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Biomedical subjects

M A Hall

Publications and source records attributed to M A Hall.

At least 91 records · Page 5Linked to original sources
PubMed1993

Medical technology assessment and practice guidelines: their day in court.

There is the expectation that outcomes research and the promulgation of medical practice guidelines will be able to identify and hopefully reduce the amount of unnecessary or inappropriate medical care through a variety of methods, including utilization review. However, past efforts by public and private insurers to deny claims on the basis of formal technology assessments or practice guidelines have frequently been overturned by the courts for multifarious reasons. This paper examines the court's reluctance to accept a variety of technology assessment methods in coverage policy decisions. The paper reviews the options that have been proposed to restrict judicial involvement in the formulation of coverage policy and then proposes a new option that employs a more precise taxonomy of medical practice assessment.

Complementary Therapies↗
PubMed1993

Informed consent to rationing decisions.

The prevailing legal and ethical opinion that rationing decisions must always be disclosed to patients is countered. Although conventional informed consent law could theoretically extend to decisions to decline treatment because of costs, it has not yet done so. Moreover, abandonment law does not prohibit declining treatment for economic reasons. A new theory of economic informed consent would stipulate that when patients make informed decisions to purchase less expensive health insurance, they are consenting in advance either to limiting marginally beneficial treatment or to waiving their right to be informed of particular decisions not to treat. Whether this will prove workable or will be accepted by the courts depends on the specifics of the enrollment disclosures, the range of choices given to subscribers, and their capacity to understand them.

Choice Behavior↗
PubMed1992

HLA class II alleles associated with celiac disease susceptibility in a southern European population.

Susceptibility to celiac disease in Northern Europe is associated with the human leukocyte antigens (HLA) B8, DR3 and DQ2, which exist together on an extended haplotype. The strong predominance of this haplotype within the Northern European celiac populations, together with the linkage disequilibrium which occurs between these loci, does not allow identification of the gene(s) primarily associated with disease susceptibility. Studies from Southern Europe using both serology and examination of restriction fragment length polymorphisms (RFLP) have demonstrated associations with DR3, DR7 and DQ2, suggesting that the DQ locus is primarily involved. We investigated 43 celiac patients and 41 healthy controls from Rome, Italy, using sequence-specific oligonucleotide (SSO) probes, in conjunction with gene amplification by the polymerase chain reaction (PCR), to determine alleles at the DRB, DQA1, DQB1 and DPB1 loci: 19% of celiac patients possessed the alleles DRB1*0301 DRB3*0101, 33% DRB1*0301 DRB3*0201 and 33% of celiac patients were heterozygous for DRB1*1101-1201/DRB1*0701. The strongest association with celiac disease susceptibility was the combination of alleles DQA1*0501 DQB1*0201 (91% celiac patients vs. 12% controls; p = 0.000002). There was no additional susceptibility associated with alleles at the DPB locus. This study confirms the hypothesis that susceptibility is associated with a particular combination of DQ alleles and the ethnic variation in DR frequencies is secondary to linkage disequilibrium with these DQ alleles.

Adolescent↗
PubMed1992

Complement and antibody participation in opsonophagocytosis of type IV and V group B streptococci.

Requirements for complement and antibody in neutrophil-mediated killing of serotype IV and V group B streptococci were investigated. Neutrophils from adults were tested in an opsonophagocytic assay with sera from healthy adults, healthy newborns, and hypogammaglobulinemic, agammaglobulinemic, and C4-deficient patients. For all serum sources, the bactericidal index for both serotypes exceeded 84% after 40 min of incubation. Heat inactivation of sera ablated killing. Blockade of neutrophil receptor FcIII effected a maximum of 16% inhibition of opsonophagocytosis, and FcII receptor blockade demonstrated negligible inhibition. When neutrophil complement receptor 1 or 3 blockade was employed, the maximum inhibition detected was 26%. Simultaneous blockade of complement receptors 1 and 3 effected maximum inhibition levels of 25 and 65% for serotypes IV and V, respectively. Blockade of complement receptor 3 and neutrophil receptor FcIII inhibited opsonophagocytosis by 56% for both serotypes. When serum complement concentrations were restricted, neutrophil-mediated killing diminished but was restored by the addition of hyperimmune rabbit antiserum. These findings suggest that complement and antibody are major participants in the opsonophagocytosis of serotypes IV and V group B streptococci. A low prevalence of carriage or mediation of efficient phagocytosis by interactions of neutrophil complement and Fc receptors may contribute to the rarity of human infections caused by these two serotypes.

