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Biomedical subjects

A M Connolly

Publications and source records attributed to A M Connolly.

32 records · Page 2Linked to original sources
PubMed1997

Trauma and pregnancy.

Trauma and/or accidental injury complicates 6-7% of all pregnancies. The management protocols for trauma in pregnancy are based largely on case reports and small series. The purposes of this study were to: describe the demographics of pregnant trauma patients at a tertiary care center and a large community hospital; identify variables predictive of fetal outcome including an examination of Kleihauer-Betke and nonstress testing; and recommend an evaluation and management protocol after trauma based on empirical data rather than anecdotal reports. Data from pregnancies complicated by trauma from July 1987 through October 1993 were retrospectively reviewed. Statistical analysis included Chi-square and Kruskall-Wallis testing. There were 476 medical records available for review. Of the trauma cases, 54.6% were motor vehicle accidents, 22.3% were domestic abuse and assaults, 21.8% were associated with falls, and 1.3% were secondary to burns, puncture wounds, or animal bites. Mean maternal age was 24 years, 49.9% were Caucasian, and 43% were primigravid. Mean gestational age at occurrence of trauma was 25.9 weeks and mean gestational age of delivery was 37.9 weeks. Domestic abuse occurred most frequently before 18 weeks, falls between 20-30 weeks' gestation, and motor vehicle accidents occurred with equal frequency throughout gestation. Uterine contractions occurred in 39.8% of patients and as often as every 1 to 5 min in 18% of patients. Preterm labor occurred in 11.4%, preterm delivery in 25%, and abruptions in 1.58% of the trauma population. Fetal heart rate monitoring was abnormal in 3% of cases. Twenty-seven perinatal deaths were noted and in 14 pregnancies the deaths were related to trauma. Eight of these perinatal deaths were associated with motor vehicle accidents, four with domestic violence, and two with falls. The only preventable perinatal deaths were a twin pregnancy transferred with nonreassuring fetal heart tones. Early warning symptoms of vaginal bleeding, uterine contractions, and/or abdominal and/or uterine tenderness were not predictive of either preterm delivery or adverse pregnancy outcome, sensitivity 52%, specificity 48%. Abnormal monitoring and positive Kleihauer-Betke tests were also not predictive of adverse pregnancy outcome. However, there were no adverse outcomes directly related to trauma when monitoring was normal and early warning symptoms were absent (negative predictive value 100%). Two hundred eighty-nine Kleihauer-Betke tests were performed and only one affected management. Repetitive monitoring over several days did not uncover any patients whose heart rate tracings evolved from normal to abnormal monitoring. Given our findings that prolonged monitoring was not helpful in management of pregnant trauma patients, we support the recommendation that initial external fetal monitoring be performed for 4 hr, and, if reassuring, the patient may be sent home with precautions. We also recommend an Rh-immunoglobulin work-up for all Rh-negative pregnant trauma patients, but do not recommend Kleihauer-Betke testing for Rh-positive women. Given the frequency with which trauma affects pregnancy and the difficulty encountered with identifying variables predictive of pregnancy outcome, there may be great benefits of incorporating trauma prevention into routine prenatal care.

Adolescent↗
PubMed1997

Anti-tubulin autoantibodies in acquired demyelinating polyneuropathies.

Selective high-titer anti-tubulin autoantibodies are associated with Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP). Low-titer anti-tubulin autoantibodies are a normal component of some human sera. Analysis of 7 human sera with monoclonal anti-tubulin autoantibodies showed that the epitopes recognized by these antibodies are within central, conserved regions of tubulin. Sera from 3 patients with IgM monoclonal antibodies and CIDP reacted to an epitope spanning aa 301-314 of beta-tubulin, which has some sequence homology to several human viruses. Natural polyclonal anti-tubulin antibodies also bind to central regions of tubulin. In contrast, polyclonal tubulin antibodies induced in mice react to epitopes on the amino- or carboxy-terminal. Selective polyclonal anti-tubulin autoantibodies with low reactivity to other neural antigens are found in about one-half of patients with CIDP.

Animals↗
PubMed1997

Serum IgM monoclonal autoantibody binding to the 301 to 314 amino acid epitope of beta-tubulin: clinical association with slowly progressive demyelinating polyneuropathy.

