Letters To The Editor

To the Editor: In the article, “Menstrual manipulation: Options for suppressing the cycle,”¹ the authors described advantages and disadvantages of various hormone-based methods of menstrual manipulation, including prolonged use of oral contraceptives. We believe the authors underemphasized the risks associated with oral contraceptives. Blood clots, stroke, and death are often included in print and television ads by law firms recruiting patients harmed by these drugs. In addition, the authors failed to mention the risk of premenopausal breast cancer due to oral contraceptives, which are now classified as group 1 carcinogens by the World Health Organization.²

In October 2006, we published the most current meta-analysis to date regarding oral contraceptive use and the risk of premenopausal breast cancer.³ We found that 21 out of 23 studies showed a positive trend or positive risk for premenopausal breast cancer with oral contraceptive use prior to first-term pregnancy. This resulted in a highly statistically significant cumulative risk of 44% (ie, odds ratio 1.44, 95% confidence interval 1.24–1.68). Our meta-analysis remains the most recent study in this area and updates the Oxford pooled analysis,⁴ which relied on older studies with older women (two-thirds of whom were over age 45).

A more recent collaborative study coauthored by investigators from the National Cancer Institute, the Hutchinson Cancer Research Center, and the University of Washington includes oral contraceptives in the list of risk factors for breast cancer in younger women.⁵ We ask your readers to consider that patients are entitled to know about this important risk factor before making a decision regarding hormonal menstrual manipulation.

To the Editor: In the article, “Menstrual manipulation: Options for suppressing the cycle,”¹ the authors described advantages and disadvantages of various hormone-based methods of menstrual manipulation, including prolonged use of oral contraceptives. We believe the authors underemphasized the risks associated with oral contraceptives. Blood clots, stroke, and death are often included in print and television ads by law firms recruiting patients harmed by these drugs. In addition, the authors failed to mention the risk of premenopausal breast cancer due to oral contraceptives, which are now classified as group 1 carcinogens by the World Health Organization.²

In October 2006, we published the most current meta-analysis to date regarding oral contraceptive use and the risk of premenopausal breast cancer.³ We found that 21 out of 23 studies showed a positive trend or positive risk for premenopausal breast cancer with oral contraceptive use prior to first-term pregnancy. This resulted in a highly statistically significant cumulative risk of 44% (ie, odds ratio 1.44, 95% confidence interval 1.24–1.68). Our meta-analysis remains the most recent study in this area and updates the Oxford pooled analysis,⁴ which relied on older studies with older women (two-thirds of whom were over age 45).

A more recent collaborative study coauthored by investigators from the National Cancer Institute, the Hutchinson Cancer Research Center, and the University of Washington includes oral contraceptives in the list of risk factors for breast cancer in younger women.⁵ We ask your readers to consider that patients are entitled to know about this important risk factor before making a decision regarding hormonal menstrual manipulation.

To the Editor: In the article, “Menstrual manipulation: Options for suppressing the cycle,”¹ the authors described advantages and disadvantages of various hormone-based methods of menstrual manipulation, including prolonged use of oral contraceptives. We believe the authors underemphasized the risks associated with oral contraceptives. Blood clots, stroke, and death are often included in print and television ads by law firms recruiting patients harmed by these drugs. In addition, the authors failed to mention the risk of premenopausal breast cancer due to oral contraceptives, which are now classified as group 1 carcinogens by the World Health Organization.²

In October 2006, we published the most current meta-analysis to date regarding oral contraceptive use and the risk of premenopausal breast cancer.³ We found that 21 out of 23 studies showed a positive trend or positive risk for premenopausal breast cancer with oral contraceptive use prior to first-term pregnancy. This resulted in a highly statistically significant cumulative risk of 44% (ie, odds ratio 1.44, 95% confidence interval 1.24–1.68). Our meta-analysis remains the most recent study in this area and updates the Oxford pooled analysis,⁴ which relied on older studies with older women (two-thirds of whom were over age 45).

A more recent collaborative study coauthored by investigators from the National Cancer Institute, the Hutchinson Cancer Research Center, and the University of Washington includes oral contraceptives in the list of risk factors for breast cancer in younger women.⁵ We ask your readers to consider that patients are entitled to know about this important risk factor before making a decision regarding hormonal menstrual manipulation.

