The American Journal of Medicine Blog http://amjmed.org 'The Green Journal' Sat, 07 Jul 2018 00:11:12 +0000 en-US hourly 1 https://wordpress.org/?v=3.9.25 Cervical Cancer Screening: What’s New? Updates for the Busy Clinician http://amjmed.org/cervical-cancer-screening-whats-new-updates-for-the-busy-clinician/ http://amjmed.org/cervical-cancer-screening-whats-new-updates-for-the-busy-clinician/#comments Fri, 08 Jun 2018 13:43:12 +0000 http://amjmed.org/?p=4929 senior woman about to get a diagnostic test

In the United States, 12,000 women are diagnosed with cervical cancer each year, even though the screening for this disease is safe and effective. There are 3 types of screening options available: cervical cytology (Papanicolaou or “Pap” test), Pap/HPV (human papillomavirus) co-test, and HPV-only test. With simplified options such as HPV-only screening, providers who have been reluctant to incorporate cervical cancer screening into their primary care practice may feel more comfortable with offering these services to women. In this article we review the different cervical cancer screening options that are now available and summarize the various changes in guidelines over the last decade.

Background

Although cervical cancer screening is effective and safe, almost one-quarter of women aged 45-64 years in the United States have not received timely screening in the prior 3 years.1 Oncogenic “high-risk” human papillomavirus (HPV) subtypes are responsible for nearly all cervical cancers and a variable percentage of anal, vaginal, penile, vulvar, and oropharyngeal cancers.2 The subtypes of HPV 16 and 18 account for 65%-75% of cervical cancers, whereas 12 other high-risk genotypes account for the rest.3 Though immunization (primary prevention) for cervical cancer has the potential to prevent up to 70% of cervical cancers due to HPV,4 screening (secondary prevention) is still a critical strategy for identifying cervical dysplasia and invasive cervical cancer precursors.

Currently, approximately 7% of US women between the ages of 21 and 65 years have never received a screening test in their lifetime, especially foreign-born women who have lived less than 25% of their lifetime in the United States.5 Other under-screened populations include minorities, those with low social–economic status, those with multiple chronic conditions, and those who lack medical access or insurance.167 With simplified options such as HPV-only screening, providers who have been reluctant to incorporate cervical cancer screening into their primary care practice may feel more comfortable with offering these services to women. In this review article, we aim to provide an update on the different cervical cancer screening options that are now available and summarize the various changes in guidelines over the last decade.

Screening Strategies

There are 3 types of screening options available: cervical cytology (Papanicolaou or “Pap” test), Pap/HPV co-test, and HPV-only test (Table). Though there are differences between the 3 strategies, the goal of each recommendation is the same: to identify cervical dysplasia or precancerous lesions in their early stages, before they progress to cervical cancer. We recommend that providers choose the screening strategy that fits best with their practice, because it is most important that women are screened, not how they are screened.

To read this article in its entirety please visit our website.

-Salina Zhang, BS, Megan McNamara, MD, MSc, Pelin Batur, MD

This article originally appeared in the June issue  of The American Journal of Medicine.

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Cigarette Smoking in Persons Living with Hepatitis C: The National Health and Nutrition Examination Survey (NHANES), 1999-2014 http://amjmed.org/cigarette-smoking-in-persons-living-with-hepatitis-c-the-national-health-and-nutrition-examination-survey-nhanes-1999-2014/ http://amjmed.org/cigarette-smoking-in-persons-living-with-hepatitis-c-the-national-health-and-nutrition-examination-survey-nhanes-1999-2014/#comments Thu, 07 Jun 2018 13:43:11 +0000 http://amjmed.org/?p=4928

smoking cigarette in the hand of young man close up

Cigarette smoking is common in persons living with hepatitis C (hepatitis C+), but national statistics on this harmful practice are lacking. A better understanding of smoking behaviors in hepatitis C+ individuals may help in the development of targeted treatment strategies.

Methods

We extracted data from the National Health and Nutrition Examination Survey (NHANES) between 1999 and 2014. Hepatitis C+ were compared with hepatitis C− adults in the entire sample and in the subset of current smokers. Measures included demographics, current smoking, cigarettes/day, nicotine dependence, other tobacco use, substance use, and medical and psychiatric comorbidities.

Results

Complete smoking and hepatitis C virus (HCV) data were available for 39,472 (90.1%) of 43,793 adult participants in NHANES during the study years. Hepatitis C+ smoked at almost triple the rate of hepatitis C− adults (62.4% vs 22.9%), with no significant difference between hepatitis C+ men and women (64.5% vs 58.2%). Hepatitis C+ smokers were more likely to smoke daily than hepatitis C− smokers (87.5% vs 80.0%), but had similar levels of nicotine dependence. Hepatitis C+ smokers were more likely to be older (mean age: 47.1 vs 41.5 years), male (69.4% vs 54.4%), Black (21.2% vs 12.1%), less educated (any college: 31.8% vs 42.9%), poor (mean family monthly poverty index: 1.80 vs 2.47), uninsured (43.9% vs 30.4%), use drugs (cocaine: 11.1% vs 3.2%; heroin: 4.0% vs 0.6%), and be depressed (33.2% vs 13.5%). Multivariate analyses revealed significant associations of both hepatitis C infection and cigarette smoking with current depression and hypertension.

