Background Metastatic castration-resistant prostate cancer (mCRPC) is typically associated with declining health-related quality of life (HR-QoL).

Objective To assess patient experience with abiraterone acetate (hereafter abiraterone) plus prednisone longitudinally.

Methods COU-AA-302 was a phase 3, multinational, randomized, double-blind study that enrolled asymptomatic or mildly symptomatic, chemotherapy-naïve patients with mCRPC. Patients were randomized to 1 g abiraterone daily plus 5 mg prednisone BID (n = 546) or placebo plus prednisone (n = 542) in continuous 28-day cycles. Patient-reported outcomes (PROs) were collected using the Functional Assessment of Cancer Therapy-Prostate (FACT-P) questionnaire, consisting of 4 well-being subscales (physical, social/family, emotional, functional) and a prostate cancer-specific subscale (PCS). The trial outcome index (TOI) is a composite of the physical well-being, functional well-being, and PCS scores. Least squares mean change from baseline at each cycle up to 1 year (cycle13) was compared between treatment arms using a mixed-effects model for repeated measures, which assumed that data were “missing at random.” A pattern-mixture model (PMM) with multiple imputation was performed to address the assumption that data were “missing not at random.”

Results Significant differences favoring abiraterone-prednisone were observed for FACT-P total, TOI, and PCS scores, and for all well-being subscales except social/family well-being over the first year of treatment. These results were supported by the PMM with multiple imputation.

Limitations Attrition after 1 year limited our ability to analyze the PRO data beyond that time point.

Conclusions Abiraterone-prednisone confers sustained HR-QoL benefits over the course of treatment.

Funding Janssen Research & Development

Click on the PDF icon at the top of this introduction to read the full article.

Background Metastatic castration-resistant prostate cancer (mCRPC) is typically associated with declining health-related quality of life (HR-QoL).

Objective To assess patient experience with abiraterone acetate (hereafter abiraterone) plus prednisone longitudinally.

Methods COU-AA-302 was a phase 3, multinational, randomized, double-blind study that enrolled asymptomatic or mildly symptomatic, chemotherapy-naïve patients with mCRPC. Patients were randomized to 1 g abiraterone daily plus 5 mg prednisone BID (n = 546) or placebo plus prednisone (n = 542) in continuous 28-day cycles. Patient-reported outcomes (PROs) were collected using the Functional Assessment of Cancer Therapy-Prostate (FACT-P) questionnaire, consisting of 4 well-being subscales (physical, social/family, emotional, functional) and a prostate cancer-specific subscale (PCS). The trial outcome index (TOI) is a composite of the physical well-being, functional well-being, and PCS scores. Least squares mean change from baseline at each cycle up to 1 year (cycle13) was compared between treatment arms using a mixed-effects model for repeated measures, which assumed that data were “missing at random.” A pattern-mixture model (PMM) with multiple imputation was performed to address the assumption that data were “missing not at random.”

Results Significant differences favoring abiraterone-prednisone were observed for FACT-P total, TOI, and PCS scores, and for all well-being subscales except social/family well-being over the first year of treatment. These results were supported by the PMM with multiple imputation.

Limitations Attrition after 1 year limited our ability to analyze the PRO data beyond that time point.

Conclusions Abiraterone-prednisone confers sustained HR-QoL benefits over the course of treatment.

Funding Janssen Research & Development

Click on the PDF icon at the top of this introduction to read the full article.

Background Metastatic castration-resistant prostate cancer (mCRPC) is typically associated with declining health-related quality of life (HR-QoL).

Objective To assess patient experience with abiraterone acetate (hereafter abiraterone) plus prednisone longitudinally.

Methods COU-AA-302 was a phase 3, multinational, randomized, double-blind study that enrolled asymptomatic or mildly symptomatic, chemotherapy-naïve patients with mCRPC. Patients were randomized to 1 g abiraterone daily plus 5 mg prednisone BID (n = 546) or placebo plus prednisone (n = 542) in continuous 28-day cycles. Patient-reported outcomes (PROs) were collected using the Functional Assessment of Cancer Therapy-Prostate (FACT-P) questionnaire, consisting of 4 well-being subscales (physical, social/family, emotional, functional) and a prostate cancer-specific subscale (PCS). The trial outcome index (TOI) is a composite of the physical well-being, functional well-being, and PCS scores. Least squares mean change from baseline at each cycle up to 1 year (cycle13) was compared between treatment arms using a mixed-effects model for repeated measures, which assumed that data were “missing at random.” A pattern-mixture model (PMM) with multiple imputation was performed to address the assumption that data were “missing not at random.”

Results Significant differences favoring abiraterone-prednisone were observed for FACT-P total, TOI, and PCS scores, and for all well-being subscales except social/family well-being over the first year of treatment. These results were supported by the PMM with multiple imputation.

Limitations Attrition after 1 year limited our ability to analyze the PRO data beyond that time point.

Conclusions Abiraterone-prednisone confers sustained HR-QoL benefits over the course of treatment.

Funding Janssen Research & Development

Click on the PDF icon at the top of this introduction to read the full article.

Background Concurrent chemotherapy radiation therapy may result in significant nausea and vomiting. There have been few studies reporting effective interventions for preventing treatment-related nausea and vomiting.

Objective To compare olanzapine with fosaprepitant for the prevention of nausea and vomiting in patients receiving concurrent highly emetogenic chemotherapy (HEC) and radiotherapy for locally advanced head and neck or esophageal cancer.

Methods 120 chemotherapy and radiotherapy naïve patients with head and neck cancer who were receiving concurrent local radiation and cisplatin were randomized to receive either olanzapine or fosaprepitant in combination with palonosetron and dexamethasone for the prevention of chemotherapy- and radiation-induced nausea and vomiting. The olanzapine, palonosetron, dexamethasone (OPD) regimen was 10 mg oral olanzapine , 0.25 mg IV palonosetron, and 20 mg IV dexamethasone before chemotherapy on day 1, and 10 mg/day of oral olanzapine before chemotherapy on days 2-4. The fosaprepitant, palonosetron, dexamethasone (FPD) regimen was 150 mg IV fosaprepitant, 0.25 mg IV palonosetron, and 12 mg IV dexamethasone before chemotherapy on day 1, and 4 mg dexamethasone PO BID, before chemotherapy days 2 and 3.

Results 101 of the 120 patients were evaluable. In 51 patients who received the OPD regimen, the complete response (CR; no emesis, no rescue medication) rate was 88% for the acute period (24 h after chemotherapy), 76% for the delayed period (days 2-5), and 76% for the overall period (0-120 h). In 50 patients who received the FPD regimen, the CR was 84% acute, 74% delayed, and 74% overall (P > .01 for all periods). Patients with no nausea (0, on a scale 0-10, visual analogue scale) were: OPD: 86% acute, 71% delayed, 71% overall; FPD: 78% acute, 40% delayed, 40% overall (P > .01 for acute; P < .01 for delayed and overall) There were no grade 3 or 4 toxicities.

