Biomedical subjects

Mark L Britton

Publications and source records attributed to Mark L Britton.

4 recordsLinked to original sources

PubMed2005

Antidepressant-induced sweating.

OBJECTIVE: To report a case of excessive sweating probably caused by paroxetine, review the literature on antidepressant-induced sweating, and provide recommendations for the management of antidepressant-induced sweating. CASE SUMMARY: A 59-year-old white female presented to a pharmacist-staffed pharmacotherapy clinic with episodes of excessive sweating. The episodes occurred primarily on her head and back of the neck. Other etiologies were ruled out and paroxetine was discontinued. Paroxetine had been initiated at least 7 months prior to the reporting of symptoms. Sweating symptoms gradually improved until resolution 5 weeks following discontinuation of paroxetine. The Naranjo probability scale indicated a causal relationship is probable. DISCUSSION: Excessive sweating has been associated with antidepressants including tricyclic antidepressants, selective serotonin-reuptake inhibitors, and venlafaxine. In some patients, these symptoms require therapeutic intervention such as dose reduction, antidepressant substitution, antidepressant discontinuation, or addition of an agent to control sweating. Agents that have been reported successful in controlling the sweating include benztropine and cyproheptadine. CONCLUSIONS: We recommend a patient-specific approach for the management of antidepressant-induced sweating. First, consider dose reduction or a trial off antidepressant medication. In patients in whom this is inappropriate or ineffective, substitution of another antidepressant should be considered. If episodes of excessive sweating persist, consider treatment of sweating symptoms with benztropine or cyproheptadine in the absence of contraindications.

Antidepressive Agents↗

PubMed2005

Angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers for prevention and treatment of nephropathy associated with type 2 diabetes mellitus.

Renal complications resulting from type 2 diabetes mellitus are costly and common. Finding optimal therapy is important for the prevention and management of diabetic nephropathy. Research has focused on antihypertensive agents that modify the renin-angiotensin-aldosterone system. Because of their effects on the glomerulus, angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) have been studied as interventions at various stages of diabetic nephropathy. The ACE inhibitors may delay the progression to microalbuminuria and then clinical albuminuria. The ARBs decrease albuminuria in patients with microalbuminuria and decrease adverse renal events, specifically the progression to end-stage renal disease in patients with clinical albuminuria and hypertension. Limited data suggest that combination therapy with ACE inhibitors and ARBs may slow the progression of microalbuminuria to clinical albuminuria. Because of the variability in degree of albuminuria evaluated and in study designs (numbers of patients, study duration, drug dosages, and outcomes measured), a detailed review of the available literature about ACE inhibitors and ARBs in the prevention or treatment of diabetic nephropathy may provide insight to clinicians.

Albuminuria↗

PubMed2004

Second-generation thiazolidinediones and hepatotoxicity.

OBJECTIVE: To report a case of hepatotoxicity probably caused by pioglitazone, summarize case reports of hepatotoxicity induced by rosiglitazone or pioglitazone, and make recommendations regarding routine liver enzyme measurement in patients taking these agents. CASE SUMMARY: A 39-year-old black woman with type 2 diabetes mellitus, hypertension, and congestive heart failure presented to a pharmacist-staffed diabetes comanagement service. She reported fatigue, dark brown urine, nausea, itching, and loss of appetite. Pioglitazone was promptly discontinued because her symptoms were consistent with those of hepatic dysfunction and pioglitazone was identified as a potential cause. The patient was referred to her physician. Liver enzyme levels were checked 13 days after initial presentation and found to be abnormal: alanine aminotransferase 490 U/L, aspartate aminotransferase 360 U/L, alkaline phosphatase 851 U/L, total bilirubin 3.1 mg/dL, direct bilirubin 2.0 mg/dL, and indirect bilirubin 1.1 mg/dL. Within 2(1/2) months of discontinuing pioglitazone, the patient's symptoms resolved and liver enzyme levels returned to normal. DISCUSSION: Troglitazone, a thiazolidinedione (TZD), was removed from the market because of hepatotoxicity. Reported cases involving the newer TZDs, rosiglitazone and pioglitazone, have been few in number and less severe in consequence. Six cases of rosiglitazone-induced hepatotoxicity and 5 of pioglitazone-induced hepatotoxicity have been reported. Most patients improved symptomatically 2-4 weeks following discontinuation of the offending TZD, with normalization of liver enzyme levels in 2 weeks to 6 months following TZD discontinuation. CONCLUSIONS: Although the timeline and extent of liver enzyme elevation in this case are unclear, the Naranjo probability scale suggests that a causal relationship between pioglitazone and liver disease is probable. Patients with previous TZD-induced hepatotoxicity should not be rechallenged. Cases of hepatotoxicity with second generation TZDs, although clearly linked, have been few in number and less severe in consequence when compared to troglitazone. We agree with current package labeling that requires baseline and then periodic measurement of liver enzymes in patients taking pioglitazone or rosiglitazone.

Adult↗

PubMed2004

Diabetes mellitus non-glucose monitoring: point-of-care testing.

OBJECTIVE: To review and evaluate reimbursable point-of-care testing devices yielding immediate results, other than glucometers, that are available to evaluate and monitor diabetes and its complications and to describe how pharmacists may use these devices. DATA SOURCES: A MEDLINE search (1966-March 2003) was performed using the following search terms: point-of-care systems, clinical diabetes monitoring, decision support systems, glycosylated hemoglobin, and microalbumin. Pertinent company and product Web sites and customer service departments were accessed for information about point-of-care devices and supplies. STUDY SELECTION AND DATA EXTRACTION: All descriptive, evaluative, and comparative articles and product information were reviewed, and relevant information was included. DATA SYNTHESIS: Diabetes mellitus is a complex, chronic metabolic disease that is a challenging management problem and requires routine monitoring for disease control and screening for complications. Point-of-care tests are available to monitor hemoglobin A(1c), glucose, fructosamine, ketones, lipid profiles, urinary microalbumin concentrations, and alanine aminotransferase concentrations. Many of these tests are Clinical Laboratory Improvement Amendments (CLIA)-waived and, therefore, practical for pharmacists to use in a variety of settings. Tests for measuring sensation are also discussed. Pharmacists should consider each of these tests in the establishment of a comprehensive diabetes care service. CONCLUSIONS: The availability of many new point-of-care testing methods creates new opportunities for pharmacists to monitor drug therapy and screen for complications in patients with diabetes. Reimbursement is possible since many of these tests are CLIA-waived.

Albuminuria↗