Making best practice, everyday practice

Login Register

IN PHARMACY: Statin intolerance in high cardiovascular risk Case Study

Read below to complete the CPD questions

Introduction:

This case study reflects clinical challenges in the diagnosis and management of familial hypercholesterolaemia (FH). Pharmacists can play a key role in the care of FH patients, counselling on the safe and effective use of pharmacotherapy as well as ensuring effective outcomes through monitoring for safety, medication adherence, adverse events and therapeutic efficacy.1

In this case study, once the diagnosis is made, there are points of pharmacist intervention that will contribute to the health of the patient and his family.

NOTE: This case study was sponsored by an unrestricted grant from CIPLA which had no control over the content and the experts participated voluntarily.

When answering the CPD questions you MUST read the expert comment as this is essential to the understanding of the Case Study.

Presenter:

Dr Dirk Blom Head of Division of Lipidology
FCP(SA) PhD
Head
Division of Lipidology
Department of Medicine
University of Cape Town
Cape Town


With comment from:

Dr Natie Finkelstein
Hons-BSc (Med Sci)
MSc, PhD, FPS (SA)
FRPharmS, FIPharmM, MSAChem
Visiting Professor: Faculty of Pharmacy
Rhodes University
Grahamstown


Patient: Mr S, 42-year-old male, Civil engineer

  • Married with one son aged 12 years
  • Never smoked
  • Drinks one glass of wine with meals during the week, three to four glasses on weekend nights when socialising
  • Jogs for 45 minutes five days of the week
  • Admits to ‘not paying any attention to his diet’ and ‘eating what he likes’. He is particularly fond of cheese, bacon and pork ribs.

Reason for visit

Mr. S recently moved to a new town following a promotion, seeking new medical care

Medical history

  • Seasonal allergic rhinitis for which he uses an antihistamine as necessary
  • Hypercholesterolaemia: He first became aware of high cholesterol at the age of 17 when his father, who was then 42 years old, had a myocardial infarction and he and his siblings had their cholesterol tested on the advice of their father’s cardiologist. Although his previous doctor advised him to take lipid-lowering medication he only did so briefly several years ago. His main reasons for not taking lipid-lowering medication are that he felt the medication ‘did not agree with him’ and he thought it not necessary because he was a non-smoker and exercised regularly.

Medication

Cetirizine 10mg/daily as needed

Family history

  • Father: Myocardial infarction at age 42, untreated total cholesterol of 10.9mmol/l with triglycerides of 3.0mmol/l, PCI and stent insertion at age 45 followed by a CABG at age 52, takes rosuvastatin 40mg/day and ezetimibe 10mg/day for lipid control
  • Paternal grandmother died suddenly at age 50 of a suspected myocardial infarction
  • Mother: Well with no significant medical problems
  • Siblings: One of four children. Older brother takes atorvastatin 40mg/daily for hypercholesterolaemia Older sister’s total cholesterol is 3.8mmol/l without medication Younger sister has a total cholesterol of 7.9mmol/l but will only take homeopathic remedies

Clinical Examination

  • Height: 1.93m
  • Weight: 90kg
  • BMI: 24.2kg/m2
  • Waist circumference: 94cm
  • Pulse: 62 beats per minute
  • Blood pressure: 122/74mmHg
  • Bilateral inferior arcus cornealis
  • Small nodule in right Achilles tendon
  • Other systems: No abnormalities found

Initial Investigations (following an overnight fast)

Investigation Result Interpretation
Triglycerides 1.1mmol/l Normal
Total cholesterol 10.4mmol/l Increased
HDL-cholesterol 1.3mmol/l Average
LDL-cholesterol 8.6mmol/l Increased
Lipoprotein (a) 225nmol/l Increased
Urine dipstick Normal Normal
Creatinine 82μmol/l Normal
Glucose 4.0mmol/l Normal
Creatinine kinase 88U/l Normal
AST 12U/l Normal
ALT 18U/l Normal

CLINICAL DIAGNOSIS

This patient has the phenotype of heterozygous FH. There is a family history of autosomal dominant hypercholesterolaemia and/or premature cardiovascular disease spanning at least three generations. He also has an Achilles tendon xanthoma. Tendon xanthomata are the most useful clinical sign for the diagnosis of FH. Although tendon xanthomata are not found in all patients with FH, their presence in the setting of autosomal dominant LDL hypercholesterolaemia confirms the diagnosis.

Patients with familial combined hyperlipidaemia (FCH) or polygenic hypercholesterolaemia may have severe hypercholesterolaemia and a positive family history but do not have tendon xanthomata. Although diet can influence serum lipids, such marked elevation of LDL-C cannot be ascribed to diet alone. Triglycerides may be modestly elevated in some patients with FH (e.g. if they are obese or have insulin resistance) and the fact that his father has modest hypertriglyceridaemia does not detract from the diagnosis of FH. Framingham risk scoring underestimates risk markedly in patients with FH and should not be performed. Patients with FH are at high cardiac risk and vascular imaging is not routinely required to make treatment decisions.

Following the history and examination, the patient is told that he has FH, based on the family history of autosomal dominant LDL hypercholesterolaemia, premature coronary artery disease and the tendon xanthoma. His cardiovascular risk is very high and lipid-lowering therapy is required in addition to lifestyle changes.

The patient agrees to see a dietitian for advice on improving his diet and also agrees to try taking lipid-lowering medication again. Because of his previous negative experience with statins he is started on a relatively low statin dose and prescribed atorvastatin 20mg/day with the aim of titrating the dose at four-weekly intervals depending on tolerability and LDL response. The patient is told that although there is quite a wide variation in individual statin responses, he will almost certainly require a high-dose statin because of his very high baseline LDL-C.

THE PHARMACIST’S PERSPECTIVE AND CONTRIBUTION TO THIS PATIENT’S CARE

Mr S arrives at the pharmacy and expresses his concern about taking statins again because of his FH. He is worried about the diagnosis, about taking statins and the implications of this condition for his teenage son.

Dr Finkelstein comments

The most important role of the pharmacist as part of the health care team is to encourage adherence to therapy.1

The pharmacist points out that Mr S was previously on simvastatin 40mg/day and that the dosage of atorvastatin, a more powerful statin in terms of its cholesterol-lowering effect, will result in lower statin levels in the blood and probably fewer side-effects. Also, he recommends that Mr S take his medication at night which may also reduce the risks of side-effects. He points out that adverse effects are normally transitory and research has shown that nonspecific muscle or joint aches and pains only occur in 5% of patients on statin therapy.2

With regard to the risk that his son carries the gene for FH, the pharmacist describes the risk and what can be done to determine this risk.


This section is ONLY for Pharmacy professionals

Intended for Pharmacy professionals registered with the Pharmacy Council and has NOT been accredited for other Health Care Professionals registered with the HPCSA

Do you like this? Share with a colleague