A spike in later-stage breast cancers is a potential byproduct of the Republican-proposed Medicaid reductions, according to Wafa Tarazi, PhD, and her colleagues.

The team looked at breast cancer stage at diagnosis following the 2005 Medicaid disenrollment of nearly 170,000 nonelderly adults in Tennessee that occurred because of state financial issues.

“Overall, nonelderly women in Tennessee were diagnosed at later stages of disease and experienced more delays in treatment in the period after disenrollment,” wrote Dr. Tarazi of Virginia Commonwealth University, Richmond, and her colleagues. “Disenrollment was found to be associated with a 3.3 percentage point increase in late stage of disease at the time of diagnosis” (Cancer 2016 June 26. doi: 10.1002/cncr.30771).

The investigators offered a few explanations for why this could be the case.

sndr/istockphoto.com

[email protected]

A spike in later-stage breast cancers is a potential byproduct of the Republican-proposed Medicaid reductions, according to Wafa Tarazi, PhD, and her colleagues.

The team looked at breast cancer stage at diagnosis following the 2005 Medicaid disenrollment of nearly 170,000 nonelderly adults in Tennessee that occurred because of state financial issues.

“Overall, nonelderly women in Tennessee were diagnosed at later stages of disease and experienced more delays in treatment in the period after disenrollment,” wrote Dr. Tarazi of Virginia Commonwealth University, Richmond, and her colleagues. “Disenrollment was found to be associated with a 3.3 percentage point increase in late stage of disease at the time of diagnosis” (Cancer 2016 June 26. doi: 10.1002/cncr.30771).

The investigators offered a few explanations for why this could be the case.

sndr/istockphoto.com

[email protected]

A spike in later-stage breast cancers is a potential byproduct of the Republican-proposed Medicaid reductions, according to Wafa Tarazi, PhD, and her colleagues.

The team looked at breast cancer stage at diagnosis following the 2005 Medicaid disenrollment of nearly 170,000 nonelderly adults in Tennessee that occurred because of state financial issues.

“Overall, nonelderly women in Tennessee were diagnosed at later stages of disease and experienced more delays in treatment in the period after disenrollment,” wrote Dr. Tarazi of Virginia Commonwealth University, Richmond, and her colleagues. “Disenrollment was found to be associated with a 3.3 percentage point increase in late stage of disease at the time of diagnosis” (Cancer 2016 June 26. doi: 10.1002/cncr.30771).

The investigators offered a few explanations for why this could be the case.

sndr/istockphoto.com

[email protected]

MADRID – Bisphosphonates mitigate the damaging effects of glucocorticoid on bone, boosting bone mineral density and reducing the risk of fracture by up to 33%, compared with placebo, according to a systematic review and meta-analysis.

The review of 11 randomized, controlled trials found that bisphosphonates consistently improved bone outcomes among patients taking prednisone, Anas Makhzoum, MD, said at the European Congress of Rheumatology.

[email protected]

On Twitter @alz_gal

MADRID – Bisphosphonates mitigate the damaging effects of glucocorticoid on bone, boosting bone mineral density and reducing the risk of fracture by up to 33%, compared with placebo, according to a systematic review and meta-analysis.

The review of 11 randomized, controlled trials found that bisphosphonates consistently improved bone outcomes among patients taking prednisone, Anas Makhzoum, MD, said at the European Congress of Rheumatology.

[email protected]

On Twitter @alz_gal

MADRID – Bisphosphonates mitigate the damaging effects of glucocorticoid on bone, boosting bone mineral density and reducing the risk of fracture by up to 33%, compared with placebo, according to a systematic review and meta-analysis.

The review of 11 randomized, controlled trials found that bisphosphonates consistently improved bone outcomes among patients taking prednisone, Anas Makhzoum, MD, said at the European Congress of Rheumatology.

[email protected]

On Twitter @alz_gal

The Diagnosis: Dermatofibroma

Dermatofibroma (DF) is a commonly encountered lesion. Although usually a straightforward clinical diagnosis, histopathological diagnosis is sometimes required. Conventional histologic findings of DF are hyperkeratosis, induction of the epidermis with acanthosis, and basal layer hyperpigmentation.^1,2 Within the dermis there usually is proliferation of fibroblasts, histiocytes, and blood vessels that sometimes spares the overlying papillary dermis. Nomenclature of specific variants may be assigned based on the predominant component (eg, nodular subepidermal fibrosis, histiocytoma, sclerosing hemangioma) or histologic findings (eg, fibrocollagenous, sclerotic, cellular, histiocytic, lipidized, angiomatous, aneurysmal, clear cell, monster cell, myxoid, keloidal, palisading, osteoclastic, epithelioid).^3-5 Of the histologic variants, fibrocollagenous is most common, but knowledge of other variants is important for accurate diagnosis, especially to exclude malignancy.

The sclerosing hemangioma variant of DF may pre-sent a diagnostic dilemma. In addition to typical features of DF, pseudovascular spaces, abundant hemosiderin, and reactive-appearing spindled cells are histologically demonstrated. The marked sclerosis and pigment deposition may mimic a blue nevus, and the dilated pseudovascular spaces may be reminiscent of a vascular neoplasm such as angiosarcoma or Kaposi sarcoma. However, the presence of characteristic features such as peripheral collagen trapping and overlying epidermal hyperplasia provide important clues for correct diagnosis. 

Angiosarcomas (Figure 1) are malignant neoplasms with vascular differentiation. Cutaneous angiosarcomas present as purple plaques or nodules on the head and/or neck in elderly individuals as well as in patients with chronic lymphedema or prior radiation exposure.^6-9 They are aggressive neoplasms with high rates of recurrence and metastases. Microscopically, the tumor is composed of anastomosing vascular channels lined by atypical endothelial cells with a multilayered appearance. There is frequent red blood cell extravasation, and substantial hemosiderin deposition may be noted in long-standing lesions. Neoplastic cells are positive for vascular markers (CD34, CD31, ETS-related gene transcription factor). Notably, cases associated with radiation exposure and chronic lymphedema are positive for MYC.¹⁰

Blue nevi (Figure 2) are benign melanocytic tumors that occur most frequently in children but may pre-sent in any age group. Clinical presentation is a blue to black, slightly raised papule that may be found on any site of the body. Biopsy typically shows a wedge-shaped infiltrate of spindled melanocytes with elongated dendritic processes in a sclerotic collagenous stroma. There frequently is a striking population of heavily pigmented melanophages. The melanocytes are positive for melanoma antigen recognized by T cells (MART-1)/melan-A, S-100, and transcription factor SOX-10. In contrast to other benign nevi, human melanoma black-45 will be positive in the dermal component.

Dermatofibrosarcoma protuberans (Figure 3) is a dermal-based tumor of intermediate malignant potential with a high rate of local recurrence and potential for sarcomatous transformation. Dermatofibrosarcoma protuberans most commonly presents in young adults as firm, pink to brown plaques and can occur on any site of the body. Histologically, they show a dermal proliferation of spindled cells that infiltrate in a storiform fashion into the subcutaneous adipose tissue,¹¹ which imparts a honeycomb or Swiss cheese pattern. The tumor characteristically demonstrates positive staining for CD34. Loss of CD34 staining, increased mitoses, nuclear atypia, and fascicular growth are features suggestive of sarcomatous transformation.^11,12 Dermatofibrosarcoma protuberans is associated with chromosomal abnormalities of chromosomes 17 and 22, resulting in COL1A1 (collagen type 1 alpha 1 chain) and PDGF-β (platelet-derived growth factor subunit B) gene fusion.¹³

Sclerotic fibromas (also known as storiform collagenomas)(Figure 4) may represent regressed DFs and are frequently associated with prior trauma to the affected area.^14,15 They usually appear as flesh-colored papules or nodules on the face and trunk. The presence of multiple sclerotic fibromas is associated with Cowden syndrome.^16,17 Histologically, the lesions present as well-demarcated, nonencapsulated, dermal nodules composed of a storiform or whorled arrangement of collagen with spindled fibroblasts. The sclerotic collagen bundles often are separated by small clefts imparting a plywoodlike pattern.¹⁶

The differential diagnosis for DF expands once atypical clinical and histopathological findings are present. In this case, the nodule was much larger and darker than the usual appearance of DF (3-10 mm).^2,4 Given the lesion's nodularity, the clinical dimple sign on lateral compression could not be seen. On biopsy, the predominance of blood vessels and sclerosis further complicated the diagnostic picture. In unusual cases such as this one, correlation of clinical history, histology, and immunophenotype is ever important.

The Diagnosis: Dermatofibroma

Dermatofibroma (DF) is a commonly encountered lesion. Although usually a straightforward clinical diagnosis, histopathological diagnosis is sometimes required. Conventional histologic findings of DF are hyperkeratosis, induction of the epidermis with acanthosis, and basal layer hyperpigmentation.^1,2 Within the dermis there usually is proliferation of fibroblasts, histiocytes, and blood vessels that sometimes spares the overlying papillary dermis. Nomenclature of specific variants may be assigned based on the predominant component (eg, nodular subepidermal fibrosis, histiocytoma, sclerosing hemangioma) or histologic findings (eg, fibrocollagenous, sclerotic, cellular, histiocytic, lipidized, angiomatous, aneurysmal, clear cell, monster cell, myxoid, keloidal, palisading, osteoclastic, epithelioid).^3-5 Of the histologic variants, fibrocollagenous is most common, but knowledge of other variants is important for accurate diagnosis, especially to exclude malignancy.