Conclusions

There is a cigarette smoking epidemic embedded within the hepatitis C epidemic in the United States. The sociodemographic profile of hepatitis C+ smokers suggests that the implementation of effective tobacco treatment will be challenging. Thoughtful treatment strategies that are mindful of the unique characteristics of this group are needed.

To read this article in its entirety please visit our website.

-Ryung S. Kim, PhD, Andrea H. Weinberger, PhD, Geetanjali Chander, MD, MPH, Mark S. Sulkowski, MD, Brianna Norton, DO, Jonathan Shuter, MD

This article originally appeared in the June issue  of The American Journal of Medicine.

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Do Not Resuscitate Tattoos http://amjmed.org/do-not-resuscitate-tattoos/ http://amjmed.org/do-not-resuscitate-tattoos/#comments Wed, 06 Jun 2018 13:43:10 +0000 http://amjmed.org/?p=4927 man holding his chest

A recent New England Journal of Medicine letter gained national attention by describing an emergency room visit by a patient with a tattoo on his chest, “Do Not Resuscitate.” The article told how the emergency room physicians, who had not encountered this issue before, contacted their medical ethics specialists to make sure they were complying with their state’s informed consent law.1

I had a similar experience after we opened the then-new University of Arizona College of Medicine Hospital in Tucson, a half-century ago. The first physician in charge of our “Emergency Room” was a tough, “crusty,” and beloved veteran, who had served in a Mobile Army Surgical Hospital unit in the Korean War. At that time, the “Emergency Room” was a subset of the Department of Surgery. When there was a cardiac arrest, a “code blue” was announced over the hospital loudspeaker. On those occasions some of our house staff—and during the day I—would often run, often down several flights of stairs, to help with the “code.”

This “Emergency Room” physician eventually had a baseball cap embroidered with the title, “CODE CAPTAIN”; and whenever I or another cardiologist showed up, he would slap that cap on our head so that he could continue running the “Emergency Room” while we ran the “code.” He was a colorful character, who had a tattoo on his chest that implied, “DO NOT DEFIBRILLATE.” His tattoo showed 2 defibrillator paddles, surrounded by a red circle and diagonal line, the “international prohibition sign” for not doing something! This was before the days of written “advanced directives.” In fact, decades later he did come into our Emergency Department with cardiac arrest. None of his academic colleagues defied his tattooed “advanced directive.”

This experience emphasizes the importance of having a written official advanced directive, so physicians do not have to relay on interpreting the presence or absence of a tattoo.

To read this article in its entirety please visit our website.

-Gordon A. Ewy, MD, DSc

This article originally appeared in the June issue  of The American Journal of Medicine.

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Candid to the Bitter End: Indiscriminate Disclosures http://amjmed.org/candid-to-the-bitter-end-indiscriminate-disclosures/ http://amjmed.org/candid-to-the-bitter-end-indiscriminate-disclosures/#comments Mon, 04 Jun 2018 13:32:37 +0000 http://amjmed.org/?p=4912 nurse showing an elderly woman something on a tablet in office

 

The physician’s obligation to tell the patient the full truth about his or her condition has become an established ethical principle, enabling patients’ autonomy, shared decision-making, and patient-centered care. However, indiscriminate application of this obligation may at times be harmful to the patient, contradicting the old Hippocratic imperative of “first do no harm” (“Primum non nocere”), as our 2 recent short patient histories demonstrate.

Patient 1

A 65-year-old father of 6 was diagnosed with urothelial (transitional cell) carcinoma of the urinary bladder. He was a past smoker (46 pack-years) with hypertension, dyslipidemia, and a remote history of myocardial infarction. Disease was T1N0 (stage I) and treated by transurethral resection and intravesical therapy. A second-look operation and imaging revealed no evidence of disease. One year later right loin pain developed, and computed tomography revealed right hydroureter and minimal hydronephrosis without discernible cause. Results on cystoscopy were normal, but magnetic resonance imaging suggested fullness of the right ureteral outlet. Serum creatinine increased (2.0 mg/dL), ureteral infiltration by transitional cell carcinoma was demonstrated, and nephrostomy was performed with ureteropelvic junction stent placement, creatinine normalization, and nephrostomy removal. However, he was soon readmitted with recurrent vomiting, and retroperitoneal involvement, bilateral ureteral obstruction, and creatinine 3.7 mg/dL were found. After drainage he was referred to a tertiary care center and left us very sick but hopeful. On the third hospital day he was suddenly and bluntly told by a physician, who had seen him once, that a team of oncologists, urologists, and radiologists had reviewed his data, that he had extensive unresponsive disease, and that nothing could be done. He listened in silence. A few hours later a blood pressure of 250/115 was recorded, and atherothrombotic hemiplegia developed. He was sent back to the referring hospital, where we found a broken man.

