- Email: [email protected]
Mycobacterial Lung Infections
Mayo Clin Proc, July 1999, Vol 74
Letters to the Editor
REFERENCES 1. 2. 3. 4.
3.
Movsas B, Raffin TA, Epstein AH, Link CJ Jr. Pulmonary radiation injury. Chest. 1997;111:1061-1076. Gibson PG, Bryant DH, Morgan GW, et al. Radiation-induced lung injury: a hypersensitivity pneumonitis? Ann Intern Med. 1988;109: 288-291. Roberts CM, Foulcher E, Zaunders 11,et al. Radiation pneumonitis: a possible lymphocyte-mediated hypersensitivity reaction. Ann Intern Med. 1993;118:696-700. Nakayama Y, Makino S, Fukuda Y, Min KY, Shimizu A, OhsawaN. Activation of lavage lymphocytes in lung injuries caused by radiotherapy for lung cancer.Int J Radiat Oneal Bioi Phys. 1996;34:459467.
In reply: My coauthors and I thank Dr Satoh and colleagues for
their interest in our article on radiation-induced organizing pneumonia. The cases described by Satoh and associates seem to represent acute radiation-induced pneumonitis, even though the involvement was noted in the nonirradiated lung. With regard to clinical features and outcome, acute radiation-induced pneumonitis is distinctly different from the delayed form of organizing pneumonia described in our 6 patients. Therefore, a comparison of the responses to systemic corticosteroid therapy and mortality rates in these 2 groups of patients is not appropriate. Acute radiation-induced pneumonitis is far more serious than radiationinduced organizing pneumonia and is associated with high morbidity and mortality. Indeed, the letter by Satoh and colleagues seems to indicate that 17 of their 21 patients died of acute radiation-induced pneumonitis. In contrast, almost all the patients with radiation-induced organizing pneumonia occurring in the nonirradiated lung that have been reported in the literature have responded to systemic corticosteroid therapy. )-5 Although my colleagues and I have encountered many cases of both acute radiation-induced pneumonitis and chronic radiation-induced pulmonary fibrosis leading to respiratory failure in patients with lung cancer, we have not seen the radiation-induced migratory type of organized pneumonia occurring in the nonirradiated lung of patients with lung cancer. The cause of this rare type of radiation-induced organizing pneumonia is believed to be related to radiation "priming" of the lymphocytes. This process leads to a hypersensitivity-type reaction that ultimately results in organizing pneumonia in both the radiated and nonirradiated lung." Based on the cases reported in the literature, the term "radiation-induced organizing pneumonitis" seems to be an appropriate description for such cases. Udaya B. S. Prakash, MD Mayo Clinic Rochester Rochester, Minn
REFERENCES I.
2.
Bayle JY, Nesme P, Bejui-Thivolet F, Loire R, Guerin JC, Cordier JF. Migratory organizing pneumonitis "primed" by radiation therapy. Eur Respir J. 1995;8:322-326. Crestani B, Kambouchner M, Soler P, et al. Migratory bronchiolitis obliterans organizing pneumonia after unilateral radiation therapy for breast carcinoma. Eur Respir J. 1995;8:318321.
4.
5. 6.
744
Gibson PG, Bryant DH, Morgan GW, et al. Radiation-induced lung injury: a hypersensitivity pneumonitis? Ann Intern Med. 1988;109: 288-291. Crestani B, Valeyre D, Roden S, Wallaert B, Dalphin JC, Cordier JF, Groupe d'Etudes et de Recherche sur les Maladies Orphelines Pulmonaires. Bronchiolitis obliterans organizing pneumonia syndrome primed by radiation therapy to the breast. Am J Respir Crit Care Med. 1998;158:1929-1935. Martin C, Romero S, Sanchez-Paya J, Massuti B, Arriero JA, Hernandez L. Bilateral lymphocytic alveolitis: a common hypersensitivity reaction after unilateral thoracic radiation. Eur Respir J. In press. Prakash UBS. Radiation-induced injury in the "nonirradiated" lung [editorial]. Eur Respir J. In press.