The sclerosing hemangioma variant of DF may pre-sent a diagnostic dilemma. In addition to typical features of DF, pseudovascular spaces, abundant hemosiderin, and reactive-appearing spindled cells are histologically demonstrated. The marked sclerosis and pigment deposition may mimic a blue nevus, and the dilated pseudovascular spaces may be reminiscent of a vascular neoplasm such as angiosarcoma or Kaposi sarcoma. However, the presence of characteristic features such as peripheral collagen trapping and overlying epidermal hyperplasia provide important clues for correct diagnosis. 

Angiosarcomas (Figure 1) are malignant neoplasms with vascular differentiation. Cutaneous angiosarcomas present as purple plaques or nodules on the head and/or neck in elderly individuals as well as in patients with chronic lymphedema or prior radiation exposure.^6-9 They are aggressive neoplasms with high rates of recurrence and metastases. Microscopically, the tumor is composed of anastomosing vascular channels lined by atypical endothelial cells with a multilayered appearance. There is frequent red blood cell extravasation, and substantial hemosiderin deposition may be noted in long-standing lesions. Neoplastic cells are positive for vascular markers (CD34, CD31, ETS-related gene transcription factor). Notably, cases associated with radiation exposure and chronic lymphedema are positive for MYC.¹⁰

Blue nevi (Figure 2) are benign melanocytic tumors that occur most frequently in children but may pre-sent in any age group. Clinical presentation is a blue to black, slightly raised papule that may be found on any site of the body. Biopsy typically shows a wedge-shaped infiltrate of spindled melanocytes with elongated dendritic processes in a sclerotic collagenous stroma. There frequently is a striking population of heavily pigmented melanophages. The melanocytes are positive for melanoma antigen recognized by T cells (MART-1)/melan-A, S-100, and transcription factor SOX-10. In contrast to other benign nevi, human melanoma black-45 will be positive in the dermal component.

Dermatofibrosarcoma protuberans (Figure 3) is a dermal-based tumor of intermediate malignant potential with a high rate of local recurrence and potential for sarcomatous transformation. Dermatofibrosarcoma protuberans most commonly presents in young adults as firm, pink to brown plaques and can occur on any site of the body. Histologically, they show a dermal proliferation of spindled cells that infiltrate in a storiform fashion into the subcutaneous adipose tissue,¹¹ which imparts a honeycomb or Swiss cheese pattern. The tumor characteristically demonstrates positive staining for CD34. Loss of CD34 staining, increased mitoses, nuclear atypia, and fascicular growth are features suggestive of sarcomatous transformation.^11,12 Dermatofibrosarcoma protuberans is associated with chromosomal abnormalities of chromosomes 17 and 22, resulting in COL1A1 (collagen type 1 alpha 1 chain) and PDGF-β (platelet-derived growth factor subunit B) gene fusion.¹³

Sclerotic fibromas (also known as storiform collagenomas)(Figure 4) may represent regressed DFs and are frequently associated with prior trauma to the affected area.^14,15 They usually appear as flesh-colored papules or nodules on the face and trunk. The presence of multiple sclerotic fibromas is associated with Cowden syndrome.^16,17 Histologically, the lesions present as well-demarcated, nonencapsulated, dermal nodules composed of a storiform or whorled arrangement of collagen with spindled fibroblasts. The sclerotic collagen bundles often are separated by small clefts imparting a plywoodlike pattern.¹⁶

The differential diagnosis for DF expands once atypical clinical and histopathological findings are present. In this case, the nodule was much larger and darker than the usual appearance of DF (3-10 mm).^2,4 Given the lesion's nodularity, the clinical dimple sign on lateral compression could not be seen. On biopsy, the predominance of blood vessels and sclerosis further complicated the diagnostic picture. In unusual cases such as this one, correlation of clinical history, histology, and immunophenotype is ever important.

The Diagnosis: Dermatofibroma

Dermatofibroma (DF) is a commonly encountered lesion. Although usually a straightforward clinical diagnosis, histopathological diagnosis is sometimes required. Conventional histologic findings of DF are hyperkeratosis, induction of the epidermis with acanthosis, and basal layer hyperpigmentation.^1,2 Within the dermis there usually is proliferation of fibroblasts, histiocytes, and blood vessels that sometimes spares the overlying papillary dermis. Nomenclature of specific variants may be assigned based on the predominant component (eg, nodular subepidermal fibrosis, histiocytoma, sclerosing hemangioma) or histologic findings (eg, fibrocollagenous, sclerotic, cellular, histiocytic, lipidized, angiomatous, aneurysmal, clear cell, monster cell, myxoid, keloidal, palisading, osteoclastic, epithelioid).^3-5 Of the histologic variants, fibrocollagenous is most common, but knowledge of other variants is important for accurate diagnosis, especially to exclude malignancy.

The sclerosing hemangioma variant of DF may pre-sent a diagnostic dilemma. In addition to typical features of DF, pseudovascular spaces, abundant hemosiderin, and reactive-appearing spindled cells are histologically demonstrated. The marked sclerosis and pigment deposition may mimic a blue nevus, and the dilated pseudovascular spaces may be reminiscent of a vascular neoplasm such as angiosarcoma or Kaposi sarcoma. However, the presence of characteristic features such as peripheral collagen trapping and overlying epidermal hyperplasia provide important clues for correct diagnosis. 

Angiosarcomas (Figure 1) are malignant neoplasms with vascular differentiation. Cutaneous angiosarcomas present as purple plaques or nodules on the head and/or neck in elderly individuals as well as in patients with chronic lymphedema or prior radiation exposure.^6-9 They are aggressive neoplasms with high rates of recurrence and metastases. Microscopically, the tumor is composed of anastomosing vascular channels lined by atypical endothelial cells with a multilayered appearance. There is frequent red blood cell extravasation, and substantial hemosiderin deposition may be noted in long-standing lesions. Neoplastic cells are positive for vascular markers (CD34, CD31, ETS-related gene transcription factor). Notably, cases associated with radiation exposure and chronic lymphedema are positive for MYC.¹⁰

Blue nevi (Figure 2) are benign melanocytic tumors that occur most frequently in children but may pre-sent in any age group. Clinical presentation is a blue to black, slightly raised papule that may be found on any site of the body. Biopsy typically shows a wedge-shaped infiltrate of spindled melanocytes with elongated dendritic processes in a sclerotic collagenous stroma. There frequently is a striking population of heavily pigmented melanophages. The melanocytes are positive for melanoma antigen recognized by T cells (MART-1)/melan-A, S-100, and transcription factor SOX-10. In contrast to other benign nevi, human melanoma black-45 will be positive in the dermal component.

Dermatofibrosarcoma protuberans (Figure 3) is a dermal-based tumor of intermediate malignant potential with a high rate of local recurrence and potential for sarcomatous transformation. Dermatofibrosarcoma protuberans most commonly presents in young adults as firm, pink to brown plaques and can occur on any site of the body. Histologically, they show a dermal proliferation of spindled cells that infiltrate in a storiform fashion into the subcutaneous adipose tissue,¹¹ which imparts a honeycomb or Swiss cheese pattern. The tumor characteristically demonstrates positive staining for CD34. Loss of CD34 staining, increased mitoses, nuclear atypia, and fascicular growth are features suggestive of sarcomatous transformation.^11,12 Dermatofibrosarcoma protuberans is associated with chromosomal abnormalities of chromosomes 17 and 22, resulting in COL1A1 (collagen type 1 alpha 1 chain) and PDGF-β (platelet-derived growth factor subunit B) gene fusion.¹³

Sclerotic fibromas (also known as storiform collagenomas)(Figure 4) may represent regressed DFs and are frequently associated with prior trauma to the affected area.^14,15 They usually appear as flesh-colored papules or nodules on the face and trunk. The presence of multiple sclerotic fibromas is associated with Cowden syndrome.^16,17 Histologically, the lesions present as well-demarcated, nonencapsulated, dermal nodules composed of a storiform or whorled arrangement of collagen with spindled fibroblasts. The sclerotic collagen bundles often are separated by small clefts imparting a plywoodlike pattern.¹⁶

The differential diagnosis for DF expands once atypical clinical and histopathological findings are present. In this case, the nodule was much larger and darker than the usual appearance of DF (3-10 mm).^2,4 Given the lesion's nodularity, the clinical dimple sign on lateral compression could not be seen. On biopsy, the predominance of blood vessels and sclerosis further complicated the diagnostic picture. In unusual cases such as this one, correlation of clinical history, histology, and immunophenotype is ever important.

The presence of cirrhosis in patients with autoimmune hepatitis markedly increased their risk of hepatocellular carcinoma, according to a systematic review and meta-analysis of 25 cohort studies and 6,528 patients.

Estimated rates of hepatocellular carcinoma (HCC) were 10.1 (6.9-14.7) cases per 1,000 person-years in these patients versus 1.1 (0.6-2.2) cases per 1,000 person-years in patients without cirrhosis at diagnosis, Aylin Tansel, MD, of Baylor College of Medicine in Houston, and associates reported in Clinical Gastroenterology and Hepatology (doi: 10.1016/j.cgh.2017.02.006). Thus, surveillance for HCC “might be cost effective in this population,” they wrote. “However, patients with AIH [autoimmune hepatitis] without cirrhosis at index diagnosis, particularly those identified from general populations, are at an extremely low risk of HCC.”

