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Biomedical subjects

William L Isley

Publications and source records attributed to William L Isley.

27 records · Page 2Linked to original sources
PubMed2002

Growth hormone therapy for adults: not ready for prime time?

Human growth hormone is now readily available and approved for treatment of the growth hormone deficiency syndrome in adults. However, physicians have been slow to adopt this therapeutic modality. Reasons for skepticism about the use of growth hormone for the growth hormone deficiency syndrome include doubts about whether growth hormone deficiency causes increased morbidity and mortality in patients with hypopituitarism; availability of highly efficacious, easier to use, and less expensive agents for certain aspects of the growth hormone deficiency syndrome, especially cardiovascular disease; and concerns about possible toxicity in adults. Long-term studies in patients receiving appropriate comprehensive management for other hormonal deficiencies and for concomitant abnormalities will be required to convince physicians of the utility and safety of growth hormone replacement therapy.

Adult↗
PubMed2002

Novel mutations of APOB cause ApoB truncations undetectable in plasma and familial hypobetalipoproteinemia.

Familial hypobetalipoproteinemia (FHBL) is a genetic disorder characterized by low levels of apoB-100 and LDL cholesterol. Truncation-producing mutations of apoB (chromosome 2) are among several potential causes of FHBL in patients. Ten new families with FHBL linked to chromosome 2 were identified. In Family 8, a 4432delT in exon 26 produces a frame-shift and a premature stop codon predicted to produce a truncated apoB-30.9. Even though this truncation is just 10 amino acid shorter than the well-documented apoB-31, which is readily detectable in plasma, apoB-30.9 is undetectable. Most truncations shorter than apoB-30 are not detectable in plasma. In Family 34, an acceptor splicing mutation at position -1 of exon 14 changes the acceptor splice site AG to AA. Two families (Family 50 and 52) had mutations (apoB-9 and apoB-29) reported previously. In Family 98, a novel point mutation in exon 26 (11163T>G) causes a premature stop codon, and produces a truncated apoB-80.5 readily detectable in plasma. Sequencing of the ApoB gene in families 1, 5, 18, 58, and 59 did not reveal mutations.

Adult↗
PubMedDate not supplied

Hyperthyroidism: a "curable" cause of congestive heart failure--three case reports and a review of the literature.

With the increasing incidence of coronary artery disease and the aging population, the prevalence of congestive heart failure (CHF) is increasing. In the majority of these cases the etiology is underlying coronary artery disease. Other less common causes of CHF include valvular heart disease, hypertension, alcoholic cardiomyopathy, and dilated cardiomyopathy. In addition, there are rare causes, one of which is hyperthyroidism. Hyperthyroidism can affect the cardiovascular system in a variety of ways. The cardiovascular manifestations range from sinus tachycardia to atrial fibrillation and from a high cardiac output state to CHF due to systolic left ventricular dysfunction. If the underlying hyperthyroidism is recognized and treated early the CHF in such cases can be cured. The authors present three cases of CHF due to systolic left ventricular dysfunction secondary to hyperthyroidism, which showed considerable improvement in the left ventricular function once the hyperthyroidism was treated.

Adult↗