Patient 2

A 69-year-old practicing lawyer was admitted after acute onset of severe vertigo associated with nausea, vomiting, and sweating. She was a past smoker and was diagnosed with diabetes mellitus, dyslipidemia, and hypertension 8 years prior, both well-controlled. Examination showed unilateral horizontal nystagmus and gait instability with neither hearing loss nor other neurologic signs. Head computerized tomography revealed generalized brain atrophy. Acute vestibular neuronitis was diagnosed, and she gradually made full recovery. However, although she did not ask, the neuroimaging findings were described by the attending physician and featured among the International Classification of Diseases, Ninth Revision coded diagnoses at the head of the discharge summary (code 331.9) handed to her. From then on, every minor forgetfulness was taken by her to signify creeping dementia. Soon she stopped working and became withdrawn and depressed, seldom going out or meeting her friends. Explanations, favorable second opinion, encouragement, and treatment failed to bring about an improvement.

Comment

In a hurry to comply with the ethical paradigm of the patient’s autonomy and right to know, physicians’ beneficence may sometimes be forgotten. Patient 1 was aware of the diagnosis and the spread of cancer obstructing drainage of both kidneys. At the same time, however, he had some hope, and even if self-deception was involved, it served a purpose and had a positive role, helping to maintain a fragile balance essential to the quality of his remaining lifespan.1 The price of instantaneously extinguishing hope by following protocol without heeding the patient’s feelings may be heavy, although the evidence is mostly anecdotal.2 Here we had an unusually striking example of a mind–body response that seems intimately and pathophysiologically linked—an emotionally triggered hypertensive emergency and a devastating cerebrovascular accident.3

At other times, it is “only” the quality of life that deteriorates irrevocably (patient 2). “Incidental” imaging information not amenable to treatment was provided to the patient, although she did not ask for it and although its clinical significance remains uncertain and highly variable.4 The patient, who was admitted with a benign self-limited condition and who made a full recovery, left the hospital convinced that she is doomed to become afflicted with devastating dementia very soon. Her life changed irrevocably. The physician’s words had in fact become for her a self-fulfilling prophecy. Indeed, negative information provided by the physician (eg, about possible adverse effects of drugs) may in itself affect outcomes and induce adverse effects that would not have occurred without this information, through expectancy mechanisms (so called “nocebo effects”).5

Without compromising our basic obligation to be truthful to our patients and their families, a more gradual and gentle approach, taking into account the potential impact of the information from the patient’s point of view, may be the better option. Even going as far as suggesting a trial of treatment, acknowledging that its chances to alter anything are very slim, might allow the patient and family time to adjust and come to grips with the grim reality (patient 1). Downplaying the neuroimaging finding of brain atrophy while stressing the absence of focal lesions, for example (patient 2), might have been far more considerate of the patient’s best interests. This approach may have to be frequently considered nowadays, when sophisticated imaging and laboratory tests reveal countless “incidental” findings, from cerebral changes through minor pulmonary nodules to the detection of autoantibodies in asymptomatic patients. Not all patients necessarily want to know everything about their prognosis or about future implications that may never materialize. A substantial minority of patients (up to 20%, according to several studies) prefers to remain ignorant of “hopeless” conditions6 and may find the uncertainty involved in some findings as a cause of intolerable anxiety. Even among patients who express a desire to receive as much information as possible about their illness, there is little evidence to support that they actually implement this desire in encounters with their physicians. Physicians seem well aware of this wish for the confinement of dire news, and 49% (of 710 oncologists studied) express their reluctance in providing “uninhibited” information of their own initiative.7 Moreover, a quarter of physicians were uncertain whether they would like to be told of their own prognosis were they diagnosed with advanced cancer.

Thus, the prevailing policy of absolute disclosure to each and every patient needs to be individualized and patient-tailored like any other medical decision, because its indiscriminate, undiscerning application may have prolonged deleterious effects on some patients. These adverse effects of “total” unselective truth disclosure may be prevented by tailoring information to patients’ wishes and keeping in mind the immense value of hope in medical care. Patient-centered care mandates taking heed of the patient’s values and preferences. When these include not wishing to know the “whole” truth, we need to be sensitive enough to discern it and use our best judgment to provide care without extinguishing every remnant of hope (patient 1) or supplying potentially harmful but uncertain and unsolicited information (patient 2). Thus, physicians should be cognizant of the fact that too much information of ominous or uncertain prognostic significance may be a double-edged sword for quite a few patients. Rather than unwavering “total” disclosure, probing patients’ preferences first16 will allow for true patient-centered sensitive disclosures of diagnostic and prognostic information. More information may translate into lesser-quality care for some patients.

To read this article in its entirety please visit our website.

-Ami Schattner, MD

This article originally appeared in the June issue  of The American Journal of Medicine.

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Oxygen Therapy in Patients with Acute Myocardial Infarction: A Systemic Review and Meta-Analysis http://amjmed.org/oxygen-therapy-in-patients-with-acute-myocardial-infarction-a-systemic-review-and-meta-analysis/ http://amjmed.org/oxygen-therapy-in-patients-with-acute-myocardial-infarction-a-systemic-review-and-meta-analysis/#comments Sun, 03 Jun 2018 22:32:36 +0000 http://amjmed.org/?p=4911

man holding chest and woman offering him water

 

Oxygen therapy is frequently used for patients with acute myocardial infarction. The aim of this study is to perform a systematic review and meta-analysis to compare the outcomes of oxygen therapy versus no oxygen therapy in post–acute myocardial infarction settings.

