reasonable one. In his consideration of my comments concerning the patient's leukemia, Dr Schwarz seems to have missed the word not in my leading sentence. It reads, "Lead is not known to be leuke-
mogenic."
William H. Crosby, MD Scripps Clinic and Research Foundation La Jolla, Calif
Marrow Examination the Editor.\p=m-\The
To
case
report
"Chlorpropamide-Induced Agranulocytosis" (238:422, 1977) contains a deficiency. Description of hypocellular marrow on bone marrow aspiration, with a photograph (Fig 2) of marrow diluted by peripheral blood, hardly documents "a marked reduction in the myeloid series." The necessity of marrow sectioning in assessing aplasia is well known,1 and the techniques and advantages of marrow coring are well described.2 Marrow aplasia as a cause for inadequate marrow aspiration is far less common in our experience than lymphoma, hairy cell disease, fibrosis, or
replacement by tumor.
David A. Mulkey, MD Southern Nevada Memorial
Hospital Vegas
single axillary mass that had been biopsied. The second and third cases might have been more definitively clar¬ ified by comparison of the histology of the primary breast lesions and the
métastases. In the last two cases, the absence of estrogen receptors did not contribute to their management. The
interpretation by the authors of the fifth case is particularly distressing in that they assume the chest wall recur¬ rence from breast cancer was estrogenreceptor positive just because it re¬ sponded to estrogens, and concerning the second primary, there is in¬ adequate evidence at present of estro¬ gen receptor status in patients on hormonal treatment. They present very little evidence in their patients with positive receptors to substantiate their conclusions, and inferences about tumors with negative receptors cannot be made when the original tumors were not studied for estrogen receptors, as reiterated in Jensen's editorial (238:59-60,1977). Charles K. Tashima, MD
Medical Breast Service The University of Texas
Cancer Center
System
Houston 1. McClendon JE,
Appleby D, Claudon DB, et al: Colonic neoplasms: Tissue estrogen receptor and carcinoembryonic antigen. Arch Surg 112:240-241, 1977.
Las
1. Ellis LD, Jensen WN, Westman MP: Needle biopsy of bone and marrow. Arch Intern Med 114:213-221, 1964. 2. Block MH: Atlas of Hematology. Philadelphia, Lea and Febiger Publishers, 1976, pp 5-9.
Estrogen Receptor Assay To the Editor.\p=m-\Kiang and Kennedy (238:59-60, 1977) have presented an interesting idea that may prove to be useful in the differential diagnosis of adenocarcinomas of unknown primary site. Unfortunately, however, the evidence offered hardly appears to justify their claim that positive estrogen indicate that metastases arose from breast cancer. Of the 295 patients in whom estro-
receptor assays
can
receptor assays were performed, only 45 patients had cancers of other origin besides breast. A total of six patients with colon cancer is certainly not a substantial sample from which to draw any conclusions, particularly in view of reports such as that of gen
McClendon et al,1 who found estrogen receptor protein in five of 21 colonic
neoplasms.
A review of the five
Reply.\p=m-\Twocrucial points regarding the use and interpretation of
In
estrogen receptor results should be
brought up after reading Dr Tashima's letter: (1) one should not accept the receptor results readily without understanding the method of assays, and (2) one should not depend on estrogen receptor assay solely and neglect the importance of clinical information as a whole in the management of patients. In the quoted report of McClendon et al,1 "estrogen receptor" in five colonic neoplasms were all less than 70 fmole/g of tissue. According to our experience and that of others,2 a substantial 8 S receptor peak usually
could not be identified with confidence by sucrose gradient method when the receptor level was below 3 fmole/mg cytosol protein, or equivalent to about 100 fmole/g of tissue. Any claim for the presence of estrogen receptors below this level should be supported by Scatchard analysis and Kd (dissociation constant). These confirmatory data
unfortunately not described; therefore, their results,1 in our opinion, were difficult to interpret. The com¬ plexity of various assay techniques and different criteria in interpretation fur¬ ther accentuates the importance of the knowledge on the methodology of were
case
reports in
Kiang and Kennedy's article shows extenuating circumstances that prevent justification of their claim. In case 1, the only evidence that the patient might have had breast cancer was the response to estrogen therapy of a
estrogen receptor assay.
