Chronic obstructive pulmonary disease with tracheostomy: report of case involving endodontic treatment

Modern medicine has made many advances in the capability to sustain life. The dental profession needs to keep up to date with these changes and be creative in caring for these individuals who are medically compromised and who require special care.¹¹ This sometimes requires the purchase of new equipment; other times it means modifying that which exists. In all instances, the level of care for these individuals requires a team approach and mandates education of all team members. In the case presented, the medical problems necessitated such a team effort to achieve optimal care.     

Reduction of Mortality in the Stockholm Ischaemic Heart Disease Secondary Prevention Study by Combined Treatment with Clofibrate and Nicotinic Acid

Consecutive survivors of a myocardial infarction from the Southern Hospital, below 70 years of age, were randomized into a Control group (n=276) and a Treatment group (n=279). The latter was openly prescribed the combination of clofibrate and nicotinic acid for serum lipid lowering. Each patient should remain in the study for 5 years and be seen regularly every 4 months at a special IHD outpatient clinic within the hospital. The concentration of serum cholesterol and triglyceride was lowered by 13% and 19%, respectively, in the Treatment group compared to the Control group. Total mortality was 82 cases in the Control group and 61 in the Treatment group, a 26% reduction (p<0.05). For patients above 60 years of age in the Treatment group the reduction in mortality was 28% (p<0.05). IHD mortality was reduced by 36% (p<0.01)in the Treatment group compared to the Control group. The beneficial effect of the serum lipid lowering treatment was related to the serum triglyceride concentration in two ways. First, it only occurred in patients with a triglyceride level >1.5 mmol/l (n=216). Secondly, it was most pronounced in the 44% of the treated patients who had a lowering of the serum triglyceride concentration by 30% or more, and in this subgroup the reduction of IHD mortality was 60% (p<0.01). For serum cholesterol there were no such relations. The difference between serum triglycerides and cholesterol concerning these relations to the treatment outcome may be due to the fact that hypertriglyceridaemia was the most common hyperlipidaemia among our patients, occurring in 50%, while hypercholesterolaemia only occurred in 13 %. Caution should be exercised in the interpretation of the results as the trial was not blind. However, the fact that the decrease in IHD deaths was directly related to the degree of serum triglyceride lowering indicates that it was the drug effect on serum lipids that was reponsible for the beneficial effect of the treatment.     

Interferon Alfa-2b or Not 2b? Significant Differences Exist in the Decision-Making Process between Melanoma Patients Who Accept or Decline High-Dose Adjuvant Interferon Alfa-2b Treatment

BACKGROUND: Patients with thick (Breslow>4 mm) primary melanoma and/or regional nodal metastasis have a high risk of tumor recurrence. High-dose adjuvant interferon (IFN) alfa-2b offers/=50% risk of recurrence/disease-related mortality and offered IFN. Telephone surveys delineated reasons behind patients' decisions to accept IFN. RESULTS: Acceptors, 60 of 135 (45%), decided to take IFN alfa-2b whereas 75 of 135 (55%) declined. Being female (OR, 2.4; 95% CI, 1.17-5.03; p=.017) and positive SLN status (OR, 2.2; 95% CI, 1.01-4.97; p=.048) were strongly associated with patients who chose IFN. Acceptors of IFN were younger, more influenced by physicians, and less affected by depression and side effect profile (p<.05 for all). Decliners were more concerned by strained relationships with family and social life (p<.05). CONCLUSIONS: Gender and positive SLN were predictive of high-risk melanoma patients' acceptance of IFN treatment. Physician insight into melanoma patients' therapeutic decision-making process can guide patients through this difficult disease.     

Effects of Glycerol on Lung and Liver Tumor Development

Mice of several strains(A/J, SWR, MaMyJ, BALB/cByJ, 129J, andC57BL/6J) were treated with the carcinogens 3-methylcholanthrene,urethane, and 4-nitroquinoline 1 -oxide and then given 1 or5% glycerol in the drinking water for up to 4 months. Effectsof glycerol on lung tumor multiplicity and incidence were evaluated.The effects of glycerol were variable, and in the majority ofexperiments glycerol failed to enhance tumor development inmouse lung. Analysis of cell kinetics did not show a proliferativeresponse of alveolar or bronchiolar cells to glycerol. In rats,glycerol did not enhance the appearance of putative preneoplasticliver foci, and in C3H mice it did not increase the incidenceof spontaneously occurring liver tumors. It is concluded thatglycerol does not increase number or incidence of lung tumorsin the mouse strains used, whether the animals are pretreatedwith a carcinogen or not. Glycerol does not affect liver tumordevelopment.     

Acute effects of acetazolamide on cerbral blood flow in man

We have followed the time course of the effect of the carbonic anhydrase inhibitor acetazolamide injected i. v. in unanesthetized healthy human beings. The dose administered was 500 mg as a bolus. Cerebral blood flow (CBF) was measured continuously before, during and after the injection, using a pulsed ultrasound doppler system, which measured the instantaneous mean velocity across the lumen of the internal carotid artery, just below its entrance into the skull. Ventilation, heart-rate, end-expiratory PCO₂- arterial PCO₂, pH and systemic blood pressure was also measured. We found that acetazolamide caused a rise in CBF which could be detected as early as 2 min after the injection. A maximal average response of 75% increase in CBF was seen after 25 min. The half-time of the declining phase of the response was 95 min. There were no systematic differences in the CO₂ reactivities, given as ACBF/ΔPACO₂ in % of CBF at normocapnia, before and after acetazolamide injection, regardless of the absolute PACO₂ level. The present dose of the drug caused no change in ventilation, alveolar and arterial PCO₂ or in arterial blood pH indicating that the carbonic anhydrase was not fully inhibited. Our observations show that acetazolamide nevertheless caused a rapid vasodilation in the brain and over a wide range of PCO₂′s. We suggest that this agent has a local vasodilator effect on the cerebral arterioles, unrelated to its specific effects as a carbonic anhydrase inhibitor.     

