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Diagnosing Syncope
To the Editor: Having read the position paper on diagnosing syncope (1), I question the advice given for the use of 24-hour Holter monitoring as opposed to long-term ambulatory loop electrocardiogramt monitoring). According to the data presented in this article, it is clear that the overall diagnostic yield of loop recording far exceeds that of 24-hour Holter mon- itoring (24% to 47% compared with 19%). The value of this increased diagnostic yield of loop recording far outweighs the diagnostic yield of 14% for asymptomatic arrhythmia seen on 24-hour Holter monitoring.
I believe that loop recording should replace 24-hour Holter monitoring as the outpatient monitoring test of choice in patients with organic heart disease (branch 1 of the figure in the position paper) as well as in those without suspected heart disease. The article also states that in patients with a high pretest probability of arrhythmia and a negative result on 24-hour Holter monitor- ing, further evaluation for arrhythmia should be pursued by event monitoring or electrophysiologic study. Why not do the event monitoring initially?
The authors also state that loop recording is most beneficial in patients with frequent episodes of syncope. Because loop record- ing is usually done for 30 days, it seems that this would be a much better method for diagnosing infrequent syncope than 24- hour Holter monitoring.
This article confirms my experience that for the diagnosis of syncope in a compliant patient not requiring in-patient monitor- ing, 30-day event recording is a much better and more cost- effective test than 24-hour Holter monitoring.
G. Truett Jarrard Jr., MD Papp Clinic Newnan, GA 30263
Reference
1. Linzer M, Yang EH, Estes NA 3d, Wang P, Vorperian VR, Kapoor WN. Diagnosing syncope. Part 2: Unexplained syncope. Ann Intern Med. 1997;127:76-86.
To the Editor: The 15 June 1997 issue of Annals contained an interesting juxtaposition of articles. The first is a position paper produced by the Clinical Efficacy Assessment Project of the American College of Physicians (1) on diagnosing syncope. An expert panel reviewed the appropriate workup for patients with syncope and noted that “routine use of basic laboratory tests is not recommended… ” Immediately following this position paper is an essay, “What’s Wrong with This Picture?” (2), that de-
scribes a patient with isolated syncope. This patient has a thor- ough cardiac evaluation that fails to detect his colon carcinoma. One wonders whether a routine laboratory test, the complete blood count, if properly assessed, would have led to an earlier diagnosis of colon cancer. It is well recognized that colonic neoplasms are associated with gastrointestinal bleeding. Right- sided lesions, in particular, are often asymptomatic until signifi- cant anemia develops. It is likely that Dr. Brody’s patient had iron deficiency. Even if the patient did not have a textbook picture of hypochromia and microcytosis, I would expect an increased red cell deviation. Any of these findings should have alerted his physicians to the possibility of gastrointestinal blood loss.
I was trained in an era when a complete patient evaluation included a set of routine laboratory tests. These tests were non- invasive and were designed to screen the patient for otherwise silent disease. Linzer and colleagues (1) noted that the most common cause of syncope is “unknown” (their Table 1). Routine laboratory testing may help diagnose clinically occult bleeding and other hidden conditions and should remain part of our approach to patients with serious medical symptoms.
Paul 1. Roda, MD North East Medical Oncology Hazleton, PA 18201
References
1. Linzer M, Yang EH, Estes NA 3d, Wang P, Vorperian VR, Kapoor WN. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiogramn Intern Med. 1997;126:989-96.
2. Brody SA. What’s wrong with this picture? Ann Intern Med. 1997;126: 997-8.
In response: Dr. Jarrard suggests that loop monitoring should replace 24-hour Holter monitoring in patients with syncope. The problem with this point of view is that a patient needs to be symptomatic while wearing a loop monitor for the test to provide any useful information. Because 85% of patients with a first episode of syncope will not faint again within the next 6 months (1), loop monitoring would be of no benefit in these patients. However, Holter monitoring can document background rhythm disturbances (such as sinus pauses or nonsustained bouts of ventricular tachycardia) that, although nondiagnostic, might prompt further evaluation and subsequent diagnosis. Loop mon- itoring has the most benefit in patients with relatively frequent bouts of syncope or palpitations.