To the Editor: I wish to point out an error in the excellent review of MAO inhibitors published in the December 2010 issue of the Cleveland Clinic Journal of Medicine. The authors state, “The only selective MAO inhibitor now available in the United States is selegiline, which inhibits MAO-B at low doses but loses its selectivity at dosages greater than 20 mg/day” (on page 861). In fact, a second selective MAO inhibitor has been available in the United States for several years. Rasagiline, developed by Teva Pharmaceuticals and marketed under the brand name Azilect, is a highly selective MAO-B inhibitor indicated for treating the symptoms of Parkinson disease, either as monotherapy or as adjunct therapy to carbidopa-levodopa. However, rasagiline is not indicated for the treatment of depression. Perhaps the authors meant to say that selegiline is the only selective MAO-B inhibitor indicated for treating depression in the United States.

To the Editor: I wish to point out an error in the excellent review of MAO inhibitors published in the December 2010 issue of the Cleveland Clinic Journal of Medicine. The authors state, “The only selective MAO inhibitor now available in the United States is selegiline, which inhibits MAO-B at low doses but loses its selectivity at dosages greater than 20 mg/day” (on page 861). In fact, a second selective MAO inhibitor has been available in the United States for several years. Rasagiline, developed by Teva Pharmaceuticals and marketed under the brand name Azilect, is a highly selective MAO-B inhibitor indicated for treating the symptoms of Parkinson disease, either as monotherapy or as adjunct therapy to carbidopa-levodopa. However, rasagiline is not indicated for the treatment of depression. Perhaps the authors meant to say that selegiline is the only selective MAO-B inhibitor indicated for treating depression in the United States.

To the Editor: I wish to point out an error in the excellent review of MAO inhibitors published in the December 2010 issue of the Cleveland Clinic Journal of Medicine. The authors state, “The only selective MAO inhibitor now available in the United States is selegiline, which inhibits MAO-B at low doses but loses its selectivity at dosages greater than 20 mg/day” (on page 861). In fact, a second selective MAO inhibitor has been available in the United States for several years. Rasagiline, developed by Teva Pharmaceuticals and marketed under the brand name Azilect, is a highly selective MAO-B inhibitor indicated for treating the symptoms of Parkinson disease, either as monotherapy or as adjunct therapy to carbidopa-levodopa. However, rasagiline is not indicated for the treatment of depression. Perhaps the authors meant to say that selegiline is the only selective MAO-B inhibitor indicated for treating depression in the United States.

In Reply: Dr. Keller is correct, and we thank him for the clarification. We meant to say that selegiline is the only selective MAO-B inhibitor indicated for treating depression in the United States.

In Reply: Dr. Keller is correct, and we thank him for the clarification. We meant to say that selegiline is the only selective MAO-B inhibitor indicated for treating depression in the United States.

In Reply: Dr. Keller is correct, and we thank him for the clarification. We meant to say that selegiline is the only selective MAO-B inhibitor indicated for treating depression in the United States.

To the Editor: Thank you for the thorough review of gout and chronic kidney disease in the December 2010 issue of Cleveland Clinic Journal of Medicine.

Table 2 displays results from the Febuxostat Versus Allopurinol Controlled Trial (FACT), in which we see that 76% of patients treated with febuxostat 80 mg per day achieved a serum uric acid level of less than 6 mg/dL at week 28. With a dose of febuxostat 240 mg per day, 94% of patients were able to reduce their serum uric acid below 6 mg/dL, the threshold needed to prevent precipitation of uric acid crystals. However, the maximum daily dose recommended in the product information for Uloric (febuxostat) is 80 mg, at which approximately 24% of patients failed to lower their serum uric acid levels to less than 6 mg/dL.

When encountering such patients in clinical practice, would the authors advise pushing the daily dose of febuxostat up to 240 mg, if needed? Alternatively, is there any role for combination therapy with both febuxostat and allopurinol for gout patients with severe resistant hyperuricemia?

To the Editor: Thank you for the thorough review of gout and chronic kidney disease in the December 2010 issue of Cleveland Clinic Journal of Medicine.

Table 2 displays results from the Febuxostat Versus Allopurinol Controlled Trial (FACT), in which we see that 76% of patients treated with febuxostat 80 mg per day achieved a serum uric acid level of less than 6 mg/dL at week 28. With a dose of febuxostat 240 mg per day, 94% of patients were able to reduce their serum uric acid below 6 mg/dL, the threshold needed to prevent precipitation of uric acid crystals. However, the maximum daily dose recommended in the product information for Uloric (febuxostat) is 80 mg, at which approximately 24% of patients failed to lower their serum uric acid levels to less than 6 mg/dL.

