Letters To The Editor

In Reply: I thank Drs. Bachmeyer and Gauthier for their kind comments. My review was limited to therapies currently available by prescription in the United States; therefore, strontium ranelate was not included. I agree with their comment that prospective studies are required to consider strontium ranelate as an effective therapy for glucocortocoid-induced osteoporosis.

In Reply: I thank Drs. Bachmeyer and Gauthier for their kind comments. My review was limited to therapies currently available by prescription in the United States; therefore, strontium ranelate was not included. I agree with their comment that prospective studies are required to consider strontium ranelate as an effective therapy for glucocortocoid-induced osteoporosis.

In Reply: I thank Drs. Bachmeyer and Gauthier for their kind comments. My review was limited to therapies currently available by prescription in the United States; therefore, strontium ranelate was not included. I agree with their comment that prospective studies are required to consider strontium ranelate as an effective therapy for glucocortocoid-induced osteoporosis.

To the Editor: Like Dr. Hanlon (Cleve Clin J Med 2010; 77:408–411), I too am alarmed by the inability of electronic medical records to incorporate whole language. Physicians can make treatment errors when they fail to include contextual factors in their diagnosis and treatment plans. The social and circumstantial complexities of a patient’s life cannot be parsed by computer systems that can only “search” bullet points. The current template-driven systems were originally designed for billing and now are touted for “quality measurements.” They could tell us whether a patient’s hemoglobin A_1c was at goal, or if she was “noncompliant” and hadn’t filled a prescription; they could not tell us that a psychologically abusive husband would not allow her to purchase her diabetes medications (this actually happened to one of my patients). I would argue that addressing the abuse is more important to her health. Yet we are all being pushed, like teachers teaching to a standardized test, to hit certain “benchmarks,” in order to be called “quality” physicians.

Since it is unlikely that the tide will turn back to a written record, physicians should be demanding rapid deployment of computer systems, now in development, that can analyze whole language and find information in context. This technology is out there and needs aggressive support.

Texting contractions, Twitter, and the rest are chipping away at the concept of narrative. Our patients’ lives are worthy of a narrative, not the bullet points and cut-and-paste we are forcing their lives and health into.

To the Editor: Like Dr. Hanlon (Cleve Clin J Med 2010; 77:408–411), I too am alarmed by the inability of electronic medical records to incorporate whole language. Physicians can make treatment errors when they fail to include contextual factors in their diagnosis and treatment plans. The social and circumstantial complexities of a patient’s life cannot be parsed by computer systems that can only “search” bullet points. The current template-driven systems were originally designed for billing and now are touted for “quality measurements.” They could tell us whether a patient’s hemoglobin A_1c was at goal, or if she was “noncompliant” and hadn’t filled a prescription; they could not tell us that a psychologically abusive husband would not allow her to purchase her diabetes medications (this actually happened to one of my patients). I would argue that addressing the abuse is more important to her health. Yet we are all being pushed, like teachers teaching to a standardized test, to hit certain “benchmarks,” in order to be called “quality” physicians.

Since it is unlikely that the tide will turn back to a written record, physicians should be demanding rapid deployment of computer systems, now in development, that can analyze whole language and find information in context. This technology is out there and needs aggressive support.

Texting contractions, Twitter, and the rest are chipping away at the concept of narrative. Our patients’ lives are worthy of a narrative, not the bullet points and cut-and-paste we are forcing their lives and health into.

To the Editor: Like Dr. Hanlon (Cleve Clin J Med 2010; 77:408–411), I too am alarmed by the inability of electronic medical records to incorporate whole language. Physicians can make treatment errors when they fail to include contextual factors in their diagnosis and treatment plans. The social and circumstantial complexities of a patient’s life cannot be parsed by computer systems that can only “search” bullet points. The current template-driven systems were originally designed for billing and now are touted for “quality measurements.” They could tell us whether a patient’s hemoglobin A_1c was at goal, or if she was “noncompliant” and hadn’t filled a prescription; they could not tell us that a psychologically abusive husband would not allow her to purchase her diabetes medications (this actually happened to one of my patients). I would argue that addressing the abuse is more important to her health. Yet we are all being pushed, like teachers teaching to a standardized test, to hit certain “benchmarks,” in order to be called “quality” physicians.

