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Study: Dying at home doesn’t mean dying sooner
patient’s hand
Choosing to die at home does not hasten death for patients with terminal cancer, according to a study published in Cancer.
The research showed that cancer patients who died at home lived at least as long as patients who spent their last days in hospitals.
Investigators say these results suggest oncologists should not hesitate to refer patients for home-based palliative care simply because less medical treatment may be provided.
“The cancer patient and family tend to be concerned that the quality of medical treatment provided at home will be inferior to that given in a hospital and that survival might be shortened,” said study author Jun Hamano, MD, of the University of Tsukuba in Japan.
“However, our finding—that home death does not actually have a negative influence on the survival of cancer patients at all and, rather, may have a positive influence—could suggest that the patient and family can choose the place of death in terms of their preference and values.”
Dr Hamano and his colleagues conducted this research by prospectively studying 2069 patients—1582 receiving hospital-based palliative care and 487 receiving home-based palliative care.
In all, 1607 patients died in the hospital, and 462 died at home.
Among patients thought to have only days to live, the survival of those who died at home was significantly longer than the survival of those who died in a hospital. The estimated median survival times were 13 days and 9 days, respectively (P<0.006).
Similarly, survival was significantly longer in the home group than the hospital group among patients thought to have weeks to live. The estimated median survival times were 36 days and 29 days, respectively (P<0.007).
There was no significant difference between the home and hospital groups among patients thought to have months to live. The estimated median survival times were 59 days and 62 days, respectively (P=0.925).
Finally, analyses suggested the place of death had a significant influence on the survival time in both unadjusted and adjusted models. The hazard ratios were 0.86 (P<0.01) and 0.87 (P=0.01), respectively.
Based on these findings, Dr Hamano concluded that, “Patients, families, and clinicians should be reassured that good home hospice care does not shorten patient life and even may achieve longer survival.” 
patient’s hand
Choosing to die at home does not hasten death for patients with terminal cancer, according to a study published in Cancer.
The research showed that cancer patients who died at home lived at least as long as patients who spent their last days in hospitals.
Investigators say these results suggest oncologists should not hesitate to refer patients for home-based palliative care simply because less medical treatment may be provided.
“The cancer patient and family tend to be concerned that the quality of medical treatment provided at home will be inferior to that given in a hospital and that survival might be shortened,” said study author Jun Hamano, MD, of the University of Tsukuba in Japan.
“However, our finding—that home death does not actually have a negative influence on the survival of cancer patients at all and, rather, may have a positive influence—could suggest that the patient and family can choose the place of death in terms of their preference and values.”
Dr Hamano and his colleagues conducted this research by prospectively studying 2069 patients—1582 receiving hospital-based palliative care and 487 receiving home-based palliative care.
In all, 1607 patients died in the hospital, and 462 died at home.
Among patients thought to have only days to live, the survival of those who died at home was significantly longer than the survival of those who died in a hospital. The estimated median survival times were 13 days and 9 days, respectively (P<0.006).
Similarly, survival was significantly longer in the home group than the hospital group among patients thought to have weeks to live. The estimated median survival times were 36 days and 29 days, respectively (P<0.007).
There was no significant difference between the home and hospital groups among patients thought to have months to live. The estimated median survival times were 59 days and 62 days, respectively (P=0.925).
Finally, analyses suggested the place of death had a significant influence on the survival time in both unadjusted and adjusted models. The hazard ratios were 0.86 (P<0.01) and 0.87 (P=0.01), respectively.
Based on these findings, Dr Hamano concluded that, “Patients, families, and clinicians should be reassured that good home hospice care does not shorten patient life and even may achieve longer survival.”
patient’s hand
Choosing to die at home does not hasten death for patients with terminal cancer, according to a study published in Cancer.
The research showed that cancer patients who died at home lived at least as long as patients who spent their last days in hospitals.
Investigators say these results suggest oncologists should not hesitate to refer patients for home-based palliative care simply because less medical treatment may be provided.
“The cancer patient and family tend to be concerned that the quality of medical treatment provided at home will be inferior to that given in a hospital and that survival might be shortened,” said study author Jun Hamano, MD, of the University of Tsukuba in Japan.
“However, our finding—that home death does not actually have a negative influence on the survival of cancer patients at all and, rather, may have a positive influence—could suggest that the patient and family can choose the place of death in terms of their preference and values.”
Dr Hamano and his colleagues conducted this research by prospectively studying 2069 patients—1582 receiving hospital-based palliative care and 487 receiving home-based palliative care.
In all, 1607 patients died in the hospital, and 462 died at home.
Among patients thought to have only days to live, the survival of those who died at home was significantly longer than the survival of those who died in a hospital. The estimated median survival times were 13 days and 9 days, respectively (P<0.006).
Similarly, survival was significantly longer in the home group than the hospital group among patients thought to have weeks to live. The estimated median survival times were 36 days and 29 days, respectively (P<0.007).
There was no significant difference between the home and hospital groups among patients thought to have months to live. The estimated median survival times were 59 days and 62 days, respectively (P=0.925).
Finally, analyses suggested the place of death had a significant influence on the survival time in both unadjusted and adjusted models. The hazard ratios were 0.86 (P<0.01) and 0.87 (P=0.01), respectively.
Based on these findings, Dr Hamano concluded that, “Patients, families, and clinicians should be reassured that good home hospice care does not shorten patient life and even may achieve longer survival.”
Another Spin
A previously healthy 11‐year‐old boy presented to the emergency department after referral from his pediatrician for 1 week of fevers. Seven days prior to admission he developed a fever to 40.8C, vomiting, and mild left knee pain. The vomiting resolved within 2 days. Five days prior to admission he developed a pruritic, pinpoint rash over his abdomen that resolved within 24 hours. He also developed red, cracked lips, redness of his tongue, redness surrounding his eyes, and slight swelling of his hands. Three days prior to admission his pediatrician noted a 1‐cm anterior cervical lymph node. His fevers occurred throughout each of the prior 7 days without a discernible pattern, and his mild knee pain persisted at the time of presentation.
This preteen has had high fevers for 1 week associated with arthralgia, pruritic rash, emesis, and oral mucosal erythema. His rash, lip and tongue erythema, and swollen hands are classic features of Kawasaki disease (KD), but he lacks the other characteristic physical examination findings. The diagnosis of KD requires fever for at least 5 days accompanied by 4 of the following 5 signs: polymorphous rash, oral mucous membrane changes, peripheral extremity changes such as swelling or skin desquamation, bilateral bulbar conjunctival injection, and cervical lymphadenopathy >1.5 cm in diameter. Children meeting fewer than 4 of these criteria may have an incomplete form of KD.
Because most patients with KD (80%) are under 5 years old, alternative diagnoses such as autoimmune illnesses or a hypersensitivity reaction should be considered. Travel, medication, and animal exposure histories may reveal clues to an infectious or drug‐induced etiology of his fever. Immunization status should be assessed, as measles is also associated with fever, rash, and mucosal changes. Arthralgia or arthritis may occur in KD, but these findings suggest the need to entertain other possibilities, including bone or joint infection, infective endocarditis, inflammatory bowel disease, juvenile idiopathic arthritis (JIA), or systemic lupus erythematosus (SLE).
The child's only past medical history was an episode of croup as an infant. There was no family history of autoimmune diseases. He was not taking any medications and had no known allergies. His immunizations were up to date, including measles, mumps, rubella, and varicella. He lived with his parents and his dog. He swam in fresh water during a trip to Maine 2 months earlier. Neither he nor his family recalled a tick bite. He had no exposure to raw meat or unpasteurized dairy products.
The travel to New England raises the possibility of Lyme disease, although a 2‐month interval between exposure and a high, prolonged fever would be very unusual. Knee arthralgia or arthritis is common in children with late‐stage Lyme disease, but can also be seen in early‐disseminated disease. The prior description of the rash is not suggestive of erythema chronicum migrans, which is seen in early‐stage Lyme disease.
C‐reactive protein (CRP) was 189 mg/L (normal <6.3 mg/L). An echocardiogram was normal. Intravenous immunoglobulin (IVIG) was administered for presumed KD, with immediate improvement of the periorbital erythema, tongue redness, and hand swelling. He was discharged the next day on aspirin with cardiology clinic follow‐up.
Improvement after IVIG supports the diagnosis of KD. It is typical to discharge KD patients from the hospital when they have been afebrile for 24 hours or when the CRP level has declined by approximately 50%.
Over the next 48 hours he felt unwell with high‐grade fevers, continued left knee pain, and new left hip pain. He was readmitted to the hospital. His temperature was 39.4C, respiratory rate was 22 breaths per minute, heart rate was 122 beats per minute, blood pressure was 103/50 mm Hg, and oxygen saturation was 100% while breathing ambient air. He appeared mildly uncomfortable. His conjunctivae were normal. His lips were dry, red, and cracked, and his tongue was red with prominent papillae. His neck was supple without lymphadenopathy. His lungs were clear to auscultation. His heart exam was without murmurs. His abdomen was soft, and the liver and spleen were not enlarged. He had no swelling or erythema of his joints; however, he experienced pain with range of motion of his left knee, and tenderness and restricted range of motion of his left hip. His neurologic exam was normal. There were no rashes.
He has persistent fever, tachycardia, and tachypnea, now without features of KD except oral mucosal changes including prominent tongue papillae consistent with a strawberry tongue. Continued or recurrent fever may suggest persistent KD with ongoing inflammation or the need to search for an alternative diagnoses. An echocardiogram should be repeated, as the coronary artery abnormalities in KD can evolve rapidly, particularly when inflammation persists. Additional findings may include decreased left ventricular function, mitral regurgitation, or pericardial effusion. A second dose of IVIG is necessary to control fever and inflammation in about 15% of patients with KD, although in this case IVIG should be withheld pending further evaluation.
Arthralgia occurs commonly in KD, whereas frank arthritis is less typical. Polyarticular or oligoarticular arthritis involving small or large joints (especially knee or ankle) affects 5% to 10% of patients. The severity of findings in his left hip warrants consideration of septic arthritis with pain referred to the knee; pelvic or femoral osteomyelitis; psoas abscess; or pyomyositis. Following basic lab tests, imaging of the left hip region is indicated.
Laboratory evaluation revealed: white blood cell (WBC) count 10,000/L (absolute neutrophil count 8,460/L, absolute lymphocyte count 530/L), hemoglobin 10.6 g/dL, platelet count 208,000/L, serum sodium 130 mmol/L, serum potassium 3.3 mmol/L, serum urea nitrogen 11 mg/dL, serum creatinine 0.54 mg/dL, aspartate transaminase (AST) 26 U/L, alanine transaminase (ALT) 31 U/L, albumin 1.7 g/dL, erythrocyte sedimentation rate (ESR) > 100 mm/h, and CRP 263 mg/L. No blast cells were seen on peripheral blood smear.
Hypoalbuminemia and markedly elevated inflammatory markers indicate an inflammatory condition that has been active for more than a week. Assessing ESR after IVIG therapy is not useful because exogenous globulins increase the ESR; however, CRP is useful to monitor inflammation and remains elevated here.
Incomplete KD is still possible. Hyponatremia, hypoalbuminemia, and anemia are all features of persistent KD, and have been utilized in several clinical scoring systems in Japan to identify KD patients at increased risk for developing coronary complications. A neoplastic process cannot be excluded, but does not appear likely based on the acuity of his presentation and peripheral blood smear review.
Upon readmission he received a second dose of 2 g/kg IVIG. He remained on aspirin and continued to have fevers. A repeat echocardiogram was normal. He had worsening pain in his left knee and hip with difficulty straightening his left leg. Physical examination was notable for tenderness to palpation over his left hip joint, refusal to bear weight, and resistance to passive range of motion. On hospital day 2, an ultrasound of his left hip and knee revealed a complex left hip effusion and small left knee effusion.
KD becomes less likely in the presence of persistent fevers after IVIG and a repeatedly normal echocardiogram. Worsening left leg symptoms including impaired hip extension with a complex hip effusion suggests an infectious process in or adjacent to the left hip, such as septic arthritis, myositis, or osteomyelitis of the pelvis or proximal femur. A complex hip effusion is less likely to be present with arthritis related to JIA or SLE. The patient needs an emergent hip aspiration and possibly magnetic resonance imaging (MRI) to evaluate adjacent structures.
Arthrotomy and open drainage of his left hip revealed purulent fluid with a WBC count of 49,000/L with 89% neutrophils and 2% lymphocytes. Gram stain was negative. A left knee aspirate demonstrated straw‐colored synovial fluid (which was not sent for cell counts). Bacterial, fungal, and acid‐fast bacilli cultures were requested from hip and knee aspirates. Intravenous ceftriaxone and vancomycin were administered.
The most likely organism in pediatric pyogenic arthritis is Staphylococcus aureus, but there is a long list of other potential pathogens, including Streptococcus pyogenes (group A streptococcus) and Streptococcus pneumoniae. Most pediatric patients with acute pyogenic arthritis have synovial fluid WBC counts in excess of 75,000 to 100,000/L. The protracted course and the initial lack of hip symptoms raise the possibility of a primary osteomyelitis of the femur (particularly the intracapsular portion of the femoral neck or head) or of the acetabulum, with subsequent extension into the hip joint. Pyogenic myositis involving muscle groups adjacent to the hip would be unlikely to spread into the hip space, but can lead to synovial irritation, characterized by sterile joint fluid and WBC counts that fall short of the usual numbers seen in septic arthritis. The blood supply to the femoral head can become compromised with prolonged inflammation and increased intracapsular pressure, resulting in aseptic necrosis.
All cultures from his hip and knee aspirations were sterile. He continued to have daily fevers and persistent tachycardia while receiving intravenous ceftriaxone and vancomycin. Additional testing was notable for: antinuclear antibody (ANA) 1:80, anti‐streptolysin O (ASO) titer 344 IU (normal <150 IU), AST and ALT within normal limits, ferritin 568 ng/mL (normal <322 ng/mL), and lactate dehydrogenase (LDH) 212 units/L (normal <257 units/L). Abdominal ultrasound revealed borderline hepatosplenomegaly. An ophthalmologic examination was normal.
On postoperative day 4 he developed left upper thigh swelling. An MRI showed rim‐enhancing juxta‐articular complex fluid collections surrounding the left femur with decreased marrow enhancement of the left proximal femur (Figure 1).
The limited rheumatologic evaluation is unrevealing; the ANA result is nondiagnostic and the ASO titer is normal for age. Laboratories generally report adult normal values for streptococcal antibodies regardless of the patient's age; children from ages 7 to 12 years are at their life peak frequency of group A streptococcal pharyngitis and typically have higher normal values of streptococcal antibodies, including ASO (up to about 480640 IU). The moderately elevated ferritin level is most likely an acute phase reactant and not high enough to suggest macrophage activation syndrome, which is unlikely with the normal AST, ALT, and LDH levels, the absence of significant splenomegaly, and the lack of cytopenias. Continued fever with progressive left upper thigh swelling point to osteomyelitis of the proximal femur, which may have initially ruptured into the hip and then infiltrated the femoral cortex and spread infection into the adjacent soft tissues. Surgical debridement is indicated.
The relative prevalence of methicillin‐sensitive S aureus (MSSA) and methicillin‐resistant S aureus vary widely with geography. MSSA strains are more likely to be highly toxigenic. The elaboration of 1 or more extracellular toxins could account for the patient's initial symptoms.
The patient was brought back to the operating room for drainage of the juxta‐articular fluid collections and a biopsy of his femur. The fluid collections were grossly purulent. His intraoperative cultures were positive for MSSA. The bone biopsy revealed necrotic tissue, acute inflammation, and bacterial colonies, consistent with acute osteomyelitis. Further testing of his S aureus isolate was positive for staphylococcal enterotoxin B. He completed a 4‐week course of oral clindamycin with subsequent normalization of his hip exam and inflammatory markers. At a follow‐up visit the patient was feeling better, but had developed skin peeling on the lateral aspects of his feet consistent with late sequelae of toxin‐mediated disease (Figure 2). Three months after discharge the patient had returned to his baseline activity level and remained asymptomatic.
COMMENTARY
The patient presented with a constellation of symptoms that was initially mistaken for incomplete KD until focal progression of his symptoms exposed an underlying femoral osteomyelitis with periarticular abscess formation. Bacterial cultures and subsequent toxin assay revealed an enterotoxin B‐producing strain of S aureus.
Certain staphylococcal strains secrete superantigens that may lead to the development of a systemic toxin‐mediated syndrome. Toxins elaborated by S aureus include toxic shock syndrome toxin‐1 (TSST‐1) and enterotoxins, which have been implicated in menstrual and nonmenstrual toxic shock syndromes.[1, 2] Enterotoxin B is a staphylococcal superantigen found in most strains of the USA400 clonal group, and has been frequently associated with skin and soft tissue infections.[3] Enterotoxin B production has been reported in nearly half of S aureus isolates from skin, soft tissue, and bone infections.[4]
Staphylococcal and streptococcal toxin‐mediated diseases can mimic vasculitis, systemic juvenile idiopathic arthritis, viral infections, and Stevens‐Johnson syndrome. Glossitis in toxin‐mediated syndromes manifests with a swollen, red tongue with overlying enlarged papillae, giving the appearance of a strawberry. Although pediatric providers often equate strawberry tongue, conjunctival injection, rash, and erythematous lips with KD, these findings are also seen in toxin‐mediated diseases, such as scarlet fever or staphylococcal toxic shock syndrome. Enterotoxin B mediated staphylococcal disease masquerading as KD has been reported in 2 cases: a 7‐month‐old boy with multifocal S aureus osteomyelitis and a 5‐year‐old boy with S aureus bacteremia. Both staphylococcal isolates produced enterotoxin B but were negative for other staphylococcus‐related toxins including TSST‐1.[5]
The Institute of Medicine (IOM) recently released its report Improving Diagnosis in Health Care, highlighting the under‐recognized quality and safety issue of diagnostic error.[6] The report uses the following broad and patient‐centered definition of diagnostic error: the failure to (a) establish an accurate and timely explanation of the patient's health problem(s) or (b) communicate that explanation to the patient. The IOM's conceptual model of diagnosis emphasizes the iterative nature of the diagnostic process, including the importance of generating a working diagnosis, gathering and incorporating new information in the reassessment of that diagnosis, and integrating treatment response into the formulation of the final diagnosis (Figure 3).