Downloaded From: http://jama.jamanetwork.com/ by a Oakland University User on 05/31/2015
Nowhere did we claim that the posi¬ tive estrogen receptor assays can indi¬ cate that métastases arose from breast cancer, without use of other supportive information. We have clearly stated that 8 S estrogen receptors were also found in the adenocarcinoma of the uterus and ovary. A clinical impression of métastases from breast cancer was reached only after carefully assessing the clinical information, the results of laboratory and roentgenographic stud¬ ies, the knowledge of the biological nature and disease pattern of various cancers, and the results of estrogen receptor studies. This method of approach was clearly demonstrated in case 1. We were glad that an incisional
biopsy was performed on a large right axillary mass, which not only provided
the information of the presence of estrogen receptor but also showed that the mass that regressed with estrogenic therapy was truly a metastatic lesion. We believe that some patients have benefitted from estrogen receptor assay when tumor histology could not pinpoint the primary site, as illus¬ trated in cases 2 and 3. In the fifth case presented, the finding of an absence of estrogen receptors in the tumor from the contralateral breast, in contrast to Dr Tashima's opinion, did help in our clin¬ ical management by continuing the estrogen therapy since estrogen was still effectively controlling metastatic disease from the first breast cancer. Furthermore, our opinion on the use of estrogen receptor assay for distin¬ guishing a new primary from metas¬ tasis in the contralateral breast was in accord with that of Jensen's editorial (238:59, 1977). Dr Tashima apparently misinterpreted the editorial. David T. Kiang, MD, PhD B. J. Kennedy, MD
University of Minnesota School of Medicine
Minneapolis 1. McClendon JE, Appleby D, Claudon DB, et al: Colonic neoplasms: Tissue estrogen receptor and carcinoembryonic antigen. Arch Surg 112:240-241, 1977. 2. McGuire WL, Pearson OH, Segaloff A: Predicting hormone responsiveness in human breast cancer, in McGuire WL, Carbone PP, Vollmer EP (eds): Estrogen Receptors In Human Breast Cancer. New York, Raven Press, 1975, pp 17-30.
Steroid Receptors To the Editor.\p=m-\We write to support
Kiang and Kennedy (238:32, 1977)
on
the usefulness of estrogen receptor analyses in the differential diagnosis of adenocarcinomas of unknown origin in female patients and want to report our finding on combined analyses for estrogen and progesterone binding in 14 ovarian tumors over the past two years.
Data from seven tumors illustrate the usefulness with this application of receptor analyses. Of three lung tumors in patients with prior histories of genital tract tumors, one of the lesions could be established as metastatic endometrial carcinoma, and another was established as metastatic ovarian disease because of the presence of high-affinity, low-capacity estrogen binding in the cytosol; in the third, the absence of detectable estrogen binding
helped
to
verify primary lung
cancer.