Mycobacterial Lung Infections To the Editor: In the article on mycobacterial lung infections by Hadjiliadis, Adlakha, and Prakash, published in the January 1999 issue of Mayo Clinic Proceedings (pages 45 to 51), achalasia often provided the reservoir for lipoid material, particularly for mineral oil. I encountered a patient with mineral oil aspiration and a giant Zenker diverticulum, and another who regurgitated mineral oil and ancient food from a massive epiphrenic diverticulum and had recurrent bezoars that blocked the esophageal lumen. A topic that most medical textbooks do not address and many physicians do not appreciate is the impact of undertreated achalasia and long-standing diverticular retention on medication decisions (including the use of mineral oil'). Particularly in patients with diverticula, multiple doses of orally administered medications can be retained. Baron? reported intractable hypothyroidism in a patient with Zenker diverticulum caused by "pooling" and then regurgitation of thyroxine tablets. Dr Stanley Hamilton of Johns Hopkins has a photograph of an epiphrenic diverticulum containing at least 25 ulcerogenic quinidine tablets in various stages of decomposition. Depending on diverticular "whims," the blood levels of quinidine in this patient could range from 0 to fatal! Because it takes decades for diverticula to achieve such size, they are found most often in elderly patients whose need for multiple pharmaceutical agents compounds the problem. The pH in the diverticula or achalasia pouch is usually similar to that of saliva, and if the patient takes antacids, it is even alkaline. Protective coatings designed for delivery to the small intestine solubilize during prolonged diverticular stasis, a process that releases active agents. "Decoating" then affects drugs inactivated by gastric acids such as pancreatic enzymes and proton pump inhibitors, changes the kinetics of the many sustainedrelease delivery systems, and risks mucosal damage from drugs requiring coatings to prevent gastrointestinal toxicity. Drugs that are toxic to the esophageal wall;' such as doxycycline, tetracycline, minocycline, potassium, some nonsteroidal anti-inflammatory drugs, phenytoin, iron, quinidine, and diphosphonate ("Fosamax esophagus"), can also be trapped. Stasis sufficient for bezoar formation or "rotten-food halitosis" predisposes the patient to contact necrosis. One of my patients had food and pills solidly impacted in a Zenker diverticulum and an asymptomatic chronic perforation allowing mediastinal visualization (topical toxicity?). In another patient, just 1 retained doxycycline tablet produced into-the-muscle circumferential
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
745
Mayo Clio Proc, July 1999, Vol 74
Letters to the Editor
debridement. Are such drugs the "X" factor in "idiopathic" diverticular ulcerations, particularly those that hemorrhage or perforate into abutting critical organs? My experience with retained medications has prompted me to recommend, when possible, liquid or chewable products followed by a liquid flush. However, physicians should be aware that, in patients with giant diverticula or undertreated achalasia in whom reliability and rapid availability of medications are essential for therapeutic success, the oral route may be too erraticassociated with unpredictable absorptive delays, "peaks and valleys" in serum levels, and risk of drug predigestion. David E. Langdon, MD Arlington, Tex
REFERENCES 1.
Langdon DE. A risk of mineral oil. N Engl J Med. 1998;339: 19471948.
2. 3.
Baron SH. Zenker's diverticulum as a cause for loss of drug availability: a "new" complication. Am J Gastroenterol. 1982;77:152-153. McCord OS, Clouse RE. Pill-induced esophageal strictures: clinical features and risk factors for development. Am J Med. 1990;88:512-518.
In reply: I thank Dr Langdon, on behalf of my coauthors, for his interest in our article and his thoughtful comments regarding the complications associated with pharyngoesophageal (Zenker) diverticulum. We agree with him about the possibility of retention oftablets in the diverticulum and resultant complications. If surgical correction is not a therapeutic option in such patients, it is important to educate them about the complications and precautions recommended by Dr Langdon.
Udaya B. S. Prakash, MD Mayo Clinic Rochester Rochester, Minn
The Editor welcomes letters and comments, particularly pertaining to recently published articles in Mayo Clinic Proceedings, as well as letters reporting original observations and research. Letters pertaining to a recently published Proceedings article should be received no later than 1 month after the article's publication. A letter should be no longer than 500 words, contain no more than 5 references and I table or figure, be signed by no more than 3 authors, be in doublespaced, typewritten format, and not be published or submitted elsewhere. The letter must be signed and include the correspondent's full address, telephone and fax numbers, and e-mail address (if available). It is assumed that appropriate letters will be published, at the Editor's discretion, unless the writer indicates otherwise. The Editor reserves the right to edit letters in accordance with Proceedings style and to abridge them if necessary. Letters may be submitted by surface mail to Letters to the Editor, Mayo Clinic Proceedings, Room 660 Siebens Building, Rochester, MN 55905; by fax to (507) 284-0252; or bye-mail to [email protected]. (Note: Authors who submit letters by fax or e-mail must also send a copy by surface mail.)