Adult↗
PubMed1992

Phosphatidylcholine composition of endotracheal tube aspirates of neonates and subsequent respiratory disease.

The phosphatidylcholine (PC) content of the initial endotracheal tube aspirate was measured in 105 infants intubated for resuscitation or for ventilation for respiratory distress syndrome, using high performance liquid chromatography and postcolumn fluorescence derivitization with diphenyl-1,3,5-hexatriene. Sixty eight had measurable PC. Of the infants who developed respiratory distress syndrome, with or without subsequent chronic lung disease, neither the percentage of dipalmitoylphosphatidylcholine (DPPC) nor the ratio of DPPC to palmitoyloleoylphosphatidylcholine (POPC), showed any correlation with gestational age. However, both parameters were significantly lower overall in this group than in the group of infants who did not develop respiratory distress syndrome. Infants with a ratio of DPPC:POPC less than 3.0 developed respiratory distress syndrome irrespective of gestational age, but there was considerable overlap between groups for values greater than this. The infants with respiratory distress syndrome who went on to develop chronic lung disease had the same initial PC profile as those with respiratory distress syndrome who did not develop chronic lung disease, but differed as a group by being lighter and more premature. The development of chronic lung disease was not associated with a particular initial PC composition. Other factors related to increasing prematurity must therefore be involved in rendering infants vulnerable to developing chronic lung disease.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1992

Turnover of exogenous artificial surfactant.

The turnover of the artificial surfactant Exosurf after its administration to infants with respiratory distress syndrome was studied. High performance liquid chromatography was used to compare the phosphatidylcholine (PC) composition of serial endotracheal tube secretions from three groups of infants. There were 22 infants who received two doses of Exosurf in 24 hours (group 1), 10 infants who received four doses in 36 hours (group 2), and 41 control infants who did not receive Exosurf. Two parameters were studied: (i) dipalmitoylphosphatidylcholine (DPPC), which is present in both Exosurf and endogenous surfactant, expressed as a percentage of total PC (% DPPC) and (ii) the ratio of DPPC to the entirely endogenous palmitoyloleoylphosphatidylcholine (DPPC:POPC ratio). The administration of Exosurf produced changes in endotracheal tube aspirate PC composition that were detectable for over one week. Four doses of Exosurf in 36 hours prolonged the persistence of these changes compared with two doses in 24 hours, but the numbers of infants were small, and should not be over-interpreted. We conclude that after giving two doses of Exosurf, further doses might best be delayed until after two days, and that further clinical evaluation of dosage regimens is required.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1992

Regional cerebral blood flow velocity changes after indomethacin infusion in preterm infants.

Cerebral blood flow velocity was assessed during infusion of indomethacin over 30 minutes. Eleven preterm infants with symptomatic patent ductus arteriosus were studied on 12 occasions. Indomethacin infusion was associated with a significant reduction in time averaged mean velocity (TAMV), peak systolic velocity (PSV), and end diastolic velocity in both the anterior cerebral artery and middle cerebral artery. The fall in the TAMV and PSV was gradual with maximal change 30-40 minutes after the start of the infusion. It was concluded that administration of indomethacin by slow infusion produces haemodynamic alterations to the cerebral circulation comparable in magnitude with changes described with bolus administration. Indomethacin remains a useful and effective treatment for patent ductus arteriosus in preterm infants, but should continue to be used with caution.

Blood Flow Velocity↗
PubMed1991

A family study confirms that the HLA-DP associations with celiac disease are the result of an extended HLA-DR3 haplotype.

