Cases Of Pityriasis Lichenoides Research Articles

Relationship Between Pityriasis Lichenoides and Mycosis Fungoides: A Clinicopathological, Immunohistochemical, and Molecular Study

Several cases of pityriasis lichenoides (PL) have been reported to evolve into mycosis fungoides (MF). To elucidate clues to this progression. Fifty-eight patients with PL between 2000 and 2013 (follow-up: 3-16 years, average: 8.3). A total of 3 (5.2%) of the 58 patients with PL developed MF after 3-11 years of prolonged clinical course. Papules and small plaques characterized PLs, and patches and larger plaques subsequent MFs. A total of 35 of 41 (85%) followed up non-MF associated patients with PL reported lasting complete remissions. Histopathologically, apoptotic keratinocytes disappeared mostly or completely in subsequent MFs. The presence of epidermotropism, folliculotropism, and epidermal lymphocytic nuclear atypia in PLs was not predictive of MF. CD8 cells were the dominant intraepidermal lymphocytes in the 3 PLs but remained so in only 1 subsequent MF. CD7 lymphocytes decreased substantially in 2 MFs, and lymphocytic nuclear atypia increased markedly in 1. T-cell receptor gene rearrangement studies demonstrated clonal populations in 1 of 2 studied PLs and in all 3 subsequent MFs. A few PLs may evolve into MF. Prolonged clinical course, appearance of patches and larger plaques, markedly increased lymphocytic nuclear atypia, marked diminution of apoptotic keratinocytes and CD7 and CD8 lymphocytes, and clonal T-cell receptor gene rearrangement may serve as clues.

A clinical and histolopathological study of pityriasis lichenoides

Pityriasis lichenoides is a papulosquamous disorder of unknown etiology with remissions and exacerbations. Histopathology helps greatly in the diagnosis of this condition. We studied clinical and histopathological features of pityriasis lichenoides in our patients. This is a 3-year retrospective and prospective, descriptive study of all patients clinically diagnosed as pityriasis lichenoides and confirmed by histopathology. All patients were studied clinically and histopathologically. There were 51 (30 males and 21 females) cases of pityriasis lichenoides in the study period. The maximum number of cases, 14 (27.45%) were in their second decade of life. Pityriasis lichenoides chronica was diagnosed in 39 cases (76.47%) and pityriasis lichenoides et varioliformis acuta (PLEVA) in 12 cases (23.53%). Histopathologically, basal cell vacuolation and perivascular infiltrate were seen in all the cases. Exocytosis was seen in 45.1% of the cases. All the cases of PLEVA showed lymphocytic vasculitis albeit without fibrinoid deposition in the vessel walls. Pityriasis lichenoides is not a rare disorder, and is not a true lymphocytic vasculitis as blood vessel damage and fibrinoid deposition in the blood vessel walls were not seen in this study.

Lack of the t(2;5) or other mutations resulting in expression of anaplastic lymphoma kinase catalytic domain in CD30+ primary cutaneous lymphoproliferative disorders and Hodgkin's disease