Source: American Gastroenterological Association

Autoimmune hepatitis may be asymptomatic at presentation or may cause severe acute hepatitis or even fulminant liver failure. Even with immunosuppressive therapy, patients progress to cirrhosis at reported annual rates of 0.1%-8%. HCC is the fastest-growing cause of cancer mortality, and the American Association for the Study of Liver Diseases (AASLD) recommends enhanced surveillance for this disease in patients whose annual estimated risk is at least 1.5%. Although the European Association for the Study of Liver Diseases recommends screening for HCC in patients with autoimmune hepatitis and cirrhosis, AASLD makes no such recommendation, the reviewers noted. To study the risk of HCC in patients with autoimmune hepatitis, they searched PubMed, Embase, and reference lists for relevant cohort studies published through June 2016. This work yielded 20 papers and five abstracts with a pooled median follow-up period of 8 years.

The overall pooled incidence of HCC was 3.1 (95% confidence interval, 2.2-4.2) cases per 1,000 person-years, or 1.007% per year, the reviewers wrote. However, the 95% confidence interval for the annual incidence rate nearly encompassed the 1.5% cutoff recommended by AASLD, they said. Furthermore, 5 of 16 studies that investigated the risk of HCC in patients with concurrent cirrhosis reported incidence rates above 1.5%. Among 93 patients who developed HCC in the meta-analysis, only 1 did not have cirrhosis by the time autoimmune hepatitis was diagnosed.

The meta-analysis also linked HCC to older age and Asian ethnicity among patients with autoimmune hepatitis, as has been reported before. Male sex only slightly increased the risk of HCC, but the studies included only about 1,130 men, the reviewers noted. Although the severity of autoimmune hepatitis varied among studies, higher rates of relapse predicted HCC in two cohorts. Additionally, one study linked alcohol abuse to a sixfold higher risk of HCC among patients with autoimmune hepatitis. “These data support careful monitoring of patients with autoimmune hepatitis, particularly older men, patients with multiple autoimmune hepatitis relapses, and those with ongoing alcohol abuse,” the investigators wrote.

They found no evidence of publication bias, but each individual study included at most 15 cases of HCC, so pooled incidence rates were probably imprecise, especially for subgroups, they said. Studies also inconsistently reported HCC risk factors, often lacked comparison groups, and usually did not report the effects of surveillance for HCC.

Dr. Tansel reported receiving support from the National Institutes of Health. The reviewers had no conflicts of interest.

The presence of cirrhosis in patients with autoimmune hepatitis markedly increased their risk of hepatocellular carcinoma, according to a systematic review and meta-analysis of 25 cohort studies and 6,528 patients.

Estimated rates of hepatocellular carcinoma (HCC) were 10.1 (6.9-14.7) cases per 1,000 person-years in these patients versus 1.1 (0.6-2.2) cases per 1,000 person-years in patients without cirrhosis at diagnosis, Aylin Tansel, MD, of Baylor College of Medicine in Houston, and associates reported in Clinical Gastroenterology and Hepatology (doi: 10.1016/j.cgh.2017.02.006). Thus, surveillance for HCC “might be cost effective in this population,” they wrote. “However, patients with AIH [autoimmune hepatitis] without cirrhosis at index diagnosis, particularly those identified from general populations, are at an extremely low risk of HCC.”

Source: American Gastroenterological Association

Autoimmune hepatitis may be asymptomatic at presentation or may cause severe acute hepatitis or even fulminant liver failure. Even with immunosuppressive therapy, patients progress to cirrhosis at reported annual rates of 0.1%-8%. HCC is the fastest-growing cause of cancer mortality, and the American Association for the Study of Liver Diseases (AASLD) recommends enhanced surveillance for this disease in patients whose annual estimated risk is at least 1.5%. Although the European Association for the Study of Liver Diseases recommends screening for HCC in patients with autoimmune hepatitis and cirrhosis, AASLD makes no such recommendation, the reviewers noted. To study the risk of HCC in patients with autoimmune hepatitis, they searched PubMed, Embase, and reference lists for relevant cohort studies published through June 2016. This work yielded 20 papers and five abstracts with a pooled median follow-up period of 8 years.

The overall pooled incidence of HCC was 3.1 (95% confidence interval, 2.2-4.2) cases per 1,000 person-years, or 1.007% per year, the reviewers wrote. However, the 95% confidence interval for the annual incidence rate nearly encompassed the 1.5% cutoff recommended by AASLD, they said. Furthermore, 5 of 16 studies that investigated the risk of HCC in patients with concurrent cirrhosis reported incidence rates above 1.5%. Among 93 patients who developed HCC in the meta-analysis, only 1 did not have cirrhosis by the time autoimmune hepatitis was diagnosed.

The meta-analysis also linked HCC to older age and Asian ethnicity among patients with autoimmune hepatitis, as has been reported before. Male sex only slightly increased the risk of HCC, but the studies included only about 1,130 men, the reviewers noted. Although the severity of autoimmune hepatitis varied among studies, higher rates of relapse predicted HCC in two cohorts. Additionally, one study linked alcohol abuse to a sixfold higher risk of HCC among patients with autoimmune hepatitis. “These data support careful monitoring of patients with autoimmune hepatitis, particularly older men, patients with multiple autoimmune hepatitis relapses, and those with ongoing alcohol abuse,” the investigators wrote.

They found no evidence of publication bias, but each individual study included at most 15 cases of HCC, so pooled incidence rates were probably imprecise, especially for subgroups, they said. Studies also inconsistently reported HCC risk factors, often lacked comparison groups, and usually did not report the effects of surveillance for HCC.

Dr. Tansel reported receiving support from the National Institutes of Health. The reviewers had no conflicts of interest.

The presence of cirrhosis in patients with autoimmune hepatitis markedly increased their risk of hepatocellular carcinoma, according to a systematic review and meta-analysis of 25 cohort studies and 6,528 patients.

Estimated rates of hepatocellular carcinoma (HCC) were 10.1 (6.9-14.7) cases per 1,000 person-years in these patients versus 1.1 (0.6-2.2) cases per 1,000 person-years in patients without cirrhosis at diagnosis, Aylin Tansel, MD, of Baylor College of Medicine in Houston, and associates reported in Clinical Gastroenterology and Hepatology (doi: 10.1016/j.cgh.2017.02.006). Thus, surveillance for HCC “might be cost effective in this population,” they wrote. “However, patients with AIH [autoimmune hepatitis] without cirrhosis at index diagnosis, particularly those identified from general populations, are at an extremely low risk of HCC.”

Source: American Gastroenterological Association

Autoimmune hepatitis may be asymptomatic at presentation or may cause severe acute hepatitis or even fulminant liver failure. Even with immunosuppressive therapy, patients progress to cirrhosis at reported annual rates of 0.1%-8%. HCC is the fastest-growing cause of cancer mortality, and the American Association for the Study of Liver Diseases (AASLD) recommends enhanced surveillance for this disease in patients whose annual estimated risk is at least 1.5%. Although the European Association for the Study of Liver Diseases recommends screening for HCC in patients with autoimmune hepatitis and cirrhosis, AASLD makes no such recommendation, the reviewers noted. To study the risk of HCC in patients with autoimmune hepatitis, they searched PubMed, Embase, and reference lists for relevant cohort studies published through June 2016. This work yielded 20 papers and five abstracts with a pooled median follow-up period of 8 years.

The overall pooled incidence of HCC was 3.1 (95% confidence interval, 2.2-4.2) cases per 1,000 person-years, or 1.007% per year, the reviewers wrote. However, the 95% confidence interval for the annual incidence rate nearly encompassed the 1.5% cutoff recommended by AASLD, they said. Furthermore, 5 of 16 studies that investigated the risk of HCC in patients with concurrent cirrhosis reported incidence rates above 1.5%. Among 93 patients who developed HCC in the meta-analysis, only 1 did not have cirrhosis by the time autoimmune hepatitis was diagnosed.

The meta-analysis also linked HCC to older age and Asian ethnicity among patients with autoimmune hepatitis, as has been reported before. Male sex only slightly increased the risk of HCC, but the studies included only about 1,130 men, the reviewers noted. Although the severity of autoimmune hepatitis varied among studies, higher rates of relapse predicted HCC in two cohorts. Additionally, one study linked alcohol abuse to a sixfold higher risk of HCC among patients with autoimmune hepatitis. “These data support careful monitoring of patients with autoimmune hepatitis, particularly older men, patients with multiple autoimmune hepatitis relapses, and those with ongoing alcohol abuse,” the investigators wrote.

They found no evidence of publication bias, but each individual study included at most 15 cases of HCC, so pooled incidence rates were probably imprecise, especially for subgroups, they said. Studies also inconsistently reported HCC risk factors, often lacked comparison groups, and usually did not report the effects of surveillance for HCC.

Dr. Tansel reported receiving support from the National Institutes of Health. The reviewers had no conflicts of interest.

The Diagnosis: Piedra

Microscopic examination of the hair shafts revealed brown to black, firmly adherent concretions (Figure 1). Scanning electron microscopy of the nodules was performed, which allowed for greater definition of the constituent hyphae and arthrospores (Figure 2). 

