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Dive into the research topics where Paul Aronowitz is active.

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Featured researches published by Paul Aronowitz.


Clinical Infectious Diseases | 2007

Overwhelming Parasitemia with Plasmodium falciparum Infection in a Patient Receiving Infliximab Therapy for Rheumatoid Arthritis

Estella M. Geraghty; Bryan Ristow; Shelley Gordon; Paul Aronowitz

We describe a 45-year-old woman receiving infliximab therapy for rheumatoid arthritis who developed an overwhelming Plasmodium falciparum infection with cerebral malaria. Physicians should be aware that patients receiving tumor necrosis factor inhibitors, such as infliximab, may be at increased risk of life-threatening malarial infections.


Hospital Practice | 2013

The Tell-Tale Heart: Aspergillus fumigatus Endocarditis in an Immunocompetent Patient

Sheba Vohra; Robert Taylor; Paul Aronowitz

Abstract Aspergillus is a saprophytic, spore-forming fungus that is ubiquitous in our daily environment. Inhalation of the airborne conidia leads to a variety of diseases, from asymptomatic colonization to disseminated disease. Immunocompromised patients are usually viewed as the population most susceptible to aspergillosis because of their lack of host immune defenses. However, a healthy immune system does not preclude an individual from susceptibility to aspergillosis. Our case illustrates an immunocompetent patient with disseminated aspergillosis involving the tricuspid valve. A high degree of suspicion is imperative in patients who present without the classic risk factors. Recognition of disseminated aspergillosis in such patients is necessary to promote early diagnosis, treatment, and improved outcomes in an otherwise fulminant, life-threatening infection.


The American Journal of Medicine | 2012

E-Learning—The New Frontier: A Report from the APDIM E-Learning Task Force

John D. Myers; Aashish Didwania; Chirayu Shah; David Jacobson; Daphne Norwood; Maniza Ehtesham; Paul Aronowitz

E-Learning—The New Frontier: A Report from the APDIM E-Learning Task Force John D. Myers, MD, Aashish Didwania, MD, Chirayu Shah, MD, David Jacobson, MD, Daphne Norwood, MD, Maniza Ehtesham, MD, Paul Aronowitz, MD Department of Medicine, Scott and White Hospital and Clinic/Texas AM Department of Medicine, orthwestern University, Feinberg School of Medicine, Chicago, Ill; Department of Medicine, Baylor College of Medicine, ouston, Texas; Department of Medicine, University of California, San Francisco; Department of Medicine, University of ennessee Graduate School of Medicine, Knoxville; Department of Medicine, University of Missouri Kansas City, Mo; Department of Medicine, California Pacific Medical Center, San Francisco.


Journal of General Internal Medicine | 2015

The Habit Tic: Onychotillomania

Shaheen Najafi; Paul Aronowitz; George R. Thompson

A 67-year-old man presented to his primary care physician for routine care. The absence of cuticles was noted on his bilateral thumbnails, and a midline crease with horizontal ridges from the proximal nail fold to the distal nail (Fig. 1). The patient stated that these changes had been present for over a year. He admitted to frequent “picking” and biting of the cuticles and repeated hand washing, as evidenced by the xerosis of his fingers. Habit-tic deformity is a type of onychodystrophy that is classified in a group of disorders known as onychotillomania, which includes entities such as nail biting (onychophagia), nail picking, and finger sucking. The deformity is the result of repetitive nail bed trauma from the conscious or unconscious manipulation of the cuticle. The characteristic findings include a midline furrow in the nail plate, often yellow in color, running the length of the nail, with a series of transverse ridges. Treatment includes physically covering the nails with bandages or glue to prevent further trauma. In addition, behavioral therapy and SSRIs have been tried, given the obsessive-compulsive nature of the habit. Cessation of the habit leads to complete resolution of the nail changes.


Journal of Hospital Medicine | 2010

Myelofibrosis with massive hepatosplenomegaly and osteolytic bone lesions

Ginger M. Merry; Paul Aronowitz

An 83-year-old man with a 7-year history of myelofibrosis presented to the hospital with progressive weakness and fatigue, which resulted in him tripping and falling onto his left hand and arm 1 day prior to admission. His past medical history was significant for transfusion-dependent anemia and hypertension. His current treatment regimen for myelofibrosis included thalidomide and darbopoetin alfa. Physical examination revealed a pale and edematous man who was holding his injured arm to his chest, but in no distress. He had massive hepatosplenomegaly (Figure 1) and pitting edema of the lower extremities that extended to his abdomen. Laboratory studies showed a white blood count of 5000, hematocrit of 29%, and platelets of 218,000. The peripheral blood smear (Figure 2) showed marked anisocytosis, poikilocytosis, and teardrop cells (Figure 2; arrow). Imaging of the left arm and hand was significant for a third metacarpal fracture and first phalanx fracture. Of note, these x-rays also revealed numerous round lucencies within the osseous structures of the left hand, wrist, and forearm (Figure 3; arrow). The patient’s hospital course was uncomplicated and included casting of the left arm, treatment of his lower extremity edema, and transfusion for a slowly declining hematocrit. He was discharged home after several days but died 1 month later. Primary myelofibrosis is a myeloproliferative disease that consists of 2 phases. The first phase is the growth and proliferation of abnormal bone marrow stem cells, which leads to ineffective erythropoiesis. This is followed by reactive myelofibrosis and extramedullary hematopoiesis. These 2 phases of the disease can lead to a constellation of findings, as illustrated in these images. The median length of survival from diagnosis is 3 to 5 years, with the main causes of death