None of three Krukenberg tumors exhibited high-affinity, low-capacity binding for estrogen or progesterone, thereby indicating them to be more likely from the gastrointestinal tract rather than from the ovary. However, we feel that the absence of estrogen and progesterone binding in the cytosol of a tumor does not preclude an origin from the reproductive tract. Involving adenocarcinoma in the ileum and liver that was confirmed by histopathological criteria to be from the endometrium, the lesions in the seventh patient were devoid of apparent estro¬ gen binding. This correlates with Kiang and Kennedy's finding for their case number 4 and emphasizes that for differential diagnoses it is the presence rather than the absence of receptors that is the more definitive and helpful to management. Jensen has also com¬ mented editorially (238:59, 1977) that "the absence of estrogen receptor does not rule out female reproductive tissues as the origin of a neoplasm of unknown ancestry." Data on the presence of steroid hormone receptor in ovarian neo¬
plasms are still sparse. Our experience with estrogen binding is similar to that of Kiang and Kennedy with 8S recep¬ tor. In addition, we have examined tumor cytosol for progesterone binding. Three of fourteen ovarian adenocarcinomas had high-affinity, low-capacity binding for both estrogen and proges¬ terone detectable by Scatchard plot analyses of dextran-coated charcoal assays in which either diethylstilbestrol or 17a,21-dimethyl-19-norpregna-
4,9-diene-3,20-dione (R 5020) were used as inhibitors; five of 14 bound only estrogen, and only one tumor bound progesterone in the absence of detect¬ able estrogen binding. In five meta¬
static lesions of ovarian carcinomas, three retained the complement of estrogen binding exhibited by the primary, and three of five retained progesterone-binding characteristic of the primary; two of five retained both the progesterone- and estrogen-binding characteristic of the primary. Whether the presence of progeste-
rone receptor as a second tumor marker in ovarian adenocarcinomas has the importance for predicting probable responses to endocrine thera¬ py as proposed for breast cancers1 remains to be elucidated. We feel that steroid hormone receptors are valuable adjunct biochemical tumor markers. For us they have proved useful to identify the tissue of origin of some tumors and to select the optimal mode of therapy. The high incidence of estrogen binding in ovarian adenocar¬ cinomas suggests that antiestrogen such as tamoxifen could prove effica¬ cious against these tumors consistent with clinical trials with estrogenreceptor-positive breast tumors,2 and in vitro experience.3 John A. Holt, PhD Thomas A. Caputo, MD Kathleen M. Kelly Neil Hellman Medical Research Building Albany Medical College Albany, NY 1. Horwitz KB, McGuire WL, Pearson OH, et al: Predicting response to endocrine therapy in human breast cancer: A hypothesis. Science 189:726, 1975.
2. Heuson JC: Current overview of EORTC clinical trials with tamoxifen. Cancer Treat Rep 60:1465, 1976. 3. Zava DT, Chamness GC, Horwitz KB, et al: Human breast cancer: Biologically active estrogen receptor in the absence of estrogen? Science 196:663, 1977.
Bone Scans To the Editor. \p=m-\Iwish to extend the
arguments of Chayes and Meyer (238: 305-306, 1977) concerning the useful-
of bone scans in cancer patients by suggesting that the clinical implicaness
tions of bone scans have yet to be exhausted. Recent reports indicate that positive bone scans may be helpful in determining prognosis in breast cancer.1,2 Bone scans can aid in the detection of other conditions besides osseous metastases, such as pulmonary calcification,3 soft tissue metastases,4 pulmonary osteoarthropathy,5 and other conditions6,7 Bone scans may be used to assess the response of metastatic disease to treatment.8 While the condition of positive bone scan, negative roentgenograms, and lack of confirmation with bone biopsy may not always indicate osseous metastases, we have encountered patients whose bone scans reverted to normal as other measurable metastatic disease responded to systemic therapy. Further difficulties with the asymptomatic bone metastases have arisen with Bonadonna's9 observation in his adjuvant studies in breast cancer: while a third of untreated patients with bone lesions were asymptomatic, two thirds of patients who were treated with cyclophosphamide, methotrexate, and fluorouracil (CMF) and who subse-
Downloaded From: http://jama.jamanetwork.com/ by a Oakland University User on 05/31/2015
quently sustained osseous métastases did not experience bone pain. It has even been suggested that there is a group of asymptomatic breast cancer patients with positive bone scans and negative bone roentgenograms who may still harbor disease in
