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A 62 years old patient presented with rapidly progressive mycosis fungoides. Lesions of the face, head, trunk and limbs exhibited numerous vesicles and erosions. Histopathology showed marked spongiosis and intraepidermal blisters, as well as invasion of the epidermis by atypical lymphocytes, which was confirmed by immunohistochemistry. The vesicular variant of mycosis fungoides is rare and associated with a poor prognosis.
The platelet cytotoxic action on tumor cells was studied in patients with mycosis fungoides and Kaposi's sarcoma. The findings evidence, that along with the known populations of cytotoxic effector cells, such as lymphocytes and monocytes, platelets may destroy tumor cells as well. Platelet ability to induce tumor cell lysis is essentially increased in mycosis fungoides patients treated according to scheme B. The data indicate that platelets from patients with mycosis fungoides and Kaposi's sarcoma are characterized by cytotoxic activity against AKL continuous tumor target cell line.
A total of 115 patients with mycosis fungoides were given total-skin electron-beam therapy (TSEB), utilizing 3.5-mev electrons at doses of 400 rads to the entire skin surface once a week for 6--8 consecutive weeks. Prompt relief of symptoms and regression of lesions were observed in all patients. Of the 81 patients at risk for 12--91 months (median, 24 months) following TSEB, initial unmaintained remission lasted 6--69 months (median, 19 months). No untoward immediate or late effects have been noted in the bone marrow or normal skin which was irradiated. The duration of remission following TSEB correlated well with lymphocyte responsiveness to various mitogens and antigens, but not with the initial response. Thymic hormone factor levels (Facteur Thymic Serique) were elevated in the majority of these patients with mycosis fungoides.
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A 43-year-old man with tumour stage mycosis fungoides developed multiple follicular pustules on the trunk during total-skin electron beam therapy. A potassium hydroxide preparation of the contents of the pustules revealed the presence of Demodex mites. The patient was treated with 6% sulphur lotion with rapid improvement of the cutaneous lesions. We believe that this case represents a pustular folliculitis caused by Demodex mites. Immunosuppression associated with mycosis fungoides and its treatment may have resulted in the proliferation of this obligate parasite of the pilosebaceous follicle, and the development of the folliculitis.
Primary cutaneous T-cell lymphomas, including lymphomatoid papulosis, mycosis fungoides and CD30+ anaplastic large cell lymphoma (ALCL) overlap clinicopathologically and form part of a spectrum of lymphoproliferative disorders. There have been several case reports of these diseases coexisting. We describe a 59-year-old Korean man who presented with a recurrent, solitary CD30+ ALCL of 25 years' duration as well as patch stage mycosis fungoides of 11 years' duration. Such occurrences may represent different clinical manifestations of the same clonal T-cell abnormality, and provide further insight into the pathogenesis of these related disorders.
A 51-year-old man with type IV skin presented for evaluation of a generalized rash associated with multiple ulcerated, nodular lesions on his legs. The nodular lesions occurred approximately 18 months after the initial onset of generalized rash, which had been diagnosed as plaque/patch stage mycosis fungoides. He continued to develop further nodular lesions on his trunk in the weeks following presentation. The nodular lesions were shown to be squamous-cell carcinoma on histopathology. He had received only topical hydrocortisone prior to the development of the second cutaneous malignancy and had no past exposure to carcinogens. His squamous cell carcinomas were treated with surgical excision and split-skin grafting. He received total skin electron-beam therapy to treat the mycosis fungoides. Second malignancy in mycosis fungoides is a recognized phenomenon and usually occurs after potentially carcinogenic therapy. This case demonstrates the occurrence of second malignancy in the absence of a precipitating factor, suggesting that there are innate, immune-mediated mechanisms in the development of cancer in patients with mycosis fungoides.
The two cases reported in this paper allow the differentiation of pagetoid reticulosis from solitary lesions of mycosis on the basis of clinical, histological ultrastructural, immunohistochemical and enzyme histochemical studies. The first patient presented with a slowly growing asymptomatic scaly plaque of 30 years duration. Histology of the lesion was typical of pagetoid reticulosis. Immunohistochemical studies showed that the abnormal cells present in the cutaneous infiltrate were not T lymphocytes and ultrastructural studies suggested these were of histocytic origin. The second patient presented with a poikilodermatous lesion present for 14 years with histology of plaque stage mycosis fungoides. Enzyme and immunohistochemistry showed the predominant T cell nature of the cutaneous infiltrate and electron microscopy showed numerous mycosis fungoides cells. In contrast to generalized forms of mycosis fungoides, no peripheral blood monocyte chemotactic defect was found in either case. Both lesions responded to radiotherapy.