When encountering such patients in clinical practice, would the authors advise pushing the daily dose of febuxostat up to 240 mg, if needed? Alternatively, is there any role for combination therapy with both febuxostat and allopurinol for gout patients with severe resistant hyperuricemia?

To the Editor: Thank you for the thorough review of gout and chronic kidney disease in the December 2010 issue of Cleveland Clinic Journal of Medicine.

Table 2 displays results from the Febuxostat Versus Allopurinol Controlled Trial (FACT), in which we see that 76% of patients treated with febuxostat 80 mg per day achieved a serum uric acid level of less than 6 mg/dL at week 28. With a dose of febuxostat 240 mg per day, 94% of patients were able to reduce their serum uric acid below 6 mg/dL, the threshold needed to prevent precipitation of uric acid crystals. However, the maximum daily dose recommended in the product information for Uloric (febuxostat) is 80 mg, at which approximately 24% of patients failed to lower their serum uric acid levels to less than 6 mg/dL.

When encountering such patients in clinical practice, would the authors advise pushing the daily dose of febuxostat up to 240 mg, if needed? Alternatively, is there any role for combination therapy with both febuxostat and allopurinol for gout patients with severe resistant hyperuricemia?

In Reply: The clinical dilemma Dr. Keller describes is the inability to lower the serum urate to a consensually accepted target level of less than 6.0 mg/dL in patients with significant gouty arthritis, when using doses of febuxostat (or for that matter allopurinol) recommended by the US Food and Drug Administration (FDA). This problem is not limited to the management of the gouty patient with renal insufficiency, and we will describe our approach.

In patients failing to meet target serum urate levels, patient adherence to the prescribed dosing should be considered first, since as many as 50% of patients do not adhere to their prescribed hypouricemic medication regimen.¹

As Dr. Keller notes, staying below the FDA-approved daily dosage (in the absence of renal insufficiency) of febuxostat (80 mg) or allopurinol (800 mg) will result in some patients not achieving adequate urate-lowering to ameliorate their gout. With clinical and laboratory monitoring for intolerance, we have increased the dose of allopurinol to above 800 mg when necessary; we have explained to patients that this was above the normally recommended dosage of the drug. Of those patients who have been truly intolerant to allopurinol whom we have needed to switch to febuxostat, there have been a few who have required greater than 80 mg daily, and we have increased the dosage, again with extra vigilance in monitoring (liver tests in particular) and after discussion with the patient. Thus far, we have been fortunate in not having had significant side effects, but we do not assume that all patients will tolerate more than 80 mg daily.

Since both febuxostat and allopurinol inhibit the same enzyme (xanthine oxidase) as their mechanism of action, we do not anticipate an advantage to using combined drug therapy, as opposed to increasing the dose of one or the other of the medications. There might even be some loss of efficacy due to inhibitor competition at the enzyme’s active site. Alternatively, in the patient with normal renal function, there might be an advantage to adding probenecid, a uricosuric drug, to either allopurinol or febuxostat, in order to gain some additional hypouricemic effect.

Finally, it is worth reemphasizing that in clinical trials, although febuxostat 80 mg may have outperformed allopurinol at a dose of 300 mg (or less), in clinical practice it is quite reasonable to significantly increase the dosage of allopurinol to at least 800 mg daily as long as it is tolerated, before switching to the very effective but much more expensive alternative. The goal of therapy is, after all, to safely lower the serum urate level to well below its saturation point. Surveys of prescribing habits indicate that physicians have been very reluctant to increase the dose of allopurinol to above 300 mg daily and, unfortunately, do not adequately monitor the efficacy of the therapy in lowering the serum urate level.

In Reply: The clinical dilemma Dr. Keller describes is the inability to lower the serum urate to a consensually accepted target level of less than 6.0 mg/dL in patients with significant gouty arthritis, when using doses of febuxostat (or for that matter allopurinol) recommended by the US Food and Drug Administration (FDA). This problem is not limited to the management of the gouty patient with renal insufficiency, and we will describe our approach.