bone after eight years.10 We continue to perform bone scans and skeletal (roentgenological) surveys on initial assessment and periodic scans and selective x-rays along with biochemical studies for a thorough evaluation of the condition of our
patients. Charles K. Tashima, MD Medical Breast Service The
University of Texas System
Cancer Center Houston 1. Galasko CSB: The
significance
of occult skeletal
metastases, detected by skeletal scintigraphy, in patients with otherwise apparently 'early' mammary carcinoma. Br J Surg 62:694-696, 1975. 2. Citrin DL, Furnival CM, Bessent RG, et al: Radioactive technetium phosphate bone scanning in preoperative assessment and follow-up study of patients with primary cancer of the breast. Surg Gynecol Obstet 143:360-364, 1976. 3. Grames GM, Sauser DD, Jansen C, et al: Radionuclide detection of diffuse interstitial pulmonary calcification. JAMA 230:992-995, 1974. 4. Richman LS, Gumerman LW, Levine G, et al: Localization of Tc99m polyphosphate in soft tissue malignancies. Am J Roentgenol 124:577-582, 1975. 5. Terry DW Jr, Isitman AT, Holmes RA: Radionuclide
images in hypertrophic pulmonary osteoarthropathy. Am J Roentgenol 124:571-576, 1975. 6. O'Mara RE: Bone scanning in osseous metastatic disease. JAMA 229:1915-1917, 1974. 7. Lentle BC, Russell AS, Percy JS, et al: Bone scinti\x=req-\ scanning updated. Ann Intern Med 84:297-303, 1976. 8. Citrin DL, Tuohy JB, Bessent RG, et al: Quantitative bone scanning: A method for assessing response of bone metastases to treatment. Lancet 1:1132-1133, 1974. 9. Bonadonna G, Rossi A, Valagussa P, et al: The CMF program for operable breast cancer with positive axillary nodes. Cancer 39:2904-2915, 1977. 10. Sklaroff RB, Sklaroff DM: Bone metastases from breast cancer at the time of radical mastectomy as detected by bone scan. Cancer 38:107-111, 1976.
Endotracheal Intubation To the Editor.\p=m-\Stauffer and Petty recently reported "Accidental Intubation of the Pyriform Sinus" (237:2324, 1977). The authors concluded that their
communication "underscores the need for improved training and skill in performing endotracheal intubation." While I completely agree with this statement, I wish the authors had stressed that it is rarely necessary to intubate a patient at the "roadside." The vast majority of these patients can be handled very easily and safely with anoral airway and an emergency resuscitation. I am well aware that Thomas Petty, MD, is an authority in the field, and I only wish he had taken the opportunity to use his stature todo a little "preaching" on unnecessary intubation. We have had similar complications in our county and are currently making an effort to review all intubations done
mogenic."
William H. Crosby, MD Scripps Clinic and Research Foundation La Jolla, Calif
Marrow Examination the Editor.\p=m-\The
To
case
report
"Chlorpropamide-Induced Agranulocytosis" (238:422, 1977) contains a deficiency. Description of hypocellular marrow on bone marrow aspiration, with a photograph (Fig 2) of marrow diluted by peripheral blood, hardly documents "a marked reduction in the myeloid series." The necessity of marrow sectioning in assessing aplasia is well known,1 and the techniques and advantages of marrow coring are well described.2 Marrow aplasia as a cause for inadequate marrow aspiration is far less common in our experience than lymphoma, hairy cell disease, fibrosis, or
replacement by tumor.
David A. Mulkey, MD Southern Nevada Memorial
Hospital Vegas
single axillary mass that had been biopsied. The second and third cases might have been more definitively clar¬ ified by comparison of the histology of the primary breast lesions and the
métastases. In the last two cases, the absence of estrogen receptors did not contribute to their management. The
interpretation by the authors of the fifth case is particularly distressing in that they assume the chest wall recur¬ rence from breast cancer was estrogenreceptor positive just because it re¬ sponded to estrogens, and concerning the second primary, there is in¬ adequate evidence at present of estro¬ gen receptor status in patients on hormonal treatment. They present very little evidence in their patients with positive receptors to substantiate their conclusions, and inferences about tumors with negative receptors cannot be made when the original tumors were not studied for estrogen receptors, as reiterated in Jensen's editorial (238:59-60,1977). Charles K. Tashima, MD
Medical Breast Service The University of Texas
Cancer Center
System
Houston 1. McClendon JE,
Appleby D, Claudon DB, et al: Colonic neoplasms: Tissue estrogen receptor and carcinoembryonic antigen. Arch Surg 112:240-241, 1977.
