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Biomedical subjects

C P Alderman

Publications and source records attributed to C P Alderman.

11 recordsLinked to original sources
PubMed1994

Abnormal bone mineral metabolism after long-term anticonvulsant treatment.

OBJECTIVE: To present a case of anticonvulsant-induced disturbances of bone mineral metabolism associated with long-term phenytoin treatment. CASE SUMMARY: An 87-year-old woman was hospitalized with generalized acroparesthesia. Her medical history was significant for grand mal epilepsy, which had been treated with phenytoin for more than ten years. On admission she was found to be hypocalcemic, and her alkaline phosphatase concentration was markedly elevated. DISCUSSION: Further investigations revealed that the patient's serum concentration of 25-hydroxycalciferol was well below the expected range. Phenytoin treatment was withdrawn, and calcitriol supplementation commenced. Ten weeks later she was normocalcemic, and the calcitriol dosage was reduced. Radiologic investigations at this time revealed an ununited hip fracture, as well as widespread evidence of bone demineralization. CONCLUSIONS: Minor elevations of liver enzymes observed in association with anticonvulsant treatment may reflect hepatic microsomal enzyme induction. Marked elevation of serum alkaline phosphatase, particularly when seen in concert with hypocalcemia, may be markers of anticonvulsant-induced bone disease. Under these circumstances, further radiologic investigations and measurement of the vitamin D serum concentration should be undertaken.

Aged↗
PubMed1993

Concurrent agranulocytosis and hepatitis secondary to clomipramine therapy.

A 67-year-old man developed concurrent severe agranulocytosis and elevation of hepatic transaminases as a result of treatment with clomipramine. Although such adverse drug reactions can be considered rare events, the potentially serious nature of these reactions vindicate the routine monitoring of blood picture, and liver function tests, after initiation of treatment with tricyclic antidepressants.

Aged↗
PubMed1992

Abnormal platelet aggregation associated with fluoxetine therapy.

OBJECTIVE: To document the development of abnormal hemostasis in a patient treated with fluoxetine. CASE SUMMARY: A 49-year-old man developed a release-type defect in platelet aggregation during treatment with fluoxetine. Abnormal platelet aggregation was observed during platelet viability testing, in which adenosine diphosphate, epinephrine, ristocetin, arachidonic acid, and collagen were used as agonists. Two days after the withdrawal of fluoxetine, platelet function returned to normal. DISCUSSION: Fluoxetine is an antidepressant that is thought to act through inhibition of serotonin reuptake in the central nervous system. Fluoxetine also inhibits the reuptake of serotonin in platelets, significantly decreasing granular storage and potentially influencing platelet aggregation characteristics. Clinical manifestations of abnormal platelet function have been reported in association with fluoxetine therapy. CONCLUSIONS: The rapid normalization of platelet aggregation after the withdrawal of fluoxetine in this patient does not conform to the known clinical pharmacokinetics of norfluoxetine. The half-life of fluoxetine is shorter, suggesting that the parent drug (rather than norfluoxetine) was the causative agent. Serum fluoxetine and norfluoxetine concentrations were not measured in this patient.

Fluoxetine↗
PubMed1990

Creutzfeldt-Jakob disease in a recipient of human pituitary-derived gonadotrophin.

A forty-year-old female presented with an unsteady gait 13 years after receiving an eight-month course of human pituitary-derived gonadotrophin injections as treatment for infertility. Over the next ten months the patient subsequently developed generalised myoclonic jerks and dementia and finally died. Neuropathological examination revealed changes in the brain consistent with Creutzfeldt-Jakob disease. This is the first reported case of Creutzfeldt-Jakob disease in a recipient of human derived gonadotrophin.

Adult↗
PubMedDate not supplied

Continuous subcutaneous heparin infusion for treatment of Trousseau's syndrome.

OBJECTIVE: To describe the use of continuous subcutaneous heparin infusion in the treatment of 2 cases of Trousseau's syndrome. CASE SUMMARIES: Two patients with metastatic carcinoma presented to the hospital with acute coagulopathies consistent with a diagnosis of Trousseau's syndrome. In both cases conventional anticoagulant therapies proved to be impractical and ineffective. DISCUSSION: Considerable literature suggests that oral anticoagulants such as warfarin are ineffective in the treatment of Trousseau's syndrome. Heparin is more effective for this purpose, although continuous intravenous infusion may prove difficult in the ambulatory setting. Intermittent subcutaneous injections of heparin or low-molecular-weight heparin may not provide reliable anticoagulation for the entire dosage interval. Although the use of continuous subcutaneous infusion of heparin has been used for anticoagulation during pregnancy, this is the first report of the use of sodium heparin administered by continuous subcutaneous infusion in the treatment of Trousseau's syndrome. CONCLUSIONS: Continuous subcutaneous heparin infusion may be an effective option for the treatment of Trousseau's syndrome in the ambulatory setting.

Aged↗
PubMedDate not supplied

The potential for teratogenicity of vitamin A and its congeners.

OBJECTIVE: To review the evidence for teratogenic potential associated with the use of vitamin A and synthetic retinoids in Australia. DATA SOURCES: Relevant indexed journal articles and standard drug information reference texts were identified by Medicine and library search. Information was also obtained from the Australian National Perinatal Statistics Unit. DATA EXTRACTION: We summarised human and animal data relating to the teratogenicity of vitamin A derivatives and synthetic retinoids, including case reports documenting systemic effects from topically administered drugs, pertinent information relating to the clinical pharmacokinetics and adverse effects of these compounds, and the approved and potential indications for the use of these agents. DATA SYNTHESIS: Extensive experimental evidence points to the teratogenicity of natural and synthetic retinoids in animals. Data confirming an effect in humans are not as good. Nevertheless case series, case reports and some epidemiological data regarding isotretinoin suggest that synthetic retinoids are similarly teratogenic in humans. Although there are extensive guidelines and legislation dealing with the use of these compounds in the United States and Australia, the potential for teratogenicity induced by vitamin A still exists. This is because retinoids and vitamin A continue to be prescribed for women of child-bearing potential and documented evidence from the United States reveals that not all prescribers comply with recommendations that minimise the risk of malformations. Non-prescription forms of vitamin A are available without a pregnancy hazard warning, and potentially teratogenic amounts are available from dietary sources. CONCLUSIONS: There exists a potential for teratogenicity in association with the use of both synthetic and natural retinoids in Australia. Monitoring systems currently in place in this country may not detect these malformations should they occur.

Abnormalities, Drug-Induced↗