We identified five patients with IgM monoclonal autoantibodies that bound to human brain tubulin. In a companion study, we found that IgM in these sera selectively recognized one of three epitopes on tubulin. IgM from three patients bound selectively to a small epitope on human beta-tubulin comprising amino acids 301 to 314. The other two sera recognized tubulin amino acids 215 to 235 and 315 to 336. In this study, we compared the clinical syndromes in these patients with the tubulin epitope recognized by their serum IgM. The three patients with IgM binding to tubulin amino acids 301 to 314 all had chronic inflammatory demyelinating polyneuropathy (CIDP) syndromes with slowly progressive weakness, hyporeflexia, and electrophysiologic studies consistent with demyelination. Two of these patients had significant asymmetry to their weakness. The two other patients had diagnoses of polyradiculopathy and amyotrophic lateral sclerosis with no evidence of peripheral nerve demyelination. We conclude that IgM monoclonal anti-tubulin antibodies have some association with demyelinating polyneuropathy syndromes, but may occur in patients with other clinical syndromes as well. A stronger association with demyelinating polyneuropathies may occur if the anti-tubulin antibodies recognize the 301 to 314 amino acid epitope on tubulin. This tubulin epitope, or a similar one on another molecule, could play an important antigenic role in the development of demyelinating polyneuropathies with features of CIDP.

Aged↗
PubMed1996

Congenital muscular dystrophy syndromes distinguished by alkaline and acid phosphatase, merosin, and dystrophin staining.

Congenital muscular dystrophy syndromes are characterized by congenital weakness, contractures, and dystrophic features on muscle biopsy. However, these syndromes are often difficult to diagnose precisely because their clinical and pathologic characteristics are not specific and resemble changes in other myopathies. We examined muscle biopsies from 20 children with a congenital muscular dystrophy syndrome. Disease controls with dystrophies or other myopathies (n=19) and normal individuals (n=15) were studied for comparison. In each biopsy we determined (1) numbers of muscle fibers with alkaline phosphatase (AlkP) staining, (2) numbers of acid phosphatase-(AcP) positive cells, (3) dystrophin levels by immunocytochemistry, and (4) the distribution of merosin and laminin-A staining. A ratio of AcP:AlkP staining was calculated for each biopsy. In nine patients with congenital muscular dystrophy (younger than 4 years of age) with normal dystrophin, the AcP:AlkP ratio was low (0.09 +/- 0.03). In contrast, in Duchenne muscular dystrophy, the AcP:AlkP ratio was 15 times higher (1.6 +/- 0.04, p=0.001). The three children with congetial muscular dystrophy syndromes and reduced dystrophin and one child with facioscapulohumeral dystrophy had AcP:AlkP ratios in the range of Duchenne muscular dystrophy patients (2.4 +/- 1.4). Low Ac:AlkP ratios were related to relative absence of AcP-positive cells. Merosin staining was absent in 5 of the 17 congenital muscular dystrophy biopsies tested. None of the 5 children with merosin-negative but all 12 with merosin-positive stains walked (p=0.0002). We conclude that a pattern of few AcP-positive cells in the setting of numerous AlkP staining muscle fibers has specificity for congenital muscular dystrophy syndromes and provides histopathologic support for the diagnosis. Reduced merosin in muscle predicts more severe weakness and long-term disability.

Acid Phosphatase↗
PubMed1996

Childhood chronic inflammatory demyelinating neuropathies: clinical course and long-term follow-up.

Chronic inflammatory demyelinating neuropathy (CIDP) is a rare disease in childhood. We reviewed the clinical characteristics, response to therapy, and long-term prognosis in 13 children (1.5 to 16 years of age) diagnosed with CIDP at Washington University Medical Center, St. Louis, and the Royal Children's Hospital, Melbourne, Australia, between 1979 and 1994. The most common presenting symptom (in 11/13 [85%]) was lower extremity weakness associated with difficulty in walking. Preceding events within 1 months of onset, mostly intercurrent infections or vaccinations, occurred in seven children (54%). The disease was monophasic in three children (23%). One relapse occurred in four (30%) and multiple relapses in six (46%). All patients had at least short-term response to steroids. Three children (23%) recovered completely during the first year. Ten children (77%) had residual weakness after an average follow-up of 6 years. There seems to be two populations of children with CIDP. One subgroup, with a favorable prognosis, progressed to peak disability over less than 3 months; these children often have a monophasic course with complete resolution of symptoms and signs and withdrawal from all medications by 1 year after onset. A second subgroup progressed for 3 months or longer; these children all required substantial does of prednisone for prolonged periods and had considerable long-term morbidity with persistent weakness.

Adolescent↗
PubMed1996

Mutations in the human skeletal muscle chloride channel gene (CLCN1) associated with dominant and recessive myotonia congenita.