Las
1. Ellis LD, Jensen WN, Westman MP: Needle biopsy of bone and marrow. Arch Intern Med 114:213-221, 1964. 2. Block MH: Atlas of Hematology. Philadelphia, Lea and Febiger Publishers, 1976, pp 5-9.
Estrogen Receptor Assay To the Editor.\p=m-\Kiang and Kennedy (238:59-60, 1977) have presented an interesting idea that may prove to be useful in the differential diagnosis of adenocarcinomas of unknown primary site. Unfortunately, however, the evidence offered hardly appears to justify their claim that positive estrogen indicate that metastases arose from breast cancer. Of the 295 patients in whom estro-
receptor assays
can
receptor assays were performed, only 45 patients had cancers of other origin besides breast. A total of six patients with colon cancer is certainly not a substantial sample from which to draw any conclusions, particularly in view of reports such as that of gen
McClendon et al,1 who found estrogen receptor protein in five of 21 colonic
neoplasms.
A review of the five
Reply.\p=m-\Twocrucial points regarding the use and interpretation of
In
estrogen receptor results should be
brought up after reading Dr Tashima's letter: (1) one should not accept the receptor results readily without understanding the method of assays, and (2) one should not depend on estrogen receptor assay solely and neglect the importance of clinical information as a whole in the management of patients. In the quoted report of McClendon et al,1 "estrogen receptor" in five colonic neoplasms were all less than 70 fmole/g of tissue. According to our experience and that of others,2 a substantial 8 S receptor peak usually
could not be identified with confidence by sucrose gradient method when the receptor level was below 3 fmole/mg cytosol protein, or equivalent to about 100 fmole/g of tissue. Any claim for the presence of estrogen receptors below this level should be supported by Scatchard analysis and Kd (dissociation constant). These confirmatory data
unfortunately not described; therefore, their results,1 in our opinion, were difficult to interpret. The com¬ plexity of various assay techniques and different criteria in interpretation fur¬ ther accentuates the importance of the knowledge on the methodology of were
case
reports in
Kiang and Kennedy's article shows extenuating circumstances that prevent justification of their claim. In case 1, the only evidence that the patient might have had breast cancer was the response to estrogen therapy of a
estrogen receptor assay.
Downloaded From: http://jama.jamanetwork.com/ by a Oakland University User on 05/31/2015
Nowhere did we claim that the posi¬ tive estrogen receptor assays can indi¬ cate that métastases arose from breast cancer, without use of other supportive information. We have clearly stated that 8 S estrogen receptors were also found in the adenocarcinoma of the uterus and ovary. A clinical impression of métastases from breast cancer was reached only after carefully assessing the clinical information, the results of laboratory and roentgenographic stud¬ ies, the knowledge of the biological nature and disease pattern of various cancers, and the results of estrogen receptor studies. This method of approach was clearly demonstrated in case 1. We were glad that an incisional
biopsy was performed on a large right axillary mass, which not only provided
the information of the presence of estrogen receptor but also showed that the mass that regressed with estrogenic therapy was truly a metastatic lesion. We believe that some patients have benefitted from estrogen receptor assay when tumor histology could not pinpoint the primary site, as illus¬ trated in cases 2 and 3. In the fifth case presented, the finding of an absence of estrogen receptors in the tumor from the contralateral breast, in contrast to Dr Tashima's opinion, did help in our clin¬ ical management by continuing the estrogen therapy since estrogen was still effectively controlling metastatic disease from the first breast cancer. Furthermore, our opinion on the use of estrogen receptor assay for distin¬ guishing a new primary from metas¬ tasis in the contralateral breast was in accord with that of Jensen's editorial (238:59, 1977). Dr Tashima apparently misinterpreted the editorial. David T. Kiang, MD, PhD B. J. Kennedy, MD
University of Minnesota School of Medicine
Minneapolis 1. McClendon JE, Appleby D, Claudon DB, et al: Colonic neoplasms: Tissue estrogen receptor and carcinoembryonic antigen. Arch Surg 112:240-241, 1977. 2. McGuire WL, Pearson OH, Segaloff A: Predicting hormone responsiveness in human breast cancer, in McGuire WL, Carbone PP, Vollmer EP (eds): Estrogen Receptors In Human Breast Cancer. New York, Raven Press, 1975, pp 17-30.