Dr. Roda’s suggestion that routine laboratory testing should be a part of the syncope workup is not supported by the literature. Anemia is not listed as a cause of syncope in most references, nor is hyponatremia, hypokalemia, or other such disorders. Pop- ulation-based studies of patients with syncope have not docu- mented the importance of routine laboratory tests (2). We be- lieve that a thorough history and physical examination, including measurement of orthostatic vital signs and, when indicated, a rectal examination, will alert the clinician to such abnormalities and prompt a more focused diagnostic evaluation.
Dr. Brody’s elderly patient who had syncope in church and aortic valve disease (3) is a provocative case (we suspect that this is why Annals decided to publish it!). This patient had intensive cardiac evaluation followed by placement of a coronary stent and a permanent pacemaker, only to eventually present with gastro- intestinal bleeding from colon cancer while receiving warfarin. Was the colon cancer missed, and would a complete blood count early on have helped to diagnose it? (In fact, it is hard to imagine that a complete blood count was not done before some of these invasive procedures.) One possible scenario would be that the patient was not anemic at the time of syncope, that the syncopal episode was due to cardiac ischemia or bradyarrhyth- mia, that the pacemaker and stent were appropriately placed, and that the colon cancer was incidentally discovered once the patient had received anticoagulation. More details about the
nature of the patient’s syncopal episodes would help sort this out (for example, were they sudden, exertional or positional, or as- sociated with chest pain?), as would more information on the patient’s presenting physical examination (for example, was pal- lor or orthostatic hypotension present?).
Mark Linzer, MD University of Wisconsin School of Medicine Madison, WI 53792
N.A. Mark Estes III, MD New England Medical Center Boston, MA 02111
Wishwa Kapoor, MD University of Pittsburgh Pittsburgh, PA 15261
References
1. Kapoor W, Peterson J, Wieand HS, Karpf M. Diagnostic and prognos- tic implications of recurrences in patients with syncope. Am J Med. 1987;83:700-8.
2. Kapoor WN. Evaluation of outcome of patients with syncope. Medicine (Baltimore). 1990;69:160-75.
3. Brody SA. What’s wrong with this picture? Ann Intern Med. 1997;126: 997-8.
Extramedullary Plasmacytoma: A Localized or Systemic Disease?
To the Editor: Extramedullary plasmacytoma is an uncommon variant of plasma cell dyscrasia that develops outside the bone; most cases (76%) occur in the upper respiratory tract (1). Lung involvement is rare; only 20 cases have been reported (2). For the definition of primary extramedullary plasmacytoma, a normal radiographic survey in the absence of bone marrow infiltration is required. The latter criterion has classically been assessed by conventional morphology. Now, however, more sensitive ap- proaches are available for the identification of bone marrow involvement. These studies would help elucidate whether ex- tramedullary plasmacytoma is a localized or an already dissemi- nated disorder.
A 70-year-old man with episodes of recurrent pneumonia had
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radiographic evidence of opacity in the lower right lobe of the lung. The IgG-A serum monoclonal component was 60.45 g/L, and no Bence Jones urinary protein or skeletal lesions were present. Bone marrow aspirate revealed less than 1% of plasma cells, as seen with May-Grünwald-Giemsa staining. Computed tomography of the chest confirmed a mass, the histology of which confirmed a proliferation of IgG-A-secreting plasma cells with amyloid deposits.
Our patient met the criteria for secretory primary pulmonary plasmacytoma (2). However, flow cytometric analysis using a propidium iodide/CD38 double-staining technique (3) showed that all plasma cells displayed DNA aneuploidy (DNA index, 1.10; Figure). On deparaffinized tissue blocks obtained from the pulmonary mass, DNA measurements by flow cytometry detected a clonal aneuploid population of plasma cells (DNA index, 1.10), and cytogenetic studies with fluorescence in situ hybridization (4) detected a trisomy of chromosome 1. The identical DNA index seen in plasma cells from both the mass and the bone marrow suggests that these cells may belong to the same clone.