Myotonia, defined as delayed relaxation of muscle after contraction, is seen in a group of genetic disorders that includes autosomal dominant myotonia congenita (Thomsen's disease) and autosomal recessive myotonia congenita (Becker's disease). Both disorders are characterized electrophysiologically by increased excitability of muscle fibers, reflected in clinical myotonia. These diseases are similar except that transient weakness is seen in patients with Becker's, but not Thomsen's disease. Becker's and Thomsen's diseases are caused by mutations in the skeletal muscle voltage-gated chloride channel gene (CLCN1). Genetic screening of a panel of 18 consecutive myotonia congenita (MC) probands for mutation in CLCN1 revealed that a novel Gln-68-Stop nonsense mutation predicts premature truncation of the chloride channel protein. Four previously reported mutations, Arg-894-stop, Arg-338-Gln, Gly-230-Glu, and del 1437-1450, were also noted in our sample set. The Arg-338-Gln and Gly-230-Glu mutations were found in patients with different phenotypes from those of previous reports. Further study of the Arg-338-Gln and Gln-230-Glu alleles may shed light on variable modes of transmission (dominant versus recessive) in different families. Physiologic study of these mutations may lead to better understanding of the pathophysiology of myotonia in these patients and of voltage-gated chloride channel structure/function relationships in skeletal muscles.

Chloride Channels↗
PubMed1994

Course and outcome of acute cerebellar ataxia.

We report a study of 73 consecutive children with acute cerebellar ataxia, representing all of the children evaluated at St. Louis Children's Hospital during a 23-year-period to whom this diagnosis could appropriately be assigned. Twenty-six percent had chickenpox, 52% had other illnesses that were presumed to be viral, and in 3% the ataxia was related to immunization. Nineteen percent had no definite prodrome. Sixty children were followed for 4 months or longer after onset of their ataxia (mean, 7.4 +/- 6.0 years). Ninety-one percent (55/60) of these, including all children with chickenpox, recovered completely from ataxia. Eighty-nine percent (39/44) of the children with non-varicella-related ataxia recovered completely from the ataxia, a much better rate of recovery than what was found in prior large studies. One fifth of the children followed for more than 4 months experienced transient behavioral or intellectual difficulties, but only 5 of the 60 children demonstrated sustained learning problems. This study represents the largest reported series of acute cerebellar ataxia and the most complete characterization of the clinical features and outcome of this illness.

Acute Disease↗
PubMed1994

The role of the pre-symptomatic food handler in a common source outbreak of food-borne SRSV gastroenteritis in a group of hospitals.

A common source outbreak of small round structure virus (SRSV) gastroenteritis affected 81 patients and 114 staff in four hospitals served by one central hospital kitchen. Eating salad items was found to be significantly associated with illness. In a cohort study of a staff buffet function eating turkey salad sandwiches was associated with illness (relative risk = 2.4; 95% CI = 1.4-4.1; P = 0.003), and a case control study of patients in one hospital showed an odds ratio of 6.6 (95% CI = 1.0-71.6; P = 0.04) for eating tuna salad and becoming ill. One of two food handlers who prepared the salads became ill the day following food preparation; she also had a young child at home who had been ill with a gastrointestinal illness during the previous two days. Contamination of food by mechanical transmission of the virus from the child via clothes and hands of the mother, or pre-symptomatic faecal excretion in the mother are possible explanations of contamination of food.

Caliciviridae Infections↗
PubMed1993

What are the complications of influenza and can they be prevented? Experience from the 1989 epidemic of H3N2 influenza A in general practice.

OBJECTIVES: In an epidemic: to measure the incidence and risk of complications of influenza; to determine the effect of pre-existing disease on complications; to estimate vaccine uptake and efficacy. DESIGN: Case-control study. SETTING: Primary care: two group practices. SUBJECTS: 342 of the 395 cases of clinically diagnosed influenza reported to the general practice surveillance of infectious diseases scheme of the Public Health Laboratory Service during the 1989 epidemic, and 342 age and sex matched controls. INTERVENTIONS: Examination of records. MAIN OUTCOME MEASURES: Documented recognised complications; hospital admission; previous vaccination. RESULTS: Of 15 recognised complications, bronchitis was the commonest (rate 190.1/1000 cases) and significantly commoner in cases (summary odds ratio 9.7) after adjusting for higher consultation rates (mean 6.1 per annum v 4.2 among controls; p < 0.0001). No deaths were recorded. The risk of bronchitis complicating influenza was higher in patients with pre-existing illnesses regarded as an indication for vaccination (odds ratio 3.3; p < 0.0001). Observed vaccination efficacy in those with pre-existing illnesses and in elderly subjects was high (63% and 77% respectively) but uptake was low (4.5% and 6.1% respectively). CONCLUSIONS: Bronchitis complicates about one fifth of all cases of influenza presenting to general practitioners. Patients with pre-existing illnesses regarded as an indication for vaccination are particularly at risk. Vaccine uptake is extremely low, precluding an unequivocal demonstration of a protective effect.