Since it is unlikely that the tide will turn back to a written record, physicians should be demanding rapid deployment of computer systems, now in development, that can analyze whole language and find information in context. This technology is out there and needs aggressive support.

Texting contractions, Twitter, and the rest are chipping away at the concept of narrative. Our patients’ lives are worthy of a narrative, not the bullet points and cut-and-paste we are forcing their lives and health into.

To the Editor: Thanks for the excellent review articles on nephrolithiasis in your October 2009 issue.^1,2

Dr. Hall¹ cites studies in which patients given the alpha blocker tamsulosin (Flomax) or the calcium channel blocker nifedipine (Procardia) had improved rates of kidney stone passage compared with placebo. As a primary care physician, I am often confronted with the challenge of managing a patient who is waiting for a kidney stone to pass while taking tamsulosin. Is Dr. Hall aware of any clinical studies, or at least theoretical reasons, which would support adding nifedipine in such cases?

Secondly, Dr. Hall cites studies that demonstrated that a higher intake of dietary calcium is actually associated with fewer calcium stone events in both men and women. An unanswered question is whether patients taking calcium supplements for osteoporosis or osteopenia can safely continue to do so after a calcium stone event, or indeed, whether calcium supplementation might actually be helpful in preventing a recurrent calcum stone.

If there is an absence of randomized studies to answer these questions, Dr. Hall’s recommendations based on his expert experience would be most welcome.

To the Editor: Thanks for the excellent review articles on nephrolithiasis in your October 2009 issue.^1,2

Dr. Hall¹ cites studies in which patients given the alpha blocker tamsulosin (Flomax) or the calcium channel blocker nifedipine (Procardia) had improved rates of kidney stone passage compared with placebo. As a primary care physician, I am often confronted with the challenge of managing a patient who is waiting for a kidney stone to pass while taking tamsulosin. Is Dr. Hall aware of any clinical studies, or at least theoretical reasons, which would support adding nifedipine in such cases?

Secondly, Dr. Hall cites studies that demonstrated that a higher intake of dietary calcium is actually associated with fewer calcium stone events in both men and women. An unanswered question is whether patients taking calcium supplements for osteoporosis or osteopenia can safely continue to do so after a calcium stone event, or indeed, whether calcium supplementation might actually be helpful in preventing a recurrent calcum stone.

If there is an absence of randomized studies to answer these questions, Dr. Hall’s recommendations based on his expert experience would be most welcome.

To the Editor: Thanks for the excellent review articles on nephrolithiasis in your October 2009 issue.^1,2

Dr. Hall¹ cites studies in which patients given the alpha blocker tamsulosin (Flomax) or the calcium channel blocker nifedipine (Procardia) had improved rates of kidney stone passage compared with placebo. As a primary care physician, I am often confronted with the challenge of managing a patient who is waiting for a kidney stone to pass while taking tamsulosin. Is Dr. Hall aware of any clinical studies, or at least theoretical reasons, which would support adding nifedipine in such cases?

Secondly, Dr. Hall cites studies that demonstrated that a higher intake of dietary calcium is actually associated with fewer calcium stone events in both men and women. An unanswered question is whether patients taking calcium supplements for osteoporosis or osteopenia can safely continue to do so after a calcium stone event, or indeed, whether calcium supplementation might actually be helpful in preventing a recurrent calcum stone.

If there is an absence of randomized studies to answer these questions, Dr. Hall’s recommendations based on his expert experience would be most welcome.

In Reply: I thank Dr. Keller for his kind letter.

With respect to expulsive therapy, Dellabella et al¹ randomly assigned 210 patients to receive nifedipine, tamsulosin, or phloroglucinol. All the patients also received a corticosteroid. The most effective therapy was tamsulosin, though this was not a placebo-controlled study. In a separate study, Borghi et al² compared methylprednisolone plus nifedipine and methylprednisolone plus placebo. The nifedipine-methylpednisolone combination seemed to result in more prompt stone passage.

