Thanh Nguyen, PharmD

Dr. Nguyen is a freelance clinical writer based in San Jose, California. 

Dr. Muzyk is a freelance clinical writer based in Tampa, Florida.

Hypertension is often a silent condition that can lead to end organ damage such as renal failure if inadequately treated.

Management of hypertension includes maintaining blood pressure (BP) at goal, preventing complications, and promoting health. According to the hypertension guidelines from the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), the goal BP should be below 140/90 mm Hg (130/80 mm Hg for patients with diabetes or chronic kidney disease).

 It is crucial that health care providers and patients work together closely to achieve and maintain treatment goals for hypertension. 

The pharmacist has many opportunities during personal interactions with a patient to establish a professional and caring relationship and become a valuable information resource for hypertension management. One of the best ways to gain respect and trust from a patient is through effective communication during patient counseling sessions. Patient counseling for managing hypertension should focus not only on improving understanding of the disease state and antihypertensive medications, but also on enhancing patients’ awareness of nonpharmacologic treatment options. 

When communicating with patients, it is important to simplify medical terminologies. If the patient is receiving an antihypertensive medication for the first time, the pharmacist should assess the patient’s knowledge about hypertension and provide a quick overview when necessary. The overview can begin with an explanation of hypertension as a condition in which BP is elevated. The pharmacist also should point out that untreated hypertension can lead to dire consequences, such as renal failure, stroke, or heart failure.

 According to a review of randomized clinical trials, antihypertensive therapy can reduce incidence of stroke by 35% to 40%, heart attack by 20% to 25%, and heart failure by >50%.

Lifestyle modification (LSM) alone can sometimes suffice in the management of hypertension. It has been shown that a healthy lifestyle can reduce BP significantly, enhance the efficacy of antihypertensive agents, and decrease cardiovascular risks.

 LSM includes increasing physical activity, smoking cessation, limiting alcohol consumption, reducing sodium intake, and adopting the Dietary Approaches to Stop Hypertension (DASH) plan.

 Pharmacists also should inform their patients that every 10 kg in weight reduction can equal a reduction of up to 20 mm Hg in systolic BP, and the   continued on page 71 66 n 12.09 | Pharmacy Times www.PharmacyTimes.com All patients on antihypertensive medications should be counseled to monitor for signs and symptoms of hypotension. DASH diet can also equal a reduction of up to 14 mm Hg in systolic BP, according to multiple long-term studies. 

In addition to LSM, some patients with hypertension also require medication( s) to achieve their BP goal. The pharmacist can help to ensure patients know how and when to administer medications correctly and what to expect from them. When taking antihypertensive medications, all patients with hypertension need to be informed about signs and symptoms of hypotension, which include dizziness, blurred vision, weakness, and confusion. Patients should be told to rise slowly from a lying or sitting position to reduce dizziness and avoid falls. 

The pharmacist and patient also need to discuss the common side effects of his or her medication and the signs and symptoms of a true allergic reaction, such as hives, wheezing, and swelling of the lips, tongue, or face. The table summarizes the general counseling points for each antihypertensive class.

Patient adherence is paramount for the treatment of hypertension. Hypertension usually does not exhibit any major symptoms, and many antihypertensive medications can have serious side effects; thus, nonadherence is very common.

The pharmacist has a vital role in stressing the importance of adherence in managing hypertension and slowing future complications. 

As well as improved understanding of drug therapy and awareness of the importance of LSM, regular self-monitoring of BP can significantly increase adherence. Self-monitoring of BP gives patients a chance to see their response to antihypertensive medications and also helps rule out white-coat syndrome. Pharmacists can provide assistance in the selection of a BP monitoring device to ensure the appropriate cuff size and proper use before purchasing. 

Pharmacists should advise patients to measure their BP at home daily and have them demonstrate the proper method to take their BP.

 All patients should be informed about their BP goal and be advised to keep a record of their BP readings, including the date and time taken. Pharmacists also should encourage patients to bring their BP record to their appointments with their primary health care provider for followup. 

In order to build a trusting relationship with patients, pharmacists must express care and sympathy, be responsive to patients’ questions, and be able to recognize their needs and concerns. As the most accessible health care professional, pharmacists can have a great impact on the outcomes of hypertension management. 

1. Remuzzi, G, Ruggenenti, P, Perico, N. Chronic renal diseases: Renoprotective benefits of renin-angiotensin system inhibition. 