Even though the patient initially had several features consistent with KD, the increasing number of atypical features could have prompted the clinical team to reconsider their working diagnosis. The patient's age was atypical for KD, he had progressive knee and hip arthritis, and his fevers persisted after IVIG. An expanded differential should have included toxic shock syndrome; the resolution of conjunctival and mucosal injection and edema after IVIG may have been the result of antibodies in the IVIG preparation with neutralizing activity against superantigens. This antitoxin activity has established a role for IVIG in the management of staphylococcal toxic shock syndrome.[7] Ultimately, his imaging and surgical drainage revealed a focal staphylococcal toxin‐producing infectious source from which his fevers, rash, and mucosal and extremity changes emanated. This case reminds us that the more atypical a working diagnosis iseither in its presentation or treatment responsethe more readily clinicians should take it for another spin around the diagnostic wheel in search of a more suitable alternative.
KEY LEARNING POINTS
- Staphylococcal toxin‐mediated disease may mimic KD, with common features including strawberry tongue, oral and conjunctival injection, and skin desquamation.
- Improvement after treatment with IVIG is characteristic but not diagnostic of KD, and may be seen in toxin‐mediated disease.
- KD may present with arthralgia or arthritis, but severe joint abnormalities warrant consideration of infectious and other autoimmune conditions.
- The more atypical a working diagnosis iseither in its presentation or treatment responsethe more readily clinicians should gather, interpret, and integrate new information in search of a more suitable alternative.
Disclosure: Nothing to report.
- . Staphylococcal enterotoxin B and toxic shock syndrome toxin‐1 are significantly associated with non‐menstrual TSS. Lancet. 1986;1:1149–1150.
- , , , , . Toxic shock syndrome caused by a strain of staphylococcus aureus that produces enterotoxin C but not toxic shock syndrome toxin‐1. Am J Dis Child. 1989;143 (7):848–849.
- , , , , , . Staphylococcus aureus isolates encode variant staphylococcal enterotoxin B proteins that are diverse in superantigenicity and lethality. PLoS One. 2012;7(7):e41157.
- , , , et al. Variability of antibiotic susceptibility and toxin production of Staphylococcal aureus stains isolated from skin, soft tissue, and bone related infections. BMC Microbiol. 2013;13:188.
- , , , , . Kawasaki syndrome‐like illness associated with infection caused by enterotoxin B‐secreting Staphylococcus aureus. Clin Microbiol Rev. 2013;26:422–447.
- National Academies of Sciences, Engineering, and Medicine. Improving Diagnosis in Health Care. Washington, DC: The National Academies Press; 2015.
- , , , et al. Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: a European randomized, double‐blind, placebo‐controlled trial. Clin Infect Dis. 2003;37(3):333–340.
A previously healthy 11‐year‐old boy presented to the emergency department after referral from his pediatrician for 1 week of fevers. Seven days prior to admission he developed a fever to 40.8C, vomiting, and mild left knee pain. The vomiting resolved within 2 days. Five days prior to admission he developed a pruritic, pinpoint rash over his abdomen that resolved within 24 hours. He also developed red, cracked lips, redness of his tongue, redness surrounding his eyes, and slight swelling of his hands. Three days prior to admission his pediatrician noted a 1‐cm anterior cervical lymph node. His fevers occurred throughout each of the prior 7 days without a discernible pattern, and his mild knee pain persisted at the time of presentation.
This preteen has had high fevers for 1 week associated with arthralgia, pruritic rash, emesis, and oral mucosal erythema. His rash, lip and tongue erythema, and swollen hands are classic features of Kawasaki disease (KD), but he lacks the other characteristic physical examination findings. The diagnosis of KD requires fever for at least 5 days accompanied by 4 of the following 5 signs: polymorphous rash, oral mucous membrane changes, peripheral extremity changes such as swelling or skin desquamation, bilateral bulbar conjunctival injection, and cervical lymphadenopathy >1.5 cm in diameter. Children meeting fewer than 4 of these criteria may have an incomplete form of KD.
Because most patients with KD (80%) are under 5 years old, alternative diagnoses such as autoimmune illnesses or a hypersensitivity reaction should be considered. Travel, medication, and animal exposure histories may reveal clues to an infectious or drug‐induced etiology of his fever. Immunization status should be assessed, as measles is also associated with fever, rash, and mucosal changes. Arthralgia or arthritis may occur in KD, but these findings suggest the need to entertain other possibilities, including bone or joint infection, infective endocarditis, inflammatory bowel disease, juvenile idiopathic arthritis (JIA), or systemic lupus erythematosus (SLE).
The child's only past medical history was an episode of croup as an infant. There was no family history of autoimmune diseases. He was not taking any medications and had no known allergies. His immunizations were up to date, including measles, mumps, rubella, and varicella. He lived with his parents and his dog. He swam in fresh water during a trip to Maine 2 months earlier. Neither he nor his family recalled a tick bite. He had no exposure to raw meat or unpasteurized dairy products.
The travel to New England raises the possibility of Lyme disease, although a 2‐month interval between exposure and a high, prolonged fever would be very unusual. Knee arthralgia or arthritis is common in children with late‐stage Lyme disease, but can also be seen in early‐disseminated disease. The prior description of the rash is not suggestive of erythema chronicum migrans, which is seen in early‐stage Lyme disease.
C‐reactive protein (CRP) was 189 mg/L (normal <6.3 mg/L). An echocardiogram was normal. Intravenous immunoglobulin (IVIG) was administered for presumed KD, with immediate improvement of the periorbital erythema, tongue redness, and hand swelling. He was discharged the next day on aspirin with cardiology clinic follow‐up.
Improvement after IVIG supports the diagnosis of KD. It is typical to discharge KD patients from the hospital when they have been afebrile for 24 hours or when the CRP level has declined by approximately 50%.
Over the next 48 hours he felt unwell with high‐grade fevers, continued left knee pain, and new left hip pain. He was readmitted to the hospital. His temperature was 39.4C, respiratory rate was 22 breaths per minute, heart rate was 122 beats per minute, blood pressure was 103/50 mm Hg, and oxygen saturation was 100% while breathing ambient air. He appeared mildly uncomfortable. His conjunctivae were normal. His lips were dry, red, and cracked, and his tongue was red with prominent papillae. His neck was supple without lymphadenopathy. His lungs were clear to auscultation. His heart exam was without murmurs. His abdomen was soft, and the liver and spleen were not enlarged. He had no swelling or erythema of his joints; however, he experienced pain with range of motion of his left knee, and tenderness and restricted range of motion of his left hip. His neurologic exam was normal. There were no rashes.
He has persistent fever, tachycardia, and tachypnea, now without features of KD except oral mucosal changes including prominent tongue papillae consistent with a strawberry tongue. Continued or recurrent fever may suggest persistent KD with ongoing inflammation or the need to search for an alternative diagnoses. An echocardiogram should be repeated, as the coronary artery abnormalities in KD can evolve rapidly, particularly when inflammation persists. Additional findings may include decreased left ventricular function, mitral regurgitation, or pericardial effusion. A second dose of IVIG is necessary to control fever and inflammation in about 15% of patients with KD, although in this case IVIG should be withheld pending further evaluation.
Arthralgia occurs commonly in KD, whereas frank arthritis is less typical. Polyarticular or oligoarticular arthritis involving small or large joints (especially knee or ankle) affects 5% to 10% of patients. The severity of findings in his left hip warrants consideration of septic arthritis with pain referred to the knee; pelvic or femoral osteomyelitis; psoas abscess; or pyomyositis. Following basic lab tests, imaging of the left hip region is indicated.
Laboratory evaluation revealed: white blood cell (WBC) count 10,000/L (absolute neutrophil count 8,460/L, absolute lymphocyte count 530/L), hemoglobin 10.6 g/dL, platelet count 208,000/L, serum sodium 130 mmol/L, serum potassium 3.3 mmol/L, serum urea nitrogen 11 mg/dL, serum creatinine 0.54 mg/dL, aspartate transaminase (AST) 26 U/L, alanine transaminase (ALT) 31 U/L, albumin 1.7 g/dL, erythrocyte sedimentation rate (ESR) > 100 mm/h, and CRP 263 mg/L. No blast cells were seen on peripheral blood smear.
Hypoalbuminemia and markedly elevated inflammatory markers indicate an inflammatory condition that has been active for more than a week. Assessing ESR after IVIG therapy is not useful because exogenous globulins increase the ESR; however, CRP is useful to monitor inflammation and remains elevated here.
Incomplete KD is still possible. Hyponatremia, hypoalbuminemia, and anemia are all features of persistent KD, and have been utilized in several clinical scoring systems in Japan to identify KD patients at increased risk for developing coronary complications. A neoplastic process cannot be excluded, but does not appear likely based on the acuity of his presentation and peripheral blood smear review.
Upon readmission he received a second dose of 2 g/kg IVIG. He remained on aspirin and continued to have fevers. A repeat echocardiogram was normal. He had worsening pain in his left knee and hip with difficulty straightening his left leg. Physical examination was notable for tenderness to palpation over his left hip joint, refusal to bear weight, and resistance to passive range of motion. On hospital day 2, an ultrasound of his left hip and knee revealed a complex left hip effusion and small left knee effusion.
KD becomes less likely in the presence of persistent fevers after IVIG and a repeatedly normal echocardiogram. Worsening left leg symptoms including impaired hip extension with a complex hip effusion suggests an infectious process in or adjacent to the left hip, such as septic arthritis, myositis, or osteomyelitis of the pelvis or proximal femur. A complex hip effusion is less likely to be present with arthritis related to JIA or SLE. The patient needs an emergent hip aspiration and possibly magnetic resonance imaging (MRI) to evaluate adjacent structures.
Arthrotomy and open drainage of his left hip revealed purulent fluid with a WBC count of 49,000/L with 89% neutrophils and 2% lymphocytes. Gram stain was negative. A left knee aspirate demonstrated straw‐colored synovial fluid (which was not sent for cell counts). Bacterial, fungal, and acid‐fast bacilli cultures were requested from hip and knee aspirates. Intravenous ceftriaxone and vancomycin were administered.
The most likely organism in pediatric pyogenic arthritis is Staphylococcus aureus, but there is a long list of other potential pathogens, including Streptococcus pyogenes (group A streptococcus) and Streptococcus pneumoniae. Most pediatric patients with acute pyogenic arthritis have synovial fluid WBC counts in excess of 75,000 to 100,000/L. The protracted course and the initial lack of hip symptoms raise the possibility of a primary osteomyelitis of the femur (particularly the intracapsular portion of the femoral neck or head) or of the acetabulum, with subsequent extension into the hip joint. Pyogenic myositis involving muscle groups adjacent to the hip would be unlikely to spread into the hip space, but can lead to synovial irritation, characterized by sterile joint fluid and WBC counts that fall short of the usual numbers seen in septic arthritis. The blood supply to the femoral head can become compromised with prolonged inflammation and increased intracapsular pressure, resulting in aseptic necrosis.
All cultures from his hip and knee aspirations were sterile. He continued to have daily fevers and persistent tachycardia while receiving intravenous ceftriaxone and vancomycin. Additional testing was notable for: antinuclear antibody (ANA) 1:80, anti‐streptolysin O (ASO) titer 344 IU (normal <150 IU), AST and ALT within normal limits, ferritin 568 ng/mL (normal <322 ng/mL), and lactate dehydrogenase (LDH) 212 units/L (normal <257 units/L). Abdominal ultrasound revealed borderline hepatosplenomegaly. An ophthalmologic examination was normal.
On postoperative day 4 he developed left upper thigh swelling. An MRI showed rim‐enhancing juxta‐articular complex fluid collections surrounding the left femur with decreased marrow enhancement of the left proximal femur (Figure 1).
The limited rheumatologic evaluation is unrevealing; the ANA result is nondiagnostic and the ASO titer is normal for age. Laboratories generally report adult normal values for streptococcal antibodies regardless of the patient's age; children from ages 7 to 12 years are at their life peak frequency of group A streptococcal pharyngitis and typically have higher normal values of streptococcal antibodies, including ASO (up to about 480640 IU). The moderately elevated ferritin level is most likely an acute phase reactant and not high enough to suggest macrophage activation syndrome, which is unlikely with the normal AST, ALT, and LDH levels, the absence of significant splenomegaly, and the lack of cytopenias. Continued fever with progressive left upper thigh swelling point to osteomyelitis of the proximal femur, which may have initially ruptured into the hip and then infiltrated the femoral cortex and spread infection into the adjacent soft tissues. Surgical debridement is indicated.
The relative prevalence of methicillin‐sensitive S aureus (MSSA) and methicillin‐resistant S aureus vary widely with geography. MSSA strains are more likely to be highly toxigenic. The elaboration of 1 or more extracellular toxins could account for the patient's initial symptoms.
The patient was brought back to the operating room for drainage of the juxta‐articular fluid collections and a biopsy of his femur. The fluid collections were grossly purulent. His intraoperative cultures were positive for MSSA. The bone biopsy revealed necrotic tissue, acute inflammation, and bacterial colonies, consistent with acute osteomyelitis. Further testing of his S aureus isolate was positive for staphylococcal enterotoxin B. He completed a 4‐week course of oral clindamycin with subsequent normalization of his hip exam and inflammatory markers. At a follow‐up visit the patient was feeling better, but had developed skin peeling on the lateral aspects of his feet consistent with late sequelae of toxin‐mediated disease (Figure 2). Three months after discharge the patient had returned to his baseline activity level and remained asymptomatic.
COMMENTARY
The patient presented with a constellation of symptoms that was initially mistaken for incomplete KD until focal progression of his symptoms exposed an underlying femoral osteomyelitis with periarticular abscess formation. Bacterial cultures and subsequent toxin assay revealed an enterotoxin B‐producing strain of S aureus.
Certain staphylococcal strains secrete superantigens that may lead to the development of a systemic toxin‐mediated syndrome. Toxins elaborated by S aureus include toxic shock syndrome toxin‐1 (TSST‐1) and enterotoxins, which have been implicated in menstrual and nonmenstrual toxic shock syndromes.[1, 2] Enterotoxin B is a staphylococcal superantigen found in most strains of the USA400 clonal group, and has been frequently associated with skin and soft tissue infections.[3] Enterotoxin B production has been reported in nearly half of S aureus isolates from skin, soft tissue, and bone infections.[4]
Staphylococcal and streptococcal toxin‐mediated diseases can mimic vasculitis, systemic juvenile idiopathic arthritis, viral infections, and Stevens‐Johnson syndrome. Glossitis in toxin‐mediated syndromes manifests with a swollen, red tongue with overlying enlarged papillae, giving the appearance of a strawberry. Although pediatric providers often equate strawberry tongue, conjunctival injection, rash, and erythematous lips with KD, these findings are also seen in toxin‐mediated diseases, such as scarlet fever or staphylococcal toxic shock syndrome. Enterotoxin B mediated staphylococcal disease masquerading as KD has been reported in 2 cases: a 7‐month‐old boy with multifocal S aureus osteomyelitis and a 5‐year‐old boy with S aureus bacteremia. Both staphylococcal isolates produced enterotoxin B but were negative for other staphylococcus‐related toxins including TSST‐1.[5]
The Institute of Medicine (IOM) recently released its report Improving Diagnosis in Health Care, highlighting the under‐recognized quality and safety issue of diagnostic error.[6] The report uses the following broad and patient‐centered definition of diagnostic error: the failure to (a) establish an accurate and timely explanation of the patient's health problem(s) or (b) communicate that explanation to the patient. The IOM's conceptual model of diagnosis emphasizes the iterative nature of the diagnostic process, including the importance of generating a working diagnosis, gathering and incorporating new information in the reassessment of that diagnosis, and integrating treatment response into the formulation of the final diagnosis (Figure 3).
Even though the patient initially had several features consistent with KD, the increasing number of atypical features could have prompted the clinical team to reconsider their working diagnosis. The patient's age was atypical for KD, he had progressive knee and hip arthritis, and his fevers persisted after IVIG. An expanded differential should have included toxic shock syndrome; the resolution of conjunctival and mucosal injection and edema after IVIG may have been the result of antibodies in the IVIG preparation with neutralizing activity against superantigens. This antitoxin activity has established a role for IVIG in the management of staphylococcal toxic shock syndrome.[7] Ultimately, his imaging and surgical drainage revealed a focal staphylococcal toxin‐producing infectious source from which his fevers, rash, and mucosal and extremity changes emanated. This case reminds us that the more atypical a working diagnosis iseither in its presentation or treatment responsethe more readily clinicians should take it for another spin around the diagnostic wheel in search of a more suitable alternative.
KEY LEARNING POINTS
- Staphylococcal toxin‐mediated disease may mimic KD, with common features including strawberry tongue, oral and conjunctival injection, and skin desquamation.
- Improvement after treatment with IVIG is characteristic but not diagnostic of KD, and may be seen in toxin‐mediated disease.
- KD may present with arthralgia or arthritis, but severe joint abnormalities warrant consideration of infectious and other autoimmune conditions.
- The more atypical a working diagnosis iseither in its presentation or treatment responsethe more readily clinicians should gather, interpret, and integrate new information in search of a more suitable alternative.
Disclosure: Nothing to report.
A previously healthy 11‐year‐old boy presented to the emergency department after referral from his pediatrician for 1 week of fevers. Seven days prior to admission he developed a fever to 40.8C, vomiting, and mild left knee pain. The vomiting resolved within 2 days. Five days prior to admission he developed a pruritic, pinpoint rash over his abdomen that resolved within 24 hours. He also developed red, cracked lips, redness of his tongue, redness surrounding his eyes, and slight swelling of his hands. Three days prior to admission his pediatrician noted a 1‐cm anterior cervical lymph node. His fevers occurred throughout each of the prior 7 days without a discernible pattern, and his mild knee pain persisted at the time of presentation.