To our knowledge, no information about cytogenetics or DNA cell content characteristics of tumor plasma cells has been re- ported for patients with extramedullary plasmacytoma. Our find- ings indicate that the DNA pattern in primary pulmonary plas- macytoma is similar to that previously seen in multiple myeloma (5); in this condition, both DNA hyperploidy and trisomy 1 are common. An additional important finding in our patient was the detection of clonal plasma cells in the bone marrow even though few normal-appearing plasma cells were seen by morphology. In summary, our results suggest that when appropriate and sensitive techniques are used, some, if not all, patients with extramedullary plasmacytoma may be found to have disseminated disease. This would indicate that both extramedullary plasmacytoma and mul- tiple myeloma are part of a continuous spectrum of plasma cell disorders rather than separate entities.
F. Javier Laso, MD, PhD M. Dolores Tabernero, MD, PhD M. Carmen Iglesias-Osma, MD, PhD University of Salamanca 37007 Salamanca, Spain
References
1. Wiltshaw E. The natural history of extramedullary plasmacytoma and its relation to solitary myeloma of bone and myelomatosis. Medicine (Baltimore). 1976;55:217-38.
2. Joseph G, Pandit M, Korfhage L. Primary pulmonary plasmacytoma. Cancer. 1993;71:721-4.
3. Orfao A, García-Sanz R, López-Berges MC, Vidriales MB, Gonzalez M, Caballero MD, et al. A new method for the analysis of plasma cell DNA content in multiple myeloma samples using a CD38/propidium iodide double staining technique, Cytometry. 1994;17:332-9.
4. Tabernero MD, San Miguel JF, García VL, García-Isidoro M, Wiegant J, Ciudad J, et al. Clinical, biological, and immunophenotypical char- acteristics of B-cell chronic lymphocytic leukemia with trisomy 12 by fluorescence in situ hybridization. Cytometry. 1995;22:217-22.
5. Tabernero MD, San Miguel JF, García-Sanz R, Najera L, García- Isidoro M, Perez-Simon JA, et al. Incidence of chromosome numerical changes in multiple myeloma: fluroescence in situ hybridization analysis using 15 chromosome-specific probes, Am J Pathol. 1996;149:153-61.
Vitamin E for Chronic Hepatitis B
To the Editor: Interferon-a for chronic hepatitis B is often ineffective and is associated with drawbacks, such as prolonged parenteral schedules, high costs, and side effects (1). Oral vitamin E is an inexpensive antioxidant that can stimulate the immune response and does not induce side effects (2). We evaluated vitamin E supplementation as therapy for chronic hepatitis B.
Twenty-four patients (12 were positive for hepatitis B e anti- gen [HBeAg] and 12 were infected by the “e” minus mutant) with elevated serum alanine aminotransferase (ALT) levels and serum hepatitis B virus DNA (Abbott Laboratories, North Chi- cago, Illinois) were randomly assigned to receive vitamin E, 300 mg twice daily for 3 months (n = 12), or no treatment (n = 12). They were followed monthly for 9 months. Nineteen patients (10 in the vitamin E group and 9 controls) had been unsuccessfully
| Variable | Patients Receiving Vitamin E | Controls | P Value |
|---|---|---|---|
| n/n (%) | |||
| After 3 months | |||
| Normalization of ALT levels | 4/12 (33) | 1/12 (8) | |
| Negative for HBV DNA | 6/12 (50) | 3/12 (25) | |
| Complete responset | 2/12 (17) | 0/12 (0) | |
| After 9 months | |||
| Normalization of ALT levels | 7/12 (58) | 1/12 (8) | 0.013 |
| Negative for HBV DNA | 7/12 (58) | 2/12 (17) | 0.044 |
| Complete responset | 5/12 (42) | 0/12 (0) | 0.019 |
* Data were analyzed by using the Fisher exact test. ALT = alanine aminotransferase; HBV = hepatitis B virus.
