Angioimmunoblastic T-cell Lymphoma Presenting as a Methotrexate-associated Lymphoproliferative Disorder with Extreme Peripheral Blood Plasmacytosis.

A 74-year-old man was admitted to our hospital because of systemic lymphadenopathy, weight loss, and a fever at night that had persisted for approximately 1 month. Blood tests revealed extreme peripheral blood plasmacytosis and hypergammaglobulinemia. A lymph node biopsy showed angioimmunoblastic T-cell lymphoma (AITL). Based on the history of methotrexate (MTX) administration, the established diagnosis was MTX-associated lymphoproliferative disorder (MTX-LPD). After MTX was discontinued, the lymphadenopathy spontaneously regressed and the plasmacytosis disappeared. He had no disease progression for three years. We found that AITL as an MTX-LPD can cause plasmacytosis, and the prognosis of this disease may not be poor.

Methotrexate-associated lymphoproliferative disorders of T-cell phenotype: clinicopathological analysis of 28 cases.

Methotrexate-associated lymphoproliferative disorders are categorized as "other immunodeficiency-associated lymphoproliferative disorders in the WHO classification. Methotrexate-associated lymphoproliferative disorder is mainly a B-cell lymphoproliferative disorders or Hodgkin lymphoma type, whereas T-cell lymphoproliferative disorders are relatively rare (4-8%). Only a small number of methotrexate-associated T-cell lymphoproliferative disorders have been detailed thus far. Because of the rarity, methotrexate-associated T-cell lymphoproliferative disorder has not been well studied and its clinicopathological characteristics are unknown. A total of 28 cases of methotrexate-associated T-cell lymphoproliferative disorders were retrospectively analyzed. Histologically and immunohistochemically, they were divided into three main types: angioimmunoblastic T-cell lymphoma (n = 19), peripheral T-cell lymphoma, NOS (n = 6), and CD8+ cytotoxic T-cell lymphoma (n = 3). Among the 28 cases, only one CD8+ cytotoxic T-cell lymphoma case was Epstein-Barr virus-positive. The other 27 cases were negative for Epstein-Barr virus on tumor cells, but scattered Epstein-Barr virus-infected B-cells were detected in 24 cases (89%), implying the reactivation of Epstein-Barr virus caused by immunodeficient status of the patients. After the diagnosis of methotrexate-associated T-cell lymphoproliferative disorder, methotrexate was immediately withdrawn in 26 cases. Twenty (77%) cases presented with spontaneous regression. Compared to methotrexate-associated B-cell lymphoproliferative disorder, patients with methotrexate-associated T-cell lymphoproliferative disorder had a significantly higher proportion of males (p = 0.035) and presence of B-symptoms (p = 0.036), and lower proportion of Epstein-Barr virus+ tumor cells (p < 0.001). Although the difference was not significant, the methotrexate-associated T-cell lymphoproliferative disorder also had more frequent spontaneous regression (p = 0.061). In conclusion, methotrexate-associated T-cell lymphoproliferative disorder was divided into three main types: angioimmunoblastic T-cell lymphoma, peripheral T-cell lymphoma, NOS, and CD8+ cytotoxic T-cell lymphoma. Angioimmunoblastic T-cell lymphoma was the most common type. Methotrexate-associated T-cell lymphoproliferative disorder was characterized by a high rate of spontaneous regression after methotrexate cessation. Epstein-Barr virus positivity was relatively rare in methotrexate-associated T-cell lymphoproliferative disorder, significantly less frequent than methotrexate-associated B-cell lymphoproliferative disorder, suggesting different pathogenesis.

Angioimmunoblastic lymphadenopathy with dysproteinemia following doxycycline administration.

