Atezolizumab-induced scleroderma: a rare complication.

Few cases of programmed death-ligand 1 inhibitor-induced scleroderma have been reported and their clinical features remain unpublished. Optimal management is, therefore, unknown and an autoantibody association has yet to be identified. We present the case of a female in her 60s who developed skin thickening after starting atezolizumab for metastatic non-small cell lung cancer. Skin biopsy 7 months after symptom onset showed histological changes consistent with scleroderma. Anti-PM/SCL-75 antibody was positive. Atezolizumab was discontinued and treatment was started with mycophenolate mofetil. After 5 months, she experienced mild improvement in skin thickening. Earlier identification of this complication may limit morbidity in this disease process, which otherwise has limited treatment options. In suspected cases, obtaining scleroderma-associated autoantibodies may help with earlier diagnosis.

Values and Limits of Telemedicine: a Case Report.

In the era of a pandemic, the utilization of telemedicine is growing at a rapid speed. This new and necessary adaption in medicine is a threat to the basics of medicine which include the physical exam. A 72-year-old woman presents for a 1-week history of cervical neck discomfort. The patient was found to be febrile with initial physical exam nonrevealing due to patient preference of not taking off hospital gown. After blood cultures grew group A beta-hemolytic streptococcus and a computed tomography scan of the abdomen and pelvis with contrast demonstrated subtle bilateral renal hypodensities suggesting possible septic emboli, a more thorough physical exam was sought out which revealed a large rodent ulcer which the patient had been hiding from her family for 2 years. Transthoracic echocardiography was done which demonstrated a vegetation on the mitral valve confirming the diagnosis of endocarditis. The source of infection was the ulcer which was biopsied and found to be basal cell carcinoma. We present a unique case of endocarditis that was reliant on the physical exam to reveal the source of infection which was a rodent basal cell carcinoma ulcer. This case reminds physicians that at the forefront of telemedicine, the physical exam should not be forgotten.

Correction: Mantle Cell Lymphoma Relapsing as Disease of Skin, Orbit and CNS: An Extremely Rare Presentation and a Review of Literature.

[This corrects the article DOI: 10.14740/jh363w.].

Vancomycin-associated Henoch-Schönlein purpura.

Intravenous vancomycin is a widely used antibiotics, but it causes different types of cutaneous hypersensitivity reactions, ranging from maculopapular rash, red-man syndrome, drug rash with eosinophilia and systemic symptoms, IgA bullous dermatosis, leukocytoclastic vasculitis, Stevens-Johnsons syndrome, to IgE-mediated anaphylaxis. We report an elderly patient with the end-stage renal disease presented with diffuse palpable purpura while receiving IV vancomycin therapy for methicillin-resistant Staphylococcus aureus septicemia. Histopathology of skin biopsy revealed perivascular infiltrates of leukocytoclastic debris with necrosis of the small-sized blood vessels. Direct immunofluorescence analysis demonstrated vivid IgA plus C3 immune-complex deposits localized to the vessel walls, and no immune complexes were noted on the dermoepidermal junction. There was no IgG or IgM immunoreactivity detected on the tissue specimen. Rheumatologic disease work-ups were negative. A diagnosis of vancomycin-associated Henoch-Schönlein variant of vasculitis was made. Vancomycin was substituted by daptomycin, and the purpuric skin rashes were resolved. Since vancomycin is a commonly used antibacterial agent, clinicians are encouraged to have a heightened awareness of this rare adverse skin reaction. Early recognition and prompt discontinuation of the medication is the key in management. As it is not an Ig-E mediated reaction, desensitization of vancomycin or re-challenge with vancomycin is not recommended as re-exposure to the drug may result in a recurrence of similar manifestations with potential permanent renal failure.

Scalp metastasis from esophageal adenocarcinoma: comparative histopathology dictates surgical approach.

Cutaneous metastasis of esophageal cancer, in particular esophageal adenocarcinoma, is rare and metastasis to the scalp is extremely rare. We describe such a case that was originally diagnosed as an adnexal carcinoma. A 77-year-old male with a history of esophageal adenocarcinoma status after esophagectomy at our institution 4.5 years prior, presented to our plastic surgery clinic with a 2-month history of 2 temporoparietal scalp lesions. He was referred to our clinic by a community dermatologist who had performed a shave biopsy of the lesions. The clinical diagnosis was adnexal cyst. The history of esophageal carcinoma was not provided to the pathologist. The dermatopathology report came back as malignant adnexal neoplasm and considerations included apocrine carcinoma. We reexamined the pathologist's slides from the outside facility, comparing them to the histopathology from his esophagectomy. Histopathologic changes were identical. Thus, our surgical and postoperative approach changed significantly. Clinical suspicion should be high for cutaneous metastases in patients with a history of solid organ cancers. It is important for clinicians to illicit a history of malignancy. A biopsy should be performed on any suspicious lesions, and clinical data along with histopathology of the prior cancer resection(s) should be provided to the pathologist for comparison. Diagnosis of the suspicious lesion should be made before definitive excision, as this may change the approach, with the potential for postoperative chemotherapy and radiation. The definitive operative approach consists of surgical debulking with the evidence of negative margins. On the scalp, we feel that 5-mm margins are appropriate to obtain clear margins. One should appreciate the subdermal extent of metastases and adjust the margins accordingly. We recommend excising the galea with the skin as an en bloc resection. This will both assure clear deep margins of resection and assist in a tension-free closure of the scalp.

Human monoclonal antibodies to Pseudomonas aeruginosa alginate that protect against infection by both mucoid and nonmucoid strains.

Two fully human mAbs specific for epitopes dependent on intact carboxylate groups on the C6 carbon of the mannuronic acid components of Pseudomonas aeruginosa alginate were found to promote phagocytic killing of both mucoid and nonmucoid strains as well as protection against both types of strains in a mouse model of acute pneumonia. The specificity of the mAbs for alginate was determined by ELISA and killing assays. Some strains of P. aeruginosa did not make detectable alginate in vitro, but in vivo protection against lethal pneumonia was obtained and shown to be due to rapid induction of expression of alginate in the murine lung. No protection against strains genetically unable to make alginate was achieved. These mAbs have potential to be passive therapeutic reagents for all strains of P. aeruginosa and the results document that alginate is a target for the proper type of protective Ab even when expressed at low levels on phenotypically nonmucoid strains.