Steroid Receptors To the Editor.\p=m-\We write to support
Kiang and Kennedy (238:32, 1977)
on
the usefulness of estrogen receptor analyses in the differential diagnosis of adenocarcinomas of unknown origin in female patients and want to report our finding on combined analyses for estrogen and progesterone binding in 14 ovarian tumors over the past two years.
Data from seven tumors illustrate the usefulness with this application of receptor analyses. Of three lung tumors in patients with prior histories of genital tract tumors, one of the lesions could be established as metastatic endometrial carcinoma, and another was established as metastatic ovarian disease because of the presence of high-affinity, low-capacity estrogen binding in the cytosol; in the third, the absence of detectable estrogen binding
helped
to
verify primary lung
cancer.
None of three Krukenberg tumors exhibited high-affinity, low-capacity binding for estrogen or progesterone, thereby indicating them to be more likely from the gastrointestinal tract rather than from the ovary. However, we feel that the absence of estrogen and progesterone binding in the cytosol of a tumor does not preclude an origin from the reproductive tract. Involving adenocarcinoma in the ileum and liver that was confirmed by histopathological criteria to be from the endometrium, the lesions in the seventh patient were devoid of apparent estro¬ gen binding. This correlates with Kiang and Kennedy's finding for their case number 4 and emphasizes that for differential diagnoses it is the presence rather than the absence of receptors that is the more definitive and helpful to management. Jensen has also com¬ mented editorially (238:59, 1977) that "the absence of estrogen receptor does not rule out female reproductive tissues as the origin of a neoplasm of unknown ancestry." Data on the presence of steroid hormone receptor in ovarian neo¬
plasms are still sparse. Our experience with estrogen binding is similar to that of Kiang and Kennedy with 8S recep¬ tor. In addition, we have examined tumor cytosol for progesterone binding. Three of fourteen ovarian adenocarcinomas had high-affinity, low-capacity binding for both estrogen and proges¬ terone detectable by Scatchard plot analyses of dextran-coated charcoal assays in which either diethylstilbestrol or 17a,21-dimethyl-19-norpregna-
4,9-diene-3,20-dione (R 5020) were used as inhibitors; five of 14 bound only estrogen, and only one tumor bound progesterone in the absence of detect¬ able estrogen binding. In five meta¬
static lesions of ovarian carcinomas, three retained the complement of estrogen binding exhibited by the primary, and three of five retained progesterone-binding characteristic of the primary; two of five retained both the progesterone- and estrogen-binding characteristic of the primary. Whether the presence of progeste-
rone receptor as a second tumor marker in ovarian adenocarcinomas has the importance for predicting probable responses to endocrine thera¬ py as proposed for breast cancers1 remains to be elucidated. We feel that steroid hormone receptors are valuable adjunct biochemical tumor markers. For us they have proved useful to identify the tissue of origin of some tumors and to select the optimal mode of therapy. The high incidence of estrogen binding in ovarian adenocar¬ cinomas suggests that antiestrogen such as tamoxifen could prove effica¬ cious against these tumors consistent with clinical trials with estrogenreceptor-positive breast tumors,2 and in vitro experience.3 John A. Holt, PhD Thomas A. Caputo, MD Kathleen M. Kelly Neil Hellman Medical Research Building Albany Medical College Albany, NY 1. Horwitz KB, McGuire WL, Pearson OH, et al: Predicting response to endocrine therapy in human breast cancer: A hypothesis. Science 189:726, 1975.
2. Heuson JC: Current overview of EORTC clinical trials with tamoxifen. Cancer Treat Rep 60:1465, 1976. 3. Zava DT, Chamness GC, Horwitz KB, et al: Human breast cancer: Biologically active estrogen receptor in the absence of estrogen? Science 196:663, 1977.