With respect to calcium supplements in calcium kidney stone disease, Curhan et al³ prospectively examined stone risk associated with dietary calcium as well as calcium supplements. This seemed to show that with calcium supplements there was no increased risk, and there may have even been some benefit. In another study by Borghi et al,⁴ normal dietary calcium intake was shown to be associated with lower stone risk than a low calcium intake. Further, the study by Curhan et al³ seemed to indicate the same.

In Reply: I thank Dr. Keller for his kind letter.

With respect to expulsive therapy, Dellabella et al¹ randomly assigned 210 patients to receive nifedipine, tamsulosin, or phloroglucinol. All the patients also received a corticosteroid. The most effective therapy was tamsulosin, though this was not a placebo-controlled study. In a separate study, Borghi et al² compared methylprednisolone plus nifedipine and methylprednisolone plus placebo. The nifedipine-methylpednisolone combination seemed to result in more prompt stone passage.

With respect to calcium supplements in calcium kidney stone disease, Curhan et al³ prospectively examined stone risk associated with dietary calcium as well as calcium supplements. This seemed to show that with calcium supplements there was no increased risk, and there may have even been some benefit. In another study by Borghi et al,⁴ normal dietary calcium intake was shown to be associated with lower stone risk than a low calcium intake. Further, the study by Curhan et al³ seemed to indicate the same.

In Reply: I thank Dr. Keller for his kind letter.

With respect to expulsive therapy, Dellabella et al¹ randomly assigned 210 patients to receive nifedipine, tamsulosin, or phloroglucinol. All the patients also received a corticosteroid. The most effective therapy was tamsulosin, though this was not a placebo-controlled study. In a separate study, Borghi et al² compared methylprednisolone plus nifedipine and methylprednisolone plus placebo. The nifedipine-methylpednisolone combination seemed to result in more prompt stone passage.

With respect to calcium supplements in calcium kidney stone disease, Curhan et al³ prospectively examined stone risk associated with dietary calcium as well as calcium supplements. This seemed to show that with calcium supplements there was no increased risk, and there may have even been some benefit. In another study by Borghi et al,⁴ normal dietary calcium intake was shown to be associated with lower stone risk than a low calcium intake. Further, the study by Curhan et al³ seemed to indicate the same.

To the Editor: I was pleased to see my article on fragility fractures in patients with chronic kidney disease (CKD) in the Cleveland Clinic Journal of Medicine¹ and your preamble Letter from the Editor.²

However, Dr. Coco’s accompanying editorial³ misquoted a particular point I cautiously and consistently make—not only in the CCJM article, but in other invited papers on the topic of fractures in CKD. I specifically state that bisphosphonates should only be considered in stage 4–5 CKD in fracturing patients, not just those with “low bone mineral density,” who have clear-cut osteoporosis by exclusion of other causes of fractures in this population. Hence, Dr. Coco’s statement that “… the author advocates the use of bisphosphonate therapy in patients with chronic kidney disease who have low bone mineral density” is inaccurate.

If one carefully reads the last four paragraphs of my paper on page 721, one will see that I emphasize this caution repeatedly and even specifically state: “Treating only on the basis of low bone mineral density and other risk factors seems to be associated with greater risk than benefit.”

Thank you for your consideration.

To the Editor: I was pleased to see my article on fragility fractures in patients with chronic kidney disease (CKD) in the Cleveland Clinic Journal of Medicine¹ and your preamble Letter from the Editor.²

However, Dr. Coco’s accompanying editorial³ misquoted a particular point I cautiously and consistently make—not only in the CCJM article, but in other invited papers on the topic of fractures in CKD. I specifically state that bisphosphonates should only be considered in stage 4–5 CKD in fracturing patients, not just those with “low bone mineral density,” who have clear-cut osteoporosis by exclusion of other causes of fractures in this population. Hence, Dr. Coco’s statement that “… the author advocates the use of bisphosphonate therapy in patients with chronic kidney disease who have low bone mineral density” is inaccurate.

