Letters to the Editor

Physicians Should Counsel Patients About Exercise

TO THE EDITOR: We enjoyed reading the article "Counseling for Physical Activity in Overweight and Obese Patients."¹ We would like to make some further observations. The prevalence of obesity and being overweight is significantly higher in the United States compared with Spain, where the prevalence of obesity among persons 25 to 60 years of age is 13.3 percent for men and 15.7 percent for women.² However, the particular problem of a lack of exercise counseling by health professionals seems to be similar in these two countries. In a nonpublished, community-based, cross-sectional survey conducted in 2002 in our Family Medicine Teaching Unit, we found that fewer than 36 percent of the 481 adult subjects interviewed received counseling on physical activity from their primary care physician. This resulted in fewer than 21 percent of the subjects increasing their amount of exercise.

Because many clinical practice guidelines recommend physical activity for patients who are obese, even when they do not lose weight, the optimal intensity level will depend on the patient’s objectives. If, as the authors state,¹ the patient is searching for weight reduction then the emphasis should be on increasing duration rather than intensity to optimize caloric expenditure. If the patient is searching to improve cardiovascular fitness, exercise should be performed at a certain intensity threshold. Different studies have determined this threshold: the Institute for Aerobics Research² established a fitness threshold of 10 metabolic equivalents (METs) oxygen consumption for men and 9 METs for women; the Harvard study³ set a caloric expenditure threshold of at least 1,500 extra calories for physical activity per week. This implies the need to report the prevalence of active and nonactive people, and to quantify and analyze their level of activity.

It is surprising how infrequently an intervention with such a positive cost-benefit effect is implemented in general practice. Some authors⁴ in Spain try to explain this situation with the following reasons: lack of formal training in health professionals; busy practice; inadequate institutional support; little interest in research; lack of coordination between health professionals and physical activity specialists; and lack of support from mass media. Research and promotion campaigns should be encouraged if physicians want to achieve the goals presented in the article by McInnis and colleagues.¹

GUSTAVO DE TERESA, M.D.
CAROLINA BURGOS, M.D.
West Valladolid Regional Family Practice Residency Program
Gerencia de Atención Primaria
Paseo de Filipinos s/n-3^a planta
Valladolid, Spain 47007

REFERENCES

1. McInnis KJ, Franklin BA, Rippe JM. Counseling for physical activity in overweight and obese patients. Am Fam Physician 2003;67:1249-56.
2. Blair SN, Kohl HW 3d, Paffenbarger RS Jr, Clark DG, Cooper KH, Gibbons LW. Physical fitness and all-cause mortality. A prospective study of healthy men and women. JAMA 1989;262:2395-401.
3. Paffenbarger RS Jr, Kampert JB, Lee IM, Hyde RT, Leung RW, Wing AL. Changes in physical activity and other lifeway patterns influencing longevity. Med Sci Sports Exerc 1994;26:857-65.
4. Ortega Sanchez-Pinilla R. [Commentary: Physical Activity Should be Promoted More Effectively to Catch Up with the Rest of Europe] [in Spanish]. Aten Primaria 2003;31:86.

CASE STUDY

There Is No Substitute for a Thorough Drug History

TO THE EDITOR: A 78-year-old man presented with a two-month history of generalized weakness, nausea, upper abdominal discomfort, anorexia, and weight loss of 15 lb. There was no history of fever, vomiting, diarrhea, or dysuria. Medical history included hypertension, osteoarthritis, benign prostatic hypertrophy, and hypercholesterolemia. The patient denied using tobacco or alcohol, but was taking atenolol, tamsulosin, aspirin, and calcium and iron tablets.

On examination, he was afebrile with normal vital signs. Pertinent systemic examination revealed overt icterus, minimal tenderness on deep palpation in the epigastric region, and bilateral knee-high pedal edema. No hepatosplenomegaly or other stigmata of cirrhosis were appreciated.

Laboratory examinations revealed: serum aspartate transaminase, 345 U per L; alanine transaminase, 151 U per L; serum alkaline phosphatase, 2,356 U per L; total serum bilirubin, 12.4 mg per dL (212 mmol per L); conjugated bilirubin, 8 mg per dL (136.8 mmol per L); and albumin, 1.8 g per dL. Prothrombin time, partial thromboplastin time, alfa-feet protein, antimitochondrial antibodies, and complete blood count were within normal limits.

Differential diagnosis of obstructive jaundice included: carcinoma of the head, pancreas, or biliary tract; gallstones; or sludge causing bile duct obstruction. Infiltrative liver disorders and the patient’s medications were less likely to cause obstructive jaundice. Hepatobiliary ultrasound examination revealed no dilated intrahepatic ducts and normal echogenicity of liver without any solid masses. The gallbladder was minimally diseased containing some sludge. The biliary duct was not dilated. An abdominal computed tomographic scan did not reveal a pancreatic mass. Endoscopic retrograde cholangiopancreatography (ERCP) failed to demonstrate any dilation of common bile duct, with no evidence of stones. After failing to cannulate pancreatic duct, magnetic resonance imaging with ERCP revealed an atrophic pancreas without any focal masses. No dilation or distortion of pancreatic duct was observed. The liver biopsy showed normal lobular architecture with prominent cholestasis.

After an unrevealing work-up for obstructive jaundice, repeated inquiry revealed he had been taking 500 mg of sustained-released niacin twice daily for the past year. Within 12 weeks of cessation of the niacin, liver function was normal.

Hepatotoxicity associated with sustained-released niacin can be hepatocellular, cholestatic, or mixed.¹ The majority of cases of niacin-induced hepatitis are hepatocellular.^1,2 The mechanism of hepatocellular and cholestatic injuries from use of niacin is dose-related hepatotoxicity rather than hypersensitivity.² Constant exposure of hepatocytes to sustained-release niacin without a washout period between doses may account for increased chances of liver injury.³

The causative agent for the liver injury in this patient was niacin, based on the following: the temporal relation between the use of niacin and cholestasis; the fact that a full work-up for cholestatic jaundice was unrevealing; and liver function returning to normal within 12 weeks of cessation of niacin. Because cholestatic hepatitis is an uncommon adverse effect caused by sustained-release niacin, it can be easily overlooked.

With the major emphasis on lowering cholesterol levels, there is an increased interest in niacin. Physicians need to recognize sustained-release niacin-induced cholestatic jaundice by taking a thorough drug history that includes the use of vitamins.

NAGESH CHOPRA, M.D.
Southeast Colorado Hospital
373 East 10th Ave.
Springfield, CO 81073

REFERENCES

1. Reimund E, Ramos A. Niacin-induced hepatitis and thrombocytopenia after 10 years of niacin use. J Clin Gastroenterol 1994;18:270-1.
2. Clementz GL, Holmes AW. Nicotinic acid-induced fulminant hepatic failure. J Clin Gastroenterol 1987;9:582-4.
3. Lawrence SP. Transient focal hepatic defects related to sustained-release niacin. J Clin Gastroenterol 1993;16:234-6.