Methods

A systematic search of electronic databases was conducted for randomized studies, which reported cardiovascular events in oxygen versus no oxygen therapy. The evaluated outcomes were all-cause mortality, recurrent coronary events (ischemia or myocardial infarction), heart failure, and arrhythmias. Summary-adjusted risk ratios (RRs) were calculated by the random effects DerSimonian and Laird model. The risk of bias of the included studies was assessed by Cochrane scale.

Results

Our meta-analysis included a total of 7 studies with 3842 patients who received oxygen therapy and 3860 patients without oxygen therapy. Oxygen therapy did not decrease the risk of all-cause mortality (pooled RR, 0.99; 95% confidence interval [CI], 0.81-1.21; P = .43), recurrent ischemia or myocardial infarction (pooled RR, 1.19; 95% CI, 0.95-1.48; P = .75), heart failure (pooled RR, 0.94; 95% CI, 0.61-1.45; P = .348), and occurrence of arrhythmia events (pooled RR, 1.01; 95% CI, 0.85-1.2; P = .233) compared with the no oxygen arm.

Conclusions

This meta-analysis confirms the lack of benefit of routine oxygen therapy in patients with acute myocardial infarction with normal oxygen saturation levels.

Introduction

Ischemic heart disease is the most common cause of death worldwide.1 Furthermore, acute myocardial infarctions occur in approximately 790,000 Americans every year.2 Reperfusion therapy is the gold standard treatment strategy for patients who present with acute myocardial infarction.1 Other treatment therapies, such as routine oxygen therapy, have been evaluated to determine their impact on cardiovascular outcomes. Oxygen therapy in ischemic heart disease was first reported in 1900 and since that time has been incorporated in the usual care during acute treatment for patients with acute myocardial infarction.2 Previous animal and clinical studies hypothesized that supplemental oxygen up to even hyperoxic levels in patients with acute myocardial infarction would reduce myocardial injury by increasing oxygen delivery to ischemic myocardium.345 Yet, those studies were not randomized or blinded. Conversely, it has since been reported that hyperoxia may precipitate an increase in myocardial injury due to coronary vasoconstriction and oxidative stress.67 Yet the use of supplemental oxygen continued to be a routine practice in patients with cardiac disease. More important, no randomized, blinded, and controlled studies have shown an advantage in normoxemic patients, with surging evidence proving the conceivable adverse effects of hyperoxia in acute myocardial infarction.89 A Cochrane report from 2016 did not show any benefit to using oxygen in patients with acute myocardial infarction.8Additionally, a recent meta-analysis reviewed 5 randomized controlled trials and concluded that oxygen supplementation did not benefit patients with baseline normal peripheral oxygen saturations ≥90%.9

Most recently, a registry-based randomized clinical trial was performed to evaluate oxygen therapy on all-cause mortality at 1 year (The Determination of the Role of Oxygen in Suspected Acute Myocardial Infarction),10 which showed that routine supplemental oxygen in patients without hypoxemia at baseline undergoing hospitalization for acute myocardial infarction did not have a reduced 1-year all-cause mortality. This study provides definitive evidence that supplemental oxygen is not beneficial in patients who have normal baseline oxygen saturations with acute myocardial infarction.11 In this context, we performed an updated meta-analysis with the most updated evidence to evaluate the efficacy of routine oxygen supplementation in patients with acute myocardial infarction.

Methods

Data Sources

An electronic search of the MEDLINE, Web of Science, and Cochrane Collaboration of Clinical Trials was performed from inception to November 2017 without language restriction, using the keywords “acute myocardial infarction,” “oxygen therapy,” “assessment,” and “outcomes,” as illustrated in Figure 1. Bibliographies of the included studies, relevant review articles, and meta-analyses were manually searched for any potential overlooked studies. The major cardiovascular conferences and proceedings, for example, American College of Cardiology and American Heart Association conferences, were screened for any abstracts addressing this topic.

To read this article in its entirety please visit our website.

-Ahmed Abuzaid, MD, Carly Fabrizio, DO, Kevin Felpel, MD, Haitham S. Al Ashry, MD, Pragya Ranjan, MD, Ayman Elbadawi, MD, Ahmed H. Mohamed, MD, Kirolos Barssoum, MD, Islam Y. Elgendy, MD

This article originally appeared in the June issue  of The American Journal of Medicine.

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Sweet’s Syndrome Mimicking Anti-Neutrophil Cytoplasmic Antibodies–Associated Vasculitis http://amjmed.org/sweets-syndrome-mimicking-anti-neutrophil-cytoplasmic-antibodies-associated-vasculitis/ http://amjmed.org/sweets-syndrome-mimicking-anti-neutrophil-cytoplasmic-antibodies-associated-vasculitis/#comments Sun, 03 Jun 2018 13:32:35 +0000 http://amjmed.org/?p=4910 Clinical manifestations. (A) Coalescing infiltrated erythema with tense bullae (arrows) on the left arm. (B) Pustules on the erythematous plaque on the right axilla. (C) Dark-reddish purpuras and infiltrated erythemas with hemorrhagic bullae on the legs. (D) Widespread purpuras and erythemas with highly exudative erosions.