Photograph courtesy of Eric Hossler, MD (Danville, Pennsylvania).

Photograph courtesy of Fred E. Hossler, PhD (Johnson City, Tennesse).

Fungal cultures grew Trichosporon inkin along with other dematiaceous molds. The patient initially was treated with a combination of ketoconazole shampoo and weekly application of topical terbinafine. She trimmed 15.2 cm of the hair of her own volition. At 2-month follow-up the nodules were still present, though smaller and less numerous. Repeat cultures were obtained, which again grew T inkin. She then began taking oral terbinafine 250 mg daily for 6 weeks.

This case of piedra is unique in that our patient presented with black nodules clinically, but cultures grew only the causative agent of white piedra, T inkin. A search of PubMed articles indexed for MEDLINE using the terms black piedra, white piedra, or piedra, and mixed infection or coinfection yielded one other similar case.¹ Kanitakis et al¹ speculated that perhaps there was coinfection of black and white piedra and that Piedraia hortae, the causative agent of black piedra, was unable to flourish in culture facing competition from other fungi. This scenario also could apply to our patient. However, the original culture taken from our patient also grew other dematiaceous molds including Cladosporium and Exophiala species. It also is possible that these other fungi could have contributed pigment to the nodules, giving it the appearance of black piedra when only T inkin was present as the true pathogen.

White piedra is a rare fungal infection of the hair shaft caused by organisms of the genus Trichosporon, with Trichosporon ovoides most likely to infect the scalp.² Black piedra is a similar fungal infection caused by P hortae. Piedra means stone in Spanish, reflecting the appearance of these organisms on the hair shaft. It is common in tropical regions of the world such as Southeast Asia and South America, flourishing in the high temperatures and humidity.² Both infectious agents are found in the soil or in standing water.³ White piedra most commonly is found in facial, axilla, or pubic hair, while black piedra most often is found in the hair of the scalp.^2,4 Local cultural practices may contribute to transfer of Trichosporon or P hortae to the scalp, including the use of Brazilian plant oils in the hair or tying a veil or hijab to wet hair. Interestingly, some groups intentionally introduce the fungus to their hair for cosmetic reasons in endemic areas.^2,3,5

Patients with white or black piedra generally are asymptomatic.⁴ Some may notice a rough texture to the hair or hear a characteristic metallic rattling sound as the nodules make contact with brush bristles.^2,3 On inspection of the scalp, white piedra will appear to be white to light brown nodules, while black piedra presents as brown to black in color. The nodules are often firm on palpation.^2,3 The nodules of white piedra generally are easy to remove in contrast to black piedra, which involves nodules that securely attach to the hair shaft but can be removed with pressure.^3,5 Piedra has natural keratolytic activities and with prolonged infection can penetrate the hair cuticle, causing weakness and eventual breakage of the hair. This invasion into the hair cortex also can complicate treatment regimens, contributing to the chronic course of these infections.⁶ 

Diagnosis is based on clinical and microscopic findings. Nodules on hair shafts can be prepared with potassium hydroxide and placed on glass slides for examination.⁴ Dyes such as toluidine blue or chlorazol black E stain can be used to assist in identifying fungal structures.² Sabouraud agar with cycloheximide may be the best choice for culture medium.² Black piedra slowly grows into small dome-shaped colonies. White piedra will grow more quickly into cream-colored colonies with wrinkles and sometimes mucinous characteristics.³

The best treatment of black or white piedra is to cut the hair, thereby eliminating the fungi,⁷ which is not an easy option for many patients, such as ours, because of the aesthetic implications. Alternative treatments include azole shampoos such as ketoconazole.^2,4 Treatment with oral terbinafine 250 mg daily for 6 weeks has been successfully used for black piedra.⁷ Patients must be careful to thoroughly clean or discard hairbrushes, as they can serve as reservoirs of fungi to reinfect patients or spread to others.^5,7

The Diagnosis: Piedra

Microscopic examination of the hair shafts revealed brown to black, firmly adherent concretions (Figure 1). Scanning electron microscopy of the nodules was performed, which allowed for greater definition of the constituent hyphae and arthrospores (Figure 2). 

Photograph courtesy of Eric Hossler, MD (Danville, Pennsylvania).

Photograph courtesy of Fred E. Hossler, PhD (Johnson City, Tennesse).

Fungal cultures grew Trichosporon inkin along with other dematiaceous molds. The patient initially was treated with a combination of ketoconazole shampoo and weekly application of topical terbinafine. She trimmed 15.2 cm of the hair of her own volition. At 2-month follow-up the nodules were still present, though smaller and less numerous. Repeat cultures were obtained, which again grew T inkin. She then began taking oral terbinafine 250 mg daily for 6 weeks.

This case of piedra is unique in that our patient presented with black nodules clinically, but cultures grew only the causative agent of white piedra, T inkin. A search of PubMed articles indexed for MEDLINE using the terms black piedra, white piedra, or piedra, and mixed infection or coinfection yielded one other similar case.¹ Kanitakis et al¹ speculated that perhaps there was coinfection of black and white piedra and that Piedraia hortae, the causative agent of black piedra, was unable to flourish in culture facing competition from other fungi. This scenario also could apply to our patient. However, the original culture taken from our patient also grew other dematiaceous molds including Cladosporium and Exophiala species. It also is possible that these other fungi could have contributed pigment to the nodules, giving it the appearance of black piedra when only T inkin was present as the true pathogen.

White piedra is a rare fungal infection of the hair shaft caused by organisms of the genus Trichosporon, with Trichosporon ovoides most likely to infect the scalp.² Black piedra is a similar fungal infection caused by P hortae. Piedra means stone in Spanish, reflecting the appearance of these organisms on the hair shaft. It is common in tropical regions of the world such as Southeast Asia and South America, flourishing in the high temperatures and humidity.² Both infectious agents are found in the soil or in standing water.³ White piedra most commonly is found in facial, axilla, or pubic hair, while black piedra most often is found in the hair of the scalp.^2,4 Local cultural practices may contribute to transfer of Trichosporon or P hortae to the scalp, including the use of Brazilian plant oils in the hair or tying a veil or hijab to wet hair. Interestingly, some groups intentionally introduce the fungus to their hair for cosmetic reasons in endemic areas.^2,3,5

Patients with white or black piedra generally are asymptomatic.⁴ Some may notice a rough texture to the hair or hear a characteristic metallic rattling sound as the nodules make contact with brush bristles.^2,3 On inspection of the scalp, white piedra will appear to be white to light brown nodules, while black piedra presents as brown to black in color. The nodules are often firm on palpation.^2,3 The nodules of white piedra generally are easy to remove in contrast to black piedra, which involves nodules that securely attach to the hair shaft but can be removed with pressure.^3,5 Piedra has natural keratolytic activities and with prolonged infection can penetrate the hair cuticle, causing weakness and eventual breakage of the hair. This invasion into the hair cortex also can complicate treatment regimens, contributing to the chronic course of these infections.⁶ 

Diagnosis is based on clinical and microscopic findings. Nodules on hair shafts can be prepared with potassium hydroxide and placed on glass slides for examination.⁴ Dyes such as toluidine blue or chlorazol black E stain can be used to assist in identifying fungal structures.² Sabouraud agar with cycloheximide may be the best choice for culture medium.² Black piedra slowly grows into small dome-shaped colonies. White piedra will grow more quickly into cream-colored colonies with wrinkles and sometimes mucinous characteristics.³

The best treatment of black or white piedra is to cut the hair, thereby eliminating the fungi,⁷ which is not an easy option for many patients, such as ours, because of the aesthetic implications. Alternative treatments include azole shampoos such as ketoconazole.^2,4 Treatment with oral terbinafine 250 mg daily for 6 weeks has been successfully used for black piedra.⁷ Patients must be careful to thoroughly clean or discard hairbrushes, as they can serve as reservoirs of fungi to reinfect patients or spread to others.^5,7

The Diagnosis: Piedra

Microscopic examination of the hair shafts revealed brown to black, firmly adherent concretions (Figure 1). Scanning electron microscopy of the nodules was performed, which allowed for greater definition of the constituent hyphae and arthrospores (Figure 2). 

Photograph courtesy of Eric Hossler, MD (Danville, Pennsylvania).

Photograph courtesy of Fred E. Hossler, PhD (Johnson City, Tennesse).

Fungal cultures grew Trichosporon inkin along with other dematiaceous molds. The patient initially was treated with a combination of ketoconazole shampoo and weekly application of topical terbinafine. She trimmed 15.2 cm of the hair of her own volition. At 2-month follow-up the nodules were still present, though smaller and less numerous. Repeat cultures were obtained, which again grew T inkin. She then began taking oral terbinafine 250 mg daily for 6 weeks.

This case of piedra is unique in that our patient presented with black nodules clinically, but cultures grew only the causative agent of white piedra, T inkin. A search of PubMed articles indexed for MEDLINE using the terms black piedra, white piedra, or piedra, and mixed infection or coinfection yielded one other similar case.¹ Kanitakis et al¹ speculated that perhaps there was coinfection of black and white piedra and that Piedraia hortae, the causative agent of black piedra, was unable to flourish in culture facing competition from other fungi. This scenario also could apply to our patient. However, the original culture taken from our patient also grew other dematiaceous molds including Cladosporium and Exophiala species. It also is possible that these other fungi could have contributed pigment to the nodules, giving it the appearance of black piedra when only T inkin was present as the true pathogen.