	2. Weir, MR. Progressive renal and cardiovascular disease: Optimal treatment strategies. 

	3. Chobanian, AV, Bakris, GL, Black, HR, Cushman, WC. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 Report. 

	4. Levy, D, Larson, MG, Vasan, RS, et al. The progression from hypertension to congestive heart failure. 

	5. Staessen, JA, Fagard, R, Thijs, L, et al. Randomised double-blind comparison of placebo and active treatment for older patients with isolated systolic hypertension. The Systolic Hypertension in Europe (Syst-Eur) Trial Investigators. 

	6. Coresh, J, Wei, L, McQuillan, G, et al. Prevalence of high blood pressure and elevated serum creatinine level in the United States. Findings from the Third National Health and Nutrition Examination Survey (1988-1994). 

	7. Hsu, CY, McCulloch, CE, Darbinian, J, et al. Elevated blood pressure and risk of end-stage renal disease in subjects without baseline kidney disease. 

	8. Neal B, MacMahon S, Chapman N. Effects of ACE inhibitors, calcium antagonists, and other blood-pressure-lowering drugs: Results of prospectively designed overviews of randomized trials. Blood Pressure Lowering Treatment Trialists' Collaboration. 

	9. The Trials of Hypertension Prevention Collaborative Research Group. Effects of weight loss and sodium reduction intervention on blood pressure and hypertension incidence in overweight people with high-normal blood pressure. The Trials of Hypertension Prevention, phase II. 

	10. He J, Whelton PK, Appel LJ, Charleston J, Klag MJ. Long-term effects of weight loss and dietary sodium reduction on incidence of hypertension. 

	11. Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. 

	12. Vollmer WM, Sacks FM, Ard J, et al. Effects of diet and sodium intake on blood pressure: Subgroup analysis of the DASH-sodium trial. 

	13. Appel, LJ, Moore, TJ, Obarzanek, E, et al. A clinical trial of the effects of dietary patterns on blood pressure. 

	14. Wetzels, GE, Nelemans, P, Schouten, JS, Prins, MH. Facts and fiction of poor compliance as a cause of inadequate blood pressure control: A systematic review. 

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	16. Carter BL, Saseen JJ. Hypertension. In: Dipiro JT, Talbert RL, et al, eds. 

Pharmacotherapy: A Pathophysiologic Approach

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Articles

Educating patients about lifestyle changes, strict medication adherence, and home blood pressure monitoring can help them to avert complications from this often silent condition.

Hypertension: Promoting Adherence When a Condition Is "Silent" 

Dr. Nguyen is a clinical pharmacy writer based in San Jose, California. Dr. Muzyk is a freelance clinical pharmacy writer based in Tampa, Florida.

In recent years, researchers have discovered another form of diabetes, referred to as latent autoimmune diabetes in adults (LADA). Some other names for LADA include diabetes type 1.5, slow-progressing type 1 diabetes, and late-onset autoimmune diabetes.

 Although different names have caused confusion, they all refer to a subset of patients with type 2 diabetes who have antibodies and genetic factors commonly found in those with type 1 diabetes.

LADA is often misdiagnosed as type 2 diabetes because its onset occurs during adulthood.3,4 In addition, patients may still have some healthy b-cell function and thus do not require insulin therapy initially. Patients with LADA can adequately control their blood glucose by making lifestyle changes and taking oral hypoglycemic agents at early stages. Unlike patients with type 2 diabetes who may never need insulin, however, those with LADA will continue to experience a decline in b-cell function and will eventually progress toward insulin dependency.

One factor that is central to the pathophysiology of diabetes is insulin resistance. Many studies agree that insulin resistance in LADA is higher than in recent-onset type 1 diabetes and is similar to long-term type 1 diabetes.

 Some studies showed that patients with LADA have less insulin resistance, compared with those with type 2 diabetes; however, others did not find a difference between the 2 groups.

Besides having a similar clinical presentation as that of type 2 diabetes, LADA carries many immunologic and genetic features of type 1 diabetes. In classic type 1 diabetes, the 4 common islet autoantibodies responsible for attacking the b-cells include glutamic acid decarboxylase antibodies (GADAs), islet cell antibodies (ICAs), islet antigen 2 (IA-2) antibodies, and insulin autoantibodies.