Clinical manifestations. (A) Coalescing infiltrated erythema with tense bullae (arrows) on the left arm. (B) Pustules on the erythematous plaque on the right axilla. (C) Dark-reddish purpuras and infiltrated erythemas with hemorrhagic bullae on the legs. (D) Widespread purpuras and erythemas with highly exudative erosions.

 

Sweet’s syndrome is a rare neutrophilic skin disorder. The antibodies against neutrophil cytoplasmic antigens are called anti-neutrophil cytoplasmic antibodies (ANCAs). Positivity for ANCA has been reported in some nonvasculitic inflammatory disorders, including Sweet’s syndrome.12 Here we report a case of myeloperoxidase (MPO)-ANCA– and (proteinase 3) (PR3)-ANCA–positive Sweet’s syndrome presenting unusual and severe purpuras.

A 41-year-old woman presented with a 3-day history of general malaise, a fever of 39.4°C, and progressive eruptions on the whole body. Examination revealed multiple coalescing erythema and painful erythematous plaques with small pustules distributed on the neck, trunk, and upper limbs (Figure A and B). On the lower limbs, widespread purpuras, tense bullae, and erosions were observed (Figure C and D). No respiratory, gastrointestinal, ocular, neuronal, or articular symptoms were observed. Her white blood cell count was 31,300/µL, with 93% neutrophils. The erythrocyte sedimentation rate, at 23 mm/h, and the C-reactive protein, at 152 mg/L, were elevated. No evidence of infection or malignancy was observed. Serologic tests found MPO-ANCA (68.5 RU/mL; normal range, 0-20 RU/mL) and PR3-ANCA (45.8 RU/mL; normal range, 0-20 RU/mL) to be positive. Antinuclear antibody was negative. The histology of the erythematous plaque with bulla revealed subepidermal blistering due to marked edema of the upper dermis. Dense infiltration of neutrophils, but not eosinophils, was observed in the dermis. No vasculitis or granuloma was present. Immunoglobulin deposition in the vessels was not observed by immunofluorescence studies. The diagnosis of Sweet’s syndrome was made. The fever and the infiltrative erythema disappeared in a few days under systemic prednisone therapy at 1 mg/kg/d. After the treatment the white blood cell count was within normal limits, and the MPO-ANCA and PR3-ANCA titers decreased and finally became negative.

The present case fulfilled the diagnostic criteria of Sweet’s syndrome with respect to both major points: 1) the abrupt onset of tender erythematous plaques; 2) predominant neutrophilic infiltration in the dermis without vasculitis) and with respect to 3 of the 4 minor points: 1) pyrexia > 38°C; 2) laboratory abnormalities [elevated erythrocyte sedimentation rate, positive C-reactive protein, leukocytosis, and a left shift of white blood cells]; 3) an excellent response to systemic corticosteroid therapy.34 Widespread purpura in “classic” Sweet’s syndrome has not been reported; however, giant cellulitis-like Sweet’s syndrome, a rare subtype of Sweet’s syndrome, is characterized by indurated erythematous plaques with a vesicular, bullous, hemorrhagic appearance.5Widespread purpura suggests the presence of severe nonvasculitic endothelial damage from massive neutrophilic infiltration; therefore, the excess neutrophilic activation in this case may have contributed to the ANCA induction, as well as severe clinical appearance mimicking ANCA-associated vasculitis.

In conclusion, we present a case of Sweet’s syndrome that showed various severe skin symptoms and serologic positivity for both MPO-ANCA and PR3-ANCA. Clinicians should be aware of the occurrence of these striking purpuras in patients with Sweet’s syndrome.

 

To read this article in its entirety please visit our website.

-Hideyuki Kosumi, MD, Mika Watanabe, MD, PhD, Ken Natsuga, MD, PhD’Correspondence information about the author MD, PhD Ken Natsuga, Toshinari Miyauchi, MD, Chihiro Shiiya, MD, Hideyuki Ujiie, MD, PhD, Hiroshi Shimizu, MD, PhD

This article originally appeared in the June issue  of The American Journal of Medicine.

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Please Say Thank You http://amjmed.org/please-say-thank-you/ http://amjmed.org/please-say-thank-you/#comments Sat, 02 Jun 2018 13:32:34 +0000 http://amjmed.org/?p=4909 American Journal of Medicine Editor Joseph Alpert

Joseph S. Alpert, MD, AJM Editor-in-Chief

I frequently get letters from readers regarding one of my editorials or commentaries. Editorials and commentaries in The American Journal of Medicine (AJM) are expressions of opinion by the author of the piece. Of course, most observations in the Journal deal with medical topics, although occasionally they will stray into remarks about life in general or current events. As editor in chief, I feel that it is my duty to write one of these short essays nearly every month. Readers usually communicate with me by e-mail or with typed or handwritten correspondence. Usually, the letters are complimentary or point out an additional piece of information that expands on the remarks that I have made. Rarely, the reader will take me to task by disagreeing with my point of view. I answer every one of these messages either with a return letter or e-mail message, depending on the form that the reader employed. I very much appreciate these communications, both positive and negative, because they tell me that what I am writing is being read and digested and resulting in a reaction strong enough that the reader was moved to respond. At times, these letters result in a back-and-forth discussion between the reader and myself in order to clarify or amplify our opinions.