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
Letters to the Editor
REFERENCES 1. 2. 3. 4.
3.
Movsas B, Raffin TA, Epstein AH, Link CJ Jr. Pulmonary radiation injury. Chest. 1997;111:1061-1076. Gibson PG, Bryant DH, Morgan GW, et al. Radiation-induced lung injury: a hypersensitivity pneumonitis? Ann Intern Med. 1988;109: 288-291. Roberts CM, Foulcher E, Zaunders 11,et al. Radiation pneumonitis: a possible lymphocyte-mediated hypersensitivity reaction. Ann Intern Med. 1993;118:696-700. Nakayama Y, Makino S, Fukuda Y, Min KY, Shimizu A, OhsawaN. Activation of lavage lymphocytes in lung injuries caused by radiotherapy for lung cancer.Int J Radiat Oneal Bioi Phys. 1996;34:459467.
In reply: My coauthors and I thank Dr Satoh and colleagues for
their interest in our article on radiation-induced organizing pneumonia. The cases described by Satoh and associates seem to represent acute radiation-induced pneumonitis, even though the involvement was noted in the nonirradiated lung. With regard to clinical features and outcome, acute radiation-induced pneumonitis is distinctly different from the delayed form of organizing pneumonia described in our 6 patients. Therefore, a comparison of the responses to systemic corticosteroid therapy and mortality rates in these 2 groups of patients is not appropriate. Acute radiation-induced pneumonitis is far more serious than radiationinduced organizing pneumonia and is associated with high morbidity and mortality. Indeed, the letter by Satoh and colleagues seems to indicate that 17 of their 21 patients died of acute radiation-induced pneumonitis. In contrast, almost all the patients with radiation-induced organizing pneumonia occurring in the nonirradiated lung that have been reported in the literature have responded to systemic corticosteroid therapy. )-5 Although my colleagues and I have encountered many cases of both acute radiation-induced pneumonitis and chronic radiation-induced pulmonary fibrosis leading to respiratory failure in patients with lung cancer, we have not seen the radiation-induced migratory type of organized pneumonia occurring in the nonirradiated lung of patients with lung cancer. The cause of this rare type of radiation-induced organizing pneumonia is believed to be related to radiation "priming" of the lymphocytes. This process leads to a hypersensitivity-type reaction that ultimately results in organizing pneumonia in both the radiated and nonirradiated lung." Based on the cases reported in the literature, the term "radiation-induced organizing pneumonitis" seems to be an appropriate description for such cases. Udaya B. S. Prakash, MD Mayo Clinic Rochester Rochester, Minn
REFERENCES I.
2.
Bayle JY, Nesme P, Bejui-Thivolet F, Loire R, Guerin JC, Cordier JF. Migratory organizing pneumonitis "primed" by radiation therapy. Eur Respir J. 1995;8:322-326. Crestani B, Kambouchner M, Soler P, et al. Migratory bronchiolitis obliterans organizing pneumonia after unilateral radiation therapy for breast carcinoma. Eur Respir J. 1995;8:318321.
4.
5. 6.
744
Gibson PG, Bryant DH, Morgan GW, et al. Radiation-induced lung injury: a hypersensitivity pneumonitis? Ann Intern Med. 1988;109: 288-291. Crestani B, Valeyre D, Roden S, Wallaert B, Dalphin JC, Cordier JF, Groupe d'Etudes et de Recherche sur les Maladies Orphelines Pulmonaires. Bronchiolitis obliterans organizing pneumonia syndrome primed by radiation therapy to the breast. Am J Respir Crit Care Med. 1998;158:1929-1935. Martin C, Romero S, Sanchez-Paya J, Massuti B, Arriero JA, Hernandez L. Bilateral lymphocytic alveolitis: a common hypersensitivity reaction after unilateral thoracic radiation. Eur Respir J. In press. Prakash UBS. Radiation-induced injury in the "nonirradiated" lung [editorial]. Eur Respir J. In press.
