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Biomedical subjects

Alexander Fisher

Publications and source records attributed to Alexander Fisher.

7 recordsLinked to original sources

Vitamin D and parathyroid hormone in outpatients with noncholestatic chronic liver disease.

BACKGROUND & AIMS: The liver plays a central role in vitamin D metabolism. Our aim was to determine the prevalence and type of vitamin D-parathyroid hormone (PTH) disturbance in ambulatory patients with noncholestatic chronic liver disease (CLD) and its relationship with disease severity and liver function. METHODS: We studied 100 consecutive outpatients (63 men, 37 women; mean age, 49.0 +/- 12.1 [SD] y) with noncholestatic CLD caused by alcohol (n = 40), hepatitis C (n = 38), hepatitis B (n = 12), autoimmune hepatitis (n = 4), hemochromatosis (n = 4), and nonalcoholic steatohepatitis (n = 2); 51 patients had cirrhosis. Serum concentrations of 25-hydroxyvitamin D (25[OH]D), PTH, calcium, phosphate, magnesium, creatinine, and liver function tests were determined. RESULTS: Serum 25(OH)D levels were inadequate in 91 patients: vitamin D deficiency (<50 nmol/L) was found in 68 patients and vitamin D insufficiency (50-80 nmol/L) was found in 23 patients. Secondary hyperparathyroidism (serum PTH, >6.8 pmol/L) was present in 16 patients. The prevalence of vitamin D deficiency was significantly higher in cirrhotic vs noncirrhotic patients (86.3% vs 49.0%; P = .0001). In Child-Pugh class C patients, 25(OH)D levels were significantly lower than in class A patients (22.7 +/- 10.0 nmol/L vs 45.8 +/- 16.8 nmol/L; P < .001). Serum 25(OH)D independently correlated with international normalized ratio (negatively; P = .018) and serum albumin (positively; P = .007). Serum 25(OH)D levels of less than 25 nmol/L predicted coagulopathy, hyperbilirubinemia, hypoalbuminemia, increased alkaline phosphatase, and anemia and thrombocytopenia. CONCLUSIONS: Vitamin D inadequacy is common in noncholestatic CLD and correlates with disease severity, but secondary hyperparathyroidism is relatively infrequent. Management of CLD should include assessment of vitamin D status in all patients and replacement when necessary.

Adult↗

Cardiopulmonary complications of ERCP in older patients.

BACKGROUND: Biochemical markers of ERCP-related myocardial injury have not previously been investigated. OBJECTIVE: To evaluate ERCP-related cardiac troponin I (cTnI) release, myocardial ischemia, hemodynamic changes, and arterial hypoxemia in a series of consecutive patients according to age and to determine their relationship to preexisting cardiovascular risk factors (RF) and the development of post-ERCP pancreatitis. DESIGN: Prospective cohort study. SETTING: Tertiary teaching hospital, Canberra, Australia. PATIENTS: Data were collected on 130 consecutive ERCPs performed on 100 unselected patients (aged 18-93 years) by one endoscopist. Patients were divided into two groups: 65 years of age and older (group 1, n = 53; 27 women) and less than 65 years of age (group 2, n = 47; 33 women). INTERVENTIONS: ERCP. MAIN OUTCOME MEASUREMENTS: Cardiovascular RFs were identified, and electrocardiogram (ECG), cTnI, creatine kinase (CK), amylase, and lipase were measured before and 24 hours after ERCP. Oxygen saturation (SpO(2)), heart rate (HR), blood pressure (BP), and ECG were monitored continuously during each procedure. RESULTS: New ECG changes (ischemia, arrhythmias) occurred in 24% of procedures in group 1 and in 9.3% in group 2 (p = 0.168), and episodic arterial hypoxemia (SpO(2) < 90%) in 16.2% (group 1) and 21.4% (group 2) (p = 0.596). A post-ERCP rise in cTnI levels was documented in 6 patients in the older group. Two of these patients died: one from acute myocardial infarction and one from undiagnosed ascending aortic aneurysm. A cTnI rise was not related to any comorbid conditions, total number of RFs, hemodynamic or ECG changes, or arterial desaturation. In patients with a new cTnI rise, the duration of ERCP was significantly longer (59.5 vs. 26.4 minutes, p = 0.026), being 30 minutes or longer in 5 of 6 patients. Post-ERCP pancreatitis was associated with desaturation (relative risk [RR] = 5.9; 95% confidence interval [CI] [1.2, 32.0], p = 0.027) and myocardial ischemia/injury (RR = 4.4; 95% CI [1.4, 7.8]; p = 0.009). CONCLUSIONS: Although the majority of older patients tolerated ERCP well, in 8% of procedures, most of which were prolonged (>30 minutes), myocardial injury, as defined by the release of cTnI, occurred. Desaturation and myocardial ischemia/injury were associated with post-ERCP pancreatitis.

Aged↗

Entacapone-induced hepatotoxicity and hepatic dysfunction.

We describe 2 patients with Parkinson's disease who developed hepatotoxicity associated with the use of entacapone, a novel, mainly peripheral acting inhibitor of catechol-D-methyltransferase. Hepatotoxicity resolved rapidly with discontinuation of the drug. Analysis of causality in a further case initially linked to entacapone exposure was confounded by conflicting serial adverse reaction reports.

Aged↗

Citalopram-induced severe hyponatraemia with coma and seizure. Case report with literature and spontaneous reports review.

Numerous case reports of hyponatraemia followed increasing use of selective serotonin re-uptake inhibitors (SSRIs) but this adverse effect was only rarely observed in relation to citalopram. We report a case of severe hyponatraemia associated with deep coma, seizure, atrial fibrillation and muscle damage in a 92-year-old woman after only two doses of citalopram, and review 14 cases previously published in the literature and 28 cases spontaneously reported to Australian Drug Reaction Advisory Committee (ADRAC). The data presented suggest that citalopram, as well as SSRIs may cause hyponatraemia secondary to syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The majority of symptomatic cases occurred in elderly patients (79% were older than 70 years) and in women (74%). Polymedication and concomitant use of another psychotropic drug or thiazide diuretic may precipitate and/or augment the development of hyponatraemia/SIADH. In 84% of cases, the hyponatraemia associated with citalopram was detected during the first month of treatment. High level of suspicion, close and careful monitoring of serum sodium concentration particularly in elderly patients and especially in the first month of therapy with citalopram may reduce the incidence of this serious and likely not rare adverse effect.

Adult↗