As noted already, most of the letters that I receive are complimentary, and I must admit this gives me a great deal of pleasure. I always write back thanking the authors for their kind words. Responding in this way was one of the earliest lessons I learned from my mother who had been both a journalist and a high school English teacher. I still remember her saying: “Joseph, it costs you nothing to say thank you.” I have taken this coaching lesson to heart and have passed it on to my own children and my trainees. One of the best Christmas presents that I have received in recent years was a set of 2 handcrafted antique fountain pens. The calligraphy that results from writing with these instruments is nothing short of beautiful. Since receiving this gift, I now answer all my personal letters to the editor with these pens. Often, when the letter writer includes personal confidences, I will respond using a note card purchased at a museum store. These cards usually depict a painting by a well-known artist. I think my mother would have approved of this practice!

One of the best moments of my early career occurred following a lecture that I gave at medical grand rounds at the Peter Bent Brigham Hospital (now Brigham and Women’s Hospital) in Boston. The next day, I received a short handwritten note from the Chief of Medicine, Dr. Eugene Braunwald, stating that he had very much enjoyed my presentation. I was truly ecstatic when I read this short correspondence, and I have saved it to this day. This kind act led me to do a similar thing during my time as Chair of Medicine at the University of Arizona College of Medicine, congratulating young faculty following their grand rounds presentations. Dr. Braunwald’s memo helped fuel enthusiasm for my subsequent career choice, and I hope my positive messages have the same impact.

Hallmark cards, producers of time-honored greeting cards, have the following advice for first-time thank-you note writers:

  • 1. Greeting. Don’t forget to make sure you’re using the correct form and spelling of the person’s name, as well as anyone else’s mentioned in the note.
  • 2. Express your thanks. Begin with the two most important words: Thank you.
  • 3. Add specific details about the event or gift or remark for which you are expressing thanks.
  • 4. Look ahead to possible contact in the future.
  • 5. Restate your thanks.
  • 6. End with a phrase reflecting your regards such as sincerely, best wishes, or another friendly expression.1

 

Perhaps the readers of the Journal might think that this essay is a bit too simplistic and not necessarily deserving of publication. However, I disagree. Personally, I find the current public environment in the United States to be overloaded with negative and often hurtful invectives. One small attempt to change this undesirable atmosphere is to ask the readers of the Journal to please remember my mother’s dictum: “It costs you nothing to say thank you.”

And, in that spirit, my heartfelt thanks to everyone who has helped me and the Journal through the years that I have been the editor: Thanks to all authors for providing us with such excellent material and to our readers for following us; to the 2 wonderful publishers, Jane Grochowski and Pamela Poppalardo, for their help and encouragement; to Elsevier for the daily work efforts of their outstanding editorial staff and to their executive leadership for giving us total editorial independence; to the staff of the Journal here in Tucson, and the technical supervisors and technicians throughout the country who manage our cyber publishing vehicle, both groups enabling us to provide a quality publication every month; and finally, but far from least, to my family and spouse for their never-ending support and love.

As always, I look forward to hearing from our readership at our blog at amjmed.org or at my personal e-mail address: jalpert@shc.arizona.edu.

To read this article in its entirety please visit our website.

-Joseph S. Alpert, MD

This article originally appeared in the June issue  of The American Journal of Medicine.

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Severe Pulmonary Alveolar Proteinosis in a Young Adult http://amjmed.org/severe-pulmonary-alveolar-proteinosis-in-a-young-adult/ http://amjmed.org/severe-pulmonary-alveolar-proteinosis-in-a-young-adult/#comments Fri, 01 Jun 2018 13:32:33 +0000 http://amjmed.org/?p=4908 (A) Coronal computed tomography demonstrating extensive bilateral ground-glass opacification, most pronounced at the periphery, and anterior lobular septal thickening. (B) Effluent, initially noted to be milky, cleared with progressive saline infusions during lung lavage.

(A) Coronal computed tomography demonstrating extensive bilateral ground-glass opacification, most pronounced at the periphery, and anterior lobular septal thickening. (B) Effluent, initially noted to be milky, cleared with progressive saline infusions during lung lavage.

 

Pulmonary alveolar proteinosis is a rare lung disorder characterized by abnormal accumulation of surfactant within alveoli. Clinical presentation is nonspecific, but associated with characteristic radiologic findings and unique management options. We highlight a case of severe pulmonary alveolar proteinosis requiring total lung lavage in a young healthy man.

Case Report

A 37-year-old man with a history of nicotine abuse presented with a 5-month history of progressive dyspnea on exertion and 1 month of nonproductive cough. He denied associated fever, chest pain, and hemoptysis. He endorsed a history of industrial dust exposure from prior employment.