This preteen has had high fevers for 1 week associated with arthralgia, pruritic rash, emesis, and oral mucosal erythema. His rash, lip and tongue erythema, and swollen hands are classic features of Kawasaki disease (KD), but he lacks the other characteristic physical examination findings. The diagnosis of KD requires fever for at least 5 days accompanied by 4 of the following 5 signs: polymorphous rash, oral mucous membrane changes, peripheral extremity changes such as swelling or skin desquamation, bilateral bulbar conjunctival injection, and cervical lymphadenopathy >1.5 cm in diameter. Children meeting fewer than 4 of these criteria may have an incomplete form of KD.
Because most patients with KD (80%) are under 5 years old, alternative diagnoses such as autoimmune illnesses or a hypersensitivity reaction should be considered. Travel, medication, and animal exposure histories may reveal clues to an infectious or drug‐induced etiology of his fever. Immunization status should be assessed, as measles is also associated with fever, rash, and mucosal changes. Arthralgia or arthritis may occur in KD, but these findings suggest the need to entertain other possibilities, including bone or joint infection, infective endocarditis, inflammatory bowel disease, juvenile idiopathic arthritis (JIA), or systemic lupus erythematosus (SLE).
The child's only past medical history was an episode of croup as an infant. There was no family history of autoimmune diseases. He was not taking any medications and had no known allergies. His immunizations were up to date, including measles, mumps, rubella, and varicella. He lived with his parents and his dog. He swam in fresh water during a trip to Maine 2 months earlier. Neither he nor his family recalled a tick bite. He had no exposure to raw meat or unpasteurized dairy products.
The travel to New England raises the possibility of Lyme disease, although a 2‐month interval between exposure and a high, prolonged fever would be very unusual. Knee arthralgia or arthritis is common in children with late‐stage Lyme disease, but can also be seen in early‐disseminated disease. The prior description of the rash is not suggestive of erythema chronicum migrans, which is seen in early‐stage Lyme disease.
C‐reactive protein (CRP) was 189 mg/L (normal <6.3 mg/L). An echocardiogram was normal. Intravenous immunoglobulin (IVIG) was administered for presumed KD, with immediate improvement of the periorbital erythema, tongue redness, and hand swelling. He was discharged the next day on aspirin with cardiology clinic follow‐up.
Improvement after IVIG supports the diagnosis of KD. It is typical to discharge KD patients from the hospital when they have been afebrile for 24 hours or when the CRP level has declined by approximately 50%.
Over the next 48 hours he felt unwell with high‐grade fevers, continued left knee pain, and new left hip pain. He was readmitted to the hospital. His temperature was 39.4C, respiratory rate was 22 breaths per minute, heart rate was 122 beats per minute, blood pressure was 103/50 mm Hg, and oxygen saturation was 100% while breathing ambient air. He appeared mildly uncomfortable. His conjunctivae were normal. His lips were dry, red, and cracked, and his tongue was red with prominent papillae. His neck was supple without lymphadenopathy. His lungs were clear to auscultation. His heart exam was without murmurs. His abdomen was soft, and the liver and spleen were not enlarged. He had no swelling or erythema of his joints; however, he experienced pain with range of motion of his left knee, and tenderness and restricted range of motion of his left hip. His neurologic exam was normal. There were no rashes.
He has persistent fever, tachycardia, and tachypnea, now without features of KD except oral mucosal changes including prominent tongue papillae consistent with a strawberry tongue. Continued or recurrent fever may suggest persistent KD with ongoing inflammation or the need to search for an alternative diagnoses. An echocardiogram should be repeated, as the coronary artery abnormalities in KD can evolve rapidly, particularly when inflammation persists. Additional findings may include decreased left ventricular function, mitral regurgitation, or pericardial effusion. A second dose of IVIG is necessary to control fever and inflammation in about 15% of patients with KD, although in this case IVIG should be withheld pending further evaluation.
Arthralgia occurs commonly in KD, whereas frank arthritis is less typical. Polyarticular or oligoarticular arthritis involving small or large joints (especially knee or ankle) affects 5% to 10% of patients. The severity of findings in his left hip warrants consideration of septic arthritis with pain referred to the knee; pelvic or femoral osteomyelitis; psoas abscess; or pyomyositis. Following basic lab tests, imaging of the left hip region is indicated.
Laboratory evaluation revealed: white blood cell (WBC) count 10,000/L (absolute neutrophil count 8,460/L, absolute lymphocyte count 530/L), hemoglobin 10.6 g/dL, platelet count 208,000/L, serum sodium 130 mmol/L, serum potassium 3.3 mmol/L, serum urea nitrogen 11 mg/dL, serum creatinine 0.54 mg/dL, aspartate transaminase (AST) 26 U/L, alanine transaminase (ALT) 31 U/L, albumin 1.7 g/dL, erythrocyte sedimentation rate (ESR) > 100 mm/h, and CRP 263 mg/L. No blast cells were seen on peripheral blood smear.
Hypoalbuminemia and markedly elevated inflammatory markers indicate an inflammatory condition that has been active for more than a week. Assessing ESR after IVIG therapy is not useful because exogenous globulins increase the ESR; however, CRP is useful to monitor inflammation and remains elevated here.
Incomplete KD is still possible. Hyponatremia, hypoalbuminemia, and anemia are all features of persistent KD, and have been utilized in several clinical scoring systems in Japan to identify KD patients at increased risk for developing coronary complications. A neoplastic process cannot be excluded, but does not appear likely based on the acuity of his presentation and peripheral blood smear review.
Upon readmission he received a second dose of 2 g/kg IVIG. He remained on aspirin and continued to have fevers. A repeat echocardiogram was normal. He had worsening pain in his left knee and hip with difficulty straightening his left leg. Physical examination was notable for tenderness to palpation over his left hip joint, refusal to bear weight, and resistance to passive range of motion. On hospital day 2, an ultrasound of his left hip and knee revealed a complex left hip effusion and small left knee effusion.
KD becomes less likely in the presence of persistent fevers after IVIG and a repeatedly normal echocardiogram. Worsening left leg symptoms including impaired hip extension with a complex hip effusion suggests an infectious process in or adjacent to the left hip, such as septic arthritis, myositis, or osteomyelitis of the pelvis or proximal femur. A complex hip effusion is less likely to be present with arthritis related to JIA or SLE. The patient needs an emergent hip aspiration and possibly magnetic resonance imaging (MRI) to evaluate adjacent structures.
Arthrotomy and open drainage of his left hip revealed purulent fluid with a WBC count of 49,000/L with 89% neutrophils and 2% lymphocytes. Gram stain was negative. A left knee aspirate demonstrated straw‐colored synovial fluid (which was not sent for cell counts). Bacterial, fungal, and acid‐fast bacilli cultures were requested from hip and knee aspirates. Intravenous ceftriaxone and vancomycin were administered.
The most likely organism in pediatric pyogenic arthritis is Staphylococcus aureus, but there is a long list of other potential pathogens, including Streptococcus pyogenes (group A streptococcus) and Streptococcus pneumoniae. Most pediatric patients with acute pyogenic arthritis have synovial fluid WBC counts in excess of 75,000 to 100,000/L. The protracted course and the initial lack of hip symptoms raise the possibility of a primary osteomyelitis of the femur (particularly the intracapsular portion of the femoral neck or head) or of the acetabulum, with subsequent extension into the hip joint. Pyogenic myositis involving muscle groups adjacent to the hip would be unlikely to spread into the hip space, but can lead to synovial irritation, characterized by sterile joint fluid and WBC counts that fall short of the usual numbers seen in septic arthritis. The blood supply to the femoral head can become compromised with prolonged inflammation and increased intracapsular pressure, resulting in aseptic necrosis.
All cultures from his hip and knee aspirations were sterile. He continued to have daily fevers and persistent tachycardia while receiving intravenous ceftriaxone and vancomycin. Additional testing was notable for: antinuclear antibody (ANA) 1:80, anti‐streptolysin O (ASO) titer 344 IU (normal <150 IU), AST and ALT within normal limits, ferritin 568 ng/mL (normal <322 ng/mL), and lactate dehydrogenase (LDH) 212 units/L (normal <257 units/L). Abdominal ultrasound revealed borderline hepatosplenomegaly. An ophthalmologic examination was normal.
On postoperative day 4 he developed left upper thigh swelling. An MRI showed rim‐enhancing juxta‐articular complex fluid collections surrounding the left femur with decreased marrow enhancement of the left proximal femur (Figure 1).
The limited rheumatologic evaluation is unrevealing; the ANA result is nondiagnostic and the ASO titer is normal for age. Laboratories generally report adult normal values for streptococcal antibodies regardless of the patient's age; children from ages 7 to 12 years are at their life peak frequency of group A streptococcal pharyngitis and typically have higher normal values of streptococcal antibodies, including ASO (up to about 480640 IU). The moderately elevated ferritin level is most likely an acute phase reactant and not high enough to suggest macrophage activation syndrome, which is unlikely with the normal AST, ALT, and LDH levels, the absence of significant splenomegaly, and the lack of cytopenias. Continued fever with progressive left upper thigh swelling point to osteomyelitis of the proximal femur, which may have initially ruptured into the hip and then infiltrated the femoral cortex and spread infection into the adjacent soft tissues. Surgical debridement is indicated.
The relative prevalence of methicillin‐sensitive S aureus (MSSA) and methicillin‐resistant S aureus vary widely with geography. MSSA strains are more likely to be highly toxigenic. The elaboration of 1 or more extracellular toxins could account for the patient's initial symptoms.
The patient was brought back to the operating room for drainage of the juxta‐articular fluid collections and a biopsy of his femur. The fluid collections were grossly purulent. His intraoperative cultures were positive for MSSA. The bone biopsy revealed necrotic tissue, acute inflammation, and bacterial colonies, consistent with acute osteomyelitis. Further testing of his S aureus isolate was positive for staphylococcal enterotoxin B. He completed a 4‐week course of oral clindamycin with subsequent normalization of his hip exam and inflammatory markers. At a follow‐up visit the patient was feeling better, but had developed skin peeling on the lateral aspects of his feet consistent with late sequelae of toxin‐mediated disease (Figure 2). Three months after discharge the patient had returned to his baseline activity level and remained asymptomatic.
COMMENTARY
The patient presented with a constellation of symptoms that was initially mistaken for incomplete KD until focal progression of his symptoms exposed an underlying femoral osteomyelitis with periarticular abscess formation. Bacterial cultures and subsequent toxin assay revealed an enterotoxin B‐producing strain of S aureus.
Certain staphylococcal strains secrete superantigens that may lead to the development of a systemic toxin‐mediated syndrome. Toxins elaborated by S aureus include toxic shock syndrome toxin‐1 (TSST‐1) and enterotoxins, which have been implicated in menstrual and nonmenstrual toxic shock syndromes.[1, 2] Enterotoxin B is a staphylococcal superantigen found in most strains of the USA400 clonal group, and has been frequently associated with skin and soft tissue infections.[3] Enterotoxin B production has been reported in nearly half of S aureus isolates from skin, soft tissue, and bone infections.[4]
Staphylococcal and streptococcal toxin‐mediated diseases can mimic vasculitis, systemic juvenile idiopathic arthritis, viral infections, and Stevens‐Johnson syndrome. Glossitis in toxin‐mediated syndromes manifests with a swollen, red tongue with overlying enlarged papillae, giving the appearance of a strawberry. Although pediatric providers often equate strawberry tongue, conjunctival injection, rash, and erythematous lips with KD, these findings are also seen in toxin‐mediated diseases, such as scarlet fever or staphylococcal toxic shock syndrome. Enterotoxin B mediated staphylococcal disease masquerading as KD has been reported in 2 cases: a 7‐month‐old boy with multifocal S aureus osteomyelitis and a 5‐year‐old boy with S aureus bacteremia. Both staphylococcal isolates produced enterotoxin B but were negative for other staphylococcus‐related toxins including TSST‐1.[5]
The Institute of Medicine (IOM) recently released its report Improving Diagnosis in Health Care, highlighting the under‐recognized quality and safety issue of diagnostic error.[6] The report uses the following broad and patient‐centered definition of diagnostic error: the failure to (a) establish an accurate and timely explanation of the patient's health problem(s) or (b) communicate that explanation to the patient. The IOM's conceptual model of diagnosis emphasizes the iterative nature of the diagnostic process, including the importance of generating a working diagnosis, gathering and incorporating new information in the reassessment of that diagnosis, and integrating treatment response into the formulation of the final diagnosis (Figure 3).
Even though the patient initially had several features consistent with KD, the increasing number of atypical features could have prompted the clinical team to reconsider their working diagnosis. The patient's age was atypical for KD, he had progressive knee and hip arthritis, and his fevers persisted after IVIG. An expanded differential should have included toxic shock syndrome; the resolution of conjunctival and mucosal injection and edema after IVIG may have been the result of antibodies in the IVIG preparation with neutralizing activity against superantigens. This antitoxin activity has established a role for IVIG in the management of staphylococcal toxic shock syndrome.[7] Ultimately, his imaging and surgical drainage revealed a focal staphylococcal toxin‐producing infectious source from which his fevers, rash, and mucosal and extremity changes emanated. This case reminds us that the more atypical a working diagnosis iseither in its presentation or treatment responsethe more readily clinicians should take it for another spin around the diagnostic wheel in search of a more suitable alternative.
KEY LEARNING POINTS
- Staphylococcal toxin‐mediated disease may mimic KD, with common features including strawberry tongue, oral and conjunctival injection, and skin desquamation.
- Improvement after treatment with IVIG is characteristic but not diagnostic of KD, and may be seen in toxin‐mediated disease.
- KD may present with arthralgia or arthritis, but severe joint abnormalities warrant consideration of infectious and other autoimmune conditions.
- The more atypical a working diagnosis iseither in its presentation or treatment responsethe more readily clinicians should gather, interpret, and integrate new information in search of a more suitable alternative.
Disclosure: Nothing to report.
- . Staphylococcal enterotoxin B and toxic shock syndrome toxin‐1 are significantly associated with non‐menstrual TSS. Lancet. 1986;1:1149–1150.
- , , , , . Toxic shock syndrome caused by a strain of staphylococcus aureus that produces enterotoxin C but not toxic shock syndrome toxin‐1. Am J Dis Child. 1989;143 (7):848–849.
- , , , , , . Staphylococcus aureus isolates encode variant staphylococcal enterotoxin B proteins that are diverse in superantigenicity and lethality. PLoS One. 2012;7(7):e41157.
- , , , et al. Variability of antibiotic susceptibility and toxin production of Staphylococcal aureus stains isolated from skin, soft tissue, and bone related infections. BMC Microbiol. 2013;13:188.
- , , , , . Kawasaki syndrome‐like illness associated with infection caused by enterotoxin B‐secreting Staphylococcus aureus. Clin Microbiol Rev. 2013;26:422–447.
- National Academies of Sciences, Engineering, and Medicine. Improving Diagnosis in Health Care. Washington, DC: The National Academies Press; 2015.
- , , , et al. Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: a European randomized, double‐blind, placebo‐controlled trial. Clin Infect Dis. 2003;37(3):333–340.
- . Staphylococcal enterotoxin B and toxic shock syndrome toxin‐1 are significantly associated with non‐menstrual TSS. Lancet. 1986;1:1149–1150.
- , , , , . Toxic shock syndrome caused by a strain of staphylococcus aureus that produces enterotoxin C but not toxic shock syndrome toxin‐1. Am J Dis Child. 1989;143 (7):848–849.
- , , , , , . Staphylococcus aureus isolates encode variant staphylococcal enterotoxin B proteins that are diverse in superantigenicity and lethality. PLoS One. 2012;7(7):e41157.
- , , , et al. Variability of antibiotic susceptibility and toxin production of Staphylococcal aureus stains isolated from skin, soft tissue, and bone related infections. BMC Microbiol. 2013;13:188.
- , , , , . Kawasaki syndrome‐like illness associated with infection caused by enterotoxin B‐secreting Staphylococcus aureus. Clin Microbiol Rev. 2013;26:422–447.
- National Academies of Sciences, Engineering, and Medicine. Improving Diagnosis in Health Care. Washington, DC: The National Academies Press; 2015.
- , , , et al. Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: a European randomized, double‐blind, placebo‐controlled trial. Clin Infect Dis. 2003;37(3):333–340.
10 Reasons to Attend the Quality and Safety Educators Academy
Teaching quality improvement and patient safety is no longer an elective—it’s a necessity. The Quality and Safety Educators Academy (QSEA, sites.hospitalmedicine.org/qsea) provides medical educators with the knowledge and tools to integrate quality improvement and safety concepts into their curricula. This year, QSEA will be held May 23–25 at Tempe Mission Palms Hotel and Conference Center in Arizona.
Here are the top 10 reasons you can’t afford to miss it—and will be glad you went!
- Unparalleled Education: Develop and refine your knowledge in the field of quality and patient safety.
- Curriculum Development: Return to your institution with a collection of new curriculum ideas from QSEA faculty and peers.
- Professional Development: Spend focused time developing and reflecting on your career goals as a physician educator in quality and safety.
- Networking: Build a network of quality and safety educators with both faculty mentors and colleagues with similar career interests.
- Institutional Support: Learn strategies to engage your institutional and program leaders to support and implement a quality and patient safety curriculum to meet the Accreditation Council for Graduate Medical Education (ACGME) Next Accreditation System/Clinical Learning Environment Review (CLER) expectations and improve patient care.
- Hands-On Activities: Dive in to an interactive learning environment with a 10-to-1 student-to-faculty ratio, including facilitated large group sessions, small group activities, and mentor groups.
- Variety of Content: Each day features a variety of topics, such as the principles of quality improvement and patient safety, mentoring trainees in quality improvement project work, high-value care curriculum, curriculum development and assessment in medical education, and many others.