Adolescent↗
PubMed1993

High-titer selective serum anti-beta-tubulin antibodies in chronic inflammatory demyelinating polyneuropathy.

Although chronic inflammatory demyelinating polyneuropathy (CIDP) is presumed to be an autoimmune disorder, no neural antigen has been recognized as an immune target. We found that serum IgM from a patient with CIDP and an IgM paraprotein reacted with a 53-kd protein by Western blot analysis. Amino acid sequence analysis identified this protein as beta-tubulin. We then studied sera from 70 CIDP patients, 35 Guillain-Barré syndrome (GBS) patients, and 483 disease (amyotrophic lateral sclerosis, Alzheimer's disease, multiple sclerosis, diabetes, and other polyneuropathies) and normal controls for selective high-titer anti-beta-tubulin using ELISA methodology. Forty-two percent (30/70) of patients with CIDP had selective high titer IgM reactivity against beta-tubulin; 23% (16/70) had selective high-titer IgG reactivity against beta-tubulin. Overall, 57% of CIDP patients, 20% of GBS patients, and 2% of control patients had selective, high serum IgM or IgG anti-beta-tubulin reactivity. Selective high-titer serum anti-beta-tubulin antibodies occur in a majority of patients with CIDP but are rare in other chronic neuropathies or CNS disorders.

Adult↗
PubMed1992

Assessment of body composition in heart transplant patients.

Orthotopic heart transplantation (OHT) recipients often experience increased body weight (BW) following surgery. Using hydrostatic weighing (HW), this study assessed the body density (BD) and body composition of 17 white and seven black male OHT patients. It examined the cross-validity of the Jackson and Pollock seven and three site skinfold (SF) regression equations for predicting BD in these patients. We hypothesized that both prednisone (P) dose and months post-operative (MPO) would be inversely related to BD. The average of the last five of ten HW trials was used in computing BD. BW and % body fat (BF) were 88.5 +/- 17.8 kg (mean +/- SD) and 33.5 +/- 9.4%, respectively. The correlation coefficient between hydrostatically determined BD and BD determined via two of the three intercept revised Jackson and Pollock SF equations was r = 0.89, SE = 0.009. A polynomial regression model for BD using P dose and MPO provided a correlation coefficient of r = 0.71, SE = 0.015. Partial correlation techniques incorporating SF, age, MPO, and P dose indicated that neither P dose or MPO provided any significant additive effect, above SF and age, when predicting BD. We conclude that in OHT patients receiving glucocorticoids, the intercept revised Jackson and Pollock SF regression equations are generally applicable and associated with a SE of +/- 4 BF percentage points. Up to 49 months after OHT, both P dose and MPO are inversely related to BD but provide no additive value above SF for predicting BD.

Adult↗
PubMed1990

Clinical features of bilirubin encephalopathy.

Clinical features of bilirubin encephalopathy vary depending on the age of the infant and the degree of hyperbilirubinemia. In term infants with hyperbilirubinemia, three distinct clinical phases are apparent in the first weeks of life, and long-term consequences include extrapyramidal disturbances (particularly athetosis), hearing loss, gaze abnormalities (particularly limitation of upward gaze), and, in a minority, intellectual deficits. In term infants with moderate hyperbilirubinemia, minor delay in motor development during the first year has been demonstrated, but with longer follow-up this delay is not apparent. Associated conditions such as sepsis, anoxia, and acidosis may increase the likelihood of neurotoxicity of bilirubin in these infants. The clinical consequences of moderate hyperbilirubinemia in premature infants are unclear. No acute clinical syndrome is recognizable during the first weeks. The results of follow-up studies are variable. Hearing loss is the commonest consequence. Follow-up through age 2 years in one large study suggests that static encephalopathy may be a sequel. Longer follow-up is needed to understand the clinical consequences of moderate hyperbilirubinemia in this important group of infants.

Humans↗