White piedra is a rare fungal infection of the hair shaft caused by organisms of the genus Trichosporon, with Trichosporon ovoides most likely to infect the scalp.² Black piedra is a similar fungal infection caused by P hortae. Piedra means stone in Spanish, reflecting the appearance of these organisms on the hair shaft. It is common in tropical regions of the world such as Southeast Asia and South America, flourishing in the high temperatures and humidity.² Both infectious agents are found in the soil or in standing water.³ White piedra most commonly is found in facial, axilla, or pubic hair, while black piedra most often is found in the hair of the scalp.^2,4 Local cultural practices may contribute to transfer of Trichosporon or P hortae to the scalp, including the use of Brazilian plant oils in the hair or tying a veil or hijab to wet hair. Interestingly, some groups intentionally introduce the fungus to their hair for cosmetic reasons in endemic areas.^2,3,5

Patients with white or black piedra generally are asymptomatic.⁴ Some may notice a rough texture to the hair or hear a characteristic metallic rattling sound as the nodules make contact with brush bristles.^2,3 On inspection of the scalp, white piedra will appear to be white to light brown nodules, while black piedra presents as brown to black in color. The nodules are often firm on palpation.^2,3 The nodules of white piedra generally are easy to remove in contrast to black piedra, which involves nodules that securely attach to the hair shaft but can be removed with pressure.^3,5 Piedra has natural keratolytic activities and with prolonged infection can penetrate the hair cuticle, causing weakness and eventual breakage of the hair. This invasion into the hair cortex also can complicate treatment regimens, contributing to the chronic course of these infections.⁶ 

Diagnosis is based on clinical and microscopic findings. Nodules on hair shafts can be prepared with potassium hydroxide and placed on glass slides for examination.⁴ Dyes such as toluidine blue or chlorazol black E stain can be used to assist in identifying fungal structures.² Sabouraud agar with cycloheximide may be the best choice for culture medium.² Black piedra slowly grows into small dome-shaped colonies. White piedra will grow more quickly into cream-colored colonies with wrinkles and sometimes mucinous characteristics.³

The best treatment of black or white piedra is to cut the hair, thereby eliminating the fungi,⁷ which is not an easy option for many patients, such as ours, because of the aesthetic implications. Alternative treatments include azole shampoos such as ketoconazole.^2,4 Treatment with oral terbinafine 250 mg daily for 6 weeks has been successfully used for black piedra.⁷ Patients must be careful to thoroughly clean or discard hairbrushes, as they can serve as reservoirs of fungi to reinfect patients or spread to others.^5,7

SEATTLE – Statins appeared to decrease the risk of sepsis after colorectal surgery and of anastomotic leak after rectal resection in a review of 7,285 elective colorectal surgery patients at 64 Michigan hospitals.

Overall, 2,515 patients (34.5%) were on statins preoperatively and received at least one dose while in the hospital post op. Their outcomes were compared with those of the 4,770 patients (65.5%) who were not on statins.

[email protected]

SEATTLE – Statins appeared to decrease the risk of sepsis after colorectal surgery and of anastomotic leak after rectal resection in a review of 7,285 elective colorectal surgery patients at 64 Michigan hospitals.

Overall, 2,515 patients (34.5%) were on statins preoperatively and received at least one dose while in the hospital post op. Their outcomes were compared with those of the 4,770 patients (65.5%) who were not on statins.

[email protected]

SEATTLE – Statins appeared to decrease the risk of sepsis after colorectal surgery and of anastomotic leak after rectal resection in a review of 7,285 elective colorectal surgery patients at 64 Michigan hospitals.

Overall, 2,515 patients (34.5%) were on statins preoperatively and received at least one dose while in the hospital post op. Their outcomes were compared with those of the 4,770 patients (65.5%) who were not on statins.

[email protected]

Patients with cirrhosis and portal vein thrombosis (PVT) who received anticoagulation therapy had nearly fivefold greater odds of recanalization compared with untreated patients, and were no more likely to experience major or minor bleeding, in a pooled analysis of eight studies published in the August issue of Gastroenterology (doi: 10.1053/j.gastro.2017.04.042).

Rates of any recanalization were 71% in treated patients and 42% in untreated patients (P less than .0001), wrote Lorenzo Loffredo, MD, of Sapienza University, Rome, and his coinvestigators. Rates of complete recanalization were 53% and 33%, respectively (P = .002), rates of spontaneous variceal bleeding were 2% and 12% (P = .04), and bleeding affected 11% of patients in each group. Together, the findings “show that anticoagulants are efficacious and safe for treatment of portal vein thrombosis in cirrhotic patients,” although larger, interventional clinical trials are needed to pinpoint the clinical role of anticoagulation in cirrhotic patients with PVT, the reviewers reported.

Source: American Gastroenterological Association

Bleeding from portal hypertension is a major complication in cirrhosis, but PVT affects about 20% of patients and predicts poor outcomes, they noted. Anticoagulation in this setting can be difficult because patients often have concurrent coagulopathies that are hard to assess with standard techniques, such as PT-INR (international normalized ratio). Although some studies support anticoagulating these patients, data are limited. Therefore, the reviewers searched PubMed, the ISI Web of Science, SCOPUS, and the Cochrane database through Feb. 14, 2017, for trials comparing anticoagulation with no treatment in patients with cirrhosis and PVT.

This search yielded eight trials of 353 patients who received low-molecular-weight heparin, warfarin, or no treatment for about 6 months, with a typical follow-up period of 2 years. The reviewers found no evidence of publication bias or significant heterogeneity among the trials. Six studies evaluated complete recanalization, another set of six studies tracked progression of PVT, a third set of six studies evaluated major or minor bleeding events, and four studies evaluated spontaneous variceal bleeding. Compared with no treatment, anticoagulation was tied to a significantly greater likelihood of complete recanalization (pooled odds ratio, 3.4; 95% confidence interval, 1.5-7.4; P = .002), a significantly lower chance of PVT progressing (9% vs. 33%; pooled odds ratio, 0.14; 95% CI, 0.06-0.31; P less than .0001), no difference in bleeding rates (11% in each pooled group), and a significantly lower risk of spontaneous variceal bleeding (OR, 0.23; 95% CI, 0.06-0.94; P = .04).

“Metaregression analysis showed that duration of anticoagulation did not influence outcomes,” the reviewers wrote. “Low-molecular-weight heparin, but not warfarin, was significantly associated with a complete PVT resolution as compared to untreated patients, while both low-molecular-weight heparin and warfarin were effective in reducing PVT progression.” That finding merits careful interpretation, however, because most studies on warfarin were retrospective and lacked data on the quality of anticoagulation, they added.

“It is a challenge to treat patients with cirrhosis using anticoagulants because of the perception that the coexistent coagulopathy could promote bleeding,” the researchers wrote. Nonetheless, their analysis suggests that anticoagulation has significant benefits and does not increase bleeding risk, regardless of the severity of liver failure, they concluded.

The reviewers reported having no funding sources or conflicts of interest.

Patients with cirrhosis and portal vein thrombosis (PVT) who received anticoagulation therapy had nearly fivefold greater odds of recanalization compared with untreated patients, and were no more likely to experience major or minor bleeding, in a pooled analysis of eight studies published in the August issue of Gastroenterology (doi: 10.1053/j.gastro.2017.04.042).

Rates of any recanalization were 71% in treated patients and 42% in untreated patients (P less than .0001), wrote Lorenzo Loffredo, MD, of Sapienza University, Rome, and his coinvestigators. Rates of complete recanalization were 53% and 33%, respectively (P = .002), rates of spontaneous variceal bleeding were 2% and 12% (P = .04), and bleeding affected 11% of patients in each group. Together, the findings “show that anticoagulants are efficacious and safe for treatment of portal vein thrombosis in cirrhotic patients,” although larger, interventional clinical trials are needed to pinpoint the clinical role of anticoagulation in cirrhotic patients with PVT, the reviewers reported.

Source: American Gastroenterological Association

Bleeding from portal hypertension is a major complication in cirrhosis, but PVT affects about 20% of patients and predicts poor outcomes, they noted. Anticoagulation in this setting can be difficult because patients often have concurrent coagulopathies that are hard to assess with standard techniques, such as PT-INR (international normalized ratio). Although some studies support anticoagulating these patients, data are limited. Therefore, the reviewers searched PubMed, the ISI Web of Science, SCOPUS, and the Cochrane database through Feb. 14, 2017, for trials comparing anticoagulation with no treatment in patients with cirrhosis and PVT.

This search yielded eight trials of 353 patients who received low-molecular-weight heparin, warfarin, or no treatment for about 6 months, with a typical follow-up period of 2 years. The reviewers found no evidence of publication bias or significant heterogeneity among the trials. Six studies evaluated complete recanalization, another set of six studies tracked progression of PVT, a third set of six studies evaluated major or minor bleeding events, and four studies evaluated spontaneous variceal bleeding. Compared with no treatment, anticoagulation was tied to a significantly greater likelihood of complete recanalization (pooled odds ratio, 3.4; 95% confidence interval, 1.5-7.4; P = .002), a significantly lower chance of PVT progressing (9% vs. 33%; pooled odds ratio, 0.14; 95% CI, 0.06-0.31; P less than .0001), no difference in bleeding rates (11% in each pooled group), and a significantly lower risk of spontaneous variceal bleeding (OR, 0.23; 95% CI, 0.06-0.94; P = .04).