+ Defined as normalization of ALT levels and clearance of HBV DNA from serum.
treated with interferon-a. At study entry, the study groups were similar with respect to demographic, clinical, and laboratory fea- tures. Four HBeAb-positive patients discontinued vitamin E ther- apy because of severe increases in ALT levels (>10-fold the normal upper limit). A similar finding was seen in 2 controls. The biochemical and virologic responses after 3 and 9 months are shown in the Table. Of the 5 patients with complete response, 2 were positive for HBeAb and 3 were positive for HBeAg at study entry. The HBeAg-positive patients seroconverted to HBeAb during the study period, whereas none of the controls serocon- verted from HBeAg to HBeAb. Three of 5 patients with com- plete response had not responded to previous interferon-& treat- ment. Treatment with vitamin E had no side effects. These results suggest that vitamin E is a safe and useful treatment for chronic hepatitis B. Although the mechanism through which these results were achieved is unknown, the stimulatory effect of vitamin E on the immune system probably played a major role. Further studies are needed to confirm these data and to evaluate the effects of a possible combination with other antiviral drugs.
Pietro Andreone, MD Annagiulia Gramonzi Mauro Bernardi Universitá di Bologna 40138 Bologna, Italy
References
1. Lok AS. Treatment of chronic hepatitis. Br J Virol Hepatol, 1994;1: 105-24.
2. Meydani M. Vitamin E. Lancet. 1995;345:170-5.
Hyperadrenocorticism in a Patient with Esophageal Squamous-Cell Carcinoma
To the Editor: The ectopic corticotropin syndrome in associa- tion with nonpancreatic gastrointestinal tract cancer is rare. We report an unusual case of hyperadrenocorticism in a patient with metastatic esophageal squamous-cell carcinoma.
A 64-year-old man presented with a 3-month history of dys- phagia and 11.35-kg weight loss. Physical examination was re- markable for a blood pressure of 160/98 mm Hg, cachexia, nu- merous ecchymoses, and globally diminished strength and reflexes. Abnormal laboratory values included a hematocrit of 0.34; a serum potassium level of 2.1 mEq/L, a chloride level of 86 mEq/L, a bicarbonate level of 42 mEq/L, and a glucose level of 264 mg/dL.
Esophogastroduodenoscopy revealed a friable lesion in the mid-esophagus. Computed tomography showed an esophageal mass, a low-attenuation hepatic lesion, and bilateral adrenal en- largement. The following findings were diagnostic for the ectopic corticotropin syndrome: elevated urinary free cortisol excretion (4508 µg/24 hours [normal, 20 to 90 µg/24 hours]); increased late-afternoon serum adrenocorticotropic hormone (ACTH) con- centration (88 pg/mL [normal, 4 to 52 pg/mL]); low corticotrop-
in-releasing hormone level (20 pg/mL. [normal, 24 to 40 pg/mL]); and lack of suppressibility on 2-day, high-dose dexamethasone suppression testing. Pathologic examination of the esophageal tissue revealed poorly differentiated squamous-cell carcinoma. Positive results on immunohistochemical analysis for synaptophy- sin, keratin, and enolase indicated neuroendocrine differentia- tion. Staining for ACTH was negative.
Ketoconazole was administered to inhibit adrenal steroid bio- synthesis. For widespread metastases, the patient received cis- platinum and 5-fluorouracil. The patient died shortly after leav- ing the hospital against medical advice. Autopsy was refused.
Neoplasms of the lung, thymus, and pancreas are the main producers of ectopic ACTH. In 1968, Lohrenz and Custer (1) described the only other patient with the ectopic corticotropin syndrome associated with esophageal squamous-cell carcinoma.
Negative staining for ACTH in tumor tissue does not exclude ACTH biosynthesis (2). Some explanations include a predomi- nance of ACTH precursors that are not immunoreactive to a particular anti-ACTH serum and excessive hormone secretion rates leading to a reduced storage of pro-opiomelanocortin-derived peptides (3).
Neuroendocrine esophageal cancer and no evidence of a pul- monary, thymic, or pancreatic tumor render the former the most probable source of the ectopic ACTH syndrome in our patient.
Stephen Migueles, MD Susan Thompson, MD Sean McGrade, MD Georgetown University Medical Center Washington, DC 20007
References
1. Lohrenz FN, Custer GS. ACTH producing metastases from carcinoma of the esophagus. Ann Intern Med. 1965;62:1017-22.
2. Wajchenberg BL, Mendonca BB, Liberman B, Pereira MA, Carneiro PC, Wakamatsu A, et al. Ectopic adrenocorticotropic hormone syn- drome. Endocrinology Review. 1994;15:752-87.