Angioimmunoblastic lymphadenopathy with dysproteinemia (AILD) is a primary lymphoproliferative T-cell disorder, currently classified as a peripheral T-cell non-Hodgkin's lymphoma. AILD is characterized by generalized lymphadenopathy, hepatosplenomegaly, immunological abnormalities, polyclonal hypergammaglobulinemia and anemia. We report a case of AILD in an 80-year-old male who presented with a generalized pruritic maculopapular eruption and fever following doxycycline administration. The maculopapular rash progressed to formation of confluent nodules, plaques and finally erythroderma with lymphadenopathy and hepatosplenomegaly. Blood analysis revealed an elevated erythrocyte sedimentation rate and polyclonal hypergammaglobulinemia. Lymph node biopsy showed almost complete effacement of the nodal architecture with diffuse proliferation of small vessels forming an arborizing network, surrounded by atypical lymphocytes, usually CD3+ CD4+ and occasionally CD3+ CD8+. There were also larger cells (immunoblastic shape) that displayed CD20 positively, some scattered plasma cells, and eosinophils. Histology of a cutaneous lesion showed spongiosis and infiltration of the epidermis by atypical lymphocytes with large hyperchromatic nuclei, perivascular dermal lymphocytic infiltrate (CD3+) mixed with plasma cells and occasional large immunoblasts (CD20+). During hospitalization the patient developed hemolytic anemia (Coombs positive) and lung metastases. The prognosis of AILD is generally poor, with a median survival of less than 20 months. Our patient died two and a half months after the diagnosis was made due to sepsis caused by Staphylococcus aureus isolated in hemoculture.

Angioimmunoblastic lymphadenopathy following ciprofloxacin administration.

Angioimmunoblastic lymphadenopathy (AILD) is a rare disorder characterised by generalised lymphadenopathy, fever, hepatosplenomegaly, immune hemolytic anemia and polyclonal hypergammaglobulinemia. We report the occurrence of histology-proven AILD in a patient who had received ciprofloxacin. We suggest that this drug may be added to the list of agents susceptible to elicit AILD.

Sulfasalazine-induced angioimmunoblastic lymphadenopathy developing in a patient with juvenile chronic arthritis.

We describe a patient with juvenile chronic arthritis who developed reactive angioimmunoblastic lymphadenopathy, induced by sulfasalazine. Development of angioimmunoblastic lymphadenopathy although rare, is a very serious side effect of sulfasalazine treatment, and patients treated with this drug should be watched carefully.

Silicone granulomatous lymphadenopathy and siliconomas of the breast.

In the present study, two histologically-distinct cases of granulomatous lymphadenitis induced by dimethylpolysiloxane (silicone polymer) implants were studied. Four and six years after implant, and following surgery for breast cancer, painful homolateral axillary adenopathies were observed and biopsied. In both cases, histological examination led to a diagnosis of "silicone-induced granulomatous adenitis" requiring removal of implants. Foreign-body granulomas (siliconomas) were observed in surrounding tissue with no apparent rupture of implant capsules; however, visible retraction, hardening and scattered calcifications were noted. The presence of silica was revealed by incineration of a number of biopsied lymph nodes, a technique not hitherto used in the study of this pathology. A review is offered of the literature available.

Salazosulfapyridine-induced angioimmunoblastic lymphadenopathy.

A 20-year-old man with ulcerative colitis was admitted because of fever, eruption and lymphadenopathy. He had started taking salazosulfapyridine one month previously. Lymph node biopsy revealed angioimmunoblastic lymphadenopathy. Autoantibody titers were all negative, and viral antibody titers were not increased retrospectively. Rearrangement of T-cell receptor beta and chromosomal aberration were not seen on the lymph node. This case is considered not to be a peripheral T-cell lymphoma but rather salazosulfapyridine-induced angioimmunoblastic lymphadenopathy (AIL), which is the second case in English language literature.

[Angioimmunoblastic lymphadenopathy. Apropos a case with unusual clinical manifestations and evolution to T-cell lymphoma]. / Linfadenopatía angioinmunoblástica. A propósito de un caso con manifestaciones clínicas inusuales y evolución a linfoma T.

We present the case of a 67-years-old patient which, after treatment with ciprofloxacin, developed fever, exanthema, arthralgias, polyadenopathies, hepatosplenomegaly, autoimmune hemolytic anemia, hypergammaglobulinemia and severe inversion of the CD4/CD8 ratio. Latter, he developed ischemic signs in several locations (splenic and cerebral infarcts), as well as polyneuropathy and inflammatory myopathy. The diagnosis of angioimmunoblastic lymphadenopathy was established through ganglionary biopsy. The patient improved initially with the administration of corticoids, but in a few months, he developed pleomorphic T lymphoma with quick fatal evolution. We discuss the rarity of some of the clinical and laboratory manifestations in this patient and we comment on the association of ciprofloxacin and the angioimmunoblastic lymphadenopathy, which has never been previously described in the international literature.

