Paul M. Rodriguez-Waitkus, MD, PhD

To the Editor:

Cutaneous collagenous vasculopathy (CCV) is a rare idiopathic microangiopathy characterized by diffuse blanchable telangiectases that usually develop in late adulthood. It appears morphologically identical to generalized essential telangiectasia (GET), but skin biopsy characteristically shows dilated superficial blood vessels in the papillary dermis that are surrounded by a thickened layer of type IV collagen.¹ We report a case of CCV occurring in an elderly white man.

A 72-year-old man presented with an asymptomatic rash on the arms, legs, and abdomen of 3 years’ duration. His medical history was remarkable for hypothyroidism, hypertension, reflex sympathetic dystrophy syndrome, coronary artery disease, and nonmelanoma skin cancer. He denied any changes in medications or illnesses prior to onset of the rash. Physical examination revealed diffuse, erythematous, blanchable telangiectases on the arms, legs, and trunk (Figure 1). No petechiae, atrophy, or epidermal changes were appreciated. Darier sign was negative.

Skin biopsy is essential to differentiate CCV from GET, which appears morphologically identical. Cutaneous collagenous vasculopathy may be underreported as a result of clinician choice not to biopsy due to a presumptive diagnosis of GET.³ Successful treatment with a pulsed dye laser has been reported,⁷ though the extent of disease may make complete destruction of the lesions difficult to accomplish. Although it is theorized that CCV may be a marker for underlying systemic disease or even a genetic defect causing abnormal collagen deposition, its cause has yet to be ascertained.⁵ Previously reported patients have had a variety of comorbidities, including several cases of type 2 diabetes mellitus.⁶ Another patient was reported to have recently started treatment with an angiotensin receptor blocker prior to onset of CCV.⁵

Our case contributes to the small series of reported patients with this rare diagnosis and further suggests that it may be underreported at this time. Similar to previously reported cases, our patient was an elderly white individual. Although our patient had long-standing iatrogenic hypothyroidism, no recent medication changes or underlying comorbidities could be tied to the development of CCV. Further studies are needed to determine if this disease process is associated with any underlying systemic illnesses, medications, or family history.

To the Editor:

Cutaneous collagenous vasculopathy (CCV) is a rare idiopathic microangiopathy characterized by diffuse blanchable telangiectases that usually develop in late adulthood. It appears morphologically identical to generalized essential telangiectasia (GET), but skin biopsy characteristically shows dilated superficial blood vessels in the papillary dermis that are surrounded by a thickened layer of type IV collagen.¹ We report a case of CCV occurring in an elderly white man.

A 72-year-old man presented with an asymptomatic rash on the arms, legs, and abdomen of 3 years’ duration. His medical history was remarkable for hypothyroidism, hypertension, reflex sympathetic dystrophy syndrome, coronary artery disease, and nonmelanoma skin cancer. He denied any changes in medications or illnesses prior to onset of the rash. Physical examination revealed diffuse, erythematous, blanchable telangiectases on the arms, legs, and trunk (Figure 1). No petechiae, atrophy, or epidermal changes were appreciated. Darier sign was negative.

Skin biopsy is essential to differentiate CCV from GET, which appears morphologically identical. Cutaneous collagenous vasculopathy may be underreported as a result of clinician choice not to biopsy due to a presumptive diagnosis of GET.³ Successful treatment with a pulsed dye laser has been reported,⁷ though the extent of disease may make complete destruction of the lesions difficult to accomplish. Although it is theorized that CCV may be a marker for underlying systemic disease or even a genetic defect causing abnormal collagen deposition, its cause has yet to be ascertained.⁵ Previously reported patients have had a variety of comorbidities, including several cases of type 2 diabetes mellitus.⁶ Another patient was reported to have recently started treatment with an angiotensin receptor blocker prior to onset of CCV.⁵

Our case contributes to the small series of reported patients with this rare diagnosis and further suggests that it may be underreported at this time. Similar to previously reported cases, our patient was an elderly white individual. Although our patient had long-standing iatrogenic hypothyroidism, no recent medication changes or underlying comorbidities could be tied to the development of CCV. Further studies are needed to determine if this disease process is associated with any underlying systemic illnesses, medications, or family history.