In patients failing to meet target serum urate levels, patient adherence to the prescribed dosing should be considered first, since as many as 50% of patients do not adhere to their prescribed hypouricemic medication regimen.¹

As Dr. Keller notes, staying below the FDA-approved daily dosage (in the absence of renal insufficiency) of febuxostat (80 mg) or allopurinol (800 mg) will result in some patients not achieving adequate urate-lowering to ameliorate their gout. With clinical and laboratory monitoring for intolerance, we have increased the dose of allopurinol to above 800 mg when necessary; we have explained to patients that this was above the normally recommended dosage of the drug. Of those patients who have been truly intolerant to allopurinol whom we have needed to switch to febuxostat, there have been a few who have required greater than 80 mg daily, and we have increased the dosage, again with extra vigilance in monitoring (liver tests in particular) and after discussion with the patient. Thus far, we have been fortunate in not having had significant side effects, but we do not assume that all patients will tolerate more than 80 mg daily.

Since both febuxostat and allopurinol inhibit the same enzyme (xanthine oxidase) as their mechanism of action, we do not anticipate an advantage to using combined drug therapy, as opposed to increasing the dose of one or the other of the medications. There might even be some loss of efficacy due to inhibitor competition at the enzyme’s active site. Alternatively, in the patient with normal renal function, there might be an advantage to adding probenecid, a uricosuric drug, to either allopurinol or febuxostat, in order to gain some additional hypouricemic effect.

Finally, it is worth reemphasizing that in clinical trials, although febuxostat 80 mg may have outperformed allopurinol at a dose of 300 mg (or less), in clinical practice it is quite reasonable to significantly increase the dosage of allopurinol to at least 800 mg daily as long as it is tolerated, before switching to the very effective but much more expensive alternative. The goal of therapy is, after all, to safely lower the serum urate level to well below its saturation point. Surveys of prescribing habits indicate that physicians have been very reluctant to increase the dose of allopurinol to above 300 mg daily and, unfortunately, do not adequately monitor the efficacy of the therapy in lowering the serum urate level.

In Reply: The clinical dilemma Dr. Keller describes is the inability to lower the serum urate to a consensually accepted target level of less than 6.0 mg/dL in patients with significant gouty arthritis, when using doses of febuxostat (or for that matter allopurinol) recommended by the US Food and Drug Administration (FDA). This problem is not limited to the management of the gouty patient with renal insufficiency, and we will describe our approach.

In patients failing to meet target serum urate levels, patient adherence to the prescribed dosing should be considered first, since as many as 50% of patients do not adhere to their prescribed hypouricemic medication regimen.¹

As Dr. Keller notes, staying below the FDA-approved daily dosage (in the absence of renal insufficiency) of febuxostat (80 mg) or allopurinol (800 mg) will result in some patients not achieving adequate urate-lowering to ameliorate their gout. With clinical and laboratory monitoring for intolerance, we have increased the dose of allopurinol to above 800 mg when necessary; we have explained to patients that this was above the normally recommended dosage of the drug. Of those patients who have been truly intolerant to allopurinol whom we have needed to switch to febuxostat, there have been a few who have required greater than 80 mg daily, and we have increased the dosage, again with extra vigilance in monitoring (liver tests in particular) and after discussion with the patient. Thus far, we have been fortunate in not having had significant side effects, but we do not assume that all patients will tolerate more than 80 mg daily.

Since both febuxostat and allopurinol inhibit the same enzyme (xanthine oxidase) as their mechanism of action, we do not anticipate an advantage to using combined drug therapy, as opposed to increasing the dose of one or the other of the medications. There might even be some loss of efficacy due to inhibitor competition at the enzyme’s active site. Alternatively, in the patient with normal renal function, there might be an advantage to adding probenecid, a uricosuric drug, to either allopurinol or febuxostat, in order to gain some additional hypouricemic effect.

Finally, it is worth reemphasizing that in clinical trials, although febuxostat 80 mg may have outperformed allopurinol at a dose of 300 mg (or less), in clinical practice it is quite reasonable to significantly increase the dosage of allopurinol to at least 800 mg daily as long as it is tolerated, before switching to the very effective but much more expensive alternative. The goal of therapy is, after all, to safely lower the serum urate level to well below its saturation point. Surveys of prescribing habits indicate that physicians have been very reluctant to increase the dose of allopurinol to above 300 mg daily and, unfortunately, do not adequately monitor the efficacy of the therapy in lowering the serum urate level.