The t(2;5) (p23;q35) chromosomal translocation has been found in a high proportion of lymph node-based CD30+ large cell lymphomas of T-cell lineage. This translocation is believed to result in the expression of a fusion protein containing the catalytic domain of anaplastic lymphoma kinase (ALK) under the control of the promoter for nucleophosmin, a nucleolar phosphoprotein. Expression of ALK activity, which does not normally occur in lymphocytes, is postulated to be involved in the pathogenesis of lymphomas bearing the t(2;5) translocation. Several primary cutaneous lymphoproliferative disorders and Hodgkin's disease are also known to contain CD30+ large lymphoid cells. To determine the role of the t(2;5) translocation in these diseases, we developed a DNA- based polymerase chain reaction (PCR)/Southern blot assay to detect this translocation at the genomic level in lymphomatoid papulosis (14 cases), primary cutaneous CD30+ large cell lymphoma of T-lineage (10 cases) and Hodgkin's disease (13 cases). Two cases of pityriasis lichenoides were also studied. The t(2;5) translocation was not present in any of these specimens. To determine if some other somatic mutation might have resulted in inappropriate expression of ALK catalytic domain, we devised an RNA-based reverse transcriptase-PCR assay to detect transcripts encoded by this ALK region. None were found in the six additional cases of lymphomatoid papulosis that were studied. In aggregate, these results strongly suggest that inappropriate expression of ALK is not involved in the pathogenesis of these CD30+ lymphoproliferative disorders, and that lymph node-based CD30+ large cell lymphoma is a disease that is biologically distinct from skin- based CD30+ lymphoproliferative disorders and Hodgkin's disease. Using methods developed for this report, we also cloned and sequenced the t(2;5) genomic junctional sequences present in the SUP-M2 and SU-DHL-1 cell lines. These intron sequences will be useful for mapping t(2;5) breakpoint clusters.

Lack of the t(2;5) or Other Mutations Resulting in Expression of Anaplastic Lymphoma Kinase Catalytic Domain in CD30+ Primary Cutaneous Lymphoproliferative Disorders and Hodgkin's Disease

The t(2;5) (p23;q35) chromosomal translocation has been found in a high proportion of lymph node-based CD30+ large cell lymphomas of T-cell lineage. This translocation is believed to result in the expression of a fusion protein containing the catalytic domain of anaplastic lymphoma kinase (ALK) under the control of the promoter for nucleophosmin, a nucleolar phosphoprotein. Expression of ALK activity, which does not normally occur in lymphocytes, is postulated to be involved in the pathogenesis of lymphomas bearing the t(2;5) translocation. Several primary cutaneous lymphoproliferative disorders and Hodgkin's disease are also known to contain CD30+ large lymphoid cells. To determine the role of the t(2;5) translocation in these diseases, we developed a DNA-based polymerase chain reaction (PCR)/Southern blot assay to detect this translocation at the genomic level in lymphomatoid papulosis (14 cases), primary cutaneous CD30+ large cell lymphoma of T-lineage (10 cases) and Hodgkin's disease (13 cases). Two cases of pityriasis lichenoides were also studied. The t(2;5) translocation was not present in any of these specimens. To determine if some other somatic mutation might have resulted in inappropriate expression of ALK catalytic domain, we devised an RNA-based reverse transcriptase-PCR assay to detect transcripts encoded by this ALK region. None were found in the six additional cases of lymphomatoid papulosis that were studied. In aggregate, these results strongly suggest that inappropriate expression of ALK is not involved in the pathogenesis of these CD30+ lymphoproliferative disorders, and that lymph node-based CD30+ large cell lymphoma is a disease that is biologically distinct from skin-based CD30+ lymphoproliferative disorders and Hodgkin's disease. Using methods developed for this report, we also cloned and sequenced the t(2;5) genomic junctional sequences present in the SUP-M2 and SU-DHL-1 cell lines. These intron sequences will be useful for mapping t(2;5) breakpoint clusters.

Two Cases of Pityriasis Lichenoides et Varioliformis Acuta were Treated by Tetracyclines, Etretinates

Two Cases of Pityriasis Lichenoides et Varioliformis Acuta were Treated by Tetracyclines, Etretinates

Mucha-Habermann's disease with oral lesions

A case of pityriasis lichenoides et varioliformis acuta (Mucha-Habermann's disease) in a 30-year-old Caucasian man is presented, along with a review of pertinent clinical and microscopic features. During a severe exacerbation of the disease, lesions of the oral mucosa were observed. Histopathologic features of the oral lesions were similar to those observed in the cutaneous lesions.

Pityriasis Lichenoides et Varioliformis Acuta and Suspected Cardiomyopathy

AbstractA case of Pityriasis lichenoides et varioliformis acuta (PLV A) is reported in whom evidence of a cardiomyopathy developed during the early stages of the disease.