Journal of General Internal Medicine | 2017

Drug-Induced Sweet‘s Syndrome

Vivian Tien; Andrew Jones; Paul Aronowitz

A 69-year-old man with ulcerative colitis presented with fever, fatigue, and rash. The patient reported onset of symptoms within 5 days of starting azathioprine. Physical examination revealed a fever of 39.5°C and a painful rash of erythematous plaques with pustules on bilateral elbows and neck (Fig. 1) and scattered macules on bilateral palms. The white blood cell count was 8000/mm with 96% neutrophils; the erythrocyte sedimentation rate was 60mm/h. Biopsy of the elbow lesion revealed a dense dermal neutrophilic infiltrate, lack of perivascular inflammation, and papillary dermal edema consistent with Sweet’s syndrome (Fig. 2). Symptoms and rash rapidly resolved after discontinuing azathioprine. Sweet’s syndrome (acute febrile neutrophilic dermatosis) is an uncommon inflammatory disorder characterized by acute onset of fever and a rash consisting of tender erythematous plaques with occasional pustules, typically distributed over the upper body and extremities, with characteristic histopathologic findings. The syndrome most often occurs secondary to malignancy or autoimmune disease such as inflammatory bowel disease, but can be associated with pregnancy, preceding infection, or drug reaction. Here, the syndrome was thought to be secondary to azathioprine, given the temporal relationship between drug exposure and symptoms, with most azathioprine-associated cases occurring within a month after exposure.


Cleveland Clinic Journal of Medicine | 2015

Retroperitoneal cyst hemorrhage in polycystic kidney disease.

Cathy I. Cheng; Nicolas Karvelas; Paul Aronowitz

Polycystic kidney disease is relatively common, and fewer than half of cases are diagnosed. The cysts often bleed.


The New England Journal of Medicine | 2012

Sigmoid Perforation in Association with Colonoscopy

Albert Lu; Paul Aronowitz

A 74-year-old woman was undergoing a screening colonoscopy when it became apparent that the rectosigmoid junction might have become perforated. The procedure was terminated, and radiographs were obtained.


Journal of Hospital Medicine | 2011

Electrocardiographic changes of severe hyperkalemia.

Ryan Wong; Rupali Banker; Paul Aronowitz

A 62-year-old woman with an extensive medical and surgical history presented with complaints of 2 days of weakness. Physical examination demonstrated a lethargic, but arousable woman in no distress. Her lower extremity motor strength was 4/5 bilaterally. The patient’s electrocardiogram (ECG) demonstrated ‘‘peaked’’ T waves (Figure 1, arrow), absence of P waves, poor R wave progression and QRS interval widening (Figure 1, 2-headed arrow.) Serum chemistries revealed a potassium level of 10.4 mmol/L and a creatinine of 0.9 mg/dL. One ampule of D50, 10 units of insulin, 1 ampule of Calcium gluconate and 1 ampule of sodium bicarbonate were given intravenously alongwith oral Kayexalate. A repeat ECG showed a return of P waves, narrowing of the QRS interval, improved R wave progression and less peaking of the Twaves (Figure 2). A repeat potassium level at that timewas 9.2mmol/L. Despite continued therapy to lower the potassium, another ECG showed a return of peaked T waves, a prolonged PR interval and marked widening of the QRS interval to 205 msec; the potassium level was now 10.0 mmol/L (Figure 3). Despite the patient’s renal function being normal, she was emergently dialyzed. After a single dialysis, the patient’s potassium level remained normal for the remainder of the hospitalization and a follow-up ECG returned to baseline (Figure 4). No physiologic explanation was found for her hyperkalemia and it was concluded, despite her denials, that she had taken large quantities of exogenous potassium she had available from previous prescriptions.


Journal of Hospital Medicine | 2010

Pneumothorax in a patient with COPD after blunt trauma

Albert Lu; Paul Aronowitz

A 53-year-old man with a history of heavy tobacco use presented with shortness of breath. Eight days prior to his presentation he was diagnosed with multiple rib fractures after suffering an assault. Since then he had developed dyspnea and a nonproductive cough. A chest x-ray revealed a large pneumothorax on the right with approximately 80% volume loss (arrow, Figure 1). Tube thoracostomy was performed. Repeat chest x-ray showed that the pneumothorax had resolved, revealing a consolidation likely caused by either reexpansion pulmonary edema or, given its location in the superior segment of the right lower lobe, aspiration pneumonia (thin arrow, Figure 2). Also seen in the x-ray is an old scar (thick arrow, Figure 2) and apical bullous changes with hyperinflated lungs suggestive of chronic obstructive pulmonary disease (COPD).

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Albert Lu

California Pacific Medical Center

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Brian Apter

California Pacific Medical Center

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Debbie C. Chen

University of California

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Neeta Jain

California Pacific Medical Center

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Shelley Gordon

California Pacific Medical Center

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Tammy Lai

California Pacific Medical Center

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Von Ta

California Pacific Medical Center

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