Conclusions CR was similar for OPD and FPD; nausea in the delayed and overall periods was signifcantly improved with OPD compared with FPD (P < .01).

Funding Reich Endowment for the Care of the Whole Patient
 

Click on the PDF icon at the top of this introduction to read the full article.
 

Background Concurrent chemotherapy radiation therapy may result in significant nausea and vomiting. There have been few studies reporting effective interventions for preventing treatment-related nausea and vomiting.

Objective To compare olanzapine with fosaprepitant for the prevention of nausea and vomiting in patients receiving concurrent highly emetogenic chemotherapy (HEC) and radiotherapy for locally advanced head and neck or esophageal cancer.

Methods 120 chemotherapy and radiotherapy naïve patients with head and neck cancer who were receiving concurrent local radiation and cisplatin were randomized to receive either olanzapine or fosaprepitant in combination with palonosetron and dexamethasone for the prevention of chemotherapy- and radiation-induced nausea and vomiting. The olanzapine, palonosetron, dexamethasone (OPD) regimen was 10 mg oral olanzapine , 0.25 mg IV palonosetron, and 20 mg IV dexamethasone before chemotherapy on day 1, and 10 mg/day of oral olanzapine before chemotherapy on days 2-4. The fosaprepitant, palonosetron, dexamethasone (FPD) regimen was 150 mg IV fosaprepitant, 0.25 mg IV palonosetron, and 12 mg IV dexamethasone before chemotherapy on day 1, and 4 mg dexamethasone PO BID, before chemotherapy days 2 and 3.

Results 101 of the 120 patients were evaluable. In 51 patients who received the OPD regimen, the complete response (CR; no emesis, no rescue medication) rate was 88% for the acute period (24 h after chemotherapy), 76% for the delayed period (days 2-5), and 76% for the overall period (0-120 h). In 50 patients who received the FPD regimen, the CR was 84% acute, 74% delayed, and 74% overall (P > .01 for all periods). Patients with no nausea (0, on a scale 0-10, visual analogue scale) were: OPD: 86% acute, 71% delayed, 71% overall; FPD: 78% acute, 40% delayed, 40% overall (P > .01 for acute; P < .01 for delayed and overall) There were no grade 3 or 4 toxicities.

Conclusions CR was similar for OPD and FPD; nausea in the delayed and overall periods was signifcantly improved with OPD compared with FPD (P < .01).

Funding Reich Endowment for the Care of the Whole Patient
 

Click on the PDF icon at the top of this introduction to read the full article.
 

Background Concurrent chemotherapy radiation therapy may result in significant nausea and vomiting. There have been few studies reporting effective interventions for preventing treatment-related nausea and vomiting.

Objective To compare olanzapine with fosaprepitant for the prevention of nausea and vomiting in patients receiving concurrent highly emetogenic chemotherapy (HEC) and radiotherapy for locally advanced head and neck or esophageal cancer.

Methods 120 chemotherapy and radiotherapy naïve patients with head and neck cancer who were receiving concurrent local radiation and cisplatin were randomized to receive either olanzapine or fosaprepitant in combination with palonosetron and dexamethasone for the prevention of chemotherapy- and radiation-induced nausea and vomiting. The olanzapine, palonosetron, dexamethasone (OPD) regimen was 10 mg oral olanzapine , 0.25 mg IV palonosetron, and 20 mg IV dexamethasone before chemotherapy on day 1, and 10 mg/day of oral olanzapine before chemotherapy on days 2-4. The fosaprepitant, palonosetron, dexamethasone (FPD) regimen was 150 mg IV fosaprepitant, 0.25 mg IV palonosetron, and 12 mg IV dexamethasone before chemotherapy on day 1, and 4 mg dexamethasone PO BID, before chemotherapy days 2 and 3.

Results 101 of the 120 patients were evaluable. In 51 patients who received the OPD regimen, the complete response (CR; no emesis, no rescue medication) rate was 88% for the acute period (24 h after chemotherapy), 76% for the delayed period (days 2-5), and 76% for the overall period (0-120 h). In 50 patients who received the FPD regimen, the CR was 84% acute, 74% delayed, and 74% overall (P > .01 for all periods). Patients with no nausea (0, on a scale 0-10, visual analogue scale) were: OPD: 86% acute, 71% delayed, 71% overall; FPD: 78% acute, 40% delayed, 40% overall (P > .01 for acute; P < .01 for delayed and overall) There were no grade 3 or 4 toxicities.

Conclusions CR was similar for OPD and FPD; nausea in the delayed and overall periods was signifcantly improved with OPD compared with FPD (P < .01).

Funding Reich Endowment for the Care of the Whole Patient
 

Click on the PDF icon at the top of this introduction to read the full article.
 

A 68-year-old Filipino man with a history of hypertension, type 2 diabetes, and osteoarthritis presented to the emergency department with a one-week history of increasing pain, swelling, erythema, and seepage of his right great toe. The patient denied paresthesias, fever, chills, night sweats, cough, dyspnea, or any change in his diet, medications (which included lisinopril, metformin, and acetaminophen as needed), or routine. Social history was negative for alcohol use and cigarette smoking.

He previously had similar symptoms in his right fourth toe that resulted in amputation. The patient was told at the time that he had a “bone infection” and amputation was necessary.

The patient was thin, alert, oriented, and in no acute distress. His vital signs and a cardiopulmonary exam were normal. The patient’s right great toe was tender to touch, with ulceration of the skin dorsally at the proximal nail fold. In addition, his toe was oozing a purulent, non-foul smelling discharge (FIGURE 1). Other pertinent findings included multiple enlarged joints on both hands with visible yellow-white subcutaneous nodules on the hands and dorsum of the forearm (FIGURE 2).

The patient’s white blood cell count was 10,800/mcL, C-reactive protein (CRP) was 18 mg/L, erythrocyte sedimentation rate (ESR) was 80 mm/hr, and uric acid was 12.5 mg/dL. His blood urea nitrogen was 52 mg/dL and creatinine was 2.5 mg/dL. A glycated hemoglobin test was 7.2%. A wound culture, aspirate from the dorsum of the toe, and x-ray were obtained.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Tophaceous gouty arthritis

The x-ray of the right great toe showed erosions of the metatarsophalangeal (MTP) joint (FIGURE 3). Given the patient’s age, underlying diabetes, skin ulceration, and elevation of CRP and ESR, the initial concern was for septic arthritis and osteomyelitis. However, the absence of leukocytosis and hyperglycemia argued against an infectious process.

The diagnosis of tophaceous gouty arthritis was confirmed by aspiration from the tophus, which demonstrated monosodium urate (MSU) crystals on polarized light microscopy. The patient presented with acute gout on the first right toe overlaying chronic tophaceous gout, complicated by renal failure.