If one carefully reads the last four paragraphs of my paper on page 721, one will see that I emphasize this caution repeatedly and even specifically state: “Treating only on the basis of low bone mineral density and other risk factors seems to be associated with greater risk than benefit.”

Thank you for your consideration.

To the Editor: I was pleased to see my article on fragility fractures in patients with chronic kidney disease (CKD) in the Cleveland Clinic Journal of Medicine¹ and your preamble Letter from the Editor.²

However, Dr. Coco’s accompanying editorial³ misquoted a particular point I cautiously and consistently make—not only in the CCJM article, but in other invited papers on the topic of fractures in CKD. I specifically state that bisphosphonates should only be considered in stage 4–5 CKD in fracturing patients, not just those with “low bone mineral density,” who have clear-cut osteoporosis by exclusion of other causes of fractures in this population. Hence, Dr. Coco’s statement that “… the author advocates the use of bisphosphonate therapy in patients with chronic kidney disease who have low bone mineral density” is inaccurate.

If one carefully reads the last four paragraphs of my paper on page 721, one will see that I emphasize this caution repeatedly and even specifically state: “Treating only on the basis of low bone mineral density and other risk factors seems to be associated with greater risk than benefit.”

Thank you for your consideration.

In Reply: Bone disease in the patient with chronic kidney disease (CKD), especially in the presence of a fracture, is indeed a vexing problem. Clinically, it is very difficult to differentiate between low bone turnover—not uncommon in patients with CKD—and patients who have osteoporosis. Clinically, these patients present similarly: both can have abnormal bone density measurements (usually low bone mineral density with T scores less than −2.5 standard deviation), and both can have fractures. But both should not be treated the same without further evidence.

In Dr. Miller’s article, bisphosphonate and other therapies are named as possible treatments for “osteoporosis” in patients with CKD stages 1 through 3. “Treatment decisions are more difficult … in stage 4 and especially stage 5 chronic kidney disease with fragility fractures…."

Dr. Miller indeed states that “patients without fractures with stage 5 … should not be given bisphosphonates …” He also states, “Treating only on the basis of low bone mineral density … seems to be associated with greater risk than benefit.” In Dr. Miller’s opinion, the latter group of patients may be treated with a bisphosphonate if there has been a fracture. However, many of these patients may have fractured because of low turnover bone disease; unfortunately, they cannot have “clear-cut osteoporosis by exclusions of other causes.” Bisphosphonate therapy may further suppress bone activity (if there is any activity left) and may predispose to extraosseous and cardiovascular calcifications and further non-bone pathology.

Dr. Miller does caution regarding unknown risks in these patients with advanced kidney disease.

Treating metabolic bone disease is certainly not straightforward, especially when present in the fracturing renal patient. We need more evidence before making treatment paradigms.

In Reply: Bone disease in the patient with chronic kidney disease (CKD), especially in the presence of a fracture, is indeed a vexing problem. Clinically, it is very difficult to differentiate between low bone turnover—not uncommon in patients with CKD—and patients who have osteoporosis. Clinically, these patients present similarly: both can have abnormal bone density measurements (usually low bone mineral density with T scores less than −2.5 standard deviation), and both can have fractures. But both should not be treated the same without further evidence.

In Dr. Miller’s article, bisphosphonate and other therapies are named as possible treatments for “osteoporosis” in patients with CKD stages 1 through 3. “Treatment decisions are more difficult … in stage 4 and especially stage 5 chronic kidney disease with fragility fractures…."

Dr. Miller indeed states that “patients without fractures with stage 5 … should not be given bisphosphonates …” He also states, “Treating only on the basis of low bone mineral density … seems to be associated with greater risk than benefit.” In Dr. Miller’s opinion, the latter group of patients may be treated with a bisphosphonate if there has been a fracture. However, many of these patients may have fractured because of low turnover bone disease; unfortunately, they cannot have “clear-cut osteoporosis by exclusions of other causes.” Bisphosphonate therapy may further suppress bone activity (if there is any activity left) and may predispose to extraosseous and cardiovascular calcifications and further non-bone pathology.