To the Editor:

Cutaneous collagenous vasculopathy (CCV) is a rare idiopathic microangiopathy characterized by diffuse blanchable telangiectases that usually develop in late adulthood. It appears morphologically identical to generalized essential telangiectasia (GET), but skin biopsy characteristically shows dilated superficial blood vessels in the papillary dermis that are surrounded by a thickened layer of type IV collagen.¹ We report a case of CCV occurring in an elderly white man.

A 72-year-old man presented with an asymptomatic rash on the arms, legs, and abdomen of 3 years’ duration. His medical history was remarkable for hypothyroidism, hypertension, reflex sympathetic dystrophy syndrome, coronary artery disease, and nonmelanoma skin cancer. He denied any changes in medications or illnesses prior to onset of the rash. Physical examination revealed diffuse, erythematous, blanchable telangiectases on the arms, legs, and trunk (Figure 1). No petechiae, atrophy, or epidermal changes were appreciated. Darier sign was negative.

Skin biopsy is essential to differentiate CCV from GET, which appears morphologically identical. Cutaneous collagenous vasculopathy may be underreported as a result of clinician choice not to biopsy due to a presumptive diagnosis of GET.³ Successful treatment with a pulsed dye laser has been reported,⁷ though the extent of disease may make complete destruction of the lesions difficult to accomplish. Although it is theorized that CCV may be a marker for underlying systemic disease or even a genetic defect causing abnormal collagen deposition, its cause has yet to be ascertained.⁵ Previously reported patients have had a variety of comorbidities, including several cases of type 2 diabetes mellitus.⁶ Another patient was reported to have recently started treatment with an angiotensin receptor blocker prior to onset of CCV.⁵

Our case contributes to the small series of reported patients with this rare diagnosis and further suggests that it may be underreported at this time. Similar to previously reported cases, our patient was an elderly white individual. Although our patient had long-standing iatrogenic hypothyroidism, no recent medication changes or underlying comorbidities could be tied to the development of CCV. Further studies are needed to determine if this disease process is associated with any underlying systemic illnesses, medications, or family history.

To the Editor:

We present a case of Mycobacterium chelonae-abscessus cutaneous infection in a sporotrichoid pattern, a rare presentation most often found in immunocompromised patients. A 34-year-old man with lupus nephritis who was taking oral prednisone, mycophenolate mofetil, and hydroxychloroquine presented with multiple erythematous fluctuant nodules and plaques on the left volar forearm in a sporotrichoid pattern of 3 months’ duration (Figure, A). He denied recent travel, exposure to fish or fish tanks, and penetrating wounds. Punch biopsy showed granulomatous inflammation and scarring with negative tissue cultures. Repeat biopsies and cultures were obtained when the lesions increased in number over 2 months.

Final biopsy showed upper dermal granulomatous inflammation with karyorrhectic debris, suggesting infection, and acid-fast bacilli. Culture grew M chelonae-abscessus on Löwenstein-Jensen agar at 37°C and blood culture media from which the complex was identified using high-performance liquid chromatography. Empiric therapy with renal dosing based on the Infectious Diseases Society of America statement of susceptibilities¹ was initiated with clarithromycin, doxycycline, and ciprofloxacin for 4 months. Furthermore, the prednisone dose was tapered to 7.5 mg daily. Two months later, the lesions regressed and ciprofloxacin was discontinued (Figure, B).