Four phases. Gout progresses through 4 phases: asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout (intervals between acute attacks), and chronic tophaceous gout.¹ Chronic tophaceous gout is characterized by tophi—collections of solid urate in connective tissues (from bone to bursa, tendons, ligaments, and entheses).² There are often multiple tophi and they may be calcified. An acute gouty attack is marked by a relatively sudden increase in pain and swelling, and may improve spontaneously over the course of 7 to 10 days.³

Gout is the most common form of inflammatory arthritis, with a prevalence in the United States of 3.9%.⁴The findings of several studies suggest that the prevalence and incidence of gout have risen in recent decades, which may be attributable to a growing aging population, the rise in obesity, increasing numbers of people who have other conditions such as heart disease, kidney disease, and/or diabetes, and the use of diuretics by individuals with cardiovascular disease.⁵

In a meta-analysis on gouty involvement of the first MTP joint, the occurrence of acute first MTP arthritis has been reported to be an independent predictor of MSU crystal presence in patients with gout.⁶ The presence of first MTP arthritis and the predilection for MSU deposition in the medial and dorsal aspects of the joint suggested an association, but no causation, between the 2 disease processes. The authors concluded that the distinction between osteoarthritis and gout as the cause of the joint damage is often difficult.

The diagnosis of gout may be made clinically based on established clinical criteria. The most commonly used are the 1977 American College of Rheumatology (ACR) criteria for the classification of acute arthritis of primary gout. (See “The 12 diagnostic criteria for gout.”⁷) However, in 2015, the ACR/European League Against Rheumatism (EULAR) published a new set of criteria that include the signs and symptoms of chronic gout, as well.⁸ (The ACR-EULAR Gout Classification Criteria Calculator may be accessed at http://goutclassificationcalculator.auckland.ac.nz/.)

Differential diagnosis includes trauma, septic and reactive arthritis

The differential diagnosis of acute gouty arthritis includes trauma, pseudogout (arthritis involving calcium pyrophosphate dehydrate), septic arthritis, reactive arthritis, post-streptococcal arthritis, and Lyme disease.

Trauma with a resulting acute or stress fracture can be determined by x-ray or magnetic resonance imaging (MRI).

Pseudogout requires aspiration of fluid and examination for calcium pyrophosphate crystals under polarizing microscopy.⁹

Septic arthritis may present in a similar manner to other causes of acute arthritis. Therefore, arthrocentesis is needed to identify the causative infectious agent.¹⁰ Septic arthritis was considered in our patient, given his age, history of diabetes mellitus, and finding of skin ulceration over the toe. However, our patient did not have systemic symptoms, and the joint aspiration did not show the presence of bacteria.

Reactive arthritis typically presents with inflammation of the ligaments and tendons at their sites of insertion into the bone, and can affect other areas of the body, such as the genitourinary and ocular systems.¹¹

Post-streptococcal arthritis (aka acute rheumatic fever [ARF]) and Lyme disease can also present with joint complaints. The arthritis in ARF is usually migratory and involves several joints. Fever, rash, and a history of group A streptococcal infection are also diagnostic features.¹² History of travel to an endemic area or seasonal exposure would further differentiate Lyme disease from other causes of arthritis.

Further inquiry during the patient’s hospitalization revealed that he ate a lot of seafood and organ meat.

Deciding on a course of treatment

Initial treatment choices for acute gout include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids.¹³ Various NSAIDs have been studied in the treatment of acute gout, but none showed absolute superiority over others. One option is naproxen 500 mg twice daily, but the choice of NSAID is mainly based on the adverse reaction profile and the physician’s preference.

Due to frequent gastrointestinal adverse effects and the concern for toxicity and drug interactions, colchicine and corticosteroids are not typically the first-line agents for acute gout treatment. Patients with frequent recurrent gouty attacks require urate-lowering therapies, such as allopurinol or probenecid. Other indications for urate-lowering therapies include evidence of tophaceous deposits in joints and soft tissues and gouty arthropathy.

Our patient’s renal failure was likely chronic, secondary to his untreated tophaceous gouty disease. Because his creatinine clearance was between 30 and 60 mL/min per 1.73 m², he was not treated with NSAIDs, but with colchicine 1.2 mg for his initial flare, followed with a single dose of 0.6 mg in one hour. The patient had dramatic improvement of his pain the following day.

Initial treatment choices for acute gout include nonsteroidal anti-inflammatory drugs, colchicine, and corticosteroids.

Patient education on chronic gout was also provided. We specifically discussed the patient’s dietary habits with him, advising him to minimize his intake of seafood, animal organs, and red meat products, which are high in purines. The patient was also told that he would need to start urate-lowering therapy to prevent recurrent gouty attacks and further complications from gout.

CORRESPONDENCE
Joseph Huang, MD, Fort Belvoir Community Hospital, Family Medicine Clinic, 1st Floor Eagle Pavilion, 9300 Dewitt Loop, Fort Belvoir, VA 22060; [email protected].

A 68-year-old Filipino man with a history of hypertension, type 2 diabetes, and osteoarthritis presented to the emergency department with a one-week history of increasing pain, swelling, erythema, and seepage of his right great toe. The patient denied paresthesias, fever, chills, night sweats, cough, dyspnea, or any change in his diet, medications (which included lisinopril, metformin, and acetaminophen as needed), or routine. Social history was negative for alcohol use and cigarette smoking.

He previously had similar symptoms in his right fourth toe that resulted in amputation. The patient was told at the time that he had a “bone infection” and amputation was necessary.

The patient was thin, alert, oriented, and in no acute distress. His vital signs and a cardiopulmonary exam were normal. The patient’s right great toe was tender to touch, with ulceration of the skin dorsally at the proximal nail fold. In addition, his toe was oozing a purulent, non-foul smelling discharge (FIGURE 1). Other pertinent findings included multiple enlarged joints on both hands with visible yellow-white subcutaneous nodules on the hands and dorsum of the forearm (FIGURE 2).

The patient’s white blood cell count was 10,800/mcL, C-reactive protein (CRP) was 18 mg/L, erythrocyte sedimentation rate (ESR) was 80 mm/hr, and uric acid was 12.5 mg/dL. His blood urea nitrogen was 52 mg/dL and creatinine was 2.5 mg/dL. A glycated hemoglobin test was 7.2%. A wound culture, aspirate from the dorsum of the toe, and x-ray were obtained.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Tophaceous gouty arthritis

The x-ray of the right great toe showed erosions of the metatarsophalangeal (MTP) joint (FIGURE 3). Given the patient’s age, underlying diabetes, skin ulceration, and elevation of CRP and ESR, the initial concern was for septic arthritis and osteomyelitis. However, the absence of leukocytosis and hyperglycemia argued against an infectious process.

The diagnosis of tophaceous gouty arthritis was confirmed by aspiration from the tophus, which demonstrated monosodium urate (MSU) crystals on polarized light microscopy. The patient presented with acute gout on the first right toe overlaying chronic tophaceous gout, complicated by renal failure.