Dr. Miller does caution regarding unknown risks in these patients with advanced kidney disease.

Treating metabolic bone disease is certainly not straightforward, especially when present in the fracturing renal patient. We need more evidence before making treatment paradigms.

In Reply: Bone disease in the patient with chronic kidney disease (CKD), especially in the presence of a fracture, is indeed a vexing problem. Clinically, it is very difficult to differentiate between low bone turnover—not uncommon in patients with CKD—and patients who have osteoporosis. Clinically, these patients present similarly: both can have abnormal bone density measurements (usually low bone mineral density with T scores less than −2.5 standard deviation), and both can have fractures. But both should not be treated the same without further evidence.

In Dr. Miller’s article, bisphosphonate and other therapies are named as possible treatments for “osteoporosis” in patients with CKD stages 1 through 3. “Treatment decisions are more difficult … in stage 4 and especially stage 5 chronic kidney disease with fragility fractures…."

Dr. Miller indeed states that “patients without fractures with stage 5 … should not be given bisphosphonates …” He also states, “Treating only on the basis of low bone mineral density … seems to be associated with greater risk than benefit.” In Dr. Miller’s opinion, the latter group of patients may be treated with a bisphosphonate if there has been a fracture. However, many of these patients may have fractured because of low turnover bone disease; unfortunately, they cannot have “clear-cut osteoporosis by exclusions of other causes.” Bisphosphonate therapy may further suppress bone activity (if there is any activity left) and may predispose to extraosseous and cardiovascular calcifications and further non-bone pathology.

Dr. Miller does caution regarding unknown risks in these patients with advanced kidney disease.

Treating metabolic bone disease is certainly not straightforward, especially when present in the fracturing renal patient. We need more evidence before making treatment paradigms.

To the Editor: Buencamino and colleagues¹ reviewed the association between menopause and periodontal disease. However, they did not mention the role of vitamin D status in this setting.

Vitamin D status is usually divided into three categories based on serum 25-hydroxyvitamin D levels: “deficient” (≤ 15 ng/mL), “insufficient” (15.1–29.9 ng/mL), and “sufficient” (≥ 30 ng/mL). Serum 25-hydroxyvitamin D levels have been decreasing significantly for more than a decade, and as a result, a majority of the US population has a vitamin D insufficiency.

In the third National Health and Nutrition Examination Survey (NHANES III), a large US population survey, a low serum 25-hydroxyvitamin D concentration was independently associated with periodontal disease.² In particular, it was significantly associated with loss of alveolar attachment in persons older than 50 years of both sexes, independent of race or ethnicity; women in the highest 25-hydroxyvitamin D quintile had, on average, 0.26 mm (95% confidence interval 0.09–0.43 mm) less mean attachment loss than did women in the lowest quintile. Furthermore, in a randomized trial, supplementation with vitamin D (700 IU/day) plus calcium (500 mg/day) has been shown to significantly reduce tooth loss in older persons over a 3-year treatment period.³

Osteoporosis and periodontal disease share several risk factors, and it might be speculated that these pathologic conditions are biologically intertwined.⁴ The decreased bone mineral density of osteoporosis can lead to an altered trabecular pattern and more rapid alveolar bone resorption, thus predisposing to periodontal disease. On the other hand, periodontal infections can increase the systemic release of inflammatory cytokines, which accelerate systemic bone resorption. Indeed, vitamin D deficiency has been associated with a cytokine profile that favors greater inflammation (eg, higher levels of C-reactive protein and interleukin 6, and lower levels of interleukin 10), and vitamin D supplementation decreases circulating inflammatory markers.⁵ This might break the vicious circle of osteoporosis, periodontal disease development, and further systemic bone resorption.

Therefore, we suggest that menopausal women should maintain an adequate vitamin D status in order to prevent and treat osteoporosis-associated periodontal disease.

To the Editor: Buencamino and colleagues¹ reviewed the association between menopause and periodontal disease. However, they did not mention the role of vitamin D status in this setting.