Primary cutaneous T- and B-cell lymphomas are a heterogeneous group of diseases with varied clinical presentations and prognosis. The use of new molecular, histological, and clinical criteria has improved their recognition. Cutaneous B-cell and T-cell lymphomas are seldom found together in the same patient. Here we report a rare case of mycosis fungoides variant of a cutaneous T-cell lymphoma (CTCL) which later developed Epstein-Barr virus (EBV) associated cutaneous B-cell lymphoproliferative disorder. The patient initially presented with generalized erythroderma, extensive plaques, and axillary lymphadenopathy. Histopathology and immunophenotyping of her tumor from the right breast nodule revealed a T-cell lymphoma consistent with mycosis fungoides. She was initially treated with pentostatin, followed by topical mechlorethamine and topical steroids. After progression of her mycosis fungoides with worsening diffuse skin lesions on this regimen, her treatments were changed to oral bexarotene with an initial partial response followed by stable disease. Three years from her initial presentation, she developed ulcerated cauliflower-like nodules on her forehead. Biopsy of these lesions revealed EBV-positive large- and medium-sized pleomorphic B-cells consistent with EBV-driven B-cell lymphoproliferative disorder. She was treated with topical acyclovir cream on the involved skin areas while continuing with oral bexarotene for mycosis fungoides. Skin lesions gradually diminished and totally disappeared after four weeks of topical acyclovir treatment. Bexarotene treatment was continued for another year until the mycosis fungoides progressed and became wide spread causing her death four and a half years after the initial diagnosis. The coexistence of two cutaneous non-Hodgkin lymphomas of different lineage in the same patient and the complete clinical response of EBV-related B-cell cutaneous component to topical acyclovir makes this rare case particularly interesting.
Cell and serum samples from 7 Hungarian patients with mycosis fungoides were examined for the presence of HTLV-I-related DNA sequences and antibodies recognizing HTLV-I antigens. DNA sequences distantly related to the proviral DNA of HTLV-I were shown by Southern blot hybridization in 3 patients. Serum samples from these patients contained antibodies reactive with the internal core polypeptides of HTLV-I and HTLV-II, but not with the env gene encoded type-specific HTLV antigens. Restriction enzyme analysis with EcoRI, PstI, BamHI and SacI revealed structural similarity of the provirus(es) integrated in the DNA of mycosis fungoides cells to HTLV-I but not to HTLV-II. Data suggest that these proviruses and HTLV-I are similar to each other along gag and pol regions.
Allelotyping studies have been extensively used in a wide variety of malignancies to define chromosomal regions of allelic loss and sites of putative tumor suppressor genes; however, until now this technique has not been used in cutaneous lymphoma. We have analyzed 51 samples from patients with mycosis fungoides and 15 with Sézary syndrome using methods to detect loss of heterozygosity. Micro satellite markers were selected on 15 chromosomal arms because of their proximity to either known tumor suppressor genes or chromosomal abnormalities identified in previous cytogenetic studies in cutaneous lymphoma. Allelic loss was present in 45% of patients with mycosis fungoides and 67% with Sézary syndrome. Loss of heterozygosity was found in over 10% of patients with mycosis fungoides on 9p, 10q, 1p, and 17p and was present in 37% with early stage (T1 and T2) and 57% with advanced disease (T3 and T4). Allelic loss on 1p and 9p were found in all stages of mycosis fungoides, whereas losses on 17p and 10q were limited to advanced disease. In Sézary syndrome high rates of loss of heterozygosity were detected on 9p (46%) and 17p (42%) with lower rates on 2p (12%), 6q (7%), and 10q (12%). There was no significant difference in the age at diagnosis or number of treatments received by those with loss of heterozygosity and those without, suggesting that increasing age and multiple treatments do not predispose to allelic loss. These results provide the basis for further studies defining more accurately chromosomal regions of deletions and candidate tumor suppressor genes involved in mycosis fungoides and Sézary syndrome.
The efficacy of topical steroids, chemotherapy, photochemotherapy, grenz-ray therapy and electron beam therapy has already been established in the treatment of mycosis fungoides. In addition, the results of dermatological climatotherapy in the high Alpine region (Davos, 1,560 m) demonstrate that natural sun irradiation in this particular climate is very effective in treating mycosis fungoides. A total of 63% out of 128 treatment cycles of 84 patients suffering from mycosis fungoides went into remission, which lasted a maximum of at least 13 months. The best results are obtained in the early stages of mycosis fungoides and if climatotherapy lasts long enough and is repeated.
OBJECTIVE: To determine the effectiveness of topical corticosteroids in the management of mycosis fungoides. DESIGN: Prospective study. SETTING: Academic referral center, Veterans Affairs Medical Center, and private practice. PATIENTS: Seventy-nine patients with patch or plaque stage of mycosis fungoides. Fifty-one were stage T1 (less than 10% of skin involved) and 28 were stage T2 (10% or more of skin involved). Seventy-five had patch-stage and 4 had plaque-stage disease as determined by histological examination. INTERVENTION: Patients were treated with topical class I to III corticosteroids. Of the stage T1 patients, all used class I corticosteroids, and 4 (8%) also used class II or III corticosteroids. Of the stage T2 patients, 19 (68%) used class I and 12 (43%) used class II or III compounds. Some patients used more than 1 class of corticosteroid. Applications were almost always twice daily. Three stage T1 and 2 stage T2 patients used plastic film occlusion. Baseline and monthly morning serum cortisol levels were obtained during treatment. MAIN OUTCOME MEASURES: Response to treatment and side effects. RESULTS: The median follow-up period was 9 months. Thirty-two (63%) of stage T1 patients achieved complete remission and 16 (31%) achieved partial remission, for a total response rate of 48 (94%). The comparable figures for stage T2 patients were 7 (25%), 16 (57%), and 23 (82%), respectively. Responses were determined by clinical examination. Thirty-nine patients achieved clinical clearing. In 7 of these, posttreatment biopsy specimens were obtained, and all showed histological clearing. Reversible depression of serum cortisol levels occurred in 10 (13%). Minor skin irritation occurred in 2 patients and localized, reversible skin atrophy in 1. CONCLUSION: Topical corticosteroids, especially class I compounds, are an effective treatment for patch-stage mycosis fungoides.