To the Editor: I have to say I am disappointed, but not surprised, at Dr. Dore’s article, “How to prevent glucocorticoid-induced osteoporosis” in your August issue.¹ The section “Estrogen is being used more selectively” was shorter and had older and out of date references compared with the section “A role for testosterone?” and it was actually blatantly sexist: the comment in the estrogen section is that “…the consensus…that hormone replacement therapy should be restricted to women with menopausal symptoms or to older women who cannot tolerate other therapies or who express a strong preference for hormone replacement therapy despite being informed about potential adverse events” [my italics],¹ while the comment in the testosterone section is that males who “… are hypogonadal, and have no contraindications to androgen replacement therapy (eg, prostate cancer) be offered testosterone therapy to preserve lean body mass and bone mineral density” [my italics].¹

While I am not arguing that menopausal hormone therapy should be used first-line for the prevention or treatment of glucocorticoid-induced osteoporosis, I would like to note the following:

First, the referenced 2002 Women’s Health Initiative study² was a prevention trial, not a therapeutic menopausal trial, and to reference it as a position statement on the use of hormone therapy is ridiculous and perpetuates misinformation about the role of menopausal hormone therapy.

Next, there has been updated information from the Women’s Health Initiative, as well as updated position statements on the use of hormone therapy—the 2010 position statement on the use of estrogen and progestogen in menopausal women³ as well as the 2008 American Association of Clinical Endocrinologists position statement⁴ noting that the benefits of hormone therapy outweigh the risks for most women under age 60. So Dr. Dore’s reference citation from 2004⁵ is hopelessly outdated.

And lastly, females, unlike males, routinely become hypogonadal at midlife. When faced with a medical condition that requires glucocorticoids that further intensifies the hypogonadal state by suppressing adrenal adrenogens, females may face a “triple whammy” on the bone.

The Women’s Health Initiative actually showed fracture reduction in postmenopausal women who did not even carry the diagnosis of osteoporosis, while the referenced studies in Dr. Dore’s article related to males admittedly “cannot be considered conclusive in view of their small size and the lack of fracture data…”¹

So what is bad (actually potentially good) for the goose is apparently just fine for the gander.

To the Editor: I have to say I am disappointed, but not surprised, at Dr. Dore’s article, “How to prevent glucocorticoid-induced osteoporosis” in your August issue.¹ The section “Estrogen is being used more selectively” was shorter and had older and out of date references compared with the section “A role for testosterone?” and it was actually blatantly sexist: the comment in the estrogen section is that “…the consensus…that hormone replacement therapy should be restricted to women with menopausal symptoms or to older women who cannot tolerate other therapies or who express a strong preference for hormone replacement therapy despite being informed about potential adverse events” [my italics],¹ while the comment in the testosterone section is that males who “… are hypogonadal, and have no contraindications to androgen replacement therapy (eg, prostate cancer) be offered testosterone therapy to preserve lean body mass and bone mineral density” [my italics].¹

While I am not arguing that menopausal hormone therapy should be used first-line for the prevention or treatment of glucocorticoid-induced osteoporosis, I would like to note the following:

First, the referenced 2002 Women’s Health Initiative study² was a prevention trial, not a therapeutic menopausal trial, and to reference it as a position statement on the use of hormone therapy is ridiculous and perpetuates misinformation about the role of menopausal hormone therapy.

Next, there has been updated information from the Women’s Health Initiative, as well as updated position statements on the use of hormone therapy—the 2010 position statement on the use of estrogen and progestogen in menopausal women³ as well as the 2008 American Association of Clinical Endocrinologists position statement⁴ noting that the benefits of hormone therapy outweigh the risks for most women under age 60. So Dr. Dore’s reference citation from 2004⁵ is hopelessly outdated.

And lastly, females, unlike males, routinely become hypogonadal at midlife. When faced with a medical condition that requires glucocorticoids that further intensifies the hypogonadal state by suppressing adrenal adrenogens, females may face a “triple whammy” on the bone.

The Women’s Health Initiative actually showed fracture reduction in postmenopausal women who did not even carry the diagnosis of osteoporosis, while the referenced studies in Dr. Dore’s article related to males admittedly “cannot be considered conclusive in view of their small size and the lack of fracture data…”¹

So what is bad (actually potentially good) for the goose is apparently just fine for the gander.