“Metaregression analysis showed that duration of anticoagulation did not influence outcomes,” the reviewers wrote. “Low-molecular-weight heparin, but not warfarin, was significantly associated with a complete PVT resolution as compared to untreated patients, while both low-molecular-weight heparin and warfarin were effective in reducing PVT progression.” That finding merits careful interpretation, however, because most studies on warfarin were retrospective and lacked data on the quality of anticoagulation, they added.

“It is a challenge to treat patients with cirrhosis using anticoagulants because of the perception that the coexistent coagulopathy could promote bleeding,” the researchers wrote. Nonetheless, their analysis suggests that anticoagulation has significant benefits and does not increase bleeding risk, regardless of the severity of liver failure, they concluded.

The reviewers reported having no funding sources or conflicts of interest.

Patients with cirrhosis and portal vein thrombosis (PVT) who received anticoagulation therapy had nearly fivefold greater odds of recanalization compared with untreated patients, and were no more likely to experience major or minor bleeding, in a pooled analysis of eight studies published in the August issue of Gastroenterology (doi: 10.1053/j.gastro.2017.04.042).

Rates of any recanalization were 71% in treated patients and 42% in untreated patients (P less than .0001), wrote Lorenzo Loffredo, MD, of Sapienza University, Rome, and his coinvestigators. Rates of complete recanalization were 53% and 33%, respectively (P = .002), rates of spontaneous variceal bleeding were 2% and 12% (P = .04), and bleeding affected 11% of patients in each group. Together, the findings “show that anticoagulants are efficacious and safe for treatment of portal vein thrombosis in cirrhotic patients,” although larger, interventional clinical trials are needed to pinpoint the clinical role of anticoagulation in cirrhotic patients with PVT, the reviewers reported.

Source: American Gastroenterological Association

Bleeding from portal hypertension is a major complication in cirrhosis, but PVT affects about 20% of patients and predicts poor outcomes, they noted. Anticoagulation in this setting can be difficult because patients often have concurrent coagulopathies that are hard to assess with standard techniques, such as PT-INR (international normalized ratio). Although some studies support anticoagulating these patients, data are limited. Therefore, the reviewers searched PubMed, the ISI Web of Science, SCOPUS, and the Cochrane database through Feb. 14, 2017, for trials comparing anticoagulation with no treatment in patients with cirrhosis and PVT.

This search yielded eight trials of 353 patients who received low-molecular-weight heparin, warfarin, or no treatment for about 6 months, with a typical follow-up period of 2 years. The reviewers found no evidence of publication bias or significant heterogeneity among the trials. Six studies evaluated complete recanalization, another set of six studies tracked progression of PVT, a third set of six studies evaluated major or minor bleeding events, and four studies evaluated spontaneous variceal bleeding. Compared with no treatment, anticoagulation was tied to a significantly greater likelihood of complete recanalization (pooled odds ratio, 3.4; 95% confidence interval, 1.5-7.4; P = .002), a significantly lower chance of PVT progressing (9% vs. 33%; pooled odds ratio, 0.14; 95% CI, 0.06-0.31; P less than .0001), no difference in bleeding rates (11% in each pooled group), and a significantly lower risk of spontaneous variceal bleeding (OR, 0.23; 95% CI, 0.06-0.94; P = .04).

“Metaregression analysis showed that duration of anticoagulation did not influence outcomes,” the reviewers wrote. “Low-molecular-weight heparin, but not warfarin, was significantly associated with a complete PVT resolution as compared to untreated patients, while both low-molecular-weight heparin and warfarin were effective in reducing PVT progression.” That finding merits careful interpretation, however, because most studies on warfarin were retrospective and lacked data on the quality of anticoagulation, they added.

“It is a challenge to treat patients with cirrhosis using anticoagulants because of the perception that the coexistent coagulopathy could promote bleeding,” the researchers wrote. Nonetheless, their analysis suggests that anticoagulation has significant benefits and does not increase bleeding risk, regardless of the severity of liver failure, they concluded.

The reviewers reported having no funding sources or conflicts of interest.

What do your patients need to know?

Vascular instability associated with rosacea is exacerbated by triggers such as sunlight, hot drinks, spicy foods, stress, and rapid changing weather, which make patients flush and blush, increase the appearance of telangiectasia, and disrupt the normal skin barrier. Because the patients feel on fire, an anti-inflammatory approach is indicated. The regimen I recommend includes mild cleansers, barrier repair creams and supplements, antioxidants (topical and oral), and sun protection, all without parabens and harsh chemicals. I always recommend a product that I dispense at the office and another one of similar effectiveness that can be found over-the-counter.

What are your go-to treatments?

Cleansing is indispensable to maintain the normal flow in and out of the skin. I recommend mild cleansers without potentially sensitizing agents such as propylene glycol or parabens. It also should have calming agents (eg, fruit extracts) that remove the contaminants from the skin surface without stripping the important layers of lipids that constitute the barrier of the skin as well as ingredients (eg, prebiotics) that promote the healthy skin biome. Selenium in thermal spring water has free radical scavenging and anti-inflammatory properties as well as protection against heavy metals.

After cleansing, I recommend a product to repair, maintain, and improve the barrier of the skin. A healthy skin barrier has an equal ratio of cholesterol, ceramides, and free fatty acids, the building blocks of the skin. In a barrier repair cream I look for ingredients that stop and prevent damaging inflammation, improve the skin's natural ability to repair and heal (eg, niacinamide), and protect against environmental insults. It should contain petrolatum and/or dimethicone to form a protective barrier on the skin to seal in moisture.

Oral niacinamide should be taken as a photoprotective agent. Oral supplementation (500 mg twice daily) is effective in reducing skin cancer. Because UV light is a trigger factor, oral photoprotection is recommended.

Topical antioxidants also are important. Free radical formation has been documented even in photoprotected skin. These free radicals have been implicated in skin cancer development and metalloproteinase production and are triggers of rosacea. As a result, I advise my patients to apply topical encapsulated vitamin C every night. The encapsulated form prevents oxidation of the product before application. In addition, I recommend oral vitamin C (1 g daily) and vitamin E (400 U daily).

For sun protection I recommend sunblocks with titanium dioxide and zinc oxide for total UVA and UVB protection. If the patient has a darker skin type, sun protection should contain iron oxide. Chemical agents can cause irritation, photocontact dermatitis, and exacerbation of rosacea symptoms. Daily application of sun protection with reapplication every 2 hours is reinforced. 

What holistic therapies do you recommend?

Stress reduction activities, including yoga, relaxation, massages, and meditation, can help. Oral consumption of trigger factors is discouraged. Antioxidant green tea is recommended instead of caffeinated beverages. 

Suggested Readings 

Baldwin HE, Bathia ND, Friedman A, et al. The role of cutaneous microbiota harmony in maintaining functional skin barrier. J Drugs Dermatol. 2017;16:12-18.

Celerier P, Richard A, Litoux P, et al. Modulatory effects of selenium and strontium salts on keratinocyte-derived inflammatory cytokines. Arch Dermatol Res. 1995;287:680-682.

Chen AC, Martin AJ, Choy B, et al. A phase 3 randomized trial of nicotinamide for skin cancer chemoprevention. N Engl J Med. 2015;373:1618-1626.

Jones D. Reactive oxygen species and rosacea. Cutis. 2004;74(suppl 3):17-20.

What do your patients need to know?

Vascular instability associated with rosacea is exacerbated by triggers such as sunlight, hot drinks, spicy foods, stress, and rapid changing weather, which make patients flush and blush, increase the appearance of telangiectasia, and disrupt the normal skin barrier. Because the patients feel on fire, an anti-inflammatory approach is indicated. The regimen I recommend includes mild cleansers, barrier repair creams and supplements, antioxidants (topical and oral), and sun protection, all without parabens and harsh chemicals. I always recommend a product that I dispense at the office and another one of similar effectiveness that can be found over-the-counter.

What are your go-to treatments?

Cleansing is indispensable to maintain the normal flow in and out of the skin. I recommend mild cleansers without potentially sensitizing agents such as propylene glycol or parabens. It also should have calming agents (eg, fruit extracts) that remove the contaminants from the skin surface without stripping the important layers of lipids that constitute the barrier of the skin as well as ingredients (eg, prebiotics) that promote the healthy skin biome. Selenium in thermal spring water has free radical scavenging and anti-inflammatory properties as well as protection against heavy metals.

After cleansing, I recommend a product to repair, maintain, and improve the barrier of the skin. A healthy skin barrier has an equal ratio of cholesterol, ceramides, and free fatty acids, the building blocks of the skin. In a barrier repair cream I look for ingredients that stop and prevent damaging inflammation, improve the skin's natural ability to repair and heal (eg, niacinamide), and protect against environmental insults. It should contain petrolatum and/or dimethicone to form a protective barrier on the skin to seal in moisture.

Oral niacinamide should be taken as a photoprotective agent. Oral supplementation (500 mg twice daily) is effective in reducing skin cancer. Because UV light is a trigger factor, oral photoprotection is recommended.

