Gender differences in the onset of diabetic neuropathy

Abstract

Objective

Diabetic neuropathy is one of the more common complications plaguing individuals with type 2 diabetes. The development and progression of such complications are responsible for much of the morbidity and mortality related to this disease. Few studies have evaluated age at onset of diabetic neuropathy between genders. A difference in the progression of diabetic neuropathy between men and women may exist. This investigation evaluated gender differences in the age at onset of neuropathy among patients with type 2 diabetes.

Methods

The study, a retrospective chart analysis, reviewed 376 inpatient and outpatient medical records between January 2004 and January 2006 from a Cleveland, Ohio, hospital. Onset of neuropathy was determined by the date the neuropathy International Classification of Diseases, Ninth Revision code was first included in the medical chart; for this study, onset was equated with the date of first identification. Data were analyzed via a tailed independent t test.

Results

Of the 376 inpatient and outpatient charts reviewed, 156 were for male patients and 220 were for female patients (41% and 59%, respectively). All patients had type 2 diabetes; however, 23% (n=86) required insulin therapy at the time of the study. Males developed neuropathic complications at 63 years, approximately 4 years earlier than did females (at 67 years). The t test revealed a statistically significant difference in age at onset of diabetic neuropathy between the male and female subjects.

Conclusions

This study demonstrates that the males in the study population developed neuropathy earlier than did the females. It may then be hypothesized that earlier interventions in the male population may improve disease outcomes.

Introduction

Type 2 diabetes mellitus (DM2), a common metabolic disorder characterized by hyperglycemia, is caused by genetics, environmental factors, and lifestyle choices. It is also characterized by insulin resistance, diminished insulin secretion, and increased hepatic glucose production (Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997, Kuzuya et al., 2002). The metabolic abnormalities that occur with DM2 cause alterations in several organ systems, place physical and emotional burdens on individuals with DM2, and negatively impact the health care system (Caro et al., 2002, Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997, Gordois et al., 2003, Shearer et al., 2003).

The metabolic alterations linked to DM result in chronic complications that account for much of the morbidity and mortality associated with this disorder (Kuzuya et al., 2002, UK Prospective Diabetes Study Group, 1998). These complications, primarily vascular in nature, may be divided into macrovascular (Andersson & Svardsudd, 1995, Dyck et al., 1995, Wandell, 1999) and microvascular (Booya et al., 2005, Bruce et al., 2005, Dyck et al., 1995, Henry, 1996, Wandell, 1999) complications. Macrovascular complications include cerebrovascular disease, coronary artery disease, and peripheral vascular disease (Gaster & Hirsch, 1998, Maser et al., 1989, Wandell, 1999), whereas microvascular complications include neuropathy, retinopathy, and nephropathy (McClean et al., 2005, Wandell, 1999).

The risk for microvascular diabetic neuropathy is directly proportional to the duration of hyperglycemia and that of diabetes (Booya et al., 2005, Bruce et al., 2005, Klein et al., 1996, Kuzuya et al., 2002). A study that compared 110 patients with DM and those without neuropathy found that hyperglycemia was the only modifiable risk factor for diabetic neuropathy. Furthermore, the study found that patients with poor glycemic control had a 0.3 times greater risk for the development of diabetic neuropathy (Booya et al., 2005). Most individuals with DM2 remain asymptomatic before being diagnosed. Many have manifestations of one or more diabetic complications at the time of diagnosis (Booya et al., 2005, Harris et al., 1992, Kramer et al., 2005, UK Prospective Diabetes Study Group, 1998); the number increases to as many as 50% of all individuals throughout the course of the disease (Pirart, 1977).

Treatment of diabetic neuropathy revolves around improved glycemic control, which may help improve nerve conduction velocity (Dyck et al., 1995, Gaster & Hirsch, 1998, Kramer et al., 2005, Tolle et al., 2006). Improved glycemic control has been shown to slow down—and possibly halt—the progression of diabetic neuropathy (Ohkubo et al., 1995, Tolle et al., 2006). In one study, intensive insulin therapy decreased the appearance of neuropathy by 69%, as evidenced by nerve conduction testing at a 5-year follow-up examination (Diabetes Control and Complications Trial Research Group, 1993). Despite adequate glucose control, the symptoms associated with neuropathy may persist. These symptoms include pain, hyperesthesia, paresthesia, allodynia, and altered sense of position (Gordois et al., 2003, Ohkubo et al., 1995). This persistence may decrease quality of life and increase the frequency of hospital and physician visits among patients (Gordois et al., 2003, UK Prospective Diabetes Study Group, 1998). Gordois et al. estimated that among the 10.27 million individuals with DM2 in the United States, $10.15 billion is expended annually in the treatment of diabetic neuropathy and its complications. As a result, early prevention of the complication of diabetic neuropathy is imperative for the health and well-being of these patients; it may also reduce the health care burden that these patients will inevitably incur (Caro et al., 2002, Gordois et al., 2003).

Early prevention may lie in identifying risk factor profiles for diabetic neuropathy. One such risk factor is total hyperglycemia exposure (Booya et al., 2005, Bruce et al., 2005, Klein et al., 1996, Kuzuya et al., 2002). Gender may also be an important factor in the development of diabetic neurologic complications. Few studies have evaluated gender as a potential risk factor for the development of neurologic symptoms in patients with diabetes (Albers et al., 1996, Booya et al., 2005, Brown et al., 2004, Diabetes Control and Complications Trial Research Group, 1993). These studies failed to either assess age at onset of diabetic neuropathic symptoms (Albers et al., 1996, Booya et al., 2005, Brown et al., 2004) or separate DM1 from DM2 (Gregersen, 1967, Valensi et al., 1997). This study differs from studies in the current literature in that it sought to evaluate gender differences in the progression and age at onset of diabetic neuropathy complications in individuals with DM2.