3. Coates PJ, Doniach I, Howlett TA, Rees LH, Besser GM. An immu- nocytochemical study of 18 tumours causing ectopic Cushing’s syn- drome. J Clin Pathol. 1986;39:955-60.
Tensions in the Racial Integration of Health Care, Then and Now
To the Editor: I read with interest the recent article by Reyn- olds (1) on the role of the federal courts in desegregating health care. The article refers to the U.S. Supreme Court as having decided, by denying a writ of certiorari in Simkins, to desegregate health care facilities. In fact, what the article details is a 1963 “decision” made by a federal appellate court (the U.S. Court of Appeals for the Fourth Circuit), after which the U.S. Supreme Court chose not to consider the case further (denying certiorari). A denial of certiorari lets a lower-court decision stand by inertia. A decision on certiorari, formally speaking, is an act of “judicial discretion” (2), and decisions to deny or grant certiorari are not an expression of either agreement or disagreement with the merits of the decision of the lower appellate court.
The distinction is more than a legalistic one. The Supreme Court had indeed made a major step in 1954 when it declared unanimously in Brown v Board of Education of Topeka, Kansas that segregated public schools were unconstitutional; however, it did not at that time call for immediate school desegregation, nor did it initially articulate the position that segregation was out- lawed in all state activity (3). It was not until 1967 that the Supreme Court made clear, for example, that a state ban on interracial marriage was unconstitutional (4). This gradual ap- proach by the Supreme Court left an important role for others in the judiciary and legislative bodies. The Simkins case discussed in Reynolds’s article illustrates the important role that the federal courts throughout the South played in shaping, consolidating, and reinforcing the push toward racial equality, both before and after the Supreme Court’s 1954 decision in Brown v Board of Education (5).
Neil J. Nusbaum, JD, MD Tulane University School of Medicine New Orleans, LA 70112
References
1. Reynolds PP. Hospitals and Civil Rights, 1945-1963: The Case of Simkins v Moses H. Cone Memorial Hospital. Ann Intern Med. 1997; 126:898-906.
2. Supreme Court of the U.S. Rule 10, Considerations Governing Review on Writ of Certiorari.
3. Brown v Board of Education of Topeka, Kansas. 347 U.S. 483 (1954).
4. Loving v. Virginia. 388 U.S. 1 (1967).
5. Kluger R. Simple Justice: The History of Brown v. Board of Education and Black America’s Struggle for Equality. New York: Alfred A. Knopf; 1976.
To the Editor: We read with interest the paper on hospitals and civil rights from 1945 to 1963 (1) and its accompanying editorial (2). We wish to indicate that a subset of African-American patients-those with sickle cell disease-continue to be the tar- get of discrimination. Recent studies (3, 4) suggest the existence of a two-tier system of health care in the United States: one for the affluent and another for the poor. Subcategories exist within each system that are based on such factors as race, diagnosis, disease chronicity, and treatment. Patients with sickle cell disease seem to occupy the lowest rank on the scale. Because these patients often have recurrent attacks of acute severe pain, have chronic pain, are poor, and frequently use relatively large amounts of opioid analgesics (5), they have been granted second- or even third-class status by the health care system. In our experience, some of the markers of negativism and their mani- festations in the delivery of care to patients with sickle disease include segregation, inadequate coverage, rationing, ultimatums, and procrastination (Table).
Issues secondary to the manifestations listed in the Table may arise. Thus, patients who are denied treatment in the emergency department because they have exceeded their prescheduled num- ber of visits have no choice but to go to other emergency departments. Such patients are accused of hospital hopping and drug-seeking behavior and are subject to further restrictions and accusations.
