Biomedical subjects

A Biddinger

Publications and source records attributed to A Biddinger.

5 recordsLinked to original sources

PubMed2002

Risk factors for spinal epidural hematoma after spinal surgery.

STUDY DESIGN: A case-control retrospective analysis comparing patients who developed a postoperative spinal epidural hematoma with patients who did not develop this complication. OBJECTIVES: To identify risk factors for the development of an epidural hematoma following spinal surgery. SUMMARY OF BACKGROUND DATA: Neurologic deterioration following spinal surgery is a rare but devastating complication. Epidural hematomas should be suspected in the patient who demonstrates a new postoperative neurologic deficit. The risk factors that predispose a patient to a postoperative spinal epidural hematoma have not been identified. METHODS: Patients who underwent spinal surgery at a single institution over a 10-year period were retrospectively reviewed. Twelve patients who demonstrated neurologic deterioration after surgery and required surgical decompression because of an epidural hematoma were identified. All cases involved lumber laminectomies. A total of 404 consecutive patients that underwent lumbar decompression and did not develop an epidural hematoma formed the control group. Factors postulated to increase the risk of postoperative spinal epidural hematoma were compared between the two groups using logistic regression. RESULTS: Multilevel procedures (P = 0.037) and the presence of a preoperative coagulopathy (P < 0.001) were significant risk factors. Age, body mass index, perioperative durotomies, and postoperative drains were not statistically significant risk factors. CONCLUSIONS: Patients who require multilevel lumbar procedures and/or have a preoperative coagulopathy are at a significantly higher risk for developing a postoperative epidural hematoma.

Blood Coagulation Disorders↗

PubMed2001

Coralline hydroxyapatite as bone substitute in orthopedic oncology.

We retrospectively reviewed the results of 71 consecutive patients managed with coralline hydroxyapatite (Pro-Osteon 500; Interpore Cross International) for bone defects produced as a result of surgical extirpation of bone tumors. All patients underwent a thorough physical examination and a radiographic evaluation at baseline and follow-up by the same senior surgeon (R.B.I.). Seventy-one patients were followed up for an average of 2.4 years (range, 8.1 months to 3.5 years); mean age of female patients was 39.8 years and that of male patients was 30 years. The functional status of patients at follow-up was evaluated based on comparison with preoperative functional status. Radiographic evaluation was performed and graded as follows: stage I (obvious margins), stage II (hazy margins), and stage III (obvious incorporation). The average time of return of preoperative function was 7.6 weeks. There were 3 major and 9 minor complications. We conclude that coralline hydroxyapatite graft in the form of Pro-Osteon 500 is a viable option for the management of bone defects in orthopedic oncology.

Adolescent↗

PubMed1997

Familial thoracic aortic dilatations and dissections: a case control study.

PURPOSE: Evidence suggesting that genetic factors contribute to the development of common disorders can be obtained by demonstrating familial aggregation of the disease. This study investigated whether thoracic aortic dilations and dissections aggregate in families by comparing the prevalence of thoracic aortic aneurysms, thoracic aortic dissections, and sudden death in first-degree relatives of patients referred for thoracic aortic surgery. METHODS: Families were ascertained through 158 nonsyndromic patients referred for surgical correction of either thoracic aortic aneurysms or dissections (probands) and their 843 first-degree relatives. A control group of 547 first-degree relatives was derived from 114 proband spouses. Groups were examined for statistical differences in the prevalence of thoracic aneurysms, thoracic aortic dissections, abdominal aortic aneurysms, sudden death, and myocardial infarctions. RESULTS: First-degree relatives of probands demonstrated a higher prevalence of thoracic aortic aneurysms and sudden death when compared with the control group. Relative risks of thoracic aortic aneurysm development in proband fathers, brothers, and sisters were 1.8, 10.9, and 1.8, respectively. A pattern of inheritance of the thoracic aortic aneurysms could not be determined. CONCLUSIONS: This study indicates proband first-degree relatives are at higher risk of thoracic aortic aneurysms and sudden death compared with a control group. This study supports the role of genetic factors in the cause of thoracic aortic aneurysms and provides important information for identifying individuals at risk.

Aged↗

PubMed1996

Fibrillin-1 (FBN1) mutations in patients with thoracic aortic aneurysms.

BACKGROUND: Mutations in the FBN1 gene are the cause of the Marfan syndrome, an autosomal dominant disorder with skeletal, ocular, and cardiovascular complications. Aneurysms or dissections of the ascending thoracic aorta are the major cardiovascular complications of the disorder. We tested the hypothesis that FBN1 mutations cause thoracic aortic aneurysms or dissections in patients who do not have the Marfan syndrome. METHODS AND RESULTS: The FBN1 gene was screened for mutations by use of genomic DNA from two patients with thoracic aortic aneurysms who did not have the Marfan syndrome. Individual FBN1 exons were amplified with intron-based exon-specific primers; the DNA fragments were screened for mutations using single-stranded conformational polymorphism analysis; and aberrantly migrating bands were sequenced directly. We identified a missense mutation in one patient, D1155N in exon 27. Dermal fibroblasts from the affected individual were used to study the effect of the missense mutation D1155N on fibrillin-1 cellular processing. The mutation decreased the amount of fibrillin-1 deposited into the pericellular matrix. A second putative FBN1 mutation was identified in the second patient, P1837S in exon 44. Although this alteration was not observed in 234 chromosomes from unrelated individuals, the alteration may represent a rare polymorphism. CONCLUSIONS: Results of these studies support the hypothesis that FBN1 mutations cause thoracic aortic aneurysms in patients who do not have the Marfan syndrome. This information is important for understanding the pathogenesis of aortic aneurysms and identification of individuals at risk for developing thoracic aortic aneurysms or dissections.

Adult↗

PubMed1996

Genetic analysis of atherosclerosis: a research paradigm for the common chronic diseases.

Rapid discoveries of novel and unexpected disease-associated genes for atherosclerotic coronary artery disease (CAD) are anticipated as genomic maps become more detailed and methods for mapping complex disease phenotypes become more refined. Although establishing association or linkage of a marker locus to a CAD susceptibility gene is an important first step, the long-term goal should be to define the underlying functional mutations and explore possible disease mechanisms, including the gene-environment interactions that culminate in clinically apparent disease. This review will define a contemporary research paradigm for study of the genetics of CAD and other common chronic diseases using the tools of modern molecular biology and human genetics.

Animals↗