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Year : 2023 | Volume
: 41
| Issue : 2 | Page : 123-124
Subcutaneous panniculitis-like T-cell lymphoma and steroid-induced depression successfully treated with prednisolone and cyclosporine
Tomoko Oshimo, Ayaki Matsumoto, Hitomi Kaiami, Daisuke Matsumoto, Jay-V James Barit, Daisuke Tsuruta
Department of Dermatology, Osaka Metropolitan University Graduate School of Medicine, Osaka, Japan
Correspondence Address:
Dr. Tomoko Oshimo
Department of Dermatology, Osaka Metropolitan University Graduate School of Medicine, Osaka, Japan, 1-4-3 Asahimachi, Abeno-Ku, Osaka 545-8585
Japan
Source of Support: None, Conflict of Interest: None
DOI: 10.4103/ds.DS-D-22-00186
Dear Editor,
Subcutaneous panniculitis-like T-cell lymphoma (SPTCL) is a subtype of cutaneous lymphoma characterized by α/β-type CD8-positive cytotoxic T-cells that infiltrate the subcutaneous fat tissue.[1] Clinically, it presents as multiple erythema nodosum-like subcutaneous nodules, predominantly on the lower legs, trunk, and face. The 5-year survival rate is approximately 80% and is lower (46%) for cases complicated by hemophagocytic syndrome (HPS), occurring in 20%–30% of patients.[1],[2] While there are no standardized treatment guidelines for SPTCL and many therapeutic options are available, systemic corticosteroids have been used successfully as a first-line single agent for SPTCL.
Here, we report a case of SPTCL treated with prednisolone that was complicated by steroid-induced depression and was successfully treated with a combination of prednisolone and cyclosporine.
A 50-year-old woman presented with numerous subcutaneous nodules on her thighs and lower extremities for 2 months. Histopathology showed a predominantly lobular panniculitis with infiltration of atypical medium-to large-sized lymphocytes that rimmed adipocytes. These atypical lymphocytes were CD4(−), CD8(+), CD56(−), βF1±, Granzyme B (+), TIA-1(−), and TCRδ(−), with no gene rearrangements in TCR cβ1 [Figure 1]. Positron emission tomography-computed tomography revealed hypermetabolic nodules with intense uptake. No obvious lymph node enlargement was detected using computed tomography. The findings from laboratory examinations were as follows: White blood cell counts (3600/μL, 4300–8000), soluble interleukin-2 receptor (588 U/mL, 204–587), lactate dehydrogenase (245U/L, 124–222), and ferritin (227.4 ng/dL, 6.23–138). Anti-nuclear and anti-ds DNA antibodies were negative, b2-microglobulin level was not tested. The symptoms indicative of HPS were not observed.
Figure 1: Subcutaneous panniculitis-like T-cell lymphoma. (a) Clinical presentation of erythematous subcutaneous nodules in the thigh, (b) Positron emission tomography images showing hypermetabolism in multiple subcutaneous nodular lesions, (c) Lobular infiltration of lymphoid cells (H and E, ×40), (d) Atypical medium-to large-sized lymphocytes rimming adipocytes (H and E, ×100), (e and f) Immunostaining for CD8 and granzyme B, and (g) CD56. The infiltrating lymphoid cells were CD8 and granzyme B positive and negative for CD56 (×400).The patient was diagnosed with SPTCL and was treated with prednisolone 30 mg/day, with gradual improvement of the lesions after 1 month. During tapering, when the prednisolone dose reached 15 mg, the patient reported feeling despondent and experienced fainting spells, consistent with an organic mood disorder. There were no other apparent problems upon neurological examination and the patient was diagnosed with steroid-induced depression by the psychiatrist. In response, prednisolone was rapidly tapered; however, the subcutaneous nodules subsequently recurred. Cyclosporine (initiated at 50 mg/day and gradually increased and continuously maintained at 125 mg/day) was added alongside prednisolone (slowly tapered from 10 mg), with significant reduction in the skin lesions after 4 weeks. Improvement of depression was observed when the prednisolone dose was eventually tapered to 6 mg/day after 4 more weeks. Because it takes time for the effects of cyclosporine to develop, we continued low-dose steroids to prevent the relapse of skin symptoms.
Various treatment modalities have been reported for SPTCL, including corticosteroids, oral immunosuppressive agents, local radiation therapy, multiagent chemotherapy, and hematopoietic stem cell transplantation. The European Society for Medical Oncology guidelines state that corticosteroids or immunosuppressive agents are the first-line treatments for SPTCL without HPS.[3]
Systemic corticosteroids alone have been reported to induce complete remission in four out of five patients (80%) diagnosed with SPTCL.[4] The regimen consisted of prednisolone 0.5–0.75 mg/kg/day for 4 weeks, tapered by 10 mg decrements weekly until 20 mg, with gradual 2.5 mg reductions. In these cases, all patients were maintained at 2.5–5 mg/day and continuous low-dose corticosteroids may be necessary to maintain remission.
Unfortunately, this case was complicated by steroid-induced depression. Although uncommon, the prevalence of major depression among individuals taking corticosteroids was reported to be 11.1% compared to 4.1% in those not taking steroids, with a higher incidence in women.[5] Steroid-induced depression is more likely to occur when steroid dosages exceed 40 mg/day.[6] Moreover, an average dose of 15.6 mg/day of corticosteroids can induce depression and is speculated to be associated with changes in hippocampal structure and function.[7] Dosage reduction and eventual discontinuation of corticosteroids serve as the primary treatment; and if such changes do not improve symptoms, appropriate drug therapy for depression is warranted.
The addition of cyclosporine for our patient allowed for further improvement of the skin lesions and permitted a simultaneous reduction in prednisolone dose to address the patient's depression. In a review of 63 SPTCL patients, 24 had been initially treated with less aggressive therapies, including combinations of prednisolone, cyclosporine, chlorambucil, methotrexate, cyclophosphamide, interferon-alpha, and gemcitabine, with response rates of up to 88%.[1],[2] Combination therapy with cyclosporine appears to be a valuable and effective therapeutic option for SPTCL when complications arise from systemic corticosteroid use.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given consent for her images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published, and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Data availability statement
All data generated or analyzed during this study are included in this published article.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References
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