OBSERVATIONS ON THE EFFECT OF MASSIVE DOSES OF IRON GIVEN INTRAVENOUSLY TO PATIENTS WITH HYPOCHROMIC ANEMIA

Massive doses of iron (from 0.608 to 1.32 Gm. as colloidal terric hydroxide orcolloidal ferric oxide) were given intravenously in single infusions to 8 differentpatients with hypochromic microcytic anemia. One patient was given a secondinjection after an interval of four months, so that nine administrations were made.The following observations were made:

1. The reticulocyte response was higher in each instance than would be expectedin oral therapy. In 3 additional patients in whom injection had to be discontinuedafter 0.070, 0.180, and 0.123 Gm. of elemental iron had respectively been given, thereticulocyte rises were higher than were the average responses reported by Heath¹⁸after optimal oral therapy. This at least suggests that "optimal" oral therapy doesnot provide a maximal stimulus to outpouring of reticulocytes from the bone marrow. Comparable doses of iron given to 3 control subjects with normal hemoglobinlevels did not cause a reticulocytosis.

2. The average rate of hemoglobin regeneration per 100 cc. of blood per day was0.224 Gm.; the lowest value was 0.16 Gm. and the highest 0.27 Gm. These figureswere calculated for the rise that occurred from the day of iron administration to thetime at which the rate of hemoglobin increase was obviously becoming slower.Since correction was not made for blood loss in 3 of the patients during the periodof regeneration, the figures for the rate of hemoglobin formation are lower thanthey otherwise would have been. Even so they are distinctly greater than thoseusually obtained following oral therapy (table 2), but no greater than is found in anoccasional patient given iron by mouth. The data suggest that the fastest rate ofhemoglobin regeneration that can be stimulated by iron in subjects with hypochromic anemia approximates 0.3 Gm. per 100 cc. per day.

3. Calculations indicated that from 71.8 to 99.7 per cent of the injected iron wasapparently used for the synthesis of hemoglobin. These figures are likewise lowerthan they would have been if several of the patients had not lost blood during therecovery period. The observation of other workers that parenterally administerediron is almost completely retained by the body and converted into hemoglobin wastherefore confirmed.

4. Toxic reactions to the injected iron are described in detail. They were severein all but two instances, and in 3 patients were so alarming that injection of ironhad to be discontinued. There can be no doubt that the reactions to iron parenterally administered in large doses are great enough to contra-indicate use of thismeasure as a therapeutic procedure.

     

A study of the antigenicity of Rickettsia helvetica proteins using two‐dimensional gel electrophoresis

Rickettsia helvetica is an obligate intracellular Gram‐negative microorganism found in Ixodes ricinus ticks. When R. helvetica was first discovered in 1979, little was known about its physiology and it fell into oblivion until it recently was suspected of being pathogenic to humans. However, all efforts to isolate R. helvetica from patients have been unsuccessful, although serological responses against R. helvetica can be demonstrated. The aim of our study was to investigate the protein profile of R. helvetica and study the antigenicity of its proteins using two‐dimensional (2D) immunoblot in order to characterize the immunological response against R. helvetica infection. Our results show that in addition to the known PS120 and OmpB antigenic R. helvetica proteins, three other antigens exist: a 60 kDa GroEL protein, a 10 kDa GroES protein and a hitherto unknown 35 kDa hypothetical protein that has similarities with ORF‐RC0799 of Rickettsia conorii. Furthermore, the lipopolysaccharide showed strong antigenicity. In this study, we present the first proteome map and the first 2D immunoblot profile of R. helvetica and finally we present the 35 kDa R. helvetica as an additional antigen to the previously known rickettsial antigens.     

Molecular characterization of CTX‐M‐15‐producing clinical isolates of Escherichia coli reveals the spread of multidrug‐resistant ST131 (O25:H4) and ST964 (O102:H6) strains in Norway

Nationwide, CTX‐M‐producing clinical Escherichia coli isolates from the Norwegian ESBL study in 2003 (n=45) were characterized on strain and plasmid levels. Bla_CTX‐M allele typing, characterization of the genetic environment, phylogenetic groups, pulsed field gel electrophoresis (PFGE), serotyping and multilocus sequence typing were performed. Plasmid analysis included S1‐nuclease‐PFGE, polymerase chain reaction‐based replicon typing, plasmid transfer and multidrug resistance profiling. Bla_CTX‐M‐15 (n=23; 51%) and bla_CTX‐M‐14 (n=11; 24%) were the major alleles of which 18 (78%) and 6 (55%), respectively, were linked to ISEcp1. Thirty‐two isolates were of phylogenetic groups B2 and D. Isolates were of 29 different XbaI‐PFGE‐types including six regional clusters. Twenty‐three different O:H serotypes were found, dominated by O25:H4 (n=9, 20%) and O102:H6 (n=9, 20%). Nineteen different STs were identified, where ST131 (n=9, 20%) and ST964 (n=7, 16%) were dominant. Bla_CTX‐M was found on ≥100 kb plasmids (39/45) of 10 different replicons dominated by IncFII (n=39, 87%), FIB (n=20, 44%) and FIA (n=19, 42%). Thirty‐nine isolates (87%) displayed co‐resistance to other classes of antibiotics. A transferable CTX‐M phenotype was observed in 9/14 isolates. This study reveals that the majority of CTX‐M‐15‐expressing strains in Norway are part of the global spread of multidrug‐resistant ST131 and ST‐complex 405, associated with ISEcp1 on transferrable IncFII plasmids.