To the Editor: I have to say I am disappointed, but not surprised, at Dr. Dore’s article, “How to prevent glucocorticoid-induced osteoporosis” in your August issue.¹ The section “Estrogen is being used more selectively” was shorter and had older and out of date references compared with the section “A role for testosterone?” and it was actually blatantly sexist: the comment in the estrogen section is that “…the consensus…that hormone replacement therapy should be restricted to women with menopausal symptoms or to older women who cannot tolerate other therapies or who express a strong preference for hormone replacement therapy despite being informed about potential adverse events” [my italics],¹ while the comment in the testosterone section is that males who “… are hypogonadal, and have no contraindications to androgen replacement therapy (eg, prostate cancer) be offered testosterone therapy to preserve lean body mass and bone mineral density” [my italics].¹

While I am not arguing that menopausal hormone therapy should be used first-line for the prevention or treatment of glucocorticoid-induced osteoporosis, I would like to note the following:

First, the referenced 2002 Women’s Health Initiative study² was a prevention trial, not a therapeutic menopausal trial, and to reference it as a position statement on the use of hormone therapy is ridiculous and perpetuates misinformation about the role of menopausal hormone therapy.

Next, there has been updated information from the Women’s Health Initiative, as well as updated position statements on the use of hormone therapy—the 2010 position statement on the use of estrogen and progestogen in menopausal women³ as well as the 2008 American Association of Clinical Endocrinologists position statement⁴ noting that the benefits of hormone therapy outweigh the risks for most women under age 60. So Dr. Dore’s reference citation from 2004⁵ is hopelessly outdated.

And lastly, females, unlike males, routinely become hypogonadal at midlife. When faced with a medical condition that requires glucocorticoids that further intensifies the hypogonadal state by suppressing adrenal adrenogens, females may face a “triple whammy” on the bone.

The Women’s Health Initiative actually showed fracture reduction in postmenopausal women who did not even carry the diagnosis of osteoporosis, while the referenced studies in Dr. Dore’s article related to males admittedly “cannot be considered conclusive in view of their small size and the lack of fracture data…”¹

So what is bad (actually potentially good) for the goose is apparently just fine for the gander.

In Reply: I could find references for the use of testosterone in glucocorticoid-induced osteoporosis and could not find any references for the use of estrogen in this condition, except for the outdated American College of Rheumatology guidelines from the 1990s, which included Dr. Nancy Lane’s work. So perhaps it is the research that is gender-biased rather than my article. I agree that in osteoporosis that is not glucocorticoid-induced, estrogen has great fracture efficacy even in those without osteoporosis, as you stated, but I tried to keep my article evidence-based and on-topic regarding glucocorticoid-induced osteoporosis. As usual, topics that involve estrogen are highly volatile, and I did not mean to fuel the fire.

In Reply: I could find references for the use of testosterone in glucocorticoid-induced osteoporosis and could not find any references for the use of estrogen in this condition, except for the outdated American College of Rheumatology guidelines from the 1990s, which included Dr. Nancy Lane’s work. So perhaps it is the research that is gender-biased rather than my article. I agree that in osteoporosis that is not glucocorticoid-induced, estrogen has great fracture efficacy even in those without osteoporosis, as you stated, but I tried to keep my article evidence-based and on-topic regarding glucocorticoid-induced osteoporosis. As usual, topics that involve estrogen are highly volatile, and I did not mean to fuel the fire.

In Reply: I could find references for the use of testosterone in glucocorticoid-induced osteoporosis and could not find any references for the use of estrogen in this condition, except for the outdated American College of Rheumatology guidelines from the 1990s, which included Dr. Nancy Lane’s work. So perhaps it is the research that is gender-biased rather than my article. I agree that in osteoporosis that is not glucocorticoid-induced, estrogen has great fracture efficacy even in those without osteoporosis, as you stated, but I tried to keep my article evidence-based and on-topic regarding glucocorticoid-induced osteoporosis. As usual, topics that involve estrogen are highly volatile, and I did not mean to fuel the fire.