- Distinguished Faculty: All sessions are led by experienced physicians known for their ability to practice and teach quality improvement and patient safety, mentor junior faculty, and guide educators in curriculum development.
- Valuable Resources: Leave with a tool kit of educational resources for quality and safety education.
- Desert Beauty: Enjoy sunny Tempe, Arizona, or travel to nearby Phoenix or Scottsdale!
It’s no surprise that QSEA sold out each of the past four years, so don’t delay—it’s almost here! Register online or via phone at 800-843-3360. Questions? Email [email protected].
Teaching quality improvement and patient safety is no longer an elective—it’s a necessity. The Quality and Safety Educators Academy (QSEA, sites.hospitalmedicine.org/qsea) provides medical educators with the knowledge and tools to integrate quality improvement and safety concepts into their curricula. This year, QSEA will be held May 23–25 at Tempe Mission Palms Hotel and Conference Center in Arizona.
Here are the top 10 reasons you can’t afford to miss it—and will be glad you went!
- Unparalleled Education: Develop and refine your knowledge in the field of quality and patient safety.
- Curriculum Development: Return to your institution with a collection of new curriculum ideas from QSEA faculty and peers.
- Professional Development: Spend focused time developing and reflecting on your career goals as a physician educator in quality and safety.
- Networking: Build a network of quality and safety educators with both faculty mentors and colleagues with similar career interests.
- Institutional Support: Learn strategies to engage your institutional and program leaders to support and implement a quality and patient safety curriculum to meet the Accreditation Council for Graduate Medical Education (ACGME) Next Accreditation System/Clinical Learning Environment Review (CLER) expectations and improve patient care.
- Hands-On Activities: Dive in to an interactive learning environment with a 10-to-1 student-to-faculty ratio, including facilitated large group sessions, small group activities, and mentor groups.
- Variety of Content: Each day features a variety of topics, such as the principles of quality improvement and patient safety, mentoring trainees in quality improvement project work, high-value care curriculum, curriculum development and assessment in medical education, and many others.
- Distinguished Faculty: All sessions are led by experienced physicians known for their ability to practice and teach quality improvement and patient safety, mentor junior faculty, and guide educators in curriculum development.
- Valuable Resources: Leave with a tool kit of educational resources for quality and safety education.
- Desert Beauty: Enjoy sunny Tempe, Arizona, or travel to nearby Phoenix or Scottsdale!
It’s no surprise that QSEA sold out each of the past four years, so don’t delay—it’s almost here! Register online or via phone at 800-843-3360. Questions? Email [email protected].
Teaching quality improvement and patient safety is no longer an elective—it’s a necessity. The Quality and Safety Educators Academy (QSEA, sites.hospitalmedicine.org/qsea) provides medical educators with the knowledge and tools to integrate quality improvement and safety concepts into their curricula. This year, QSEA will be held May 23–25 at Tempe Mission Palms Hotel and Conference Center in Arizona.
Here are the top 10 reasons you can’t afford to miss it—and will be glad you went!
- Unparalleled Education: Develop and refine your knowledge in the field of quality and patient safety.
- Curriculum Development: Return to your institution with a collection of new curriculum ideas from QSEA faculty and peers.
- Professional Development: Spend focused time developing and reflecting on your career goals as a physician educator in quality and safety.
- Networking: Build a network of quality and safety educators with both faculty mentors and colleagues with similar career interests.
- Institutional Support: Learn strategies to engage your institutional and program leaders to support and implement a quality and patient safety curriculum to meet the Accreditation Council for Graduate Medical Education (ACGME) Next Accreditation System/Clinical Learning Environment Review (CLER) expectations and improve patient care.
- Hands-On Activities: Dive in to an interactive learning environment with a 10-to-1 student-to-faculty ratio, including facilitated large group sessions, small group activities, and mentor groups.
- Variety of Content: Each day features a variety of topics, such as the principles of quality improvement and patient safety, mentoring trainees in quality improvement project work, high-value care curriculum, curriculum development and assessment in medical education, and many others.
- Distinguished Faculty: All sessions are led by experienced physicians known for their ability to practice and teach quality improvement and patient safety, mentor junior faculty, and guide educators in curriculum development.
- Valuable Resources: Leave with a tool kit of educational resources for quality and safety education.
- Desert Beauty: Enjoy sunny Tempe, Arizona, or travel to nearby Phoenix or Scottsdale!
It’s no surprise that QSEA sold out each of the past four years, so don’t delay—it’s almost here! Register online or via phone at 800-843-3360. Questions? Email [email protected].
2016 Fellows in Hospital Medicine
MHM
Tina Budnitz, MPH, MHM
Greg Maynard, MD, MHM
Eric Howell, MD, MHM
FHM
Nicole Adler, MD, FHM
Tochukwu Agbata, MD, FHM
Alka Aggarwal, MD, FHM
Gaurav Ahuja, MD, MBBS, FHM
Sameena Akhtar, MD, FHM
Karan Singh S. Alag, MD, MBBS, FHM
Venkata N. Allada, MD, FACP, FHM
Margaret M. Ameyaw, MBChB, FHM
Robert L. Anderson, MD, FHM
Jorge Arboleda, DO, FHM
Michael Aref, MD, PhD, FACP, FHM
Elizabeth M. Arias, MD, FACP, FHM
Amarpreet S. Bains, MD, FHM
Ebrahim Barkoudah, MD, MPH, FACP, FHM
Wanes Barsemian, MD, FHM
Jeffrey T. Bates, MD, FACP, FHM
John F. Bell, MD, MPH, FHM
Kjell Benson, MD, FHM
Azmina Bhaiji, MD, FHM
Sai-Sridhar Boddupalli, MD, FHM
Ani Bodoutchian, MD, MBA, FAAFP, FHM
Tanya M. Boldenow, MD, FHM
Dennis T. Bolger Jr., MD, FHM
Greg D. Bowling, MD, FHM
David A. Bozaan, MD, FHM
Marcia Carbo, MD, FAAP, FHM
Donna Cardoza, MD, FHM
Frank R. Carson Jr., MD, FHM
Kelly Caverzagie, MD, FACP, FHM
Elizabeth A. Cerceo, MD, FACP, FHM
Jeffrey M. Ceresnak, MD, FHM
Romil Chadha, MD, MPH, FACP, FHM
Charles Charman, MD, FHM
Bushra I. Chaudhry, MD, FHM
Justin J. Chow, MD, FHM
Douglas E. Cohen, MD, FHM
John M. Colombo Jr., MD, FHM
Steven Connelly, MD, FACP, FHM
David Corman, MD, FHM
Christopher C. Costa, MD, FHM
William C. Crowe Jr., DNP, ACNP, FNP, MSN, RN, FHM
Ria Dancel, MD, FAAP, FHM
Zubaer Dawlah, MD, FHM
Chandrasekhar R. Dinasarapu, MD, MBBS, MPH, FHM
Vijay Saradhi Dontu, MD, FHM
Oleg Dulkin, MD, FHM
Kevin C. Eaton, PA-C, FHM
Eric Edwards, MD, FHM
Mary E. Fedor, MD, FHM
John W. Fowler Jr., MD, FACP, FHM
Maria G. Frank, MD, FACP, FHM
Yelena Galumyan, MD, FHM
Christopher D. Gamble, MD, FACP, FHM
David J. Goldstein, MD, FHM
Kalpana Gorthi, MD, FHM
Manjula V. Gunawardane, MD, FHM
Craig G. Gunderson, MD, FHM
Theodore J. Haland, MD, FHM
Aaron C. Hamilton, MD, MBA, FHM
Anil Hanuman, DO, FHM
Catriona M. Harrop, MD, FHM
Hossan Hassan, FAAFP, FHM
Eileen Hennrikus, MD, FHM
Arif Hussain, MD, FHM
Javid Iqbal, MD, FHM
Shadi Jarjous, MD, FHM
Jeremy Jaskunas, MD, FHM
John David Johnston, MD, FHM
Gurmeet Kaur Kalra, MD, FHM
Stephen K. Keiser, FHM
Sirajabid Khatib, MD, FHM
Joanna Kipnes, MD, FHM
Mukesh Kumar, MBBS, MD, FACP, FHM
Rumman A. Langah, MD, FACP, FHM
Rebecca Lauderdale, MD, FHM
Lajide R. Lawoyin, MD, FACP, FHM
Lien Le, MD, FHM
Alex Leung, FHM
William I. Levin, MD, FHM
David Lichtman, PA, FHM
Doris Wei-Hwa Lin, MD, FHM
Caroline E. Lyon, MD, MPH, FHM
John D. Machado, DO, FHM
Yvonne Maduka, MD, FHM
Lawrence L. Magras, MD, MBA, FHM
Anamaria Massier, MD, FHM
Daniel McFarlane, MD, FHM
Tresa A. McNeal, MD, FHM
Johnny Mei, MD, MHA, FACP, FHM
Rovie Mesola, MD, FHM
Henry J. Michtalik, MD, MHS, MPH, FHM
Prateek Mishra, MD, FHM
Adrian M. Mogos, MD, FHM
Wajahath A. Mohsini, MD, FACP, FHM
Ashwin Narasimhan, MD, FACP, FHM
Sivakumar Natanasabapathy, MRCP, FHM
Monica C. Necula, MD, FHM
Naomi Nomizu, MD, FHM
Shervin Nourparvar, MD, FHM
Allan L. Ong, MD, FHM
Pia Ong, MD, FHM
Chike Onyejekwe, MD, FHM
Binu T. Pappachen, MD, FHM
Akash Parashar MD, MBBS, FHM
Hiren B. Parikh, MD, MBA, FHM
Jung Hyun Park, MD, FHM
Shailesh Mansukh Patel, DO, FHM
Frank A. Perry, MD, FHM
Jeffrey W. Petry, MD, MMM, FHM
John R. Pierce Jr., MD, MPH, FHM
Jeffrey Poulos, MD, FHM
Richard N. Pulido, MD, FHM
Charu Puri, MD, FHM
Carolyn Quan, MD, FHM
Saraswathi V. Racherla, MD, FHM
Aisha Rahim, MD, FHM
Edwin Q. Ravano, MD, FHM
Behzad Razavi, MD, FACP, FHM
Erin N. Reis, MD, FHM
Maria Anaizza Aurora Reyna, MD, FHM
Mark Safalow, MD, FHM
Javaid Saleem, MD, MBBS, FHM
Mandeep S. Saluja, MD, FHM
Edward R. Sampt, MD, FHM
Jorge Santibanez, MD, FHM
Anne E. Sayers, MD, FHM
Brian Schroeder, FACHE, MHA, FHM
Scott E. Sears, MD, FACP, FHM
Meghan M. Sebasky, MD, FHM
Patricia L. Seymour, MD, FHM
Neel B. Shah, MB, BCh, FACP, FACMG, FHM
Poonam Sharma, MD, FHM
Umesh Sharma, MD, MS, FACP, FHM
Ashwin B. Shivakumar, MD, MSPH, FHM
Mohammed Fazil Siddiqi, MD, FHM
Sonya Sidhu-Izzo, MD, FHM
Alana E. Sigmund, MD, FHM
Shantnu Singh, MBBS, FHM
Amith Skandhan, MD, FHM
Christopher G. Skinner, MD, FACP, FHM
Dustin T. Smith, MD, FHM
Todd I. Smith, MD, FHM
Jeffrey D. Solomon, MD, FHM
Alberto Enrique Soyano, MD, FHM
Rodney R. Story, MD, FHM
John R. Sullivan, MD, FHM
Joseph G. Surber, DO, FHM
Heather R. Swanson, MD, FHM
Preetham Talari, MD, FHM
Sofia Teferi, MD, FAAP, FHM
Rafael A. Teran, MD, FHM
Abey K. Thomas, MD, FACP, FHM
Anca R. Udrea, MD, FHM
Shawn N. Usery, MD, FHM
Moncy Varughese, MD, FACP, FHM
Leigh Vaughan, MD, FHM
Manivannan Veerasamy, MD, FACP, FHM
Ruvan Chandika Wickramasinghe, MD, FHM
Michael Williams, DO, FHM
Sandra C. Wilson, MD, FACP, MA, FHM
Kareem Z. Yahya, MD, FHM
Deyun Yang, MD, PhD, FACP, FHM
Hector L. Yordan, MD, FHM
Elham A. Yousef, MD, MSc, FHM
Anthony M. Zepeda, MD, FHM
SFHM
Ashfaq Ahmad, MD, MBA, SFHM
Aziz Ansari, DO, SFHM
Anna M. Arroyo Plasencia, MD, SFHM
Andy Arwari, MD, FACP, SFHM
Jonathan G. Bae, MD, SFHM
Ankush K. Bansal, MD, FACP, SFHM
Jitendra Barmecha, MD, MPH, SFHM
Bishara A. Bates, BS, MHA, SFHM
Valerie F. Briones-Pryor, MD, FACP, SFHM
Michael E. Burton, MD, SFHM
Tracy E. Cardin, ACNP-BC, SFHM
Chris Cockerham, MD, SFHM
Timothy J. Crone, MD, SFHM
Debasish Dasgupta, MBBS, MHA, FACP, FACHE, SFHM, CPE, CPHQ
Kapil J. Dave, MD, SFHM
Shaker M. Eid, MD, MBA, SFHM
Howard R. Epstein, MD, SFHM
Christopher M. Frost, MD, SFHM
Timothy M. Gawronski, PA-C, SFHM
Amy S. Giarrusso, MD, SFHM
Jeffrey A. Gindi, MD, SFHM
Jason A. Green, MD, SFHM
Paul William Helgerson, MD, SFHM
Maliha Iqbal, MD, SFHM
James J. Jeffries II, MD, FACP, SFHM
Ian H. Jenkins, MD, SFHM
Scott Kaatz, DO, MSc, FACP, SFHM
Khurram Kamran, MD, SFHM
Anand Kartha, MD, MS, SFHM
Attila Kasza, MD, SFHM
Amy M. Keech, MD, SFHM
William A. Landis, MD, SFHM
Jimmie E. Lewis Jr., MD, MHA, SFHM
James W. Leyhane, MD, SFHM
Michael Lin, MD, SFHM
Julianna Lindsey, MD, SFHM
Madaiah Lokeshwari, MD, SFHM
Laszlo I. Madaras, MD, MPH, SFHM
Murthy V. Madduri, MD, SFHM
Arun V. Mohan, MD, SFHM
David R. Munoz, MD, SFHM
Mark A. Murray, MD, SFHM
Vasantha Natarajan, MD, SFHM
G. Xon Ng, MD, SFHM
Andy Odden, MD, SFHM
Tiffani M. Panek, MA, CLHM, SFHM
Shannon Connor Phillips, MD, MPH, SFHM
Preethi Prakash, MD, FACP, SFHM
Alberto Puig, MD, PhD, SFHM
Rebecca P. Ramirez, MD, SFHM
Allen B. Repp, MD, FACP, MS, SFHM
Scott C. Rissmiller, MD, SFHM
Frank Romero Jr., MD, SFHM
Marcus Lindley Scarbrough, MD, FACP, SFHM
Anneliese M. Schleyer, MD, SFHM
Eric R. Schumacher, DO, SFHM
Noppon Pooh Setji, MD, SFHM
Mohammad R. Shaheed, MD, SFHM
Jeffrey Scott Shapiro, MD, SFHM
Ann Sheehy, MD, MS, SFHM
R. Lucas Shelly, DO, SFHM
Andres F. Soto, MD, SFHM
John R. Stephens, MD, SFHM
Camille N. Upchurch, MD, SFHM
Fernando S. Waldemar, MD, SFHM
Michael D. Wang, MD, SFHM
Charlotta Weaver, MD, SFHM
Andrew White, MD, SFHM
Anthony Williams, MD, MBA, SFHM
MHM
Tina Budnitz, MPH, MHM
Greg Maynard, MD, MHM
Eric Howell, MD, MHM
FHM
Nicole Adler, MD, FHM
Tochukwu Agbata, MD, FHM
Alka Aggarwal, MD, FHM
Gaurav Ahuja, MD, MBBS, FHM
Sameena Akhtar, MD, FHM
Karan Singh S. Alag, MD, MBBS, FHM
Venkata N. Allada, MD, FACP, FHM
Margaret M. Ameyaw, MBChB, FHM
Robert L. Anderson, MD, FHM
Jorge Arboleda, DO, FHM
Michael Aref, MD, PhD, FACP, FHM
Elizabeth M. Arias, MD, FACP, FHM
Amarpreet S. Bains, MD, FHM
Ebrahim Barkoudah, MD, MPH, FACP, FHM
Wanes Barsemian, MD, FHM
Jeffrey T. Bates, MD, FACP, FHM
John F. Bell, MD, MPH, FHM
Kjell Benson, MD, FHM
Azmina Bhaiji, MD, FHM
Sai-Sridhar Boddupalli, MD, FHM
Ani Bodoutchian, MD, MBA, FAAFP, FHM
Tanya M. Boldenow, MD, FHM