We realize that some of these attitudes are expressed by some providers because of faulty perceptions, imitations, or habit. We hope that our letter will be published so that some providers may reexamine their attitudes in the delivery of care to patients with sickle cell disease.
| Marker | Manifestation |
|---|---|
| Segregation | Establishment of nonteaching service managed by a nurse practitioner or physician assistant Exemption of hematology fellows from participating in the delivery of care on a regular basis |
| Inadequate coverage | Employment of a part-time physician to deliver cursory care for a few hours on weekdays only Inadequate or nonexistent coverage in the absence of the part-time physician |
| Rationing | Restriction of frequency of treatment of painful episodes with opioids in the emergency department on a prescheduled basis, usually once a week |
| Ultimatums | Patients denied the right to choose Mandatory compliance with "homemade" rules to avoid expulsion |
| Procrastination | Frequent denial, postponement, or last-minute cancellation of diagnostic and therapeutic interventions |
Samir K. Ballas, MD Jefferson Medical College Philadelphia, PA 19107
Roy N. Gay, MD Misericordia Hospital Philadelphia, PA 19143
References
1. Reynolds PP. Hospitals and civil rights, 1945-1963: The case of Simkins v Moses H. Cone Memorial Hospital. Ann Intern Med. 1997;26:898-906.
2. Thomson GE. Discrimination in health care [Editorial]. Ann Intern Med. 1997;26:910-2.
3. Kahn KL, Pearson ML, Harrison ER, Desmond KA, Rogers WH, Rubenstein LV, et al. Health care for black and poor hospitalized Medicare patients. JAMA. 1994;271:1169-74.
4. Gronick ME, Eggers PW, Reilly TW, Mentnech RM, Fitterman LK, Kucken LE, et al. Effects of race and income on mortality and use of services among Medicare beneficiaries. N Engl J Med. 1996;335:791-9.
5. Ballas SK. Treatment of pain in adults with sickle cell disease. Am J Hematol. 1990;34:49-54.
In response: The Supreme Court receives almost 5000 petitions for certiorari each year. The 150 cases selected for full review and argument by the Supreme Court generally involve important con- stitutional principles or are likely to reverse a lower court ruling (1).
The Simkins v Moses H. Cone Memorial Hospital case, although receiving a denial of certiorari by the Supreme Court, was con- sidered in 1963 a landmark decision for Chief Judge Simon E. Sobeloff of the 4th Circuit Court of Appeals. Judge Sobeloff received letters of accolade from citizens and esteemed law col- leagues. Initially, the five circuit-court judges voted three against and two in favor of the plaintiffs. Sobeloff worked his court, changing the majority vote in favor of denial of federal funds to hospitals that racially segregated patients or denied them access to hospital beds and that refused African-American health pro- fessionals staff and employment privileges. Newspapers and hos- pital periodicals heralded the Supreme Court’s decision to let rest the 4th Circuit Court’s ruling, and the Department of Health, Education, and Welfare swiftly moved to implement new regu- lations on the use of federal funds under Hill-Burton (2).
Civil rights activists in the 1950s and 1960s faced even stiffer barriers in moving the executive branch of the federal govern- ment to a position in which it would use its authority within the limits of the law to demand compliance with desegregation reg- ulations, such as in public education and voting rights. Conse- quently, the NAACP Legal Defense and Education Fund lawyers continued to bring forth cases to force the issue of implementa- tion and to define the concept of “equal protection” under the law; the civil rights movement expanded in order to engage a societal decision on racism (3-5).
Implementation of racial equality in patient care may reflect a similar resistance, only one that seems more difficult to solve when it involves physicians’ attitudes or when it represents bar- riers to access to patient care services because of a lack of health insurance or means of direct payment. These problems, however, are old, and although the situation today is not ideal, the quality of medical care provided to minority persons has significantly improved relative to the entire period of U.S. history before the mid-1960s. Perhaps the call to re-address racism in medicine is a reminder for us to reaffirm our professionalism and our commit- ment to serve first the needs of patients, regardless of race, sex, nationality, and socioeconomic status.
P. Preston Reynolds, MD, PhD Johns Hopkins University Baltimore, MD 21205
References
1. Ions P, Guitton S. May It Please the Court. New York: WW Norton; 1993.
2. #8908: Simkins versus Moses Cone Hospital file. Simon E. Sobeloff manuscripts. Located at National Library of Congress, Washington, DC.
3. Rowan CT. Dream Makers, Dream Breakers: The World of Justice Thurgood Marshall. Boston: Little, Brown; 1993.
4. Branch T. Parting the Waters: American in the King Years, 1954-1963. New York: Simon & Schuster; 1988.
5. Evers C, Szanton A. Have No Fear: A Black Man’s Fight for Respect in America. New York: Wiley & Sons; 1997.