Four phases. Gout progresses through 4 phases: asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout (intervals between acute attacks), and chronic tophaceous gout.¹ Chronic tophaceous gout is characterized by tophi—collections of solid urate in connective tissues (from bone to bursa, tendons, ligaments, and entheses).² There are often multiple tophi and they may be calcified. An acute gouty attack is marked by a relatively sudden increase in pain and swelling, and may improve spontaneously over the course of 7 to 10 days.³

Gout is the most common form of inflammatory arthritis, with a prevalence in the United States of 3.9%.⁴The findings of several studies suggest that the prevalence and incidence of gout have risen in recent decades, which may be attributable to a growing aging population, the rise in obesity, increasing numbers of people who have other conditions such as heart disease, kidney disease, and/or diabetes, and the use of diuretics by individuals with cardiovascular disease.⁵

In a meta-analysis on gouty involvement of the first MTP joint, the occurrence of acute first MTP arthritis has been reported to be an independent predictor of MSU crystal presence in patients with gout.⁶ The presence of first MTP arthritis and the predilection for MSU deposition in the medial and dorsal aspects of the joint suggested an association, but no causation, between the 2 disease processes. The authors concluded that the distinction between osteoarthritis and gout as the cause of the joint damage is often difficult.

The diagnosis of gout may be made clinically based on established clinical criteria. The most commonly used are the 1977 American College of Rheumatology (ACR) criteria for the classification of acute arthritis of primary gout. (See “The 12 diagnostic criteria for gout.”⁷) However, in 2015, the ACR/European League Against Rheumatism (EULAR) published a new set of criteria that include the signs and symptoms of chronic gout, as well.⁸ (The ACR-EULAR Gout Classification Criteria Calculator may be accessed at http://goutclassificationcalculator.auckland.ac.nz/.)

Differential diagnosis includes trauma, septic and reactive arthritis

The differential diagnosis of acute gouty arthritis includes trauma, pseudogout (arthritis involving calcium pyrophosphate dehydrate), septic arthritis, reactive arthritis, post-streptococcal arthritis, and Lyme disease.

Trauma with a resulting acute or stress fracture can be determined by x-ray or magnetic resonance imaging (MRI).

Pseudogout requires aspiration of fluid and examination for calcium pyrophosphate crystals under polarizing microscopy.⁹

Septic arthritis may present in a similar manner to other causes of acute arthritis. Therefore, arthrocentesis is needed to identify the causative infectious agent.¹⁰ Septic arthritis was considered in our patient, given his age, history of diabetes mellitus, and finding of skin ulceration over the toe. However, our patient did not have systemic symptoms, and the joint aspiration did not show the presence of bacteria.

Reactive arthritis typically presents with inflammation of the ligaments and tendons at their sites of insertion into the bone, and can affect other areas of the body, such as the genitourinary and ocular systems.¹¹

Post-streptococcal arthritis (aka acute rheumatic fever [ARF]) and Lyme disease can also present with joint complaints. The arthritis in ARF is usually migratory and involves several joints. Fever, rash, and a history of group A streptococcal infection are also diagnostic features.¹² History of travel to an endemic area or seasonal exposure would further differentiate Lyme disease from other causes of arthritis.

Further inquiry during the patient’s hospitalization revealed that he ate a lot of seafood and organ meat.

Deciding on a course of treatment

Initial treatment choices for acute gout include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids.¹³ Various NSAIDs have been studied in the treatment of acute gout, but none showed absolute superiority over others. One option is naproxen 500 mg twice daily, but the choice of NSAID is mainly based on the adverse reaction profile and the physician’s preference.

Due to frequent gastrointestinal adverse effects and the concern for toxicity and drug interactions, colchicine and corticosteroids are not typically the first-line agents for acute gout treatment. Patients with frequent recurrent gouty attacks require urate-lowering therapies, such as allopurinol or probenecid. Other indications for urate-lowering therapies include evidence of tophaceous deposits in joints and soft tissues and gouty arthropathy.

Our patient’s renal failure was likely chronic, secondary to his untreated tophaceous gouty disease. Because his creatinine clearance was between 30 and 60 mL/min per 1.73 m², he was not treated with NSAIDs, but with colchicine 1.2 mg for his initial flare, followed with a single dose of 0.6 mg in one hour. The patient had dramatic improvement of his pain the following day.

Initial treatment choices for acute gout include nonsteroidal anti-inflammatory drugs, colchicine, and corticosteroids.

Patient education on chronic gout was also provided. We specifically discussed the patient’s dietary habits with him, advising him to minimize his intake of seafood, animal organs, and red meat products, which are high in purines. The patient was also told that he would need to start urate-lowering therapy to prevent recurrent gouty attacks and further complications from gout.

CORRESPONDENCE
Joseph Huang, MD, Fort Belvoir Community Hospital, Family Medicine Clinic, 1st Floor Eagle Pavilion, 9300 Dewitt Loop, Fort Belvoir, VA 22060; [email protected].

A 68-year-old Filipino man with a history of hypertension, type 2 diabetes, and osteoarthritis presented to the emergency department with a one-week history of increasing pain, swelling, erythema, and seepage of his right great toe. The patient denied paresthesias, fever, chills, night sweats, cough, dyspnea, or any change in his diet, medications (which included lisinopril, metformin, and acetaminophen as needed), or routine. Social history was negative for alcohol use and cigarette smoking.

He previously had similar symptoms in his right fourth toe that resulted in amputation. The patient was told at the time that he had a “bone infection” and amputation was necessary.

The patient was thin, alert, oriented, and in no acute distress. His vital signs and a cardiopulmonary exam were normal. The patient’s right great toe was tender to touch, with ulceration of the skin dorsally at the proximal nail fold. In addition, his toe was oozing a purulent, non-foul smelling discharge (FIGURE 1). Other pertinent findings included multiple enlarged joints on both hands with visible yellow-white subcutaneous nodules on the hands and dorsum of the forearm (FIGURE 2).

The patient’s white blood cell count was 10,800/mcL, C-reactive protein (CRP) was 18 mg/L, erythrocyte sedimentation rate (ESR) was 80 mm/hr, and uric acid was 12.5 mg/dL. His blood urea nitrogen was 52 mg/dL and creatinine was 2.5 mg/dL. A glycated hemoglobin test was 7.2%. A wound culture, aspirate from the dorsum of the toe, and x-ray were obtained.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Tophaceous gouty arthritis

The x-ray of the right great toe showed erosions of the metatarsophalangeal (MTP) joint (FIGURE 3). Given the patient’s age, underlying diabetes, skin ulceration, and elevation of CRP and ESR, the initial concern was for septic arthritis and osteomyelitis. However, the absence of leukocytosis and hyperglycemia argued against an infectious process.

The diagnosis of tophaceous gouty arthritis was confirmed by aspiration from the tophus, which demonstrated monosodium urate (MSU) crystals on polarized light microscopy. The patient presented with acute gout on the first right toe overlaying chronic tophaceous gout, complicated by renal failure.