Physical examination and initial laboratory study results were unremarkable. An extensive infectious and rheumatologic workup returned negative. Chest x-ray showed bilateral lung disease, and chest computed tomography demonstrated extensive bilateral ground-glass opacification, most pronounced peripherally, and anterior lobular septal thickening (Figure A). Bronchoalveolar lavage returned positive for periodic acid–Schiff staining, consistent with pulmonary alveolar proteinosis.

The patient was scheduled for total lung lavage with supplemental vest percussion. A double-lumen endotracheal tube was used to lavage 1 lung with warmed saline while independently ventilating the other lung. Initial effluent was noted to be milky, but cleared with subsequent saline infusions (Figure B). The patient was counseled on smoking cessation and discharged after an uncomplicated postprocedural course. Postdischarge laboratory testing revealed antibodies to granulocyte-macrophage colony-stimulating factor, solidifying a diagnosis of autoimmune pulmonary alveolar proteinosis.

 

Discussion

Pulmonary alveolar proteinosis is a rare lung disease characterized by accumulation of surfactant and apoproteins in distal air spaces. Three main forms of this disorder are recognized: congenital, secondary, and autoimmune, which is the most common subtype.1 In a large cohort study of patients with autoimmune pulmonary alveolar proteinosis, patients presented at a median age of 51 years with exertional dyspnea as the most common presenting symptom. Alternative presenting symptoms included cough, increased sputum production, and fatigue. One third of patients were asymptomatic on presentation, whereas 56% reported a history of smoking and 23% endorsed a history of dust exposure.2

Although physical examination and laboratory studies commonly reveal nonspecific abnormalities, chest radiographs often exhibit alveolar opacities in a “bat wing” distribution. High-resolution computed tomography demonstrates ground-glass opacities and concurrent thickening of intralobular structures, nicknamed “crazy paving.”3 Bronchoscopy with bronchoalveolar lavage frequently exhibits periodic acid–Schiff positive proteinaceous material in alveolar spaces. Lung biopsy and measurement of antibodies to granulocyte-macrophage colony-stimulating factor may help solidify the definitive diagnosis of pulmonary alveolar proteinosis.4Treatment choice is determined by symptoms and gas exchange status: For asymptomatic patients, pulmonary function tests and chest imaging are recommended; for mild symptoms (eg, dyspnea with exertion, cough, and malaise), supportive care and supplemental oxygen are indicated; for severe symptoms (eg, dyspnea with minimal exertion or at rest), total lung lavage, granulocyte-macrophage colony-stimulating factor, and rituximab may be used.5 Total lung lavage should be pursued when patients with pulmonary alveolar proteinosis meet 1 of the following criteria: resting partial pressure of oxygen <65 mm Hg, resting alveolar-arterial oxygen gradient ≥40 mm Hg, or severe dyspnea.3

Conclusions

PAP is a rare pulmonary disease in which excessive pulmonary surfactant accumulates within the alveoli. Symptoms are nonspecific and almost one third of patients are asymptomatic. If PAP is considered in the differential, a CT scan of the chest should be pursued with subsequent bronchoscopy with BAL, PAS staining, and anti-GM-CSF antibody evaluation. Once diagnosis is established, therapeutic decisions can be determined based on the underlying etiology.

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-Alisha Kamboj, BS, Michael Lause, BS, Vijay Duggirala, MD

This article originally appeared in the May issue  of The American Journal of Medicine.

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Gas Within the Bladder http://amjmed.org/gas-within-the-bladder/ http://amjmed.org/gas-within-the-bladder/#comments Sat, 26 May 2018 13:18:19 +0000 http://amjmed.org/?p=4897 doctor gives a physical examination of a patient

To the Editor:

An 83-year-old woman with a medical history of hypertension, chronic renal failure, and diabetes mellitus came to the emergency department of our clinic after 2 days of fever, asthenia, adynamia, and hypogastric abdominal pain associated with dysuria, polyuria, and bladder tenesmus. Her family reported that she had been increasingly fatigued in the several days before presentation, and she had been experiencing hematuria as well. On physical examination she was in a regular general state, dehydrated, hypotensive, sleepy, and febrile, with tenderness to palpation over her lower hemi-abdomen, predominating in hypogastrium but without signs of peritoneal irritation. Significant laboratory results included hyperglycemia of 578 mg/dL, mild leukocytosis (11,700 cells/mL) with a left-sided deviation, and creatinine level of 3.2 mg/dL, associated with abnormal results on urinalysis (pyuria, hematuria, and bacteriuria) and a urine culture in which Klebsiella pneumoniae extended-spectrum β-lactamase was isolated.

A hyperosmolar state was diagnosed, and aggressive rehydration was started, in addition to empiric antibiotic treatment with ertapenem according to local guidelines. A urethral catheter was placed, and the nurses noted pneumaturia; then suspecting a colo-vesical fistulae, a computed tomography scan of the abdomen was performed, which showed images of gas within the bladder (Figure).