Topical antioxidants also are important. Free radical formation has been documented even in photoprotected skin. These free radicals have been implicated in skin cancer development and metalloproteinase production and are triggers of rosacea. As a result, I advise my patients to apply topical encapsulated vitamin C every night. The encapsulated form prevents oxidation of the product before application. In addition, I recommend oral vitamin C (1 g daily) and vitamin E (400 U daily).

For sun protection I recommend sunblocks with titanium dioxide and zinc oxide for total UVA and UVB protection. If the patient has a darker skin type, sun protection should contain iron oxide. Chemical agents can cause irritation, photocontact dermatitis, and exacerbation of rosacea symptoms. Daily application of sun protection with reapplication every 2 hours is reinforced. 

What holistic therapies do you recommend?

Stress reduction activities, including yoga, relaxation, massages, and meditation, can help. Oral consumption of trigger factors is discouraged. Antioxidant green tea is recommended instead of caffeinated beverages. 

Suggested Readings 

Baldwin HE, Bathia ND, Friedman A, et al. The role of cutaneous microbiota harmony in maintaining functional skin barrier. J Drugs Dermatol. 2017;16:12-18.

Celerier P, Richard A, Litoux P, et al. Modulatory effects of selenium and strontium salts on keratinocyte-derived inflammatory cytokines. Arch Dermatol Res. 1995;287:680-682.

Chen AC, Martin AJ, Choy B, et al. A phase 3 randomized trial of nicotinamide for skin cancer chemoprevention. N Engl J Med. 2015;373:1618-1626.

Jones D. Reactive oxygen species and rosacea. Cutis. 2004;74(suppl 3):17-20.

What do your patients need to know?

Vascular instability associated with rosacea is exacerbated by triggers such as sunlight, hot drinks, spicy foods, stress, and rapid changing weather, which make patients flush and blush, increase the appearance of telangiectasia, and disrupt the normal skin barrier. Because the patients feel on fire, an anti-inflammatory approach is indicated. The regimen I recommend includes mild cleansers, barrier repair creams and supplements, antioxidants (topical and oral), and sun protection, all without parabens and harsh chemicals. I always recommend a product that I dispense at the office and another one of similar effectiveness that can be found over-the-counter.

What are your go-to treatments?

Cleansing is indispensable to maintain the normal flow in and out of the skin. I recommend mild cleansers without potentially sensitizing agents such as propylene glycol or parabens. It also should have calming agents (eg, fruit extracts) that remove the contaminants from the skin surface without stripping the important layers of lipids that constitute the barrier of the skin as well as ingredients (eg, prebiotics) that promote the healthy skin biome. Selenium in thermal spring water has free radical scavenging and anti-inflammatory properties as well as protection against heavy metals.

After cleansing, I recommend a product to repair, maintain, and improve the barrier of the skin. A healthy skin barrier has an equal ratio of cholesterol, ceramides, and free fatty acids, the building blocks of the skin. In a barrier repair cream I look for ingredients that stop and prevent damaging inflammation, improve the skin's natural ability to repair and heal (eg, niacinamide), and protect against environmental insults. It should contain petrolatum and/or dimethicone to form a protective barrier on the skin to seal in moisture.

Oral niacinamide should be taken as a photoprotective agent. Oral supplementation (500 mg twice daily) is effective in reducing skin cancer. Because UV light is a trigger factor, oral photoprotection is recommended.

Topical antioxidants also are important. Free radical formation has been documented even in photoprotected skin. These free radicals have been implicated in skin cancer development and metalloproteinase production and are triggers of rosacea. As a result, I advise my patients to apply topical encapsulated vitamin C every night. The encapsulated form prevents oxidation of the product before application. In addition, I recommend oral vitamin C (1 g daily) and vitamin E (400 U daily).

For sun protection I recommend sunblocks with titanium dioxide and zinc oxide for total UVA and UVB protection. If the patient has a darker skin type, sun protection should contain iron oxide. Chemical agents can cause irritation, photocontact dermatitis, and exacerbation of rosacea symptoms. Daily application of sun protection with reapplication every 2 hours is reinforced. 

What holistic therapies do you recommend?

Stress reduction activities, including yoga, relaxation, massages, and meditation, can help. Oral consumption of trigger factors is discouraged. Antioxidant green tea is recommended instead of caffeinated beverages. 

Suggested Readings 

Baldwin HE, Bathia ND, Friedman A, et al. The role of cutaneous microbiota harmony in maintaining functional skin barrier. J Drugs Dermatol. 2017;16:12-18.

Celerier P, Richard A, Litoux P, et al. Modulatory effects of selenium and strontium salts on keratinocyte-derived inflammatory cytokines. Arch Dermatol Res. 1995;287:680-682.

Chen AC, Martin AJ, Choy B, et al. A phase 3 randomized trial of nicotinamide for skin cancer chemoprevention. N Engl J Med. 2015;373:1618-1626.

Jones D. Reactive oxygen species and rosacea. Cutis. 2004;74(suppl 3):17-20.

Myth: Itching is not a symptom of acne

Acne vulgaris typically is not considered to be a pruritic disease; however, many patients experience itching, which leads them to scratch their acne lesions, causing secondary bacterial infections and subsequent scarring, hypopigmentation, or hyperpigmentation of the involved skin. Although itching rarely is mentioned as a clinical feature of acne, pruritus can be an important contributory factor to the burden of disability and impaired quality of life in acne patients of all ages, and acne itching may be an important target for therapy.

In a descriptive study of 120 consecutive acne patients in Singapore, itch was found to be a common (70% of patients) and debilitating symptom of acne. The majority of patients (83%) reported itch at noon with severity that was comparable to a mosquito bite, and the most common physical descriptor was tickling (68%). Common aggravating factors included sweat (71%), heat (62%), and stress (31%). Fifty-five percent of patients said itching had a negative impact on their mood, and 52% reported that they had scratched or rubbed the affected area.

A study of 108 adolescents with acne limited to the face yielded half who reported itching within acne lesions. The presence of itching was unrelated to age, gender, where they lived, positive family history, or acne severity. In most patients, pruritus appeared relatively infrequently and for a short period of time: 7.4% reported itching every day, 24.1% on a weekly basis, 29.6% at least once a month, and 37.7% even less frequently. Itch episodes lasted less than 1 minute in most participants. However, 31.5% of participants sought medical treatment to reduce itching. The most important factors aggravating the intensity of itching were sweat, stress, physical effort, heat, fatigue, and dry air, respectively.

Regarding the impact of acne itching on quality of life, 29.6% of participants felt depressed and 1.8% were anxious because of their itching. Some participants also noted that itching caused difficulties in falling asleep and awakening from itching.

The pathogenesis of localized itching in acne could be connected with the change in pH of the microenvironment of the acne follicle, providing an optimal environment for the production of histamine or histaminelike products by Propionibacterium acnes. Pruritus also may be a complication of certain acne therapies. Increased awareness among patients of this potential side effect may be helpful in preventing the unnecessary discontinuation of an otherwise effective acne therapy. Understanding factors that may aggravate itching in acne lesions also may be helpful to patients.

Myth: Itching is not a symptom of acne

Acne vulgaris typically is not considered to be a pruritic disease; however, many patients experience itching, which leads them to scratch their acne lesions, causing secondary bacterial infections and subsequent scarring, hypopigmentation, or hyperpigmentation of the involved skin. Although itching rarely is mentioned as a clinical feature of acne, pruritus can be an important contributory factor to the burden of disability and impaired quality of life in acne patients of all ages, and acne itching may be an important target for therapy.

In a descriptive study of 120 consecutive acne patients in Singapore, itch was found to be a common (70% of patients) and debilitating symptom of acne. The majority of patients (83%) reported itch at noon with severity that was comparable to a mosquito bite, and the most common physical descriptor was tickling (68%). Common aggravating factors included sweat (71%), heat (62%), and stress (31%). Fifty-five percent of patients said itching had a negative impact on their mood, and 52% reported that they had scratched or rubbed the affected area.

A study of 108 adolescents with acne limited to the face yielded half who reported itching within acne lesions. The presence of itching was unrelated to age, gender, where they lived, positive family history, or acne severity. In most patients, pruritus appeared relatively infrequently and for a short period of time: 7.4% reported itching every day, 24.1% on a weekly basis, 29.6% at least once a month, and 37.7% even less frequently. Itch episodes lasted less than 1 minute in most participants. However, 31.5% of participants sought medical treatment to reduce itching. The most important factors aggravating the intensity of itching were sweat, stress, physical effort, heat, fatigue, and dry air, respectively.

Regarding the impact of acne itching on quality of life, 29.6% of participants felt depressed and 1.8% were anxious because of their itching. Some participants also noted that itching caused difficulties in falling asleep and awakening from itching.

The pathogenesis of localized itching in acne could be connected with the change in pH of the microenvironment of the acne follicle, providing an optimal environment for the production of histamine or histaminelike products by Propionibacterium acnes. Pruritus also may be a complication of certain acne therapies. Increased awareness among patients of this potential side effect may be helpful in preventing the unnecessary discontinuation of an otherwise effective acne therapy. Understanding factors that may aggravate itching in acne lesions also may be helpful to patients.