Four phases. Gout progresses through 4 phases: asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout (intervals between acute attacks), and chronic tophaceous gout.¹ Chronic tophaceous gout is characterized by tophi—collections of solid urate in connective tissues (from bone to bursa, tendons, ligaments, and entheses).² There are often multiple tophi and they may be calcified. An acute gouty attack is marked by a relatively sudden increase in pain and swelling, and may improve spontaneously over the course of 7 to 10 days.³

Gout is the most common form of inflammatory arthritis, with a prevalence in the United States of 3.9%.⁴The findings of several studies suggest that the prevalence and incidence of gout have risen in recent decades, which may be attributable to a growing aging population, the rise in obesity, increasing numbers of people who have other conditions such as heart disease, kidney disease, and/or diabetes, and the use of diuretics by individuals with cardiovascular disease.⁵

In a meta-analysis on gouty involvement of the first MTP joint, the occurrence of acute first MTP arthritis has been reported to be an independent predictor of MSU crystal presence in patients with gout.⁶ The presence of first MTP arthritis and the predilection for MSU deposition in the medial and dorsal aspects of the joint suggested an association, but no causation, between the 2 disease processes. The authors concluded that the distinction between osteoarthritis and gout as the cause of the joint damage is often difficult.

The diagnosis of gout may be made clinically based on established clinical criteria. The most commonly used are the 1977 American College of Rheumatology (ACR) criteria for the classification of acute arthritis of primary gout. (See “The 12 diagnostic criteria for gout.”⁷) However, in 2015, the ACR/European League Against Rheumatism (EULAR) published a new set of criteria that include the signs and symptoms of chronic gout, as well.⁸ (The ACR-EULAR Gout Classification Criteria Calculator may be accessed at http://goutclassificationcalculator.auckland.ac.nz/.)

Differential diagnosis includes trauma, septic and reactive arthritis

The differential diagnosis of acute gouty arthritis includes trauma, pseudogout (arthritis involving calcium pyrophosphate dehydrate), septic arthritis, reactive arthritis, post-streptococcal arthritis, and Lyme disease.

Trauma with a resulting acute or stress fracture can be determined by x-ray or magnetic resonance imaging (MRI).

Pseudogout requires aspiration of fluid and examination for calcium pyrophosphate crystals under polarizing microscopy.⁹

Septic arthritis may present in a similar manner to other causes of acute arthritis. Therefore, arthrocentesis is needed to identify the causative infectious agent.¹⁰ Septic arthritis was considered in our patient, given his age, history of diabetes mellitus, and finding of skin ulceration over the toe. However, our patient did not have systemic symptoms, and the joint aspiration did not show the presence of bacteria.

Reactive arthritis typically presents with inflammation of the ligaments and tendons at their sites of insertion into the bone, and can affect other areas of the body, such as the genitourinary and ocular systems.¹¹

Post-streptococcal arthritis (aka acute rheumatic fever [ARF]) and Lyme disease can also present with joint complaints. The arthritis in ARF is usually migratory and involves several joints. Fever, rash, and a history of group A streptococcal infection are also diagnostic features.¹² History of travel to an endemic area or seasonal exposure would further differentiate Lyme disease from other causes of arthritis.

Further inquiry during the patient’s hospitalization revealed that he ate a lot of seafood and organ meat.

Deciding on a course of treatment

Initial treatment choices for acute gout include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids.¹³ Various NSAIDs have been studied in the treatment of acute gout, but none showed absolute superiority over others. One option is naproxen 500 mg twice daily, but the choice of NSAID is mainly based on the adverse reaction profile and the physician’s preference.

Due to frequent gastrointestinal adverse effects and the concern for toxicity and drug interactions, colchicine and corticosteroids are not typically the first-line agents for acute gout treatment. Patients with frequent recurrent gouty attacks require urate-lowering therapies, such as allopurinol or probenecid. Other indications for urate-lowering therapies include evidence of tophaceous deposits in joints and soft tissues and gouty arthropathy.

Our patient’s renal failure was likely chronic, secondary to his untreated tophaceous gouty disease. Because his creatinine clearance was between 30 and 60 mL/min per 1.73 m², he was not treated with NSAIDs, but with colchicine 1.2 mg for his initial flare, followed with a single dose of 0.6 mg in one hour. The patient had dramatic improvement of his pain the following day.

Initial treatment choices for acute gout include nonsteroidal anti-inflammatory drugs, colchicine, and corticosteroids.

Patient education on chronic gout was also provided. We specifically discussed the patient’s dietary habits with him, advising him to minimize his intake of seafood, animal organs, and red meat products, which are high in purines. The patient was also told that he would need to start urate-lowering therapy to prevent recurrent gouty attacks and further complications from gout.

CORRESPONDENCE
Joseph Huang, MD, Fort Belvoir Community Hospital, Family Medicine Clinic, 1st Floor Eagle Pavilion, 9300 Dewitt Loop, Fort Belvoir, VA 22060; [email protected].

Evidence summary

A 2013 Cochrane review of 17 RCTs with 2596 patients compared corticosteroids with placebo for treating bronchiolitis in children younger than 2 years.¹ The studies used dexamethasone, prednisolone, prednisone, and budesonide delivered by oral, inhaled, intravenous (IV), or intramuscular (IM) routes, ranging between a one-day dose to a 5-day taper. Doses ranged from 0.5 to 2 mg/kg/d for oral and parenteral routes and 0.2 to 1 mg for inhalation. Outcomes were rate of admissions at Days 1 and 7 from outpatient trials and length of stay among inpatients.

Investigators found no significant difference in admission rates at Day 1 and Day 7 between children treated with corticosteroids compared with placebo (Day 1: 8 trials, 1762 patients; relative risk [RR]=0.92; 95% confidence interval [CI], 0.78-1.1; Day 7: 5 trials, 1530 patients; RR=0.86; 95% CI, 0.70-1.1). Length of hospital stay didn’t differ between children treated with corticosteroids and children who received placebo (8 trials, 633 patients; mean difference= −0.18 days; 95% CI, −0.39 to 0.04).

Corticosteroid + epinephrine can lower hospital admissions

A 2009 multicenter, double-blind RCT with 800 patients (infants 6 weeks to 12 months of age with a first episode of bronchiolitis) that was included in the 2013 Cochrane review also compared the combination of epinephrine and corticosteroid with placebo and either agent alone.²

Infants were assigned to 4 groups: oral dexamethasone alone (1 mg/kg in the emergency room [ER] on Day 1, followed by 0.6 mg/kg daily for 5 days); nebulized epinephrine alone (2 treatments of 3 mL epinephrine 1:1000 solution); combined dexamethasone and epinephrine; and placebo. The primary outcome was hospital admission as long as 7 days after being seen in the ER.

Rates of admission were similar for the dexamethasone and placebo groups (25.6% vs 26.4%, respectively; RR=0.96; 95% CI, 0.69-1.3). The epinephrine group’s rate of admission was 23.7% (RR=0.88; CI, 0.63–1.23). Only the dexamethasone-epinephrine group had a lower rate of admission compared with placebo (17% vs 26%; RR=0.65; 95% CI, 0.45-0.95). The number needed to treat with dexamethasone-epinephrine to prevent one hospital admission was 11.

Review prompts revised recommendations

Based on the Cochrane review, the American Academy of Pediatrics (AAP) revised its evidence-based clinical practice guideline in 2014 to recommend that clinicians not administer systemic corticosteroids to infants with a diagnosis of bronchiolitis in any setting (evidence quality B, strong recommendation, based on results of multiple RCTs).³ The AAP advocates additional large trials to clarify whether combination therapy (corticosteroids plus agents with α or β agonist activity) is effective.

