximum increases in bronchial reactivity. Such changes were not observed in 10 control subjects. Platelet dysfunction has been detected as a reduced aggregatory response of platelets to collagen and platelet activating factor such that up to 5 times more platelet activating factor and 1.5 times more collagen were required to elicit a threshold aggregatory response in asthmatic subjects when compared with control subjects; this difference was evident at all time points tested. Furthermore, at 4:00 AM there were significantly lower levels of intraplatelet beta-thromboglobulin corresponding to the maximum reduction in peak expiratory flow and to the maximal increase in bronchial responses to inhaled methacholine. CONCLUSIONS: These results suggest that platelet activation accompanies nocturnal asthma and further suggest that platelets may play a role in this common clinical condition.

Adult↗
PubMed1992

The pharmacological modulation of thrombin-induced cerebral thromboembolism in the rabbit.

1. Intracarotid (i.c.) administration of thrombin induced a marked accumulation of 111indium-labelled platelets and 125I-labelled fibrinogen within the cranial vasculature of anaesthetized rabbits. 2. Thrombin (100 iu kg-1, i.c.) - induced platelet accumulation was completely abolished by pretreatment with desulphatohirudin (CGP 39393; 1 mg kg-1 i.c., 1 min prior to thrombin). Administration of CGP 39393 1 or 20 min after thrombin produced a significant reduction in platelet accumulation. 3. Intravenous (i.v.) administration of the platelet activating factor (PAF) receptor antagonist BN 52021 (10 mg kg-1) 5 min prior to thrombin (100 iu kg-1, i.c.) had no effect on platelet accumulation. 4. An inhibitor of NO biosynthesis, L-NG-nitro arginine methyl ester (L-NAME; 100 mg kg-1, i.c.), had no significant effect on the cranial platelet accumulation response to thrombin (10 iu kg-1, i.c.) when administered 5 min prior to thrombin. 5. Defibrotide (32 or 64 mg kg-1 bolus i.c. followed by 32 or 64 mg kg-1 h-1, i.c., infusion for 45 min) treatment begun 20 min after thrombin (100 iu kg-1, i.c.) did not significantly modify the cranial platelet accumulation response. 6. Cranial platelet accumulation induced by thrombin (100 iu kg-1, i.c.) was significantly reversed by the fibrinolytic drugs urokinase (20 iu kg-1, i.c., infusion for 45 min), anisoylated plasminogen streptokinase activator complex (APSAC) (200 micrograms kg-1, i.v. bolus) or recombinant tissue plasminogen activator (rt-PA; 100 micrograms kg-1, i.c. bolus followed by 20 micrograms kg-1 min-1, i.c., infusion for 45 min) administered 20 min after thrombin.8. These results suggest that neither endogenous PAF nor NO modulate thrombin-induced intracranial platelet accumulation in the rabbit. However, fibrin deposition appears to play an important role as shown by the ability of fibrinolytic agents to reverse platelet and fibrinogen accumulation induced by i.c. thrombin.

Animals↗
PubMed1991

The role of nitric oxide as an endogenous regulator of platelet and neutrophil activation within the pulmonary circulation of the rabbit.

1. Intravenous (i.v.) administration of adenosine diphosphate (ADP), platelet activating factor (PAF) and thrombin induced a dose-related accumulation of 111indium-labelled platelets within the thoracic region of anaesthetized rabbits. 2. I.v. administration of the inhibitor of NO biosynthesis, L-NG-nitro arginine methyl ester (L-NAME; 10 mg kg-1) significantly potentiated the peak platelet accumulation induced by ADP, PAF and thrombin. Additionally L-NAME prolonged the disaggregation of platelets in comparison to D-NAME (10 mg kg-1). Such changes were reversible by the administration of L-arginine (900 mg kg-1). 3. I.v. administration of PAF induced a small accumulation of 111indium-labelled neutrophils within the pulmonary circulation which could be greatly potentiated by pretreatment of the animals with L-NAME. In contrast, thrombin administration did not cause significant accumulation of 11indium-labelled erythrocytes in the pulmonary circulation of anaesthetized rabbits. 4. Intracarotid (i.c.) administration of thrombin induced a marked accumulation of radiolabelled platelets within the cranial vasculature which was not potentiated by the prior administration of L-NAME (at either 10 mg kg-1 or 100 mg kg-1). 5. These results suggest that endogenous NO may regulate platelet and polymorphonuclear leukocyte activation within the pulmonary but not the cerebral circulation of rabbits.

Adenosine Diphosphate↗
PubMed1990

Vasculitis in primary biliary cirrhosis--response to prednisolone.

Immunosuppressive doses of prednisolone were used to treat severe vasculitis in two patients with early primary biliary cirrhosis. Liver-specific blood tests of both patients returned to normal. The response of both the vasculitis and liver disease is discussed and the literature is reviewed.

Aged↗
PubMed1987

The involvement of platelet activating factor in endotoxin-induced pulmonary platelet recruitment in the guinea-pig.

1 Exposure of conscious guinea-pigs to an aerosol of endotoxin (25-100 micrograms ml-1) resulted in a dose-related, progressive accumulation of platelets in the thoracic region. Accumulation of 111indium oxine labelled erythrocytes was not observed following exposure to an aerosol of endotoxin (50 micrograms ml-1). 2 Pretreatment of guinea-pigs with the selective platelet activating factor (Paf)-antagonists. CV-3988 or brotizolam resulted in a dose-related inhibition of endotoxin-induced pulmonary platelet recruitment. Pretreatment of guinea-pigs with the selective Paf-antagonist BN 52021 resulted in significant inhibition of endotoxin-induced pulmonary platelet recruitment, although the effects of BN 52021 were not dose-related. 3 Pretreatment of guinea-pigs with indomethacin at doses known to inhibit cyclo-oxygenase did not inhibit endotoxin-induced pulmonary platelet recruitment, whereas higher doses of indomethacin produced a reduction in platelet recruitment in the lung. 4 Pretreatment of guinea-pigs with the anticoagulant heparin and the prostacyclin analogue ZK 36374 inhibited endotoxin-induced platelet recruitment. 5 These observations suggest that endotoxin-induced pulmonary platelet recruitment in the guinea-pig is secondary to the release of platelet activating factor, but not to cyclo-oxygenase products of arachidonic acid and may also involve activation of the coagulation cascade.

Animals↗