The sporotrichoid spread of nodules suggests infection with mycobacteria, Sporothrix schenckii, Leishmania, Francisella tularensis, or Nocardia. Most cultures for nontuberculous mycobacteria will grow on Löwenstein-Jensen agar between 28°C and 37°C. Runyon rapidly growing (group IV) mycobacteria are defined by their ubiquitous presence in the environment and ability to develop colonies in 7 days.² Cutaneous infections are increasing in prevalence, as reported in a retrospective study spanning nearly 30 years.³ The presentation is variable but often includes the distal extremities and usually is a nodule, ulcer, or abscess at a single site; a sporotrichoid pattern is more rare. Preceding skin trauma is the major risk factor for immunocompetent hosts, and the infection can spontaneously resolve in 8 to 12 months.¹ In contrast, immunosuppressed patients may have no known source of infection and often have a progressive course with an increasing number of lesions and increased time until clearance.⁴

It is difficult to differentiate M chelonae and M abscessus based on growth characteristics, and they share the same 16S ribosomal RNA sequence commonly used to differentiate other mycobacterial species.²Mycobacterium abscessus can be more difficult to treat, thus distinction via polymerase chain reaction of the heat-shock protein 65 gene, hsp65, can be valuable in cases recalcitrant to initial therapy.¹

The likelihood of M chelonae and M abscessus isolates to be initially sensitive to clarithromycin is 100%,¹ and this antibiotic remains the cornerstone of therapy. A clinical trial of treatments for M chelonae-abscessus found that clarithromycin monotherapy can be successful or complicated by resistance⁵; therefore, multidrug therapy is recommended. The antibiotic regimen for our patient was chosen to limit renal toxicity.

In summary, we report a case of M chelonae-abscessus cutaneous infection in a sporotrichoid pattern in a patient with lupus nephritis on immunosuppressive drugs. As the incidence of rapidly growing mycobacterial cutaneous infections rises, dermatologists must be aware of this pattern of infection.

To the Editor:

We present a case of Mycobacterium chelonae-abscessus cutaneous infection in a sporotrichoid pattern, a rare presentation most often found in immunocompromised patients. A 34-year-old man with lupus nephritis who was taking oral prednisone, mycophenolate mofetil, and hydroxychloroquine presented with multiple erythematous fluctuant nodules and plaques on the left volar forearm in a sporotrichoid pattern of 3 months’ duration (Figure, A). He denied recent travel, exposure to fish or fish tanks, and penetrating wounds. Punch biopsy showed granulomatous inflammation and scarring with negative tissue cultures. Repeat biopsies and cultures were obtained when the lesions increased in number over 2 months.

Final biopsy showed upper dermal granulomatous inflammation with karyorrhectic debris, suggesting infection, and acid-fast bacilli. Culture grew M chelonae-abscessus on Löwenstein-Jensen agar at 37°C and blood culture media from which the complex was identified using high-performance liquid chromatography. Empiric therapy with renal dosing based on the Infectious Diseases Society of America statement of susceptibilities¹ was initiated with clarithromycin, doxycycline, and ciprofloxacin for 4 months. Furthermore, the prednisone dose was tapered to 7.5 mg daily. Two months later, the lesions regressed and ciprofloxacin was discontinued (Figure, B).

The sporotrichoid spread of nodules suggests infection with mycobacteria, Sporothrix schenckii, Leishmania, Francisella tularensis, or Nocardia. Most cultures for nontuberculous mycobacteria will grow on Löwenstein-Jensen agar between 28°C and 37°C. Runyon rapidly growing (group IV) mycobacteria are defined by their ubiquitous presence in the environment and ability to develop colonies in 7 days.² Cutaneous infections are increasing in prevalence, as reported in a retrospective study spanning nearly 30 years.³ The presentation is variable but often includes the distal extremities and usually is a nodule, ulcer, or abscess at a single site; a sporotrichoid pattern is more rare. Preceding skin trauma is the major risk factor for immunocompetent hosts, and the infection can spontaneously resolve in 8 to 12 months.¹ In contrast, immunosuppressed patients may have no known source of infection and often have a progressive course with an increasing number of lesions and increased time until clearance.⁴

It is difficult to differentiate M chelonae and M abscessus based on growth characteristics, and they share the same 16S ribosomal RNA sequence commonly used to differentiate other mycobacterial species.²Mycobacterium abscessus can be more difficult to treat, thus distinction via polymerase chain reaction of the heat-shock protein 65 gene, hsp65, can be valuable in cases recalcitrant to initial therapy.¹

The likelihood of M chelonae and M abscessus isolates to be initially sensitive to clarithromycin is 100%,¹ and this antibiotic remains the cornerstone of therapy. A clinical trial of treatments for M chelonae-abscessus found that clarithromycin monotherapy can be successful or complicated by resistance⁵; therefore, multidrug therapy is recommended. The antibiotic regimen for our patient was chosen to limit renal toxicity.