Evidence summary

A 2013 Cochrane review of 17 RCTs with 2596 patients compared corticosteroids with placebo for treating bronchiolitis in children younger than 2 years.¹ The studies used dexamethasone, prednisolone, prednisone, and budesonide delivered by oral, inhaled, intravenous (IV), or intramuscular (IM) routes, ranging between a one-day dose to a 5-day taper. Doses ranged from 0.5 to 2 mg/kg/d for oral and parenteral routes and 0.2 to 1 mg for inhalation. Outcomes were rate of admissions at Days 1 and 7 from outpatient trials and length of stay among inpatients.

Investigators found no significant difference in admission rates at Day 1 and Day 7 between children treated with corticosteroids compared with placebo (Day 1: 8 trials, 1762 patients; relative risk [RR]=0.92; 95% confidence interval [CI], 0.78-1.1; Day 7: 5 trials, 1530 patients; RR=0.86; 95% CI, 0.70-1.1). Length of hospital stay didn’t differ between children treated with corticosteroids and children who received placebo (8 trials, 633 patients; mean difference= −0.18 days; 95% CI, −0.39 to 0.04).

Corticosteroid + epinephrine can lower hospital admissions

A 2009 multicenter, double-blind RCT with 800 patients (infants 6 weeks to 12 months of age with a first episode of bronchiolitis) that was included in the 2013 Cochrane review also compared the combination of epinephrine and corticosteroid with placebo and either agent alone.²

Infants were assigned to 4 groups: oral dexamethasone alone (1 mg/kg in the emergency room [ER] on Day 1, followed by 0.6 mg/kg daily for 5 days); nebulized epinephrine alone (2 treatments of 3 mL epinephrine 1:1000 solution); combined dexamethasone and epinephrine; and placebo. The primary outcome was hospital admission as long as 7 days after being seen in the ER.

Rates of admission were similar for the dexamethasone and placebo groups (25.6% vs 26.4%, respectively; RR=0.96; 95% CI, 0.69-1.3). The epinephrine group’s rate of admission was 23.7% (RR=0.88; CI, 0.63–1.23). Only the dexamethasone-epinephrine group had a lower rate of admission compared with placebo (17% vs 26%; RR=0.65; 95% CI, 0.45-0.95). The number needed to treat with dexamethasone-epinephrine to prevent one hospital admission was 11.

Review prompts revised recommendations

Based on the Cochrane review, the American Academy of Pediatrics (AAP) revised its evidence-based clinical practice guideline in 2014 to recommend that clinicians not administer systemic corticosteroids to infants with a diagnosis of bronchiolitis in any setting (evidence quality B, strong recommendation, based on results of multiple RCTs).³ The AAP advocates additional large trials to clarify whether combination therapy (corticosteroids plus agents with α or β agonist activity) is effective.

Evidence summary

A 2013 Cochrane review of 17 RCTs with 2596 patients compared corticosteroids with placebo for treating bronchiolitis in children younger than 2 years.¹ The studies used dexamethasone, prednisolone, prednisone, and budesonide delivered by oral, inhaled, intravenous (IV), or intramuscular (IM) routes, ranging between a one-day dose to a 5-day taper. Doses ranged from 0.5 to 2 mg/kg/d for oral and parenteral routes and 0.2 to 1 mg for inhalation. Outcomes were rate of admissions at Days 1 and 7 from outpatient trials and length of stay among inpatients.

Investigators found no significant difference in admission rates at Day 1 and Day 7 between children treated with corticosteroids compared with placebo (Day 1: 8 trials, 1762 patients; relative risk [RR]=0.92; 95% confidence interval [CI], 0.78-1.1; Day 7: 5 trials, 1530 patients; RR=0.86; 95% CI, 0.70-1.1). Length of hospital stay didn’t differ between children treated with corticosteroids and children who received placebo (8 trials, 633 patients; mean difference= −0.18 days; 95% CI, −0.39 to 0.04).

Corticosteroid + epinephrine can lower hospital admissions

A 2009 multicenter, double-blind RCT with 800 patients (infants 6 weeks to 12 months of age with a first episode of bronchiolitis) that was included in the 2013 Cochrane review also compared the combination of epinephrine and corticosteroid with placebo and either agent alone.²

Infants were assigned to 4 groups: oral dexamethasone alone (1 mg/kg in the emergency room [ER] on Day 1, followed by 0.6 mg/kg daily for 5 days); nebulized epinephrine alone (2 treatments of 3 mL epinephrine 1:1000 solution); combined dexamethasone and epinephrine; and placebo. The primary outcome was hospital admission as long as 7 days after being seen in the ER.

Rates of admission were similar for the dexamethasone and placebo groups (25.6% vs 26.4%, respectively; RR=0.96; 95% CI, 0.69-1.3). The epinephrine group’s rate of admission was 23.7% (RR=0.88; CI, 0.63–1.23). Only the dexamethasone-epinephrine group had a lower rate of admission compared with placebo (17% vs 26%; RR=0.65; 95% CI, 0.45-0.95). The number needed to treat with dexamethasone-epinephrine to prevent one hospital admission was 11.

Review prompts revised recommendations

Based on the Cochrane review, the American Academy of Pediatrics (AAP) revised its evidence-based clinical practice guideline in 2014 to recommend that clinicians not administer systemic corticosteroids to infants with a diagnosis of bronchiolitis in any setting (evidence quality B, strong recommendation, based on results of multiple RCTs).³ The AAP advocates additional large trials to clarify whether combination therapy (corticosteroids plus agents with α or β agonist activity) is effective.

Immunotherapy using sublingual tablets containing house dust mite allergen extended the interval until patients developed a moderate asthma exacerbation in a manufacturer-sponsored clinical trial reported online April 26 in JAMA.

However, patients’ scores on both the Asthma Control Questionnaire and the Asthma Quality of Life Questionnaire showed no difference between active treatment and placebo. And 25%-27% of the study participants dropped out of the study, usually citing asthma exacerbations, adverse events, or “withdrawal of consent.” Further studies are needed to assess long-term efficacy and safety, said Dr. J. Christian Virchow of the department of pulmonology/intensive care medicine, University of Rostock (Germany), and his associates.

©Eraxion/Thinkstock

The trial, involving 834 adults with asthma related to house dust mite allergy that was not well controlled by inhaled corticosteroids and short-acting beta-agonists, was performed at 109 sites in 13 European countries during a 2-year period. These participants were randomly assigned to receive add-on daily sublingual tablets containing low-dose dust-mite extract (275 patients), high-dose extract (282 patients), or placebo (277 patients) for 7-12 months. During the final 6 months of the intervention, corticosteroids were reduced by half for 3 months and then withdrawn for 3 months.

The primary efficacy outcome (time to the first asthma exacerbation) was extended by both doses of active drug, compared with placebo, with hazard ratios of 0.69 for the lower dose and 0.66 for the higher dose, the investigators said (JAMA. 2016 Apr 26;315[16]:1715-25).