PURPOSE: To present a case of ulcerative keratitis and impending corneal perforation in a patient with mycosis fungoides (cutaneous T-cell lymphoma) that developed eyelid involvement. METHODS: Case report analysis. Cultures and biopsies of the right cornea, conjunctiva, and eyelids were obtained. Biopsy tissue was examined with histologic and immunohistologic stains. RESULTS: This patient with mycosis fungoides involving the eyelids developed corneal exposure and bacterial keratitis with impending corneal perforation. Lamellar keratoplasty and permanent tarsorrhaphy were performed to protect the globe from perforation. DISCUSSION: Mycosis fungoides involving the eyelids is capable of causing severe ocular tissue injury without direct infiltration of the malignant lymphocytes. Preventative medical and surgical measures must be taken to protect the globe.
An increased risk for a second malignancy has been reported in patients with mycosis fungoides. We describe two subjects with mycosis fungoides who developed small malignant melanoma after topical application of nitrogen mustard.
Hodgkin's disease and mycosis fungoides have been rarely reported in the same patient. This coexistence has been debated in the medical literature. We studied such a patient and report, to our knowledge, the first immunophenotypic evidence for such a coexistence. Reed-Sternberg cells and their variants stained with anti-Leu-M1, Hefi-1, anti-Tac, anti-HLA-DR, and OKT9, but were negative for T cell markers 3A1, Leu-1, Leu-2a, and Leu-3a, a phenotype typical of Hodgkin's disease; infiltrating small lymphocytes were predominantly T cells and were phenotypically normal. In the skin lesions, cells with the phenotype of Hodgkin's disease were not present; the infiltrate was composed of helper T lymphocytes that were 3A1-negative, a phenotype characteristic of the malignant cells of mycosis fungoides. Unexpectedly, a dermatopathic lymph node from the same patient showed the presence of the Leu-M1 antigen on the majority of normal-appearing interdigitating reticulum cells; this was not the case with control dermatopathic lymph nodes from patients without a malignancy. The significance, implications, and possible interrelationships of the findings are discussed.
Mycosis fungoides (MF) is morphologically similar to cutaneous lesions of adult T cell leukemia/lymphoma (ATLL) of human T-cell lymphotropic virus-type I (HTLV-1). In addition, the Th1 or Th2 characteristic of MF and ATLL is still controversial. In the present study, to discriminate MF and cutaneous lesion of ATLL using immunohistochemical markers, and to elucidate Th1 or Th2 dominancy in both disorders, CLA (cutaneous lymphocyte associated antigen) was expressed on epidermotrophic lymphoma cells in all early stage MF. In contrast, all ATLL were negative for CLA. CXCR3 was especially expressed in epidermotropic small lymphoma cells of MF. CCR5 was expressed in both disorders with variable sized lymphoma cells. ST2 was expressed on large transformed lymphoma cells with ATLL, but not in any MF cases. OX40 was expressed in the large transformed cell population in both disorders. These findings suggest that CLA and ST2 could be potentially useful immunohistochemical markers for discrimination of mycosis fungoides and cutaneous lesions of ATLL. And OX40 could be a useful immunohistochemical marker for the histopathological progression of both disorders.
Electron beam irradiation of the entire skin surface was used to treat 25 patients with mycosis fungoides from 1977 to January 1988. A plexiglas screen was used to reduce the energy of the 8 MeV beam of a Sagittaire linear accelerator to 4 MeV. A total dose of 30 Gy was delivered in 12 fractions over days. This series includes 17 men and 8 women with a mean age of 44 years (range 13-78 years) and a mean follow-up of 34 months (range 6-92 months). The following-up staging system was used: stage A: superficial lesions covering less than 50 p. 100 of the body surface; stage B: superficial lesions covering more than 50 p. 100 of the body surface; stage C: tumors of the skin, lymph nodes and/or visceral organs, Sezary's syndrome. All stage A patients achieved complete remission. One developed recurrent disease in a very limited area 17 months after radiation therapy. No stage A patient died of mycosis fungoides. 6/9 stage B patients achieved complete remission; 4 of these developed recurrent disease localized to the skin 6 to 13 months after electron therapy. These recurrences were controlled by topical nitrogen mustard, puva therapy or localized irradiation. 1 patient showed no response and died of cutaneous mycosis fungoides. 5/10 stage C patients obtained complete remission but all relapsed within a mean period of 7 months. 4/5 of the patients not responding to electron therapy died of their disease and one is alive 16 months after completion of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)