Vitamin D status is usually divided into three categories based on serum 25-hydroxyvitamin D levels: “deficient” (≤ 15 ng/mL), “insufficient” (15.1–29.9 ng/mL), and “sufficient” (≥ 30 ng/mL). Serum 25-hydroxyvitamin D levels have been decreasing significantly for more than a decade, and as a result, a majority of the US population has a vitamin D insufficiency.

In the third National Health and Nutrition Examination Survey (NHANES III), a large US population survey, a low serum 25-hydroxyvitamin D concentration was independently associated with periodontal disease.² In particular, it was significantly associated with loss of alveolar attachment in persons older than 50 years of both sexes, independent of race or ethnicity; women in the highest 25-hydroxyvitamin D quintile had, on average, 0.26 mm (95% confidence interval 0.09–0.43 mm) less mean attachment loss than did women in the lowest quintile. Furthermore, in a randomized trial, supplementation with vitamin D (700 IU/day) plus calcium (500 mg/day) has been shown to significantly reduce tooth loss in older persons over a 3-year treatment period.³

Osteoporosis and periodontal disease share several risk factors, and it might be speculated that these pathologic conditions are biologically intertwined.⁴ The decreased bone mineral density of osteoporosis can lead to an altered trabecular pattern and more rapid alveolar bone resorption, thus predisposing to periodontal disease. On the other hand, periodontal infections can increase the systemic release of inflammatory cytokines, which accelerate systemic bone resorption. Indeed, vitamin D deficiency has been associated with a cytokine profile that favors greater inflammation (eg, higher levels of C-reactive protein and interleukin 6, and lower levels of interleukin 10), and vitamin D supplementation decreases circulating inflammatory markers.⁵ This might break the vicious circle of osteoporosis, periodontal disease development, and further systemic bone resorption.

Therefore, we suggest that menopausal women should maintain an adequate vitamin D status in order to prevent and treat osteoporosis-associated periodontal disease.

To the Editor: Buencamino and colleagues¹ reviewed the association between menopause and periodontal disease. However, they did not mention the role of vitamin D status in this setting.

Vitamin D status is usually divided into three categories based on serum 25-hydroxyvitamin D levels: “deficient” (≤ 15 ng/mL), “insufficient” (15.1–29.9 ng/mL), and “sufficient” (≥ 30 ng/mL). Serum 25-hydroxyvitamin D levels have been decreasing significantly for more than a decade, and as a result, a majority of the US population has a vitamin D insufficiency.

In the third National Health and Nutrition Examination Survey (NHANES III), a large US population survey, a low serum 25-hydroxyvitamin D concentration was independently associated with periodontal disease.² In particular, it was significantly associated with loss of alveolar attachment in persons older than 50 years of both sexes, independent of race or ethnicity; women in the highest 25-hydroxyvitamin D quintile had, on average, 0.26 mm (95% confidence interval 0.09–0.43 mm) less mean attachment loss than did women in the lowest quintile. Furthermore, in a randomized trial, supplementation with vitamin D (700 IU/day) plus calcium (500 mg/day) has been shown to significantly reduce tooth loss in older persons over a 3-year treatment period.³

Osteoporosis and periodontal disease share several risk factors, and it might be speculated that these pathologic conditions are biologically intertwined.⁴ The decreased bone mineral density of osteoporosis can lead to an altered trabecular pattern and more rapid alveolar bone resorption, thus predisposing to periodontal disease. On the other hand, periodontal infections can increase the systemic release of inflammatory cytokines, which accelerate systemic bone resorption. Indeed, vitamin D deficiency has been associated with a cytokine profile that favors greater inflammation (eg, higher levels of C-reactive protein and interleukin 6, and lower levels of interleukin 10), and vitamin D supplementation decreases circulating inflammatory markers.⁵ This might break the vicious circle of osteoporosis, periodontal disease development, and further systemic bone resorption.

Therefore, we suggest that menopausal women should maintain an adequate vitamin D status in order to prevent and treat osteoporosis-associated periodontal disease.