Linfadenopatía angioinmunoblástica por ingestión prolongada de anfetamina / Angioimmunoblastic lymphadenopathy due to protractred amphetamine intake

Se presenta un paciente de 58 años con una linfadenopatía angioinmunoblástica (LAI) que ha ingerido 3 tabletas diarias de anfetamina durante 8 años.La ingestión prolongada de grandes dosis de anfetamina produce daños microvasculares un rasgo característico de la LAI. Con sólo medidas generales se observó una tendencia a la regresión de las adenopatías. El empleo del interferón alfa leucocitario pareció efectivo en el control de algunas adenopatías inguinales persistentes

Immunological adverse effects of anticonvulsants. What is their clinical relevance?

Long term administration of anticonvulsants is sometimes associated with impairment of the humoral and/or cellular immune response. Furthermore, certain well known adverse reactions to antiepileptics may have an immunotoxicological origin e.g. lymphadenopathy, pseudolymphoma and systemic lupus erythematosus. However, two important questions remain unresolved. First, the possibility that epilepsy per se might be primarily associated with immune alterations makes it difficult to assess the pathogenetic role of a specific drug, especially in a patient population usually on multiple drug therapy. Secondly, the clinical relevance of some of the observed immunological abnormalities is still highly controversial. This review is intended to give an outline of the present state of knowledge on the effects of anticonvulsants on humoral, cellular and nonspecific immunity, with particular regard to some of the major clinical conditions that have been ascribed to drug-induced immune dysregulation, such as pseudolymphoma and systemic autoimmune diseases. The immunotoxic potential of anticonvulsants appears to be low, and immunological monitoring is not usually required except in patients with known immune defects.

The role of chest computed tomography in the diagnosis of drug-related reactions.

Computed tomography (CT) of the chest provides important information toward the diagnosis of drug-induced lung disease. CT's ability to demonstrate subtle parenchymal and pleural changes, small nodules, and adenopathy is valuable in the early detection of drug-related reactions. CT is also of value in monitoring the appearance, progression, and resolution of pulmonary damage in patients receiving potentially toxic drugs. The CT appearances of specific drug reactions are reviewed, including the spectrum of CT findings in bleomycin toxicity and amiodarone-induced lung disease.

Acute lymphadenopathy complicating quinidine therapy.

A patient is described with quinidine-induced acute lymphadenopathy syndrome proven by rechallenge of the drug. Serum markers for systemic lupus were negative.

[Angioimmunoblastic lymphadenopathy with dysproteinemia. The first reported case at the "Santo Tomás" Hospital]. / Linfadenopatiá angioinmunoblástica con disproteinemia. Primer caso reportado en el Hospital "Santo Tomás".

Description of the first case of angio-immunoblastic lymphadenopathy with dysproteinemia diagnosed in a male patient 64 years old and which preceded the development of a lymphoma. The importance of this study is the association that may exist between certain drugs and the development of angioimmunoblastic lymphadenopathy, which occurred in our patient with the use of diphenylhydantoin. This disease can present itself up to 22 years after exposure to the agent.

Angioimmunoblastic lymphadenopathy, sulphasalazine exposure and villous atrophy.

A woman with inflammatory lesions in the terminal ileum was treated with sulphasalazine. Nine months later she developed angioimmunoblastic lymphadenopathy and was found to have intestinal villous atrophy. Her systemic illness partially responded to oral steroids but a gluten free diet restored clinical and biochemical well being coincident with a return of her villous pattern.

Severe pancytopenia due to marked marrow fibrosis associated with angioimmunoblastic lymphadenopathy.

A patient with angioimmunoblastic lymphadenopathy (AILD) is presented. Manifestations of the disease appeared after short-term treatment with oxprenolol hydrochloride. Following treatment with prednisone, the patient remained in remission for 25 months. The disease relapsed following reuse of oxprenolol hydrochloride. Severe pancytopenia due to bone marrow involvement by AILD and myelofibrosis led to a fatal outcome. The association of AILD and myelofibrosis has been rarely encountered and is hereby discussed. In addition, the possible relationship between AILD and oxprenolol hydrochloride is considered.