Bone Scans To the Editor. \p=m-\Iwish to extend the
arguments of Chayes and Meyer (238: 305-306, 1977) concerning the useful-
of bone scans in cancer patients by suggesting that the clinical implicaness
tions of bone scans have yet to be exhausted. Recent reports indicate that positive bone scans may be helpful in determining prognosis in breast cancer.1,2 Bone scans can aid in the detection of other conditions besides osseous metastases, such as pulmonary calcification,3 soft tissue metastases,4 pulmonary osteoarthropathy,5 and other conditions6,7 Bone scans may be used to assess the response of metastatic disease to treatment.8 While the condition of positive bone scan, negative roentgenograms, and lack of confirmation with bone biopsy may not always indicate osseous metastases, we have encountered patients whose bone scans reverted to normal as other measurable metastatic disease responded to systemic therapy. Further difficulties with the asymptomatic bone metastases have arisen with Bonadonna's9 observation in his adjuvant studies in breast cancer: while a third of untreated patients with bone lesions were asymptomatic, two thirds of patients who were treated with cyclophosphamide, methotrexate, and fluorouracil (CMF) and who subse-
Downloaded From: http://jama.jamanetwork.com/ by a Oakland University User on 05/31/2015
quently sustained osseous métastases did not experience bone pain. It has even been suggested that there is a group of asymptomatic breast cancer patients with positive bone scans and negative bone roentgenograms who may still harbor disease in
bone after eight years.10 We continue to perform bone scans and skeletal (roentgenological) surveys on initial assessment and periodic scans and selective x-rays along with biochemical studies for a thorough evaluation of the condition of our
patients. Charles K. Tashima, MD Medical Breast Service The
University of Texas System
Cancer Center Houston 1. Galasko CSB: The
significance
of occult skeletal
metastases, detected by skeletal scintigraphy, in patients with otherwise apparently 'early' mammary carcinoma. Br J Surg 62:694-696, 1975. 2. Citrin DL, Furnival CM, Bessent RG, et al: Radioactive technetium phosphate bone scanning in preoperative assessment and follow-up study of patients with primary cancer of the breast. Surg Gynecol Obstet 143:360-364, 1976. 3. Grames GM, Sauser DD, Jansen C, et al: Radionuclide detection of diffuse interstitial pulmonary calcification. JAMA 230:992-995, 1974. 4. Richman LS, Gumerman LW, Levine G, et al: Localization of Tc99m polyphosphate in soft tissue malignancies. Am J Roentgenol 124:577-582, 1975. 5. Terry DW Jr, Isitman AT, Holmes RA: Radionuclide
images in hypertrophic pulmonary osteoarthropathy. Am J Roentgenol 124:571-576, 1975. 6. O'Mara RE: Bone scanning in osseous metastatic disease. JAMA 229:1915-1917, 1974. 7. Lentle BC, Russell AS, Percy JS, et al: Bone scinti\x=req-\ scanning updated. Ann Intern Med 84:297-303, 1976. 8. Citrin DL, Tuohy JB, Bessent RG, et al: Quantitative bone scanning: A method for assessing response of bone metastases to treatment. Lancet 1:1132-1133, 1974. 9. Bonadonna G, Rossi A, Valagussa P, et al: The CMF program for operable breast cancer with positive axillary nodes. Cancer 39:2904-2915, 1977. 10. Sklaroff RB, Sklaroff DM: Bone metastases from breast cancer at the time of radical mastectomy as detected by bone scan. Cancer 38:107-111, 1976.
Endotracheal Intubation To the Editor.\p=m-\Stauffer and Petty recently reported "Accidental Intubation of the Pyriform Sinus" (237:2324, 1977). The authors concluded that their
communication "underscores the need for improved training and skill in performing endotracheal intubation." While I completely agree with this statement, I wish the authors had stressed that it is rarely necessary to intubate a patient at the "roadside." The vast majority of these patients can be handled very easily and safely with anoral airway and an emergency resuscitation. I am well aware that Thomas Petty, MD, is an authority in the field, and I only wish he had taken the opportunity to use his stature todo a little "preaching" on unnecessary intubation. We have had similar complications in our county and are currently making an effort to review all intubations done