 Two or more types of autoantibodies are often present in type 1 diabetes, whereas a single type of autoantibody is common in LADA. Many studies have shown that patients with LADA are more likely to test positive for GADAs and/or ICA than IA-2 or insulin autoantibodies.

Genetic controls, such as the frequency of immune-regulating genes in the major histocompatibility complex— human leukocyte antigen (HLA)&mdash;region and non-HLA region, play an important role in susceptibility of diseases.

 Certain allelic variations in the HLA region and non-HLA loci that contribute to the risk of type 1 diabetes are also found in patients with LADA.

 At the same time, some differences exist in the degree of immune regulation between LADA and type 1 diabetes. These differences possibly account for a more gradual progression to b-cell destruction in LADA. Some potential contributors include a less marked HLA genetic predisposition to type 1 diabetes, immune tolerance to b-cell antigens, partial regeneration of b-cells, possible protection toward b-cell destruction from certain genes, and less exposure to environmental factors that cause damage to b-cells.

 The actual pathogenesis of LADA remains unknown, however.

At this time, no specific treatment guidelines for LADA are available. In general, treatment should aim to provide metabolic control and prevent chronic complications. Current treatment options for LADA consist of therapeutic lifestyle changes, oral hypoglycemic agents, and insulin. Additionally, ongoing trials that study experimental agents to prevent the progression toward b-cell destruction may lead to a new approach in treating LADA.

First, making therapeutic lifestyle changes is crucial in the management of diabetes. A healthy diet and an active lifestyle can significantly improve therapeutic outcomes. They increase insulin sensitivity, improve blood sugar control, and reduce the risk of developing long-term complications.19 Because most likely some healthy b-cell function remains at diagnosis, many LADA patients are initiated on oral medication(s). Although commonly used hypoglycemic agents, such as sulfonylureas (SUs), metformin, or thiazolidinediones (TZDs), are beneficial in providing blood glucose control, they are used for only short-term treatment of LADA. Eventually, insulin therapy will be required.

Furthermore, the use of oral hypoglycemic agents to treat LADA may have some drawbacks. Many studies do not recommend SUs in the management of LADA. By stimulating insulin secretion, SUs may also release the granules with antigenic properties.

 This in turn amplifies the immune response toward b-cell antigens, which may lead to early exhaustion of b-cell function and can expedite the need for insulin therapy.

 Although metformin is commonly used as a first-line oral agent, it has not been shown to affect the pathogenic process that leads to b-cell destruction when tested in an experimental model of autoimmune diabetes.

 TZDs are often used to control blood glucose by improving insulin sensitivity, but they may not be as effective in treating LADA because there may be less insulin resistance in these patients compared with patients with type 2 diabetes. The comparison of insulin resistance in these 2 groups is still controversial.

Even though the benefit of insulin therapy to the remaining b-cells is unclear, many reports are in favor of early initiation of insulin in patients with LADA. To determine when to begin insulin treatment, residual b-cell function is often evaluated based on C-peptide values, which are directly proportional to levels of insulin production. 

 One study compared the effects of insulin therapy versus treatment with SUs on C-peptide secretion in patients with LADA.

 The results of the study revealed that patients treated with insulin had sustained C-peptide response and maintained better b-cell function. The results also indicated that early initiation with insulin may protect b-cell mass. Another study evaluated the rate of progression to an insulin-dependent state in patients with LADA who were on insulin treatment, compared with those on SUs.

 The results of this study showed that the progression to an insulin-dependent state was slower in the group receiving insulin therapy. Nonetheless, initiation with insulin therapy in patients with LADA may be deterred due to a moderate increase of blood glucose at early stages and reluctance toward insulin injections.

Another future approach to treating LADA is the use of vaccine-based therapy with Diapep277, an immunogenic peptide from the 60kDa heat shock protein. 

 During a phase 2 clinical trial, it has been found to preserve endogenous insulin production in patients newly diagnosed with type 1 diabetes. At this time, Diapep277 also is being explored in another phase 2 trial involving LADA patients, and a phase 3 trial is being conducted to investigate its long-term effects.

Numerous studies are ongoing to explore the distinguishable factors contributing to LADA and focus on potential treatments that can arrest b-cell destruction. Currently, many questions regarding the pathogenesis of and the best treatment for LADA remain unanswered. Nonetheless, it is crucial to accurately diagnose LADA as significant differences in its pathogenesis and treatment approach emerge.