Adverse events were significantly more frequent with active treatment, affecting 39% of patients receiving the lower dose and 46% of those receiving the higher dose of active immunotherapy, compared with only 17% of patients receiving placebo. However, this study was not adequately powered to compare adverse events across groups, Dr. Virchow and his associates noted.

The most frequently reported adverse events were oral pruritus, mouth edema, and throat irritation, which developed within a median of 1-2 minutes of taking the first dose on day 1 and persisted for a median of 4-23 days. There were 32 serious adverse events, including erosive esophagitis, hepatocellular injury, arthralgia, laryngeal edema, and asthma.

This trial was limited in that treatment duration was much shorter than that for a standard course of immunotherapy, which is often 3 years. This prevents drawing conclusions regarding the sustained effect of the treatment. “Furthermore, because the ultimate aim of allergen immunotherapy is disease modification beyond the duration of treatment, a follow-up after the end of treatment would have been relevant,” the investigators said.

This study was sponsored by the Danish pharmaceutical company ALK. Dr. Virchow reported ties to 31 industry sources; his associates also reported ties to numerous industry sources.

Immunotherapy using sublingual tablets containing house dust mite allergen extended the interval until patients developed a moderate asthma exacerbation in a manufacturer-sponsored clinical trial reported online April 26 in JAMA.

However, patients’ scores on both the Asthma Control Questionnaire and the Asthma Quality of Life Questionnaire showed no difference between active treatment and placebo. And 25%-27% of the study participants dropped out of the study, usually citing asthma exacerbations, adverse events, or “withdrawal of consent.” Further studies are needed to assess long-term efficacy and safety, said Dr. J. Christian Virchow of the department of pulmonology/intensive care medicine, University of Rostock (Germany), and his associates.

©Eraxion/Thinkstock

The trial, involving 834 adults with asthma related to house dust mite allergy that was not well controlled by inhaled corticosteroids and short-acting beta-agonists, was performed at 109 sites in 13 European countries during a 2-year period. These participants were randomly assigned to receive add-on daily sublingual tablets containing low-dose dust-mite extract (275 patients), high-dose extract (282 patients), or placebo (277 patients) for 7-12 months. During the final 6 months of the intervention, corticosteroids were reduced by half for 3 months and then withdrawn for 3 months.

The primary efficacy outcome (time to the first asthma exacerbation) was extended by both doses of active drug, compared with placebo, with hazard ratios of 0.69 for the lower dose and 0.66 for the higher dose, the investigators said (JAMA. 2016 Apr 26;315[16]:1715-25).

Adverse events were significantly more frequent with active treatment, affecting 39% of patients receiving the lower dose and 46% of those receiving the higher dose of active immunotherapy, compared with only 17% of patients receiving placebo. However, this study was not adequately powered to compare adverse events across groups, Dr. Virchow and his associates noted.

The most frequently reported adverse events were oral pruritus, mouth edema, and throat irritation, which developed within a median of 1-2 minutes of taking the first dose on day 1 and persisted for a median of 4-23 days. There were 32 serious adverse events, including erosive esophagitis, hepatocellular injury, arthralgia, laryngeal edema, and asthma.

This trial was limited in that treatment duration was much shorter than that for a standard course of immunotherapy, which is often 3 years. This prevents drawing conclusions regarding the sustained effect of the treatment. “Furthermore, because the ultimate aim of allergen immunotherapy is disease modification beyond the duration of treatment, a follow-up after the end of treatment would have been relevant,” the investigators said.

This study was sponsored by the Danish pharmaceutical company ALK. Dr. Virchow reported ties to 31 industry sources; his associates also reported ties to numerous industry sources.

Immunotherapy using sublingual tablets containing house dust mite allergen extended the interval until patients developed a moderate asthma exacerbation in a manufacturer-sponsored clinical trial reported online April 26 in JAMA.

However, patients’ scores on both the Asthma Control Questionnaire and the Asthma Quality of Life Questionnaire showed no difference between active treatment and placebo. And 25%-27% of the study participants dropped out of the study, usually citing asthma exacerbations, adverse events, or “withdrawal of consent.” Further studies are needed to assess long-term efficacy and safety, said Dr. J. Christian Virchow of the department of pulmonology/intensive care medicine, University of Rostock (Germany), and his associates.

©Eraxion/Thinkstock

The trial, involving 834 adults with asthma related to house dust mite allergy that was not well controlled by inhaled corticosteroids and short-acting beta-agonists, was performed at 109 sites in 13 European countries during a 2-year period. These participants were randomly assigned to receive add-on daily sublingual tablets containing low-dose dust-mite extract (275 patients), high-dose extract (282 patients), or placebo (277 patients) for 7-12 months. During the final 6 months of the intervention, corticosteroids were reduced by half for 3 months and then withdrawn for 3 months.

The primary efficacy outcome (time to the first asthma exacerbation) was extended by both doses of active drug, compared with placebo, with hazard ratios of 0.69 for the lower dose and 0.66 for the higher dose, the investigators said (JAMA. 2016 Apr 26;315[16]:1715-25).

Adverse events were significantly more frequent with active treatment, affecting 39% of patients receiving the lower dose and 46% of those receiving the higher dose of active immunotherapy, compared with only 17% of patients receiving placebo. However, this study was not adequately powered to compare adverse events across groups, Dr. Virchow and his associates noted.

The most frequently reported adverse events were oral pruritus, mouth edema, and throat irritation, which developed within a median of 1-2 minutes of taking the first dose on day 1 and persisted for a median of 4-23 days. There were 32 serious adverse events, including erosive esophagitis, hepatocellular injury, arthralgia, laryngeal edema, and asthma.

This trial was limited in that treatment duration was much shorter than that for a standard course of immunotherapy, which is often 3 years. This prevents drawing conclusions regarding the sustained effect of the treatment. “Furthermore, because the ultimate aim of allergen immunotherapy is disease modification beyond the duration of treatment, a follow-up after the end of treatment would have been relevant,” the investigators said.

This study was sponsored by the Danish pharmaceutical company ALK. Dr. Virchow reported ties to 31 industry sources; his associates also reported ties to numerous industry sources.

DePuy Synthes Mitek Sports Medicine
(https://www.depuysynthes.com/hcp/mitek-sports-medicine)

Gryphon® Suture Anchor with Proknot™ Technology

Paul Favorito, MD, Wellington Orthopaedic and Sports Medicine, Cincinnati, OH

The Gryphon^® suture anchor with Proknot™ technology is a doubled No. 1 Permacord^® high-strength orthopedic suture with a proprietary pre-tied sliding knot. The suture construct is loaded onto a 3.0-mm Gryphonsuture anchor (Peek or Biocryl Rapide^® biocomposite material) and has clinical indications for labral repair of the shoulder and hip. In a laboratory setting, Pro­knot technology has been tested against other high-tensile sutures and commonly tied arthroscopic knots.¹ Proknot technology demonstrated higher ultimate strength, significantly less knot volume, and better reproducibility among surgeons.