To the Editor: I read with interest the excellent review by Dr. Kashyap and coauthors of bariatric surgery for patients with type 2 diabetes.¹ I am writing to contribute an additional caveat to their otherwise detailed list of postoperative complications—the increased risk of nephrolithiasis.^2,3 The majority of kidney stones that develop after bariatric surgery tend to be composed of calcium oxalate. Increased intestinal absorption of oxalate appears to promote hyperoxaluria.^2,3

Vitamin C deficiency is not usual after bariatric surgery, and the dietary reference intake of vitamin C for adults is no more than 90 mg. Therefore, I was surprised to see Dr. Kashyap recommend supplementation with vitamin C 500 mg daily (in Table 4 of her article). In my practice I have avoided supplemental vitamin C, other than that in a multivitamin, because of the risk of increasing urinary oxalate and stone formation.⁴

Iron deficiency can be a challenge after bariatric surgery. Although they do not state it in the review, the authors may believe that additional vitamin C can improve iron absorption. However, there are no compelling data of which I am aware for this belief in patients who have undergone gastric bypass,⁵ and the benefit of taking vitamin C along with iron in otherwise normal people with iron deficiency remains controversial.⁶

To the Editor: I read with interest the excellent review by Dr. Kashyap and coauthors of bariatric surgery for patients with type 2 diabetes.¹ I am writing to contribute an additional caveat to their otherwise detailed list of postoperative complications—the increased risk of nephrolithiasis.^2,3 The majority of kidney stones that develop after bariatric surgery tend to be composed of calcium oxalate. Increased intestinal absorption of oxalate appears to promote hyperoxaluria.^2,3

Vitamin C deficiency is not usual after bariatric surgery, and the dietary reference intake of vitamin C for adults is no more than 90 mg. Therefore, I was surprised to see Dr. Kashyap recommend supplementation with vitamin C 500 mg daily (in Table 4 of her article). In my practice I have avoided supplemental vitamin C, other than that in a multivitamin, because of the risk of increasing urinary oxalate and stone formation.⁴

Iron deficiency can be a challenge after bariatric surgery. Although they do not state it in the review, the authors may believe that additional vitamin C can improve iron absorption. However, there are no compelling data of which I am aware for this belief in patients who have undergone gastric bypass,⁵ and the benefit of taking vitamin C along with iron in otherwise normal people with iron deficiency remains controversial.⁶

To the Editor: I read with interest the excellent review by Dr. Kashyap and coauthors of bariatric surgery for patients with type 2 diabetes.¹ I am writing to contribute an additional caveat to their otherwise detailed list of postoperative complications—the increased risk of nephrolithiasis.^2,3 The majority of kidney stones that develop after bariatric surgery tend to be composed of calcium oxalate. Increased intestinal absorption of oxalate appears to promote hyperoxaluria.^2,3

Vitamin C deficiency is not usual after bariatric surgery, and the dietary reference intake of vitamin C for adults is no more than 90 mg. Therefore, I was surprised to see Dr. Kashyap recommend supplementation with vitamin C 500 mg daily (in Table 4 of her article). In my practice I have avoided supplemental vitamin C, other than that in a multivitamin, because of the risk of increasing urinary oxalate and stone formation.⁴

Iron deficiency can be a challenge after bariatric surgery. Although they do not state it in the review, the authors may believe that additional vitamin C can improve iron absorption. However, there are no compelling data of which I am aware for this belief in patients who have undergone gastric bypass,⁵ and the benefit of taking vitamin C along with iron in otherwise normal people with iron deficiency remains controversial.⁶

In Reply: Although some nutritional guidelines advocate the use of vitamin C in post-bariatric patients, most data are now suggesting that it may not be indicated. We appreciate the comments provided and are in agreement with regards to the supplementation of vitamin C.

In Reply: Although some nutritional guidelines advocate the use of vitamin C in post-bariatric patients, most data are now suggesting that it may not be indicated. We appreciate the comments provided and are in agreement with regards to the supplementation of vitamin C.

In Reply: Although some nutritional guidelines advocate the use of vitamin C in post-bariatric patients, most data are now suggesting that it may not be indicated. We appreciate the comments provided and are in agreement with regards to the supplementation of vitamin C.

To the Editor: We read with great interest the excellent review by Dore¹ on the prevention of glucocorticoid-induced osteoporosis. As indicated by the author, bone loss is one of the most serious complications of corticosteroid therapy, causing significant costs, morbidity, and mortality related to vertebral and hip fractures. Therefore, prevention of bone loss is mandatory, and several drugs are available.

However, the author does not mention strontium ranelate in the armamentarium for this preventive treatment. Strontium ranelate is an orally administered treatment of postmenopausal osteoporosis, reducing the risk of vertebral and hip fractures, and its efficacy has been demonstrated in clinical and histologic studies.^2,3 It has a particular mode of action, since it simultaneously inhibits bone resorption and stimulates bone formation.^2,3 Only minor adverse effects have been reported, including gastrointestinal signs such as nausea and diarrhea (only during the first 3 months), headache, and skin lesions. Strontium ranelate is currently licensed for the treatment of postmenopausal osteoporosis, but it appears to be an effective solution for diverse fracture risks, including the treatment of glucocorticoid-induced osteoporosis.