Dennis T. Bolger Jr., MD, FHM
Greg D. Bowling, MD, FHM
David A. Bozaan, MD, FHM
Marcia Carbo, MD, FAAP, FHM
Donna Cardoza, MD, FHM
Frank R. Carson Jr., MD, FHM
Kelly Caverzagie, MD, FACP, FHM
Elizabeth A. Cerceo, MD, FACP, FHM
Jeffrey M. Ceresnak, MD, FHM
Romil Chadha, MD, MPH, FACP, FHM
Charles Charman, MD, FHM
Bushra I. Chaudhry, MD, FHM
Justin J. Chow, MD, FHM
Douglas E. Cohen, MD, FHM
John M. Colombo Jr., MD, FHM
Steven Connelly, MD, FACP, FHM
David Corman, MD, FHM
Christopher C. Costa, MD, FHM
William C. Crowe Jr., DNP, ACNP, FNP, MSN, RN, FHM
Ria Dancel, MD, FAAP, FHM
Zubaer Dawlah, MD, FHM
Chandrasekhar R. Dinasarapu, MD, MBBS, MPH, FHM
Vijay Saradhi Dontu, MD, FHM
Oleg Dulkin, MD, FHM
Kevin C. Eaton, PA-C, FHM
Eric Edwards, MD, FHM
Mary E. Fedor, MD, FHM
John W. Fowler Jr., MD, FACP, FHM
Maria G. Frank, MD, FACP, FHM
Yelena Galumyan, MD, FHM
Christopher D. Gamble, MD, FACP, FHM
David J. Goldstein, MD, FHM
Kalpana Gorthi, MD, FHM
Manjula V. Gunawardane, MD, FHM
Craig G. Gunderson, MD, FHM
Theodore J. Haland, MD, FHM
Aaron C. Hamilton, MD, MBA, FHM
Anil Hanuman, DO, FHM
Catriona M. Harrop, MD, FHM
Hossan Hassan, FAAFP, FHM
Eileen Hennrikus, MD, FHM
Arif Hussain, MD, FHM
Javid Iqbal, MD, FHM
Shadi Jarjous, MD, FHM
Jeremy Jaskunas, MD, FHM
John David Johnston, MD, FHM
Gurmeet Kaur Kalra, MD, FHM
Stephen K. Keiser, FHM
Sirajabid Khatib, MD, FHM
Joanna Kipnes, MD, FHM
Mukesh Kumar, MBBS, MD, FACP, FHM
Rumman A. Langah, MD, FACP, FHM
Rebecca Lauderdale, MD, FHM
Lajide R. Lawoyin, MD, FACP, FHM
Lien Le, MD, FHM
Alex Leung, FHM
William I. Levin, MD, FHM
David Lichtman, PA, FHM
Doris Wei-Hwa Lin, MD, FHM
Caroline E. Lyon, MD, MPH, FHM
John D. Machado, DO, FHM
Yvonne Maduka, MD, FHM
Lawrence L. Magras, MD, MBA, FHM
Anamaria Massier, MD, FHM
Daniel McFarlane, MD, FHM
Tresa A. McNeal, MD, FHM
Johnny Mei, MD, MHA, FACP, FHM
Rovie Mesola, MD, FHM
Henry J. Michtalik, MD, MHS, MPH, FHM
Prateek Mishra, MD, FHM
Adrian M. Mogos, MD, FHM
Wajahath A. Mohsini, MD, FACP, FHM
Ashwin Narasimhan, MD, FACP, FHM
Sivakumar Natanasabapathy, MRCP, FHM
Monica C. Necula, MD, FHM
Naomi Nomizu, MD, FHM
Shervin Nourparvar, MD, FHM
Allan L. Ong, MD, FHM
Pia Ong, MD, FHM
Chike Onyejekwe, MD, FHM
Binu T. Pappachen, MD, FHM
Akash Parashar MD, MBBS, FHM
Hiren B. Parikh, MD, MBA, FHM
Jung Hyun Park, MD, FHM
Shailesh Mansukh Patel, DO, FHM
Frank A. Perry, MD, FHM
Jeffrey W. Petry, MD, MMM, FHM
John R. Pierce Jr., MD, MPH, FHM
Jeffrey Poulos, MD, FHM
Richard N. Pulido, MD, FHM
Charu Puri, MD, FHM
Carolyn Quan, MD, FHM
Saraswathi V. Racherla, MD, FHM
Aisha Rahim, MD, FHM
Edwin Q. Ravano, MD, FHM
Behzad Razavi, MD, FACP, FHM
Erin N. Reis, MD, FHM
Maria Anaizza Aurora Reyna, MD, FHM
Mark Safalow, MD, FHM
Javaid Saleem, MD, MBBS, FHM
Mandeep S. Saluja, MD, FHM
Edward R. Sampt, MD, FHM
Jorge Santibanez, MD, FHM
Anne E. Sayers, MD, FHM
Brian Schroeder, FACHE, MHA, FHM
Scott E. Sears, MD, FACP, FHM
Meghan M. Sebasky, MD, FHM
Patricia L. Seymour, MD, FHM
Neel B. Shah, MB, BCh, FACP, FACMG, FHM
Poonam Sharma, MD, FHM
Umesh Sharma, MD, MS, FACP, FHM
Ashwin B. Shivakumar, MD, MSPH, FHM
Mohammed Fazil Siddiqi, MD, FHM
Sonya Sidhu-Izzo, MD, FHM
Alana E. Sigmund, MD, FHM
Shantnu Singh, MBBS, FHM
Amith Skandhan, MD, FHM
Christopher G. Skinner, MD, FACP, FHM
Dustin T. Smith, MD, FHM
Todd I. Smith, MD, FHM
Jeffrey D. Solomon, MD, FHM
Alberto Enrique Soyano, MD, FHM
Rodney R. Story, MD, FHM
John R. Sullivan, MD, FHM
Joseph G. Surber, DO, FHM
Heather R. Swanson, MD, FHM
Preetham Talari, MD, FHM
Sofia Teferi, MD, FAAP, FHM
Rafael A. Teran, MD, FHM
Abey K. Thomas, MD, FACP, FHM
Anca R. Udrea, MD, FHM
Shawn N. Usery, MD, FHM
Moncy Varughese, MD, FACP, FHM
Leigh Vaughan, MD, FHM
Manivannan Veerasamy, MD, FACP, FHM
Ruvan Chandika Wickramasinghe, MD, FHM
Michael Williams, DO, FHM
Sandra C. Wilson, MD, FACP, MA, FHM
Kareem Z. Yahya, MD, FHM
Deyun Yang, MD, PhD, FACP, FHM
Hector L. Yordan, MD, FHM
Elham A. Yousef, MD, MSc, FHM
Anthony M. Zepeda, MD, FHM
SFHM
Ashfaq Ahmad, MD, MBA, SFHM
Aziz Ansari, DO, SFHM
Anna M. Arroyo Plasencia, MD, SFHM
Andy Arwari, MD, FACP, SFHM
Jonathan G. Bae, MD, SFHM
Ankush K. Bansal, MD, FACP, SFHM
Jitendra Barmecha, MD, MPH, SFHM
Bishara A. Bates, BS, MHA, SFHM
Valerie F. Briones-Pryor, MD, FACP, SFHM
Michael E. Burton, MD, SFHM
Tracy E. Cardin, ACNP-BC, SFHM
Chris Cockerham, MD, SFHM
Timothy J. Crone, MD, SFHM
Debasish Dasgupta, MBBS, MHA, FACP, FACHE, SFHM, CPE, CPHQ
Kapil J. Dave, MD, SFHM
Shaker M. Eid, MD, MBA, SFHM
Howard R. Epstein, MD, SFHM
Christopher M. Frost, MD, SFHM
Timothy M. Gawronski, PA-C, SFHM
Amy S. Giarrusso, MD, SFHM
Jeffrey A. Gindi, MD, SFHM
Jason A. Green, MD, SFHM
Paul William Helgerson, MD, SFHM
Maliha Iqbal, MD, SFHM
James J. Jeffries II, MD, FACP, SFHM
Ian H. Jenkins, MD, SFHM
Scott Kaatz, DO, MSc, FACP, SFHM
Khurram Kamran, MD, SFHM
Anand Kartha, MD, MS, SFHM
Attila Kasza, MD, SFHM
Amy M. Keech, MD, SFHM
William A. Landis, MD, SFHM
Jimmie E. Lewis Jr., MD, MHA, SFHM
James W. Leyhane, MD, SFHM
Michael Lin, MD, SFHM
Julianna Lindsey, MD, SFHM
Madaiah Lokeshwari, MD, SFHM
Laszlo I. Madaras, MD, MPH, SFHM
Murthy V. Madduri, MD, SFHM
Arun V. Mohan, MD, SFHM
David R. Munoz, MD, SFHM
Mark A. Murray, MD, SFHM
Vasantha Natarajan, MD, SFHM
G. Xon Ng, MD, SFHM
Andy Odden, MD, SFHM
Tiffani M. Panek, MA, CLHM, SFHM
Shannon Connor Phillips, MD, MPH, SFHM
Preethi Prakash, MD, FACP, SFHM
Alberto Puig, MD, PhD, SFHM
Rebecca P. Ramirez, MD, SFHM
Allen B. Repp, MD, FACP, MS, SFHM
Scott C. Rissmiller, MD, SFHM
Frank Romero Jr., MD, SFHM
Marcus Lindley Scarbrough, MD, FACP, SFHM
Anneliese M. Schleyer, MD, SFHM
Eric R. Schumacher, DO, SFHM
Noppon Pooh Setji, MD, SFHM
Mohammad R. Shaheed, MD, SFHM
Jeffrey Scott Shapiro, MD, SFHM
Ann Sheehy, MD, MS, SFHM
R. Lucas Shelly, DO, SFHM
Andres F. Soto, MD, SFHM
John R. Stephens, MD, SFHM
Camille N. Upchurch, MD, SFHM
Fernando S. Waldemar, MD, SFHM
Michael D. Wang, MD, SFHM
Charlotta Weaver, MD, SFHM
Andrew White, MD, SFHM
Anthony Williams, MD, MBA, SFHM
MHM
Tina Budnitz, MPH, MHM
Greg Maynard, MD, MHM
Eric Howell, MD, MHM
FHM
Nicole Adler, MD, FHM
Tochukwu Agbata, MD, FHM
Alka Aggarwal, MD, FHM
Gaurav Ahuja, MD, MBBS, FHM
Sameena Akhtar, MD, FHM
Karan Singh S. Alag, MD, MBBS, FHM
Venkata N. Allada, MD, FACP, FHM
Margaret M. Ameyaw, MBChB, FHM
Robert L. Anderson, MD, FHM
Jorge Arboleda, DO, FHM
Michael Aref, MD, PhD, FACP, FHM
Elizabeth M. Arias, MD, FACP, FHM
Amarpreet S. Bains, MD, FHM
Ebrahim Barkoudah, MD, MPH, FACP, FHM
Wanes Barsemian, MD, FHM
Jeffrey T. Bates, MD, FACP, FHM
John F. Bell, MD, MPH, FHM
Kjell Benson, MD, FHM
Azmina Bhaiji, MD, FHM
Sai-Sridhar Boddupalli, MD, FHM
Ani Bodoutchian, MD, MBA, FAAFP, FHM
Tanya M. Boldenow, MD, FHM
Dennis T. Bolger Jr., MD, FHM
Greg D. Bowling, MD, FHM
David A. Bozaan, MD, FHM
Marcia Carbo, MD, FAAP, FHM
Donna Cardoza, MD, FHM
Frank R. Carson Jr., MD, FHM
Kelly Caverzagie, MD, FACP, FHM
Elizabeth A. Cerceo, MD, FACP, FHM
Jeffrey M. Ceresnak, MD, FHM
Romil Chadha, MD, MPH, FACP, FHM
Charles Charman, MD, FHM
Bushra I. Chaudhry, MD, FHM
Justin J. Chow, MD, FHM
Douglas E. Cohen, MD, FHM
John M. Colombo Jr., MD, FHM
Steven Connelly, MD, FACP, FHM
David Corman, MD, FHM
Christopher C. Costa, MD, FHM
William C. Crowe Jr., DNP, ACNP, FNP, MSN, RN, FHM
Ria Dancel, MD, FAAP, FHM
Zubaer Dawlah, MD, FHM
Chandrasekhar R. Dinasarapu, MD, MBBS, MPH, FHM
Vijay Saradhi Dontu, MD, FHM
Oleg Dulkin, MD, FHM
Kevin C. Eaton, PA-C, FHM
Eric Edwards, MD, FHM
Mary E. Fedor, MD, FHM
John W. Fowler Jr., MD, FACP, FHM
Maria G. Frank, MD, FACP, FHM
Yelena Galumyan, MD, FHM
Christopher D. Gamble, MD, FACP, FHM
David J. Goldstein, MD, FHM
Kalpana Gorthi, MD, FHM
Manjula V. Gunawardane, MD, FHM
Craig G. Gunderson, MD, FHM
Theodore J. Haland, MD, FHM
Aaron C. Hamilton, MD, MBA, FHM
Anil Hanuman, DO, FHM
Catriona M. Harrop, MD, FHM
Hossan Hassan, FAAFP, FHM
Eileen Hennrikus, MD, FHM
Arif Hussain, MD, FHM
Javid Iqbal, MD, FHM
Shadi Jarjous, MD, FHM
Jeremy Jaskunas, MD, FHM
John David Johnston, MD, FHM
Gurmeet Kaur Kalra, MD, FHM
Stephen K. Keiser, FHM
Sirajabid Khatib, MD, FHM
Joanna Kipnes, MD, FHM
Mukesh Kumar, MBBS, MD, FACP, FHM
Rumman A. Langah, MD, FACP, FHM
Rebecca Lauderdale, MD, FHM
Lajide R. Lawoyin, MD, FACP, FHM
Lien Le, MD, FHM
Alex Leung, FHM
William I. Levin, MD, FHM
David Lichtman, PA, FHM
Doris Wei-Hwa Lin, MD, FHM
Caroline E. Lyon, MD, MPH, FHM
John D. Machado, DO, FHM
Yvonne Maduka, MD, FHM
Lawrence L. Magras, MD, MBA, FHM
Anamaria Massier, MD, FHM
Daniel McFarlane, MD, FHM
Tresa A. McNeal, MD, FHM
Johnny Mei, MD, MHA, FACP, FHM
Rovie Mesola, MD, FHM
Henry J. Michtalik, MD, MHS, MPH, FHM
Prateek Mishra, MD, FHM
Adrian M. Mogos, MD, FHM
Wajahath A. Mohsini, MD, FACP, FHM
Ashwin Narasimhan, MD, FACP, FHM
Sivakumar Natanasabapathy, MRCP, FHM
Monica C. Necula, MD, FHM
Naomi Nomizu, MD, FHM
Shervin Nourparvar, MD, FHM
Allan L. Ong, MD, FHM
Pia Ong, MD, FHM
Chike Onyejekwe, MD, FHM
Binu T. Pappachen, MD, FHM
Akash Parashar MD, MBBS, FHM
Hiren B. Parikh, MD, MBA, FHM
Jung Hyun Park, MD, FHM
Shailesh Mansukh Patel, DO, FHM
Frank A. Perry, MD, FHM
Jeffrey W. Petry, MD, MMM, FHM
John R. Pierce Jr., MD, MPH, FHM
Jeffrey Poulos, MD, FHM
Richard N. Pulido, MD, FHM
Charu Puri, MD, FHM
Carolyn Quan, MD, FHM
Saraswathi V. Racherla, MD, FHM
Aisha Rahim, MD, FHM
Edwin Q. Ravano, MD, FHM
Behzad Razavi, MD, FACP, FHM
Erin N. Reis, MD, FHM
Maria Anaizza Aurora Reyna, MD, FHM
Mark Safalow, MD, FHM
Javaid Saleem, MD, MBBS, FHM
Mandeep S. Saluja, MD, FHM
Edward R. Sampt, MD, FHM
Jorge Santibanez, MD, FHM
Anne E. Sayers, MD, FHM
Brian Schroeder, FACHE, MHA, FHM
Scott E. Sears, MD, FACP, FHM
Meghan M. Sebasky, MD, FHM
Patricia L. Seymour, MD, FHM
Neel B. Shah, MB, BCh, FACP, FACMG, FHM
Poonam Sharma, MD, FHM
Umesh Sharma, MD, MS, FACP, FHM
Ashwin B. Shivakumar, MD, MSPH, FHM
Mohammed Fazil Siddiqi, MD, FHM
Sonya Sidhu-Izzo, MD, FHM
Alana E. Sigmund, MD, FHM
Shantnu Singh, MBBS, FHM
Amith Skandhan, MD, FHM
Christopher G. Skinner, MD, FACP, FHM
Dustin T. Smith, MD, FHM
Todd I. Smith, MD, FHM
Jeffrey D. Solomon, MD, FHM
Alberto Enrique Soyano, MD, FHM
Rodney R. Story, MD, FHM
John R. Sullivan, MD, FHM
Joseph G. Surber, DO, FHM
Heather R. Swanson, MD, FHM
Preetham Talari, MD, FHM
Sofia Teferi, MD, FAAP, FHM
Rafael A. Teran, MD, FHM
Abey K. Thomas, MD, FACP, FHM
Anca R. Udrea, MD, FHM
Shawn N. Usery, MD, FHM
Moncy Varughese, MD, FACP, FHM
Leigh Vaughan, MD, FHM
Manivannan Veerasamy, MD, FACP, FHM
Ruvan Chandika Wickramasinghe, MD, FHM
Michael Williams, DO, FHM
Sandra C. Wilson, MD, FACP, MA, FHM
Kareem Z. Yahya, MD, FHM
Deyun Yang, MD, PhD, FACP, FHM
Hector L. Yordan, MD, FHM
Elham A. Yousef, MD, MSc, FHM
Anthony M. Zepeda, MD, FHM
SFHM
Ashfaq Ahmad, MD, MBA, SFHM
Aziz Ansari, DO, SFHM
Anna M. Arroyo Plasencia, MD, SFHM
Andy Arwari, MD, FACP, SFHM
Jonathan G. Bae, MD, SFHM
Ankush K. Bansal, MD, FACP, SFHM
Jitendra Barmecha, MD, MPH, SFHM
Bishara A. Bates, BS, MHA, SFHM
Valerie F. Briones-Pryor, MD, FACP, SFHM
Michael E. Burton, MD, SFHM
Tracy E. Cardin, ACNP-BC, SFHM
Chris Cockerham, MD, SFHM
Timothy J. Crone, MD, SFHM
Debasish Dasgupta, MBBS, MHA, FACP, FACHE, SFHM, CPE, CPHQ
Kapil J. Dave, MD, SFHM
Shaker M. Eid, MD, MBA, SFHM
Howard R. Epstein, MD, SFHM
Christopher M. Frost, MD, SFHM
Timothy M. Gawronski, PA-C, SFHM
Amy S. Giarrusso, MD, SFHM
Jeffrey A. Gindi, MD, SFHM
Jason A. Green, MD, SFHM
Paul William Helgerson, MD, SFHM
Maliha Iqbal, MD, SFHM
James J. Jeffries II, MD, FACP, SFHM
Ian H. Jenkins, MD, SFHM
Scott Kaatz, DO, MSc, FACP, SFHM
Khurram Kamran, MD, SFHM
Anand Kartha, MD, MS, SFHM
Attila Kasza, MD, SFHM
Amy M. Keech, MD, SFHM
William A. Landis, MD, SFHM
Jimmie E. Lewis Jr., MD, MHA, SFHM
James W. Leyhane, MD, SFHM
Michael Lin, MD, SFHM
Julianna Lindsey, MD, SFHM
Madaiah Lokeshwari, MD, SFHM
Laszlo I. Madaras, MD, MPH, SFHM
Murthy V. Madduri, MD, SFHM
Arun V. Mohan, MD, SFHM
David R. Munoz, MD, SFHM
Mark A. Murray, MD, SFHM
Vasantha Natarajan, MD, SFHM
G. Xon Ng, MD, SFHM
Andy Odden, MD, SFHM
Tiffani M. Panek, MA, CLHM, SFHM
Shannon Connor Phillips, MD, MPH, SFHM
Preethi Prakash, MD, FACP, SFHM
Alberto Puig, MD, PhD, SFHM
Rebecca P. Ramirez, MD, SFHM
Allen B. Repp, MD, FACP, MS, SFHM
Scott C. Rissmiller, MD, SFHM
Frank Romero Jr., MD, SFHM
Marcus Lindley Scarbrough, MD, FACP, SFHM
Anneliese M. Schleyer, MD, SFHM
Eric R. Schumacher, DO, SFHM
Noppon Pooh Setji, MD, SFHM
Mohammad R. Shaheed, MD, SFHM
Jeffrey Scott Shapiro, MD, SFHM
Ann Sheehy, MD, MS, SFHM
R. Lucas Shelly, DO, SFHM
Andres F. Soto, MD, SFHM
John R. Stephens, MD, SFHM
Camille N. Upchurch, MD, SFHM
Fernando S. Waldemar, MD, SFHM
Michael D. Wang, MD, SFHM
Charlotta Weaver, MD, SFHM
Andrew White, MD, SFHM
Anthony Williams, MD, MBA, SFHM
EC grants gene therapy orphan designation for hemophilia A
The European Commission (EC) has granted orphan designation to BMN 270, an investigational gene therapy, for the treatment of patients with hemophilia A.