Myth: Itching is not a symptom of acne

Acne vulgaris typically is not considered to be a pruritic disease; however, many patients experience itching, which leads them to scratch their acne lesions, causing secondary bacterial infections and subsequent scarring, hypopigmentation, or hyperpigmentation of the involved skin. Although itching rarely is mentioned as a clinical feature of acne, pruritus can be an important contributory factor to the burden of disability and impaired quality of life in acne patients of all ages, and acne itching may be an important target for therapy.

In a descriptive study of 120 consecutive acne patients in Singapore, itch was found to be a common (70% of patients) and debilitating symptom of acne. The majority of patients (83%) reported itch at noon with severity that was comparable to a mosquito bite, and the most common physical descriptor was tickling (68%). Common aggravating factors included sweat (71%), heat (62%), and stress (31%). Fifty-five percent of patients said itching had a negative impact on their mood, and 52% reported that they had scratched or rubbed the affected area.

A study of 108 adolescents with acne limited to the face yielded half who reported itching within acne lesions. The presence of itching was unrelated to age, gender, where they lived, positive family history, or acne severity. In most patients, pruritus appeared relatively infrequently and for a short period of time: 7.4% reported itching every day, 24.1% on a weekly basis, 29.6% at least once a month, and 37.7% even less frequently. Itch episodes lasted less than 1 minute in most participants. However, 31.5% of participants sought medical treatment to reduce itching. The most important factors aggravating the intensity of itching were sweat, stress, physical effort, heat, fatigue, and dry air, respectively.

Regarding the impact of acne itching on quality of life, 29.6% of participants felt depressed and 1.8% were anxious because of their itching. Some participants also noted that itching caused difficulties in falling asleep and awakening from itching.

The pathogenesis of localized itching in acne could be connected with the change in pH of the microenvironment of the acne follicle, providing an optimal environment for the production of histamine or histaminelike products by Propionibacterium acnes. Pruritus also may be a complication of certain acne therapies. Increased awareness among patients of this potential side effect may be helpful in preventing the unnecessary discontinuation of an otherwise effective acne therapy. Understanding factors that may aggravate itching in acne lesions also may be helpful to patients.

Ankle effusions can be quite debilitating, causing band-like swelling and stiffness to the anterior aspect of ankle at the tibiotalar joint. Significant swelling can impair ankle dorsiflexion and plantar flexion. The differential diagnosis for joint effusions is wide, and includes traumatic effusion; gout; osteoarthritis; rheumatoid arthritis; and septic arthritis, which is one of the most important diagnoses for the emergency physician (EP) to identify and initiate prompt treatment to reduce the risk of serious morbidity and mortality. Differentiating these conditions requires joint aspiration and synovial fluid analysis. While a large effusion will be palpable and likely ballotable, smaller effusions are more challenging clinically. In such cases, point-of-care (POC) ultrasound can be a valuable tool in confirming a joint effusion.

Identifying Landmarks and Tibiotalar Joint

To access the tibiotalar joint space, it is important to identify useful landmarks.¹ This is best accomplished by having the patient in the supine position, with the affected knee flexed approximately 90° and plantar surface of the foot lying flat on the bed (Figure 1).

Performing the Arthrocentesis

The arthrocentesis is performed under sterile conditions using the high-frequency linear probe. A sterile probe cover is highly recommended if the operator will be using ultrasound to guide the procedure in real time.² Using the palpable landmarks as a guide, the clinician should align the probe just medial to the tibialis anterior tendon with the probe marker oriented cephalad; scanning should begin superior to the ankle joint. The tibia will appear as a hyperechoic stripe just under a thin soft tissue layer. When the tibia is visible, the clinician should then slide the probe distally. The joint space will demonstrated by visualization of the distal tibia and talus bone (Figure 3).

Pearls and Pitfalls

Point-of-care ultrasound is not only useful to guide arthrocentesis of joint effusions, but also to confirm the presence of an effusion prior to aspiration. At our institution, we have had many cases in which POC ultrasound demonstrated an absence of effusion, and we were able to avoid an unnecessary joint aspiration. Moreover, when an effusion is present, POC ultrasound-guided aspiration avoids complications. The use of POC ultrasound can also increase the confidence of the provider performing arthrocentesis of joints less commonly aspirated.

Summary

Joint aspiration is an important procedural tool for EPs, especially when used to rule out life-threatening conditions such as septic arthritis. Deeper joints and small fluid collections, however, can be difficult to access without image guidance. In the ED setting, POC ultrasound provides a widely available, easy-to-use, low-cost tool to increase the likelihood of success while minimizing damage to adjacent structures.

Ankle effusions can be quite debilitating, causing band-like swelling and stiffness to the anterior aspect of ankle at the tibiotalar joint. Significant swelling can impair ankle dorsiflexion and plantar flexion. The differential diagnosis for joint effusions is wide, and includes traumatic effusion; gout; osteoarthritis; rheumatoid arthritis; and septic arthritis, which is one of the most important diagnoses for the emergency physician (EP) to identify and initiate prompt treatment to reduce the risk of serious morbidity and mortality. Differentiating these conditions requires joint aspiration and synovial fluid analysis. While a large effusion will be palpable and likely ballotable, smaller effusions are more challenging clinically. In such cases, point-of-care (POC) ultrasound can be a valuable tool in confirming a joint effusion.

Identifying Landmarks and Tibiotalar Joint

To access the tibiotalar joint space, it is important to identify useful landmarks.¹ This is best accomplished by having the patient in the supine position, with the affected knee flexed approximately 90° and plantar surface of the foot lying flat on the bed (Figure 1).

Performing the Arthrocentesis

The arthrocentesis is performed under sterile conditions using the high-frequency linear probe. A sterile probe cover is highly recommended if the operator will be using ultrasound to guide the procedure in real time.² Using the palpable landmarks as a guide, the clinician should align the probe just medial to the tibialis anterior tendon with the probe marker oriented cephalad; scanning should begin superior to the ankle joint. The tibia will appear as a hyperechoic stripe just under a thin soft tissue layer. When the tibia is visible, the clinician should then slide the probe distally. The joint space will demonstrated by visualization of the distal tibia and talus bone (Figure 3).

Pearls and Pitfalls

Point-of-care ultrasound is not only useful to guide arthrocentesis of joint effusions, but also to confirm the presence of an effusion prior to aspiration. At our institution, we have had many cases in which POC ultrasound demonstrated an absence of effusion, and we were able to avoid an unnecessary joint aspiration. Moreover, when an effusion is present, POC ultrasound-guided aspiration avoids complications. The use of POC ultrasound can also increase the confidence of the provider performing arthrocentesis of joints less commonly aspirated.

Summary

Joint aspiration is an important procedural tool for EPs, especially when used to rule out life-threatening conditions such as septic arthritis. Deeper joints and small fluid collections, however, can be difficult to access without image guidance. In the ED setting, POC ultrasound provides a widely available, easy-to-use, low-cost tool to increase the likelihood of success while minimizing damage to adjacent structures.

Ankle effusions can be quite debilitating, causing band-like swelling and stiffness to the anterior aspect of ankle at the tibiotalar joint. Significant swelling can impair ankle dorsiflexion and plantar flexion. The differential diagnosis for joint effusions is wide, and includes traumatic effusion; gout; osteoarthritis; rheumatoid arthritis; and septic arthritis, which is one of the most important diagnoses for the emergency physician (EP) to identify and initiate prompt treatment to reduce the risk of serious morbidity and mortality. Differentiating these conditions requires joint aspiration and synovial fluid analysis. While a large effusion will be palpable and likely ballotable, smaller effusions are more challenging clinically. In such cases, point-of-care (POC) ultrasound can be a valuable tool in confirming a joint effusion.

Identifying Landmarks and Tibiotalar Joint

To access the tibiotalar joint space, it is important to identify useful landmarks.¹ This is best accomplished by having the patient in the supine position, with the affected knee flexed approximately 90° and plantar surface of the foot lying flat on the bed (Figure 1).

Performing the Arthrocentesis

The arthrocentesis is performed under sterile conditions using the high-frequency linear probe. A sterile probe cover is highly recommended if the operator will be using ultrasound to guide the procedure in real time.² Using the palpable landmarks as a guide, the clinician should align the probe just medial to the tibialis anterior tendon with the probe marker oriented cephalad; scanning should begin superior to the ankle joint. The tibia will appear as a hyperechoic stripe just under a thin soft tissue layer. When the tibia is visible, the clinician should then slide the probe distally. The joint space will demonstrated by visualization of the distal tibia and talus bone (Figure 3).

Pearls and Pitfalls

Point-of-care ultrasound is not only useful to guide arthrocentesis of joint effusions, but also to confirm the presence of an effusion prior to aspiration. At our institution, we have had many cases in which POC ultrasound demonstrated an absence of effusion, and we were able to avoid an unnecessary joint aspiration. Moreover, when an effusion is present, POC ultrasound-guided aspiration avoids complications. The use of POC ultrasound can also increase the confidence of the provider performing arthrocentesis of joints less commonly aspirated.

Summary

Joint aspiration is an important procedural tool for EPs, especially when used to rule out life-threatening conditions such as septic arthritis. Deeper joints and small fluid collections, however, can be difficult to access without image guidance. In the ED setting, POC ultrasound provides a widely available, easy-to-use, low-cost tool to increase the likelihood of success while minimizing damage to adjacent structures.