Mycobacterial Lung Infections To the Editor: In the article on mycobacterial lung infections by Hadjiliadis, Adlakha, and Prakash, published in the January 1999 issue of Mayo Clinic Proceedings (pages 45 to 51), achalasia often provided the reservoir for lipoid material, particularly for mineral oil. I encountered a patient with mineral oil aspiration and a giant Zenker diverticulum, and another who regurgitated mineral oil and ancient food from a massive epiphrenic diverticulum and had recurrent bezoars that blocked the esophageal lumen. A topic that most medical textbooks do not address and many physicians do not appreciate is the impact of undertreated achalasia and long-standing diverticular retention on medication decisions (including the use of mineral oil'). Particularly in patients with diverticula, multiple doses of orally administered medications can be retained. Baron? reported intractable hypothyroidism in a patient with Zenker diverticulum caused by "pooling" and then regurgitation of thyroxine tablets. Dr Stanley Hamilton of Johns Hopkins has a photograph of an epiphrenic diverticulum containing at least 25 ulcerogenic quinidine tablets in various stages of decomposition. Depending on diverticular "whims," the blood levels of quinidine in this patient could range from 0 to fatal! Because it takes decades for diverticula to achieve such size, they are found most often in elderly patients whose need for multiple pharmaceutical agents compounds the problem. The pH in the diverticula or achalasia pouch is usually similar to that of saliva, and if the patient takes antacids, it is even alkaline. Protective coatings designed for delivery to the small intestine solubilize during prolonged diverticular stasis, a process that releases active agents. "Decoating" then affects drugs inactivated by gastric acids such as pancreatic enzymes and proton pump inhibitors, changes the kinetics of the many sustainedrelease delivery systems, and risks mucosal damage from drugs requiring coatings to prevent gastrointestinal toxicity. Drugs that are toxic to the esophageal wall;' such as doxycycline, tetracycline, minocycline, potassium, some nonsteroidal anti-inflammatory drugs, phenytoin, iron, quinidine, and diphosphonate ("Fosamax esophagus"), can also be trapped. Stasis sufficient for bezoar formation or "rotten-food halitosis" predisposes the patient to contact necrosis. One of my patients had food and pills solidly impacted in a Zenker diverticulum and an asymptomatic chronic perforation allowing mediastinal visualization (topical toxicity?). In another patient, just 1 retained doxycycline tablet produced into-the-muscle circumferential
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
745
Mayo Clio Proc, July 1999, Vol 74
Letters to the Editor
debridement. Are such drugs the "X" factor in "idiopathic" diverticular ulcerations, particularly those that hemorrhage or perforate into abutting critical organs? My experience with retained medications has prompted me to recommend, when possible, liquid or chewable products followed by a liquid flush. However, physicians should be aware that, in patients with giant diverticula or undertreated achalasia in whom reliability and rapid availability of medications are essential for therapeutic success, the oral route may be too erraticassociated with unpredictable absorptive delays, "peaks and valleys" in serum levels, and risk of drug predigestion. David E. Langdon, MD Arlington, Tex
REFERENCES 1.
Langdon DE. A risk of mineral oil. N Engl J Med. 1998;339: 19471948.
2. 3.
Baron SH. Zenker's diverticulum as a cause for loss of drug availability: a "new" complication. Am J Gastroenterol. 1982;77:152-153. McCord OS, Clouse RE. Pill-induced esophageal strictures: clinical features and risk factors for development. Am J Med. 1990;88:512-518.
In reply: I thank Dr Langdon, on behalf of my coauthors, for his interest in our article and his thoughtful comments regarding the complications associated with pharyngoesophageal (Zenker) diverticulum. We agree with him about the possibility of retention oftablets in the diverticulum and resultant complications. If surgical correction is not a therapeutic option in such patients, it is important to educate them about the complications and precautions recommended by Dr Langdon.
Udaya B. S. Prakash, MD Mayo Clinic Rochester Rochester, Minn
The Editor welcomes letters and comments, particularly pertaining to recently published articles in Mayo Clinic Proceedings, as well as letters reporting original observations and research. Letters pertaining to a recently published Proceedings article should be received no later than 1 month after the article's publication. A letter should be no longer than 500 words, contain no more than 5 references and I table or figure, be signed by no more than 3 authors, be in doublespaced, typewritten format, and not be published or submitted elsewhere. The letter must be signed and include the correspondent's full address, telephone and fax numbers, and e-mail address (if available). It is assumed that appropriate letters will be published, at the Editor's discretion, unless the writer indicates otherwise. The Editor reserves the right to edit letters in accordance with Proceedings style and to abridge them if necessary. Letters may be submitted by surface mail to Letters to the Editor, Mayo Clinic Proceedings, Room 660 Siebens Building, Rochester, MN 55905; by fax to (507) 284-0252; or bye-mail to [email protected]. (Note: Authors who submit letters by fax or e-mail must also send a copy by surface mail.)
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.