BMN 270 is an adeno-associated virus-factor VIII (FVIII) vector designed to restore FVIII plasma concentrations in these patients.
The EC grants orphan designation to products intended to treat, prevent, or diagnose a life-threatening condition affecting up to 5 in 10,000 people in the European Union.
The product must provide significant benefit to those affected by the condition.
Orphan designation from the EC provides companies with certain development incentives, including protocol assistance, a type of scientific advice specific for orphan drugs, and 10 years of market exclusivity once the drug is approved for use.
BMN 270 is under development by BioMarin Pharmaceutical Inc.
BioMarin is conducting a phase 1/2 study to evaluate the safety and efficacy of BMN 270 in up to 12 patients with severe hemophilia A.
Researchers are assessing the safety of a single infusion of BMN 270 and the change in FVIII expression level from baseline to 16 weeks after infusion.
The group is also assessing the impact of BMN 270 on the frequency of FVIII replacement therapy, the number of bleeding episodes requiring treatment, and any potential immune responses.
Patients will be monitored for safety and durability of effect for 5 years. BioMarin plans to provide an update on this trial in April.
BMN 270 also has orphan designation in the US.
The European Commission (EC) has granted orphan designation to BMN 270, an investigational gene therapy, for the treatment of patients with hemophilia A.
BMN 270 is an adeno-associated virus-factor VIII (FVIII) vector designed to restore FVIII plasma concentrations in these patients.
The EC grants orphan designation to products intended to treat, prevent, or diagnose a life-threatening condition affecting up to 5 in 10,000 people in the European Union.
The product must provide significant benefit to those affected by the condition.
Orphan designation from the EC provides companies with certain development incentives, including protocol assistance, a type of scientific advice specific for orphan drugs, and 10 years of market exclusivity once the drug is approved for use.
BMN 270 is under development by BioMarin Pharmaceutical Inc.
BioMarin is conducting a phase 1/2 study to evaluate the safety and efficacy of BMN 270 in up to 12 patients with severe hemophilia A.
Researchers are assessing the safety of a single infusion of BMN 270 and the change in FVIII expression level from baseline to 16 weeks after infusion.
The group is also assessing the impact of BMN 270 on the frequency of FVIII replacement therapy, the number of bleeding episodes requiring treatment, and any potential immune responses.
Patients will be monitored for safety and durability of effect for 5 years. BioMarin plans to provide an update on this trial in April.
BMN 270 also has orphan designation in the US.
The European Commission (EC) has granted orphan designation to BMN 270, an investigational gene therapy, for the treatment of patients with hemophilia A.
BMN 270 is an adeno-associated virus-factor VIII (FVIII) vector designed to restore FVIII plasma concentrations in these patients.
The EC grants orphan designation to products intended to treat, prevent, or diagnose a life-threatening condition affecting up to 5 in 10,000 people in the European Union.
The product must provide significant benefit to those affected by the condition.
Orphan designation from the EC provides companies with certain development incentives, including protocol assistance, a type of scientific advice specific for orphan drugs, and 10 years of market exclusivity once the drug is approved for use.
BMN 270 is under development by BioMarin Pharmaceutical Inc.
BioMarin is conducting a phase 1/2 study to evaluate the safety and efficacy of BMN 270 in up to 12 patients with severe hemophilia A.
Researchers are assessing the safety of a single infusion of BMN 270 and the change in FVIII expression level from baseline to 16 weeks after infusion.
The group is also assessing the impact of BMN 270 on the frequency of FVIII replacement therapy, the number of bleeding episodes requiring treatment, and any potential immune responses.
Patients will be monitored for safety and durability of effect for 5 years. BioMarin plans to provide an update on this trial in April.
BMN 270 also has orphan designation in the US.
HM16 Speakers, Attendees Focus on Training, Advancement, Work-Life Balance
SAN DIEGO — If you arrived late, or even right on time, to the session on becoming a better attending, you’d better have been ready to find a clear spot on the floor or have had the energy to stand for an hour.
Read more about the speakers at HM16.
But the dynamic talk, you could even say performance, by Jeffrey Wiese, MD, MHM, crackled with energy, so there was plenty of it to go around. The session, in its 10th year and now practically an institution of its own at the annual meeting, was a highlight among the offerings on career development at HM16.
Dr. Wiese liberally seasoned the session with role-playing and humor—the “patient” on the session-room floor but without a pillow meant “Press Ganey’s going to take a hit on this one,” he joked. He emphasized the importance of attending physicians to give reasons to support the expectations they have for their trainees.
“The key piece is giving that rationale. Once they have a reason for why they’re going to do it, now the expectation’s grounded, now it actually makes sense,” said Dr. Wiese, professor of medicine at Tulane University Health Sciences Center in New Orleans and a past SHM president. “You don’t do that, they’re going to fill in the gaps with their own expectations.”
Other points of emphasis:
- The importance of autonomy and choice so that trainees have a sense of purpose;
- The transition from self-interested medical students to residents who are concerned with the well-being of team members;
- The assurance of an endpoint so that hectic periods don’t spiral out of control; and
- Acts of ritual, such as using Purell before entering a patient’s room, as moments of “genuflect” to regain perspective.
Charles Kast, MD, an attending physician at Long Island Jewish Medical Center in New Hyde Park, N.Y., said the relationship theme resonated with him the most.
“It’s more the relationships the attendings have with their residents and with their students, and it’s more of an emotional connection,” he said. “Whether it’s education or mentoring or what have you, it’s all about developing that trust between the resident and the attending.”
But it’s a gradual process.
“It’s baby steps,” Dr. Kast added. “There were 17 different lists in there, right? So you’ve got to pick one and kind of go with it. I think it’s kind of an organic process, where one thing kind of leads to the next.”
Tactics to avoid burnout—by cultivating a sense of purpose while understanding and relating to trainees’ concerns—were a key part of Dr. Wiese’s message. Burnout was a topic that HM16 attendees returned to again and again when discussing their take-homes from the meeting. The subject popped up in almost every session to one degree or another.
David Nevin, MD, a hospitalist at ThedaCare in Wisconsin, said that he was reminded in one session—“Staying in the Game: Self-Care for Hospitalists”—that taking even brief moments for yourself can make a difference.
“Focusing on the positive for a moment and what’s good about your life, and doing that kind of exercise, helps sort of deal with burnout and bring things into perspective,” he said. “You get sort of worn down, you’re not as sharp, you miss things when you’re not at your peak in terms of looking at things.”
Ariana Peters, DO, who works at Mayo Clinic in Scottsdale, Ariz., said a similar message resonated with her, as well. There are ample situations when, if she doesn’t consciously take time for herself, things will seem to mushroom.
In just one recent example, she reflected on an especially difficult day.
“I had 18 patients, and it was horrible,” she said. “I left my office in the morning and didn’t come back until 8 p.m. that night. I was literally eating peanut butter and graham crackers on the floor.
“It doesn’t take long to just stop and take a breath. Twenty seconds is not a long time.”
Waiting for a session on personal productivity to start, Adam Garber, MD, assistant professor at Virginia Commonwealth University in Richmond, said that he found the introduction to the SMART approach (Specific, Measurable, Achievable, Relevant, and Time-Bound), meaning being able to be done within a certain period, was a good guideline to approaching projects of all kinds.
“I think you can apply it to any problem and career-development project you want to work on,” he said. “It just kind of gives you that framework of how to organize it, present it logically, and carry it out.” TH
SAN DIEGO — If you arrived late, or even right on time, to the session on becoming a better attending, you’d better have been ready to find a clear spot on the floor or have had the energy to stand for an hour.
Read more about the speakers at HM16.
But the dynamic talk, you could even say performance, by Jeffrey Wiese, MD, MHM, crackled with energy, so there was plenty of it to go around. The session, in its 10th year and now practically an institution of its own at the annual meeting, was a highlight among the offerings on career development at HM16.
Dr. Wiese liberally seasoned the session with role-playing and humor—the “patient” on the session-room floor but without a pillow meant “Press Ganey’s going to take a hit on this one,” he joked. He emphasized the importance of attending physicians to give reasons to support the expectations they have for their trainees.
“The key piece is giving that rationale. Once they have a reason for why they’re going to do it, now the expectation’s grounded, now it actually makes sense,” said Dr. Wiese, professor of medicine at Tulane University Health Sciences Center in New Orleans and a past SHM president. “You don’t do that, they’re going to fill in the gaps with their own expectations.”
Other points of emphasis:
- The importance of autonomy and choice so that trainees have a sense of purpose;
- The transition from self-interested medical students to residents who are concerned with the well-being of team members;
- The assurance of an endpoint so that hectic periods don’t spiral out of control; and
- Acts of ritual, such as using Purell before entering a patient’s room, as moments of “genuflect” to regain perspective.
Charles Kast, MD, an attending physician at Long Island Jewish Medical Center in New Hyde Park, N.Y., said the relationship theme resonated with him the most.
“It’s more the relationships the attendings have with their residents and with their students, and it’s more of an emotional connection,” he said. “Whether it’s education or mentoring or what have you, it’s all about developing that trust between the resident and the attending.”
But it’s a gradual process.
“It’s baby steps,” Dr. Kast added. “There were 17 different lists in there, right? So you’ve got to pick one and kind of go with it. I think it’s kind of an organic process, where one thing kind of leads to the next.”
Tactics to avoid burnout—by cultivating a sense of purpose while understanding and relating to trainees’ concerns—were a key part of Dr. Wiese’s message. Burnout was a topic that HM16 attendees returned to again and again when discussing their take-homes from the meeting. The subject popped up in almost every session to one degree or another.
David Nevin, MD, a hospitalist at ThedaCare in Wisconsin, said that he was reminded in one session—“Staying in the Game: Self-Care for Hospitalists”—that taking even brief moments for yourself can make a difference.
“Focusing on the positive for a moment and what’s good about your life, and doing that kind of exercise, helps sort of deal with burnout and bring things into perspective,” he said. “You get sort of worn down, you’re not as sharp, you miss things when you’re not at your peak in terms of looking at things.”
Ariana Peters, DO, who works at Mayo Clinic in Scottsdale, Ariz., said a similar message resonated with her, as well. There are ample situations when, if she doesn’t consciously take time for herself, things will seem to mushroom.
In just one recent example, she reflected on an especially difficult day.
“I had 18 patients, and it was horrible,” she said. “I left my office in the morning and didn’t come back until 8 p.m. that night. I was literally eating peanut butter and graham crackers on the floor.
“It doesn’t take long to just stop and take a breath. Twenty seconds is not a long time.”
Waiting for a session on personal productivity to start, Adam Garber, MD, assistant professor at Virginia Commonwealth University in Richmond, said that he found the introduction to the SMART approach (Specific, Measurable, Achievable, Relevant, and Time-Bound), meaning being able to be done within a certain period, was a good guideline to approaching projects of all kinds.
“I think you can apply it to any problem and career-development project you want to work on,” he said. “It just kind of gives you that framework of how to organize it, present it logically, and carry it out.” TH
SAN DIEGO — If you arrived late, or even right on time, to the session on becoming a better attending, you’d better have been ready to find a clear spot on the floor or have had the energy to stand for an hour.
Read more about the speakers at HM16.
But the dynamic talk, you could even say performance, by Jeffrey Wiese, MD, MHM, crackled with energy, so there was plenty of it to go around. The session, in its 10th year and now practically an institution of its own at the annual meeting, was a highlight among the offerings on career development at HM16.
Dr. Wiese liberally seasoned the session with role-playing and humor—the “patient” on the session-room floor but without a pillow meant “Press Ganey’s going to take a hit on this one,” he joked. He emphasized the importance of attending physicians to give reasons to support the expectations they have for their trainees.
“The key piece is giving that rationale. Once they have a reason for why they’re going to do it, now the expectation’s grounded, now it actually makes sense,” said Dr. Wiese, professor of medicine at Tulane University Health Sciences Center in New Orleans and a past SHM president. “You don’t do that, they’re going to fill in the gaps with their own expectations.”
Other points of emphasis:
- The importance of autonomy and choice so that trainees have a sense of purpose;
- The transition from self-interested medical students to residents who are concerned with the well-being of team members;
- The assurance of an endpoint so that hectic periods don’t spiral out of control; and
- Acts of ritual, such as using Purell before entering a patient’s room, as moments of “genuflect” to regain perspective.
Charles Kast, MD, an attending physician at Long Island Jewish Medical Center in New Hyde Park, N.Y., said the relationship theme resonated with him the most.
“It’s more the relationships the attendings have with their residents and with their students, and it’s more of an emotional connection,” he said. “Whether it’s education or mentoring or what have you, it’s all about developing that trust between the resident and the attending.”
But it’s a gradual process.
“It’s baby steps,” Dr. Kast added. “There were 17 different lists in there, right? So you’ve got to pick one and kind of go with it. I think it’s kind of an organic process, where one thing kind of leads to the next.”
Tactics to avoid burnout—by cultivating a sense of purpose while understanding and relating to trainees’ concerns—were a key part of Dr. Wiese’s message. Burnout was a topic that HM16 attendees returned to again and again when discussing their take-homes from the meeting. The subject popped up in almost every session to one degree or another.
David Nevin, MD, a hospitalist at ThedaCare in Wisconsin, said that he was reminded in one session—“Staying in the Game: Self-Care for Hospitalists”—that taking even brief moments for yourself can make a difference.
“Focusing on the positive for a moment and what’s good about your life, and doing that kind of exercise, helps sort of deal with burnout and bring things into perspective,” he said. “You get sort of worn down, you’re not as sharp, you miss things when you’re not at your peak in terms of looking at things.”
Ariana Peters, DO, who works at Mayo Clinic in Scottsdale, Ariz., said a similar message resonated with her, as well. There are ample situations when, if she doesn’t consciously take time for herself, things will seem to mushroom.
In just one recent example, she reflected on an especially difficult day.
“I had 18 patients, and it was horrible,” she said. “I left my office in the morning and didn’t come back until 8 p.m. that night. I was literally eating peanut butter and graham crackers on the floor.
“It doesn’t take long to just stop and take a breath. Twenty seconds is not a long time.”
Waiting for a session on personal productivity to start, Adam Garber, MD, assistant professor at Virginia Commonwealth University in Richmond, said that he found the introduction to the SMART approach (Specific, Measurable, Achievable, Relevant, and Time-Bound), meaning being able to be done within a certain period, was a good guideline to approaching projects of all kinds.
“I think you can apply it to any problem and career-development project you want to work on,” he said. “It just kind of gives you that framework of how to organize it, present it logically, and carry it out.” TH
Drug exhibits preclinical activity against MDS
Researchers have found the fusion protein APG101 can rescue erythropoiesis in bone marrow samples from patients with lower-risk myelodysplastic syndromes (MDS).
Previous research suggested that CD95—a receptor that can induce apoptosis when triggered by the CD95 ligand—is overexpressed in two-thirds of patients with lower-risk MDS, and overexpression of CD95 is predictive of a lower response to erythropoiesis-stimulating agents (ESAs).
APG101, which consists of the extracellular domain of the CD95 receptor and the Fc domain of an IgG antibody, is designed to block the CD95 ligand.
The new study showed that APG101 can inhibit apoptosis in erythrocyte precursor cells and improve their overall proliferation rate. The drug increased the number of burst-forming unit-erythroid (BFU-E) progenitors in samples from MDS patients with low BFU-E numbers at baseline.
“APG101 added to cellular assays efficiently rescued the growth of erythroid progenitors in MDS patients harboring a profound defect of erythropoiesis, independent of the expression level of CD95 or CD95 ligand,” said Michaela Fontenay, MD, PhD, of the Institut Cochin in Paris, France.