In a 2-year observational, controlled study that included 107 patients with glucocorticoid-induced osteoporosis treated with strontium ranelate or risedronate, there was a significantly higher increase in lumbar spine and total hip bone mineral density and a stronger reduction in back pain in the group of patients treated with strontium ranelate than in the group of patients under risedronate therapy, but the number of patients with no new fractures was similar in both treatment groups.⁴

In an animal model, strontium ranelate was significantly superior to alendronate in the prevention of glucocorticoid-induced osteopenia according to bone mineral density and histomorphometric analysis.⁵

Therefore, we consider that strontium ranelate could also be effective in glucocorticoid-induced osteopenia prevention, but prospective studies are required.

To the Editor: We read with great interest the excellent review by Dore¹ on the prevention of glucocorticoid-induced osteoporosis. As indicated by the author, bone loss is one of the most serious complications of corticosteroid therapy, causing significant costs, morbidity, and mortality related to vertebral and hip fractures. Therefore, prevention of bone loss is mandatory, and several drugs are available.

However, the author does not mention strontium ranelate in the armamentarium for this preventive treatment. Strontium ranelate is an orally administered treatment of postmenopausal osteoporosis, reducing the risk of vertebral and hip fractures, and its efficacy has been demonstrated in clinical and histologic studies.^2,3 It has a particular mode of action, since it simultaneously inhibits bone resorption and stimulates bone formation.^2,3 Only minor adverse effects have been reported, including gastrointestinal signs such as nausea and diarrhea (only during the first 3 months), headache, and skin lesions. Strontium ranelate is currently licensed for the treatment of postmenopausal osteoporosis, but it appears to be an effective solution for diverse fracture risks, including the treatment of glucocorticoid-induced osteoporosis.

In a 2-year observational, controlled study that included 107 patients with glucocorticoid-induced osteoporosis treated with strontium ranelate or risedronate, there was a significantly higher increase in lumbar spine and total hip bone mineral density and a stronger reduction in back pain in the group of patients treated with strontium ranelate than in the group of patients under risedronate therapy, but the number of patients with no new fractures was similar in both treatment groups.⁴

In an animal model, strontium ranelate was significantly superior to alendronate in the prevention of glucocorticoid-induced osteopenia according to bone mineral density and histomorphometric analysis.⁵

Therefore, we consider that strontium ranelate could also be effective in glucocorticoid-induced osteopenia prevention, but prospective studies are required.

To the Editor: We read with great interest the excellent review by Dore¹ on the prevention of glucocorticoid-induced osteoporosis. As indicated by the author, bone loss is one of the most serious complications of corticosteroid therapy, causing significant costs, morbidity, and mortality related to vertebral and hip fractures. Therefore, prevention of bone loss is mandatory, and several drugs are available.

However, the author does not mention strontium ranelate in the armamentarium for this preventive treatment. Strontium ranelate is an orally administered treatment of postmenopausal osteoporosis, reducing the risk of vertebral and hip fractures, and its efficacy has been demonstrated in clinical and histologic studies.^2,3 It has a particular mode of action, since it simultaneously inhibits bone resorption and stimulates bone formation.^2,3 Only minor adverse effects have been reported, including gastrointestinal signs such as nausea and diarrhea (only during the first 3 months), headache, and skin lesions. Strontium ranelate is currently licensed for the treatment of postmenopausal osteoporosis, but it appears to be an effective solution for diverse fracture risks, including the treatment of glucocorticoid-induced osteoporosis.

In a 2-year observational, controlled study that included 107 patients with glucocorticoid-induced osteoporosis treated with strontium ranelate or risedronate, there was a significantly higher increase in lumbar spine and total hip bone mineral density and a stronger reduction in back pain in the group of patients treated with strontium ranelate than in the group of patients under risedronate therapy, but the number of patients with no new fractures was similar in both treatment groups.⁴

In an animal model, strontium ranelate was significantly superior to alendronate in the prevention of glucocorticoid-induced osteopenia according to bone mineral density and histomorphometric analysis.⁵

Therefore, we consider that strontium ranelate could also be effective in glucocorticoid-induced osteopenia prevention, but prospective studies are required.