Genotyping for HLA-DR, -DQ, and -DP antigens by restriction fragment length polymorphism (RFLP) analysis along with identification of restriction fragments associated with celiac disease (CD) were undertaken in 13 families in which more than one member had CD. Major histocompatibility complex class II haplotypes for the family members were constructed which included both genotypes and RFLP markers. In 12 of the families all the affected members shared an HLA haplotype which included HLA-DR3a, DQw2 and a BglII 4.0-kb DQA fragment. Eight of these 12 haplotypes also included HLA-DPw1 and both a RsaI 4.0-kb DPB fragment and an XbaI 16.0-kb DPA fragment. In one family, the two affected members shared an HLA-DR7, DQw2 haplotype, although both their second haplotypes included HLA-DR3a and -DQw2. The results suggest that HLA-DP genes do not play an independent predisposing role in the etiology of CD but do mark a disease-associated extended haplotype. This haplotype contains genes coding for specific HLA products which may be necessary for the disease to develop. The findings support the hypothesis that the presence of a specific DQ alpha/DQ beta heterodimer, encoded in a cis arrangement on HLA-DR3a haplotypes, predisposes to celiac disease.

Adolescent↗
PubMed1991

Strong primary selection for the Dw4 subtype of DR4 accounts for the HLA-DQw7 association with Felty's syndrome.

Felty's syndrome (FS) is a rare complication of rheumatoid arthritis (RA) previously shown to be strongly associated with HLA-DR4 and less significantly with HLA-DQw7. To map more precisely the HLA locus responsible for susceptibility to FS, we have examined HLA-DR4 and DQ beta-chain polymorphisms in FS patients and controls using restriction fragment length polymorphism analysis and polymerase chain reaction amplification in conjunction with oligonucleotide probing. The increased frequency of DR4 in FS (93% vs. 32% controls) was due almost entirely to enrichment for the Dw4 subtype (88% vs. 20% controls) with a secondary increase of the Dw14 subtype. Dw10 and Dw13 subtypes of DR4 were absent from the patient group. Increase in DQw7 frequency among DR4 FS patients could be accounted for by linkage disequilibrium between Dw4 and DQw7 alleles. Whereas susceptibility to RA is strongly associated with a conserved HLA-DR beta epitope associated with several DRB1 alleles, it is primarily the Dw4 allele which is associated with progression to Felty's syndrome. The finding that amino acid sequence variation at the DR4B1 locus rather than DQB1 is associated with development of FS will have important implications for the development of novel immunotherapies which are major histocompatibility complex allele-dependent.

Amino Acids↗
PubMed1991

The wrist in juvenile arthritis.

Patients with juvenile arthritis affecting the wrist have been reviewed six months or more after treatment, which has included steroid injection, synovectomy, arthroplasty, arthrodesis and distraction lengthening of the ulna. The pattern of wrist involvement is described, the general management reviewed, and the indications, techniques and results of these various procedures are presented.

Arthritis, Juvenile↗
PubMed1991

Role of neutrophil receptors in opsonophagocytosis of coagulase-negative staphylococci.

The role of neutrophil complement receptors in the opsonophagocytosis of 10 strains of coagulase-negative staphylococci was investigated. Polymorphonuclear leukocytes from adults as well as term and premature newborn infants were tested with normal human serum, adult hypogammaglobulinemic serum, and pooled premature infant serum in an opsonophagocytic assay. Neutrophils from premature infants demonstrated significantly lower killing capacity (62%) than neutrophils from adults (86%) or term infants (84%; P less than 0.02). Maximum inhibition of opsonophagocytosis by adult or infant neutrophils occurred with an FcIII receptor blockade (80%), whereas a blockade of complement receptors produced minimal inhibition. Opsonophagocytic activity for the coagulase-negative staphylococci was not influenced by the serum source but was influenced by reducing the serum concentration below 5%. Abrogation of the complement activity of normal human serum by heating or the addition of ethylenediamine tetraacetate reduced opsonophagocytosis by 100 and 96%, respectively, whereas selective inhibition of the classical complement pathway reduced opsonophagocytosis by only 40%. Thus, opsonophagocytosis of coagulase-negative staphylococci by human sera appears to be mediated primarily by neutrophil Fc receptors, but complement is also required. The inefficiency of these interactions with neutrophils from premature infants may partially explain the enhanced susceptibility of very-low-birth-weight neonates to disseminated, coagulase-negative staphylococcal infections.

Adult↗