Dr Fontenay and her colleagues described these results in Oncotarget. The research was funded by Apogenix, the company developing APG101.
By comparing bone marrow samples from MDS patients and healthy control subjects, the researchers found that CD95, but not CD95 ligand, was overexpressed in patients with lower-risk MDS.
Further analysis revealed that a patient’s CD95 expression level at diagnosis could predict response to an ESA. Specifically, CD95 overexpression was predictive of a lower response rate to ESAs in patients with low- or intermediate-1-risk MDS.
Next, the researchers tested bone marrow erythroid progenitors from 3 control subjects and 5 patients with MDS and found that CD95 expression increased during MDS erythroid progenitor amplification but remained lower in control cultures.
On day 5 of culture, the mean number of BFU-Es was significantly lower in MDS patient samples than in controls. And treatment with APG101 prompted a dose-dependent increase in BFU-E growth in MDS samples but not in controls.
When the researchers added APG101 (at 10 μg/mL) to the cultures over 7 days, they observed an improvement in the proliferation of erythroblasts but no significant effect on the kinetics of differentiation.
They also found that APG101 reduced apoptosis in immature precursors by 30% but had no effect on apoptosis in mature precursors.
Baseline BFU-E number affects response
The researchers then assessed the effects of APG101 in samples from 5 control subjects and 20 MDS patients with varying responses to ESAs and varying baseline levels of BFU-Es.
Fifteen of the MDS patients had a significantly lower number of baseline BFU-Es than controls (P=0.005), but 5 MDS patients had a mean number of BFU-Es that was comparable to controls (P=0.429). There was no significant difference in WHO classification or CD95 expression between the 2 groups of MDS patients (P=0.612).
However, 11 of the 15 patients with low erythropoiesis had received an ESA, and all of them were resistant to this treatment. In all, 15 of the MDS patients had received an ESA, and 14 were resistant to it (6 primary and 8 secondary).
The researchers found that APG101 induced a dose-dependent increase of BFU-Es in samples from the 15 MDS patients with low erythropoiesis but not in samples from the 5 patients with normal erythropoiesis or in the control samples (P<0.001).
The team said that a low BFU-E number at baseline was significantly associated with in vitro response to APG101 among the 20 MDS patients (P=0.031) and the 14 ESA-resistant patients (P=0.027).
Further investigation confirmed that a low clonogenic progenitor number at baseline, but not the level of CD95 or CD95 ligand expression, was predictive of the response to APG101.
“This study provides a rationale for further clinical investigation of this potential new therapeutic option in patients with severely impaired erythropoiesis who are resistant to erythropoiesis-stimulating agents,” Dr Fontenay said.
Apogenix has conducted a phase 1 trial of APG101 in transfusion-dependent patients with low- to intermediate-1-risk MDS. The company expects the results of this trial will be available in the coming months.
Researchers have found the fusion protein APG101 can rescue erythropoiesis in bone marrow samples from patients with lower-risk myelodysplastic syndromes (MDS).
Previous research suggested that CD95—a receptor that can induce apoptosis when triggered by the CD95 ligand—is overexpressed in two-thirds of patients with lower-risk MDS, and overexpression of CD95 is predictive of a lower response to erythropoiesis-stimulating agents (ESAs).
APG101, which consists of the extracellular domain of the CD95 receptor and the Fc domain of an IgG antibody, is designed to block the CD95 ligand.
The new study showed that APG101 can inhibit apoptosis in erythrocyte precursor cells and improve their overall proliferation rate. The drug increased the number of burst-forming unit-erythroid (BFU-E) progenitors in samples from MDS patients with low BFU-E numbers at baseline.
“APG101 added to cellular assays efficiently rescued the growth of erythroid progenitors in MDS patients harboring a profound defect of erythropoiesis, independent of the expression level of CD95 or CD95 ligand,” said Michaela Fontenay, MD, PhD, of the Institut Cochin in Paris, France.
Dr Fontenay and her colleagues described these results in Oncotarget. The research was funded by Apogenix, the company developing APG101.
By comparing bone marrow samples from MDS patients and healthy control subjects, the researchers found that CD95, but not CD95 ligand, was overexpressed in patients with lower-risk MDS.
Further analysis revealed that a patient’s CD95 expression level at diagnosis could predict response to an ESA. Specifically, CD95 overexpression was predictive of a lower response rate to ESAs in patients with low- or intermediate-1-risk MDS.
Next, the researchers tested bone marrow erythroid progenitors from 3 control subjects and 5 patients with MDS and found that CD95 expression increased during MDS erythroid progenitor amplification but remained lower in control cultures.
On day 5 of culture, the mean number of BFU-Es was significantly lower in MDS patient samples than in controls. And treatment with APG101 prompted a dose-dependent increase in BFU-E growth in MDS samples but not in controls.
When the researchers added APG101 (at 10 μg/mL) to the cultures over 7 days, they observed an improvement in the proliferation of erythroblasts but no significant effect on the kinetics of differentiation.
They also found that APG101 reduced apoptosis in immature precursors by 30% but had no effect on apoptosis in mature precursors.
Baseline BFU-E number affects response
The researchers then assessed the effects of APG101 in samples from 5 control subjects and 20 MDS patients with varying responses to ESAs and varying baseline levels of BFU-Es.
Fifteen of the MDS patients had a significantly lower number of baseline BFU-Es than controls (P=0.005), but 5 MDS patients had a mean number of BFU-Es that was comparable to controls (P=0.429). There was no significant difference in WHO classification or CD95 expression between the 2 groups of MDS patients (P=0.612).
However, 11 of the 15 patients with low erythropoiesis had received an ESA, and all of them were resistant to this treatment. In all, 15 of the MDS patients had received an ESA, and 14 were resistant to it (6 primary and 8 secondary).
The researchers found that APG101 induced a dose-dependent increase of BFU-Es in samples from the 15 MDS patients with low erythropoiesis but not in samples from the 5 patients with normal erythropoiesis or in the control samples (P<0.001).
The team said that a low BFU-E number at baseline was significantly associated with in vitro response to APG101 among the 20 MDS patients (P=0.031) and the 14 ESA-resistant patients (P=0.027).
Further investigation confirmed that a low clonogenic progenitor number at baseline, but not the level of CD95 or CD95 ligand expression, was predictive of the response to APG101.
“This study provides a rationale for further clinical investigation of this potential new therapeutic option in patients with severely impaired erythropoiesis who are resistant to erythropoiesis-stimulating agents,” Dr Fontenay said.
Apogenix has conducted a phase 1 trial of APG101 in transfusion-dependent patients with low- to intermediate-1-risk MDS. The company expects the results of this trial will be available in the coming months.
Researchers have found the fusion protein APG101 can rescue erythropoiesis in bone marrow samples from patients with lower-risk myelodysplastic syndromes (MDS).
Previous research suggested that CD95—a receptor that can induce apoptosis when triggered by the CD95 ligand—is overexpressed in two-thirds of patients with lower-risk MDS, and overexpression of CD95 is predictive of a lower response to erythropoiesis-stimulating agents (ESAs).
APG101, which consists of the extracellular domain of the CD95 receptor and the Fc domain of an IgG antibody, is designed to block the CD95 ligand.
The new study showed that APG101 can inhibit apoptosis in erythrocyte precursor cells and improve their overall proliferation rate. The drug increased the number of burst-forming unit-erythroid (BFU-E) progenitors in samples from MDS patients with low BFU-E numbers at baseline.
“APG101 added to cellular assays efficiently rescued the growth of erythroid progenitors in MDS patients harboring a profound defect of erythropoiesis, independent of the expression level of CD95 or CD95 ligand,” said Michaela Fontenay, MD, PhD, of the Institut Cochin in Paris, France.
Dr Fontenay and her colleagues described these results in Oncotarget. The research was funded by Apogenix, the company developing APG101.
By comparing bone marrow samples from MDS patients and healthy control subjects, the researchers found that CD95, but not CD95 ligand, was overexpressed in patients with lower-risk MDS.
Further analysis revealed that a patient’s CD95 expression level at diagnosis could predict response to an ESA. Specifically, CD95 overexpression was predictive of a lower response rate to ESAs in patients with low- or intermediate-1-risk MDS.
Next, the researchers tested bone marrow erythroid progenitors from 3 control subjects and 5 patients with MDS and found that CD95 expression increased during MDS erythroid progenitor amplification but remained lower in control cultures.
On day 5 of culture, the mean number of BFU-Es was significantly lower in MDS patient samples than in controls. And treatment with APG101 prompted a dose-dependent increase in BFU-E growth in MDS samples but not in controls.
When the researchers added APG101 (at 10 μg/mL) to the cultures over 7 days, they observed an improvement in the proliferation of erythroblasts but no significant effect on the kinetics of differentiation.
They also found that APG101 reduced apoptosis in immature precursors by 30% but had no effect on apoptosis in mature precursors.
Baseline BFU-E number affects response
The researchers then assessed the effects of APG101 in samples from 5 control subjects and 20 MDS patients with varying responses to ESAs and varying baseline levels of BFU-Es.
Fifteen of the MDS patients had a significantly lower number of baseline BFU-Es than controls (P=0.005), but 5 MDS patients had a mean number of BFU-Es that was comparable to controls (P=0.429). There was no significant difference in WHO classification or CD95 expression between the 2 groups of MDS patients (P=0.612).
However, 11 of the 15 patients with low erythropoiesis had received an ESA, and all of them were resistant to this treatment. In all, 15 of the MDS patients had received an ESA, and 14 were resistant to it (6 primary and 8 secondary).
The researchers found that APG101 induced a dose-dependent increase of BFU-Es in samples from the 15 MDS patients with low erythropoiesis but not in samples from the 5 patients with normal erythropoiesis or in the control samples (P<0.001).
The team said that a low BFU-E number at baseline was significantly associated with in vitro response to APG101 among the 20 MDS patients (P=0.031) and the 14 ESA-resistant patients (P=0.027).
Further investigation confirmed that a low clonogenic progenitor number at baseline, but not the level of CD95 or CD95 ligand expression, was predictive of the response to APG101.
“This study provides a rationale for further clinical investigation of this potential new therapeutic option in patients with severely impaired erythropoiesis who are resistant to erythropoiesis-stimulating agents,” Dr Fontenay said.
Apogenix has conducted a phase 1 trial of APG101 in transfusion-dependent patients with low- to intermediate-1-risk MDS. The company expects the results of this trial will be available in the coming months.
CDC updates advice on preventing sexual transmission of Zika virus
Men potentially exposed to Zika virus should use a condom during all sex or abstain from sex for at least 8 weeks, according to new recommendations from the Centers for Disease Control and Prevention on reducing the risk of sexual transmission of the virus.
Men with confirmed infections or clinical symptoms of Zika should similarly abstain or use a condom for at least 6 months, the CDC recommends in the Morbidity and Mortality Weekly Report released on March 25 (MMWR 2016. Mar 25. doi: http://dx.doi.org/10.15585/mmwr.mm6512e3er).
These recommendations update and replace those issued by the CDC on Feb. 5 and include new guidance for men who live in, or have traveled to, an area with active Zika virus transmission. The recommendations apply to all types of sexual activity involving the penis, including vaginal intercourse, anal intercourse, or fellatio.
“The previous recommendations focused on women who were already pregnant,” Dr. Denise J. Jamieson, co-lead of the Pregnancy and Birth Defects Team of the CDC Zika Virus Response Team, said during a press briefing. “What’s new is that we are now concerned about the periconceptional period, around the time the woman conceives.”
For men with pregnant sex partners, the agency recommends consistent and accurate use of condoms during any type of sex, or abstinence during the length of the pregnancy.
“This course is the best way to avoid even a minimal risk of sexual transmission of Zika virus, which could have adverse fetal effects when contracted during pregnancy,” the CDC report states, adding that pregnant women should ask their male sex partners about recent travel to areas with currently circulating Zika virus.
For couples not expecting a child, but concerned about sexual transmission of Zika, men with a confirmed Zika infection or clinical symptoms of Zika infection should consider using condoms or abstaining from sex for at least 6 months after their symptoms appear. This recommendation is based on tripling 62 days – the longest time interval after infection during which the virus was successfully isolated from semen.
If men have traveled to areas with active Zika transmission but have not developed symptoms, the CDC recommends condom use or abstinence for at least 8 weeks after leaving the area. Those living in areas with active transmission should also consider condom use during sex or abstaining from sex until active transmission has ceased.
These recommendations come as more evidence points to a link between Zika infection and fetal abnormalities, including microcephaly and fetal mortality.
“I think we’re learning more every day, and I think the evidence of a link between Zika and a range of poor pregnancy outcomes is becoming stronger and stronger,” Dr. Jamieson said. “At this point, we’re not using causal language, but the evidence is mounting.”
The CDC also released two other reports focusing on the need to increase access to contraception for residents of Puerto Rico and interim guidance for health care providers of women of childbearing age who have been potentially exposed to Zika virus.
As of March 25, the CDC has reported 273 U.S. cases of Zika virus infections from 35 states and Washington, D.C. All of these – except six sexually transmitted cases – are travel related.
Additionally, Puerto Rico’s most recent case total is 261, all locally transmitted by mosquitoes, except for three travel-associated cases. American Samoa has 14 cases, and the U.S. Virgin Islands have 11 cases, all thought to be locally transmitted.
“Long-acting contraception methods are not readily available in Puerto Rico, and from our health care provider colleagues in Puerto Rico, there is a desire to provide a more broad range of contraception options to women in Puerto Rico,” Dr. Jamieson said.
She said the CDC is developing a plan to make long-acting contraceptive methods more available in Puerto Rico.
When advising couples who wish to become pregnant after the man has had confirmed or suspected Zika infection, the CDC recommends waiting at least 6 months after the man’s onset of Zika symptoms or confirmed infection before attempting to conceive.
Although no evidence suggests that Zika virus will cause congenital infections in pregnancies conceived after a woman’s infection has resolved, data on the virus’s incubation period is limited, according to the CDC.
“Women with Zika virus disease should wait until at least 8 weeks after symptom onset before attempting conception,” wrote Dr. Emily E. Petersen and her colleagues in the guidance on caring for women of reproductive age with possible Zika virus exposure. “No data are available regarding the risk for congenital infection among pregnant women with asymptomatic infection.”
Similarly, asymptomatic women potentially exposed to Zika virus should also wait at least 8 weeks after the possible exposure date before trying to conceive.
Men potentially exposed to Zika virus should use a condom during all sex or abstain from sex for at least 8 weeks, according to new recommendations from the Centers for Disease Control and Prevention on reducing the risk of sexual transmission of the virus.
Men with confirmed infections or clinical symptoms of Zika should similarly abstain or use a condom for at least 6 months, the CDC recommends in the Morbidity and Mortality Weekly Report released on March 25 (MMWR 2016. Mar 25. doi: http://dx.doi.org/10.15585/mmwr.mm6512e3er).
These recommendations update and replace those issued by the CDC on Feb. 5 and include new guidance for men who live in, or have traveled to, an area with active Zika virus transmission. The recommendations apply to all types of sexual activity involving the penis, including vaginal intercourse, anal intercourse, or fellatio.
“The previous recommendations focused on women who were already pregnant,” Dr. Denise J. Jamieson, co-lead of the Pregnancy and Birth Defects Team of the CDC Zika Virus Response Team, said during a press briefing. “What’s new is that we are now concerned about the periconceptional period, around the time the woman conceives.”
For men with pregnant sex partners, the agency recommends consistent and accurate use of condoms during any type of sex, or abstinence during the length of the pregnancy.
“This course is the best way to avoid even a minimal risk of sexual transmission of Zika virus, which could have adverse fetal effects when contracted during pregnancy,” the CDC report states, adding that pregnant women should ask their male sex partners about recent travel to areas with currently circulating Zika virus.
For couples not expecting a child, but concerned about sexual transmission of Zika, men with a confirmed Zika infection or clinical symptoms of Zika infection should consider using condoms or abstaining from sex for at least 6 months after their symptoms appear. This recommendation is based on tripling 62 days – the longest time interval after infection during which the virus was successfully isolated from semen.
If men have traveled to areas with active Zika transmission but have not developed symptoms, the CDC recommends condom use or abstinence for at least 8 weeks after leaving the area. Those living in areas with active transmission should also consider condom use during sex or abstaining from sex until active transmission has ceased.
These recommendations come as more evidence points to a link between Zika infection and fetal abnormalities, including microcephaly and fetal mortality.
“I think we’re learning more every day, and I think the evidence of a link between Zika and a range of poor pregnancy outcomes is becoming stronger and stronger,” Dr. Jamieson said. “At this point, we’re not using causal language, but the evidence is mounting.”
The CDC also released two other reports focusing on the need to increase access to contraception for residents of Puerto Rico and interim guidance for health care providers of women of childbearing age who have been potentially exposed to Zika virus.
As of March 25, the CDC has reported 273 U.S. cases of Zika virus infections from 35 states and Washington, D.C. All of these – except six sexually transmitted cases – are travel related.
Additionally, Puerto Rico’s most recent case total is 261, all locally transmitted by mosquitoes, except for three travel-associated cases. American Samoa has 14 cases, and the U.S. Virgin Islands have 11 cases, all thought to be locally transmitted.
“Long-acting contraception methods are not readily available in Puerto Rico, and from our health care provider colleagues in Puerto Rico, there is a desire to provide a more broad range of contraception options to women in Puerto Rico,” Dr. Jamieson said.
She said the CDC is developing a plan to make long-acting contraceptive methods more available in Puerto Rico.
When advising couples who wish to become pregnant after the man has had confirmed or suspected Zika infection, the CDC recommends waiting at least 6 months after the man’s onset of Zika symptoms or confirmed infection before attempting to conceive.
Although no evidence suggests that Zika virus will cause congenital infections in pregnancies conceived after a woman’s infection has resolved, data on the virus’s incubation period is limited, according to the CDC.