In summary, we report a case of M chelonae-abscessus cutaneous infection in a sporotrichoid pattern in a patient with lupus nephritis on immunosuppressive drugs. As the incidence of rapidly growing mycobacterial cutaneous infections rises, dermatologists must be aware of this pattern of infection.

To the Editor:

We present a case of Mycobacterium chelonae-abscessus cutaneous infection in a sporotrichoid pattern, a rare presentation most often found in immunocompromised patients. A 34-year-old man with lupus nephritis who was taking oral prednisone, mycophenolate mofetil, and hydroxychloroquine presented with multiple erythematous fluctuant nodules and plaques on the left volar forearm in a sporotrichoid pattern of 3 months’ duration (Figure, A). He denied recent travel, exposure to fish or fish tanks, and penetrating wounds. Punch biopsy showed granulomatous inflammation and scarring with negative tissue cultures. Repeat biopsies and cultures were obtained when the lesions increased in number over 2 months.

Final biopsy showed upper dermal granulomatous inflammation with karyorrhectic debris, suggesting infection, and acid-fast bacilli. Culture grew M chelonae-abscessus on Löwenstein-Jensen agar at 37°C and blood culture media from which the complex was identified using high-performance liquid chromatography. Empiric therapy with renal dosing based on the Infectious Diseases Society of America statement of susceptibilities¹ was initiated with clarithromycin, doxycycline, and ciprofloxacin for 4 months. Furthermore, the prednisone dose was tapered to 7.5 mg daily. Two months later, the lesions regressed and ciprofloxacin was discontinued (Figure, B).

The sporotrichoid spread of nodules suggests infection with mycobacteria, Sporothrix schenckii, Leishmania, Francisella tularensis, or Nocardia. Most cultures for nontuberculous mycobacteria will grow on Löwenstein-Jensen agar between 28°C and 37°C. Runyon rapidly growing (group IV) mycobacteria are defined by their ubiquitous presence in the environment and ability to develop colonies in 7 days.² Cutaneous infections are increasing in prevalence, as reported in a retrospective study spanning nearly 30 years.³ The presentation is variable but often includes the distal extremities and usually is a nodule, ulcer, or abscess at a single site; a sporotrichoid pattern is more rare. Preceding skin trauma is the major risk factor for immunocompetent hosts, and the infection can spontaneously resolve in 8 to 12 months.¹ In contrast, immunosuppressed patients may have no known source of infection and often have a progressive course with an increasing number of lesions and increased time until clearance.⁴

It is difficult to differentiate M chelonae and M abscessus based on growth characteristics, and they share the same 16S ribosomal RNA sequence commonly used to differentiate other mycobacterial species.²Mycobacterium abscessus can be more difficult to treat, thus distinction via polymerase chain reaction of the heat-shock protein 65 gene, hsp65, can be valuable in cases recalcitrant to initial therapy.¹

The likelihood of M chelonae and M abscessus isolates to be initially sensitive to clarithromycin is 100%,¹ and this antibiotic remains the cornerstone of therapy. A clinical trial of treatments for M chelonae-abscessus found that clarithromycin monotherapy can be successful or complicated by resistance⁵; therefore, multidrug therapy is recommended. The antibiotic regimen for our patient was chosen to limit renal toxicity.

In summary, we report a case of M chelonae-abscessus cutaneous infection in a sporotrichoid pattern in a patient with lupus nephritis on immunosuppressive drugs. As the incidence of rapidly growing mycobacterial cutaneous infections rises, dermatologists must be aware of this pattern of infection.