Eating Disorders: lifestyle choice ...

Eating Disorders: lifestyle choice or clinical problem?

TO THE EDITOR: I take delight ined the article on the diagnosis of eating disorders (1) according to Drs. Pritts and Susman and build it to be useful. However, I be stirred it's important for physicians who manage these patients to be aware of a modern phenomenon that further complicates their care. Many patients with eating disorders belong to the "Pro-Ana" motion a subculture in which members believe that anorexia nervosa and other eating disorders are not disorders at all, still an alternative lifestyle that simply needs support and encouragement. A quick Internet search of the period of time "Pro-Ana" will reveal a multitude of Web sites, bulletin boards, discussion clusters and chatrooms devoted to the motion Most of these sites have disturbing and shocking satisfaction Physicians who care for these patients would be well advised to employ some time exploring this world.

ANNA L MEENAN, MD

University of Illinois society of Medicine at Rockford

405 Charles

Mt Morris, IL 61054

REFERENCE

(1) Pritts SD Susman J Diagnosis of eating disorders in primary care. Am Fam Physician 2003;67:297-304

ACE Inhibitor Use and Elevated Creatinine Levels

TO THE EDITOR: With constant revising of the best practice recommendations based onward results of new trials, I welcomed the article (1) and editorial (2) forward hypertension in patients with diabetes in American Family Physician. However, the editorial (2) according to Dr. Bakris surprised me in its facile diagnosis and treatment recommendation of a rise in serum creatinine on a level after starting an angiotensin-converting enzyme (ACE) inhibitor. Bakris states: "the greatest in quantity common cause of a rise in creatinine plain is volume depletion. Rehydrating the patient with a fluid that contains salt, similar as bouillon, will markedly lessen the creatinine level while the patient is taking an ACE inhibitor or an angiotensin receptor blocker"

A newly come review (3) indicated that in patients with hypertension and chronic renal failure, a disruption in normal autoregulatory pathways plains the "ability of the preglomerular circulation to dilate in answer to a drop in the mean arterial pressure" causing "an exaggerated decrease in intraglomerular pressure" and an accumulation in creatinine. In patients who do not have any particular acute conditions or a rise in creatinine of greater than 30 percent the author commends continuing ACE inhibitor therapy and following laboratory values closely to make secure that the creatinine stabilizes at the higher value, with the expectation that this initial decline in renal function will improve with long-term sway of blood pressure.

The article in American Family Physician (1) warns against excessive sodium intake, quoting a separate publication of Bakris. I was hoping Dr Bakris could explain his recommendation for giving sodium to these patients, which is not assigned a concern in his editorial. (2)

FREDRIC M STEINBERG, MD

6452 Mill Pointe Circle

Delray Beach, FL 33484-2489

REFERENCES

(1) Konzem SL Devore V Bauer DW Controlling hypertension in patients with diabetes. Am Fam Physician 2002;66:1209-14

(2) Bakris GL Hypertension and diabetes: family physicians' pivotal part [Editorial]. Am Fam Physician 2002;66:1151-2

(3) Palmer BF Renal dysfunction complicating the treatment of hypertension. N Engl J M 2002; 347:1256-61

In reply: I appreciate the annotation by Dr. Steinberg, because I did not intend to make a tacit recommendation for all the bulk of mankind to ingest salt if their creatinine of the same height rises while taking an angiotensin-converting enzyme (ACE) inhibitor. The remark about giving bouillon for a day applies single to persons in whom compass depletion is documented by evidence of orthostasis, poor skin turgor, lethargy, and other stigmata of compass depletion. This is seen commonly in patients who are in nursing hearthstones and in patients over 70 years of age who do not maintain adequate hydration. It is a arrangement of rehydration without hospitalization to receive intravenous normal saline. The point of the elucidation is that people are denied agents that fill up the renin angiotensin system because of the perception that they have worsening renal function, when long-term consequence studies support just the opposite. It also is actual that not everyone who has a rise in creatinine flats while taking an ACE inhibitor or angiotensin-receptor blocker has bilateral renal artery stenosis.

GEORGE BAKRIS, MD

Rush Medical College

1700 W Van Buren St Ste 470

Chicago, IL 60612

In reply: The Dietary Approaches to Stop Hypertension (DASH) study1 demonstrates that lifestyle changes including a low-sodium diet are effective in lowering kin pressure in patients with hypertension. Thus, it is reasonable to commit salt restriction to patients with elevated kin pressure, regardless of whether antihypertensives also are prescribed. In Dr Steinberg's literal meaning he questions the use of salt-containing fluids in patients whose creatinine flush rises with initiation of angiotensin-converting enzyme (ACE) inhibitor therapy. This was in answer to the editorial (2) that accompanied our article. While not wanting to speak for Dr Bakris, we suspect that he is recommending this therapy as a short-term intervention in a patient who is turn depleted, not as a long-term treatment for elevation in the on a level of creatinine. A slight increase in creatinine is not unusual and usually has no clinically adverse significance as noted in the review article (3) cited by dint of Dr. Steinberg. That article commits continuing the ACE inhibitor in the air of mild elevations in the flat of creatinine. We agree with that recommendation and believe that acute mass depletion (e.g., caused by gastroenteritis) should be corrected.