Emphysematous cystitis (EC) is a rare urinary tract infection caused by gas-producing bacteria colonizing the urinary bladder. It is characterized by the presence of air within the urinary bladder wall and/or the presence of intraluminal air within the bladder.1 Typical symptoms are similar to those of uncomplicated urinary tract infections, including dysuria, hematuria, urinary frequency, fever, and possible suprapubic pain. Pneumaturia, although more specific, is a much less common presenting symptom. Some patients might be completely asymptomatic at the time of incidental diagnosis.2 Although the overall incidence of EC is unknown, it has a female predominance of 2:1. Other predisposing risk factors include being elderly or debilitated, bladder outlet obstruction, chronic urinary tract infections, neurogenic bladder, chronic indwelling bladder catheters, and immune deficiency. The management of EC has remained unchanged over the past 30 years, with broad-cover intravenous antibiotics being used until urinary pathogen sensitivities are known. Concurrently the bladder should be drained, and blood glucose levels should be controlled. Between 10% and 20% of documented patients with EC have undergone surgical debridement.3

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-Juan Carlos Cataño, MD, Diego E. Giraldo, MD

This article originally appeared in the May issue  of The American Journal of Medicine.

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Thoracoabdominal Aneurysm in a Professional Body Builder http://amjmed.org/thoracoabdominal-aneurysm-in-a-professional-body-builder-2/ http://amjmed.org/thoracoabdominal-aneurysm-in-a-professional-body-builder-2/#comments Thu, 24 May 2018 13:18:18 +0000 http://amjmed.org/?p=4895 (A) Three-dimensional reconstruction of the computed tomography scan demonstrating aneurysmal dilation of the entire length of descending thoracic and abdominal aorta. (B) Computed tomography angiogram showing thoracic aorta aneurysm. (C) Computed tomography angiogram showing abdominal aortic aneurysm with a focal saccular aneurysm in the infrarenal part with periaortic stranding (arrow).

(A) Three-dimensional reconstruction of the computed tomography scan demonstrating aneurysmal dilation of the entire length of descending thoracic and abdominal aorta. (B) Computed tomography angiogram showing thoracic aorta aneurysm. (C) Computed tomography angiogram showing abdominal aortic aneurysm with a focal saccular aneurysm in the infrarenal part with periaortic stranding (arrow).

To the Editor:

A 33-year-old otherwise healthy man presented with worsening epigastric and flank pain for 3 weeks. He denied having vomiting, diarrhea, fever, urinary symptoms, or history of kidney stones. His vital signs were significant for a blood pressure of 140/72 mm Hg and pulse rate of 94 beats/min. Acute coronary syndrome was excluded by electrocardiography. A computed tomography scan of the chest and abdomen with contrast demonstrated aneurysmal dilation of the entire length of descending thoracic and abdominal aorta with the proximal descending thoracic aorta measuring approximately 4.8 cm in diameter (Figure). There was a focal saccular aneurysm in the infrarenal part with periaortic stranding suspicious for mycotic aneurysm, for which he was started on antibiotics. There were no stigmata of Marfan syndrome on physical examination, and serologic testing for syphilis was negative. His total cholesterol level was 144 mg/dL (reference: 140-199), low-density lipoprotein was 85 mg/dL (optimal: <100), and high-density lipoprotein was 41 mg/dL (optimal: >40). Vasculitic workup was negative. He was a bodybuilder by profession, and on further questioning, he admitted to 10-year use of anabolic androgenic steroids including stanozolol, oxymetholone, and testosterone, together with human growth hormone in cycles, which is the likely cause of his aortic aneurysm. His plasma testosterone level was low at 144 ng/dL (reference: 230-800), consistent with long-term exogenous androgen use. The infrarenal aneurysm was treated with resection and aortoiliac tube graft. Histologic examination showed dense adventitial fibrosis and lymphoplasmacytic infiltrate in the aortic wall.

Anabolic androgenic steroids are a group of hormones that include testosterone and a set of synthetic testosterone analogs, clinically used to treat conditions such as reproductive organ dysfunction, breast cancer, and anemia.1 Because these drugs increase lean muscle mass and strength while promoting fat loss, professional bodybuilders, weightlifters, football players, and many more athletes abuse them. Moreover, their use is increasing among the general population, including high school students, who just want to “look good.”2 In a meta-analysis, the global lifetime prevalence rate of anabolic steroid use was found to be 3.3%, with men accounting for 6.4% and women accounting for 1.6%.1 There have been reports of acute myocardial infarction and aortic dissection with cystic medial degeneration of the aortic wall in young patients using these drugs.34Although anabolic steroids promote atherosclerosis by increasing low-density lipoprotein and decreasing high-density lipoprotein cholesterol levels, which in turn predisposes to aneurysm formation and dissection, these were normal in our patient. The exact mechanism is not clear, but there is emerging evidence that androgen/androgen receptor signaling stimulates the initiation and progression of aortic aneurysm. Androgen receptor is thought to modulate aneurysm formation through inflammation and fibrosis mediated by interleukin 1 alpha and transforming growth factor beta, respectively.5 It is important to raise awareness among the general population about these potentially life-threatening complications of anabolic steroid use.

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-Gajapathiraju Chamarthi, MD, Abhilash Koratala, MD

This article originally appeared in the May issue  of The American Journal of Medicine.

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