“Women with Zika virus disease should wait until at least 8 weeks after symptom onset before attempting conception,” wrote Dr. Emily E. Petersen and her colleagues in the guidance on caring for women of reproductive age with possible Zika virus exposure. “No data are available regarding the risk for congenital infection among pregnant women with asymptomatic infection.”
Similarly, asymptomatic women potentially exposed to Zika virus should also wait at least 8 weeks after the possible exposure date before trying to conceive.
Men potentially exposed to Zika virus should use a condom during all sex or abstain from sex for at least 8 weeks, according to new recommendations from the Centers for Disease Control and Prevention on reducing the risk of sexual transmission of the virus.
Men with confirmed infections or clinical symptoms of Zika should similarly abstain or use a condom for at least 6 months, the CDC recommends in the Morbidity and Mortality Weekly Report released on March 25 (MMWR 2016. Mar 25. doi: http://dx.doi.org/10.15585/mmwr.mm6512e3er).
These recommendations update and replace those issued by the CDC on Feb. 5 and include new guidance for men who live in, or have traveled to, an area with active Zika virus transmission. The recommendations apply to all types of sexual activity involving the penis, including vaginal intercourse, anal intercourse, or fellatio.
“The previous recommendations focused on women who were already pregnant,” Dr. Denise J. Jamieson, co-lead of the Pregnancy and Birth Defects Team of the CDC Zika Virus Response Team, said during a press briefing. “What’s new is that we are now concerned about the periconceptional period, around the time the woman conceives.”
For men with pregnant sex partners, the agency recommends consistent and accurate use of condoms during any type of sex, or abstinence during the length of the pregnancy.
“This course is the best way to avoid even a minimal risk of sexual transmission of Zika virus, which could have adverse fetal effects when contracted during pregnancy,” the CDC report states, adding that pregnant women should ask their male sex partners about recent travel to areas with currently circulating Zika virus.
For couples not expecting a child, but concerned about sexual transmission of Zika, men with a confirmed Zika infection or clinical symptoms of Zika infection should consider using condoms or abstaining from sex for at least 6 months after their symptoms appear. This recommendation is based on tripling 62 days – the longest time interval after infection during which the virus was successfully isolated from semen.
If men have traveled to areas with active Zika transmission but have not developed symptoms, the CDC recommends condom use or abstinence for at least 8 weeks after leaving the area. Those living in areas with active transmission should also consider condom use during sex or abstaining from sex until active transmission has ceased.
These recommendations come as more evidence points to a link between Zika infection and fetal abnormalities, including microcephaly and fetal mortality.
“I think we’re learning more every day, and I think the evidence of a link between Zika and a range of poor pregnancy outcomes is becoming stronger and stronger,” Dr. Jamieson said. “At this point, we’re not using causal language, but the evidence is mounting.”
The CDC also released two other reports focusing on the need to increase access to contraception for residents of Puerto Rico and interim guidance for health care providers of women of childbearing age who have been potentially exposed to Zika virus.
As of March 25, the CDC has reported 273 U.S. cases of Zika virus infections from 35 states and Washington, D.C. All of these – except six sexually transmitted cases – are travel related.
Additionally, Puerto Rico’s most recent case total is 261, all locally transmitted by mosquitoes, except for three travel-associated cases. American Samoa has 14 cases, and the U.S. Virgin Islands have 11 cases, all thought to be locally transmitted.
“Long-acting contraception methods are not readily available in Puerto Rico, and from our health care provider colleagues in Puerto Rico, there is a desire to provide a more broad range of contraception options to women in Puerto Rico,” Dr. Jamieson said.
She said the CDC is developing a plan to make long-acting contraceptive methods more available in Puerto Rico.
When advising couples who wish to become pregnant after the man has had confirmed or suspected Zika infection, the CDC recommends waiting at least 6 months after the man’s onset of Zika symptoms or confirmed infection before attempting to conceive.
Although no evidence suggests that Zika virus will cause congenital infections in pregnancies conceived after a woman’s infection has resolved, data on the virus’s incubation period is limited, according to the CDC.
“Women with Zika virus disease should wait until at least 8 weeks after symptom onset before attempting conception,” wrote Dr. Emily E. Petersen and her colleagues in the guidance on caring for women of reproductive age with possible Zika virus exposure. “No data are available regarding the risk for congenital infection among pregnant women with asymptomatic infection.”
Similarly, asymptomatic women potentially exposed to Zika virus should also wait at least 8 weeks after the possible exposure date before trying to conceive.
ECCMID 2016: Antimicrobial resistance, the microbiome and systems vaccinology
The global infectious disease and clinical microbiology community meets every year at the European Congress of Clinical Microbiology and Infectious Diseases (ECCMID), the world’s largest congress on infectious diseases and medical microbiology, to present and discuss recent research results and to offer solutions to the most pressing infection problems.
The 2016 ECCMID annual conference, organized by the European Society of Clinical Microbiology and Infectious Diseases (ESCMID), will take place April 9-12 in Amsterdam. Discussions at this event not only help translate research findings into diagnostic tools, guidelines, best practices, and international policies; they also raise awareness of emerging health care challenges.
At ECCMID 2016, researchers will present more than 3,000 abstracts with the latest findings and recommendations to help improve diagnosis, prevention, and the clinical care given to patients. The Congress offers more than 150 oral presentations, including keynote lectures, symposia, oral sessions, educational workshops, and meet-the-experts sessions, as well as more than 2,000 poster presentations.
The main topics this year are strategies to detect and tackle antimicrobial resistance in various settings, approaches for prevention involving vaccines and infection control, as well as descriptions of novel diagnostic technologies. Always among the most popular sessions are lectures by winners of the ESCMID Award for Excellence and the Young Investigator Awards, as well as oral presentations on groundbreaking research, and late-breaking abstracts.
Also included will be mini oral “e-poster” presentations. Printed posters will be presented, but they will also be available at e-poster viewing stations, where visitors can scroll through abstracts of paper presentations.
Keynote speeches this year will feature innovative approaches to vaccines; microbiome and tuberculosis therapies; lectures on how nonhuman antibiotics affect public health; and an economic perspective on antimicrobial resistance.
Special topics
This year, the ECCMID Program Committee has decided to offer two special tracks for the late-breaking abstract sessions, focused on topics requiring a coordinated response from infection specialists across all disciplines.
The first topic is refugee and migrant health. The thousands of people who are currently migrating challenge public health systems in transition and the host countries. Clinicians and public health specialists need to develop strategies for the screening, prevention, and treatment of infectious diseases that were largely eradicated in Europe but are now gradually being reintroduced.
The second focus of the late-breaking abstracts is on emerging colistin resistance. Reports about the emergence of plasmid-borne resistance to this last-resort antibiotic have come from China, Canada, the United Kingdom, and most countries in continental Europe. Colistin resistance can spread easily between different types of bacteria, says Dr. Murat Akova, current ESCMID president and professor of medicine at Hacettepe University in Ankara, Turkey, and the world needs to wake up and take note.
In terms of viral infections, experts at the Congress will evaluate HIV and hepatitis C treatments in several interesting sessions. Researchers will also present results on emerging infections, including those caused by the Zika virus. Dr. Jean Paul Stahl, vice chairman of the ESCMID Study Group for Infectious Diseases of the Brain and professor of infectious diseases at University Hospital in Grenoble, France, says the current Zika virus epidemic is an important example of the great need we have for new evidence-based approaches on how to best manage emerging infections.
The outbreaks of Zika and Ebola in the last few years have seen the international community mobilize on infectious disease issues in a more collaborative manner than ever before, which should help reduce the severity of future outbreaks. But viral infections extend far beyond the recent outbreaks of unusual pathologies, and there are a number of important developments taking place among some of the more common viruses.
For more information on ECCMID 2016, visit http://www.eccmid.org/.
Dr. Winfried V. Kern is professor of medicine at the Albert Ludwigs University of Freiburg and head of the division of infectious diseases, department of medicine, and Centre for Infectious Diseases and Travel Medicine, University Hospital, Freiburg, Germany. His professional interests include bacterial multidrug resistance mechanisms and epidemiology, hospital antibiotic stewardship programs, health care–associated infections including infections in the immunocompromised host.
The global infectious disease and clinical microbiology community meets every year at the European Congress of Clinical Microbiology and Infectious Diseases (ECCMID), the world’s largest congress on infectious diseases and medical microbiology, to present and discuss recent research results and to offer solutions to the most pressing infection problems.
The 2016 ECCMID annual conference, organized by the European Society of Clinical Microbiology and Infectious Diseases (ESCMID), will take place April 9-12 in Amsterdam. Discussions at this event not only help translate research findings into diagnostic tools, guidelines, best practices, and international policies; they also raise awareness of emerging health care challenges.
At ECCMID 2016, researchers will present more than 3,000 abstracts with the latest findings and recommendations to help improve diagnosis, prevention, and the clinical care given to patients. The Congress offers more than 150 oral presentations, including keynote lectures, symposia, oral sessions, educational workshops, and meet-the-experts sessions, as well as more than 2,000 poster presentations.
The main topics this year are strategies to detect and tackle antimicrobial resistance in various settings, approaches for prevention involving vaccines and infection control, as well as descriptions of novel diagnostic technologies. Always among the most popular sessions are lectures by winners of the ESCMID Award for Excellence and the Young Investigator Awards, as well as oral presentations on groundbreaking research, and late-breaking abstracts.
Also included will be mini oral “e-poster” presentations. Printed posters will be presented, but they will also be available at e-poster viewing stations, where visitors can scroll through abstracts of paper presentations.
Keynote speeches this year will feature innovative approaches to vaccines; microbiome and tuberculosis therapies; lectures on how nonhuman antibiotics affect public health; and an economic perspective on antimicrobial resistance.
Special topics
This year, the ECCMID Program Committee has decided to offer two special tracks for the late-breaking abstract sessions, focused on topics requiring a coordinated response from infection specialists across all disciplines.
The first topic is refugee and migrant health. The thousands of people who are currently migrating challenge public health systems in transition and the host countries. Clinicians and public health specialists need to develop strategies for the screening, prevention, and treatment of infectious diseases that were largely eradicated in Europe but are now gradually being reintroduced.
The second focus of the late-breaking abstracts is on emerging colistin resistance. Reports about the emergence of plasmid-borne resistance to this last-resort antibiotic have come from China, Canada, the United Kingdom, and most countries in continental Europe. Colistin resistance can spread easily between different types of bacteria, says Dr. Murat Akova, current ESCMID president and professor of medicine at Hacettepe University in Ankara, Turkey, and the world needs to wake up and take note.
In terms of viral infections, experts at the Congress will evaluate HIV and hepatitis C treatments in several interesting sessions. Researchers will also present results on emerging infections, including those caused by the Zika virus. Dr. Jean Paul Stahl, vice chairman of the ESCMID Study Group for Infectious Diseases of the Brain and professor of infectious diseases at University Hospital in Grenoble, France, says the current Zika virus epidemic is an important example of the great need we have for new evidence-based approaches on how to best manage emerging infections.
The outbreaks of Zika and Ebola in the last few years have seen the international community mobilize on infectious disease issues in a more collaborative manner than ever before, which should help reduce the severity of future outbreaks. But viral infections extend far beyond the recent outbreaks of unusual pathologies, and there are a number of important developments taking place among some of the more common viruses.
For more information on ECCMID 2016, visit http://www.eccmid.org/.
Dr. Winfried V. Kern is professor of medicine at the Albert Ludwigs University of Freiburg and head of the division of infectious diseases, department of medicine, and Centre for Infectious Diseases and Travel Medicine, University Hospital, Freiburg, Germany. His professional interests include bacterial multidrug resistance mechanisms and epidemiology, hospital antibiotic stewardship programs, health care–associated infections including infections in the immunocompromised host.
The global infectious disease and clinical microbiology community meets every year at the European Congress of Clinical Microbiology and Infectious Diseases (ECCMID), the world’s largest congress on infectious diseases and medical microbiology, to present and discuss recent research results and to offer solutions to the most pressing infection problems.
The 2016 ECCMID annual conference, organized by the European Society of Clinical Microbiology and Infectious Diseases (ESCMID), will take place April 9-12 in Amsterdam. Discussions at this event not only help translate research findings into diagnostic tools, guidelines, best practices, and international policies; they also raise awareness of emerging health care challenges.
At ECCMID 2016, researchers will present more than 3,000 abstracts with the latest findings and recommendations to help improve diagnosis, prevention, and the clinical care given to patients. The Congress offers more than 150 oral presentations, including keynote lectures, symposia, oral sessions, educational workshops, and meet-the-experts sessions, as well as more than 2,000 poster presentations.
The main topics this year are strategies to detect and tackle antimicrobial resistance in various settings, approaches for prevention involving vaccines and infection control, as well as descriptions of novel diagnostic technologies. Always among the most popular sessions are lectures by winners of the ESCMID Award for Excellence and the Young Investigator Awards, as well as oral presentations on groundbreaking research, and late-breaking abstracts.
Also included will be mini oral “e-poster” presentations. Printed posters will be presented, but they will also be available at e-poster viewing stations, where visitors can scroll through abstracts of paper presentations.
Keynote speeches this year will feature innovative approaches to vaccines; microbiome and tuberculosis therapies; lectures on how nonhuman antibiotics affect public health; and an economic perspective on antimicrobial resistance.
Special topics
This year, the ECCMID Program Committee has decided to offer two special tracks for the late-breaking abstract sessions, focused on topics requiring a coordinated response from infection specialists across all disciplines.
The first topic is refugee and migrant health. The thousands of people who are currently migrating challenge public health systems in transition and the host countries. Clinicians and public health specialists need to develop strategies for the screening, prevention, and treatment of infectious diseases that were largely eradicated in Europe but are now gradually being reintroduced.
The second focus of the late-breaking abstracts is on emerging colistin resistance. Reports about the emergence of plasmid-borne resistance to this last-resort antibiotic have come from China, Canada, the United Kingdom, and most countries in continental Europe. Colistin resistance can spread easily between different types of bacteria, says Dr. Murat Akova, current ESCMID president and professor of medicine at Hacettepe University in Ankara, Turkey, and the world needs to wake up and take note.
In terms of viral infections, experts at the Congress will evaluate HIV and hepatitis C treatments in several interesting sessions. Researchers will also present results on emerging infections, including those caused by the Zika virus. Dr. Jean Paul Stahl, vice chairman of the ESCMID Study Group for Infectious Diseases of the Brain and professor of infectious diseases at University Hospital in Grenoble, France, says the current Zika virus epidemic is an important example of the great need we have for new evidence-based approaches on how to best manage emerging infections.
The outbreaks of Zika and Ebola in the last few years have seen the international community mobilize on infectious disease issues in a more collaborative manner than ever before, which should help reduce the severity of future outbreaks. But viral infections extend far beyond the recent outbreaks of unusual pathologies, and there are a number of important developments taking place among some of the more common viruses.
For more information on ECCMID 2016, visit http://www.eccmid.org/.
Dr. Winfried V. Kern is professor of medicine at the Albert Ludwigs University of Freiburg and head of the division of infectious diseases, department of medicine, and Centre for Infectious Diseases and Travel Medicine, University Hospital, Freiburg, Germany. His professional interests include bacterial multidrug resistance mechanisms and epidemiology, hospital antibiotic stewardship programs, health care–associated infections including infections in the immunocompromised host.
David Henry's JCSO podcast, March 2016
In the March podcast for The Journal of Community and Supportive Oncology, Dr David Henry discusses a number of articles that center on patient quality of life and overall quality of care, among them, an article on opioid risk assessment in palliative care and three Original Reports, one on the impact of trimodality treatment on arm function and QoL in patients with superior sulcus tumors, a second on patient perceptions and the challenges of oral anticancer therapy, and a third on the use of voluntary reporting to assess symptom burden in cancer patients. A Review article by Jose de Souza and colleagues on financial toxicity in cancer care spans the QoL and quality of care spectrum as it details the implications of the increasing cost of cancer care for the delivery of high-quality, patient-centered care and discusses potential predictors of financial toxicity and instruments that could help quantify financial burden. Also in the line-up are articles on encapsulated irinotecan for hard-to-treat cancer and Case Reports on an uncommon presentation of lung cancer and on acute promyelocytic leukemia presenting as a paraspinal mass.
Listen to the podcast below.
In the March podcast for The Journal of Community and Supportive Oncology, Dr David Henry discusses a number of articles that center on patient quality of life and overall quality of care, among them, an article on opioid risk assessment in palliative care and three Original Reports, one on the impact of trimodality treatment on arm function and QoL in patients with superior sulcus tumors, a second on patient perceptions and the challenges of oral anticancer therapy, and a third on the use of voluntary reporting to assess symptom burden in cancer patients. A Review article by Jose de Souza and colleagues on financial toxicity in cancer care spans the QoL and quality of care spectrum as it details the implications of the increasing cost of cancer care for the delivery of high-quality, patient-centered care and discusses potential predictors of financial toxicity and instruments that could help quantify financial burden. Also in the line-up are articles on encapsulated irinotecan for hard-to-treat cancer and Case Reports on an uncommon presentation of lung cancer and on acute promyelocytic leukemia presenting as a paraspinal mass.
Listen to the podcast below.
In the March podcast for The Journal of Community and Supportive Oncology, Dr David Henry discusses a number of articles that center on patient quality of life and overall quality of care, among them, an article on opioid risk assessment in palliative care and three Original Reports, one on the impact of trimodality treatment on arm function and QoL in patients with superior sulcus tumors, a second on patient perceptions and the challenges of oral anticancer therapy, and a third on the use of voluntary reporting to assess symptom burden in cancer patients. A Review article by Jose de Souza and colleagues on financial toxicity in cancer care spans the QoL and quality of care spectrum as it details the implications of the increasing cost of cancer care for the delivery of high-quality, patient-centered care and discusses potential predictors of financial toxicity and instruments that could help quantify financial burden. Also in the line-up are articles on encapsulated irinotecan for hard-to-treat cancer and Case Reports on an uncommon presentation of lung cancer and on acute promyelocytic leukemia presenting as a paraspinal mass.
Listen to the podcast below.