Surgical pearl: I use the Gryphon Proknot suture anchor for all shoulder Bankart and superior labral anterior to posterior (SLAP) repairs. I have colleagues who also use this anchor for hip arthroscopy.

Once opened on the back table, the surgical assistant may ink the free limb of suture for easy arthroscopic identification. The anchor is placed and, in the case of hard bone frequently encountered in younger patients, a 2.5-mm drill bit may be substituted for the usual 2.4-mm. One important goal of any labral repair is to position knots away from the articular surface. The free suture limb is passed through the labrum, retrieved, and delivered through the open, pre-tied knot on the suture card.

Once the knot is released and dressed, the knot pusher is placed over the suture and the knot is advanced and preliminarily tensioned medial to the articular surface. The suture limbs are separated and one limb of the suture is removed from the knot pusher. As few as 1, or up to 3, half hitches may be placed to secure the knot, taking care to direct it away from the joint surface. The result is a strong but well-positioned knot with minimal mass securing the soft tissue.

DePuy Synthes Mitek Sports Medicine
(https://www.depuysynthes.com/hcp/mitek-sports-medicine)

Gryphon® Suture Anchor with Proknot™ Technology

Paul Favorito, MD, Wellington Orthopaedic and Sports Medicine, Cincinnati, OH

The Gryphon^® suture anchor with Proknot™ technology is a doubled No. 1 Permacord^® high-strength orthopedic suture with a proprietary pre-tied sliding knot. The suture construct is loaded onto a 3.0-mm Gryphonsuture anchor (Peek or Biocryl Rapide^® biocomposite material) and has clinical indications for labral repair of the shoulder and hip. In a laboratory setting, Pro­knot technology has been tested against other high-tensile sutures and commonly tied arthroscopic knots.¹ Proknot technology demonstrated higher ultimate strength, significantly less knot volume, and better reproducibility among surgeons.

Surgical pearl: I use the Gryphon Proknot suture anchor for all shoulder Bankart and superior labral anterior to posterior (SLAP) repairs. I have colleagues who also use this anchor for hip arthroscopy.

Once opened on the back table, the surgical assistant may ink the free limb of suture for easy arthroscopic identification. The anchor is placed and, in the case of hard bone frequently encountered in younger patients, a 2.5-mm drill bit may be substituted for the usual 2.4-mm. One important goal of any labral repair is to position knots away from the articular surface. The free suture limb is passed through the labrum, retrieved, and delivered through the open, pre-tied knot on the suture card.

Once the knot is released and dressed, the knot pusher is placed over the suture and the knot is advanced and preliminarily tensioned medial to the articular surface. The suture limbs are separated and one limb of the suture is removed from the knot pusher. As few as 1, or up to 3, half hitches may be placed to secure the knot, taking care to direct it away from the joint surface. The result is a strong but well-positioned knot with minimal mass securing the soft tissue.

DePuy Synthes Mitek Sports Medicine
(https://www.depuysynthes.com/hcp/mitek-sports-medicine)

Gryphon® Suture Anchor with Proknot™ Technology

Paul Favorito, MD, Wellington Orthopaedic and Sports Medicine, Cincinnati, OH

The Gryphon^® suture anchor with Proknot™ technology is a doubled No. 1 Permacord^® high-strength orthopedic suture with a proprietary pre-tied sliding knot. The suture construct is loaded onto a 3.0-mm Gryphonsuture anchor (Peek or Biocryl Rapide^® biocomposite material) and has clinical indications for labral repair of the shoulder and hip. In a laboratory setting, Pro­knot technology has been tested against other high-tensile sutures and commonly tied arthroscopic knots.¹ Proknot technology demonstrated higher ultimate strength, significantly less knot volume, and better reproducibility among surgeons.

Surgical pearl: I use the Gryphon Proknot suture anchor for all shoulder Bankart and superior labral anterior to posterior (SLAP) repairs. I have colleagues who also use this anchor for hip arthroscopy.

Once opened on the back table, the surgical assistant may ink the free limb of suture for easy arthroscopic identification. The anchor is placed and, in the case of hard bone frequently encountered in younger patients, a 2.5-mm drill bit may be substituted for the usual 2.4-mm. One important goal of any labral repair is to position knots away from the articular surface. The free suture limb is passed through the labrum, retrieved, and delivered through the open, pre-tied knot on the suture card.

Once the knot is released and dressed, the knot pusher is placed over the suture and the knot is advanced and preliminarily tensioned medial to the articular surface. The suture limbs are separated and one limb of the suture is removed from the knot pusher. As few as 1, or up to 3, half hitches may be placed to secure the knot, taking care to direct it away from the joint surface. The result is a strong but well-positioned knot with minimal mass securing the soft tissue.

ORLANDO, FL—Using arthroscopic superior capsule reconstruction (ASCR) to treat patients with massive rotator cuff tears can improve shoulder strength and function, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.

Researchers used ASCR to treat 100 patients (average age: 66) who had irreparable rotator cuff tears that failed during previous treatment. Physical exams, x-rays, and magnetic resonance imaging were performed before surgery, at 3, 6 and 12 months following surgery, and on a yearly basis thereafter. Rates of return to work or sport were analyzed in 34 patients who were employed and 26 patients who were recreational athletes before the rotator cuff tear.

Overall, 92% of patients significantly improved their strength and shoulder function. In all, 32 patients returned fully to their previous work and 2 patients returned with reduced hours and workloads. All 26 patients who played sports prior to injury fully returned to their activities.

ORLANDO, FL—Using arthroscopic superior capsule reconstruction (ASCR) to treat patients with massive rotator cuff tears can improve shoulder strength and function, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.

Researchers used ASCR to treat 100 patients (average age: 66) who had irreparable rotator cuff tears that failed during previous treatment. Physical exams, x-rays, and magnetic resonance imaging were performed before surgery, at 3, 6 and 12 months following surgery, and on a yearly basis thereafter. Rates of return to work or sport were analyzed in 34 patients who were employed and 26 patients who were recreational athletes before the rotator cuff tear.

Overall, 92% of patients significantly improved their strength and shoulder function. In all, 32 patients returned fully to their previous work and 2 patients returned with reduced hours and workloads. All 26 patients who played sports prior to injury fully returned to their activities.

ORLANDO, FL—Using arthroscopic superior capsule reconstruction (ASCR) to treat patients with massive rotator cuff tears can improve shoulder strength and function, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.

Researchers used ASCR to treat 100 patients (average age: 66) who had irreparable rotator cuff tears that failed during previous treatment. Physical exams, x-rays, and magnetic resonance imaging were performed before surgery, at 3, 6 and 12 months following surgery, and on a yearly basis thereafter. Rates of return to work or sport were analyzed in 34 patients who were employed and 26 patients who were recreational athletes before the rotator cuff tear.

Overall, 92% of patients significantly improved their strength and shoulder function. In all, 32 patients returned fully to their previous work and 2 patients returned with reduced hours and workloads. All 26 patients who played sports prior to injury fully returned to their activities.