Pathology spectrum of kidney damage in Hodgkin’s lymphoma, non-Hodgkin lymphoma/leukemia, and lymphoplasmacytic lymphoma in the real practice

2021 ◽  
pp. 239936932110400
Author(s):  
Elena V Zakharova ◽  
Tatyana A Makarova ◽  
Ekaterina S Stolyarevich ◽  
Olga A Vorobyeva

Background: Kidney damage in lymphomas/leukemia’s presents with either acute kidney injury (AKI), chronic kidney disease (CKD), or both; and whilst AKI leads to evaluation often based on the clinical data, in some AKI and in almost all CKD cases kidney biopsy gives a clue to the diagnosis. Methods: A single center non-interventional retrospective study identified 36 patients with biopsy-proven kidney damage: 6 with Hodgkin’s lymphoma (HL), 18 with non-Hodgkin’s lymphoma/leukemia (NHL/CLL), and 12 with lymphoplasmacytic lymphoma (LPL). Results: Fifty-eight percent males and 42% females mean age 56.2 ± 17.4 years, presented with nephrotic syndrome in 47.2%, and with AKI in 11.1% of cases; 75% of patients diagnosed with CKD; in 13.9% AKI was superimposed on CKD. Patients with NHL/CLL presented with AKI significantly more often compared to HL and LPL—44% versus 16.6% versus 0 respectively. Monoclonal immunoglobulin (MIg) related glomerulopathies (GP) were found in 83.3% versus 16.6% cases in the LPL and NHL/CLL sub-groups, respectively ( p = 0.013). Patterns of damage included intracapillary monoclonal deposition disease, light and heavy chain amyloidosis, monotypic membranous nephropathy (MN), cryoglobulinemic glomerulonephritis (GN) and C3-GN in the LPL; and monotypic MN and proliferative GN with MIg deposits in the NHL/CLL sub-groups respectively. Paraneoplastic GPs were found in 83.3%, 38.8%, and 16.6% of patients with HL, NHL/CLL, LPL, respectively (HL vs LPL, p < 0.001), and included minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), and IgA-nephropathy in the HL; membranoproliferative GN, MN, and MCD in NHL/CLL; and FSGS in the LPL sub-groups. Tubulointerstitial damage revealed in NHL/CLL sub-group only, and found in every other case with 80% of lymphoid infiltration. Conclusions: Pattern glomerular damage depends on lymphoma type: paraneoplastic GPs are typical for HL, MIg-related GPs dominate in LPL, NHL/CLL presents mainly as paraneoplastic with single MIg-related patterns. Tubulointerstitial damage due to specific kidney infiltration attributable to NHL/CLL.

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Owrang Eilami ◽  
Max Igor Banks Ferreira Lopes ◽  
Ronaldo Cesar Borges Gryschek ◽  
Kaveh Taghipour

Abstract Background The current literature is scarce as to the outcomes of COVID-19 infection in non-Hodgkin's lymphoma patients and whether immunosuppressive or chemotherapeutic agents can cause worsening of the patients’ condition during COVID-19 infection. Case presentation Our case is a 59-year-old gentleman who presented to the Emergency Department of the Cancer Institute of Hospital das Clínicas da Universidade de São Paulo, São Paulo, Brazil on 10th May 2020 with a worsening dyspnea and chest pain which had started 3 days prior to presentation to the Emergency Department. He had a past history of non-Hodgkin's lymphoma for which he was receiving chemotherapy. Subsequent PCR testing demonstrated that our patient was SARS-CoV-2 positive. Conclusion In this report, we show a patient with non-Hodgkin lymphoma in the middle of chemotherapy, presented a mild clinical course of COVID-19 infection.


2014 ◽  
Vol 2014 ◽  
pp. 1-4
Author(s):  
Susan Ziolkowski ◽  
Catherine Moore

Acute interstitial nephritis (AIN) is a common cause of acute kidney injury and has been associated with a variety of medications. This is the case of 30-year-old man with Hodgkin’s lymphoma who on routine labs before chemotherapy was found to have acute nonoliguric renal failure. A kidney biopsy was performed and confirmed the diagnosis of acute interstitial nephritis. The patient had taken several medications including a higher dose of Carnivora, a Venus flytrap extract, composed of numerous amino acids. The medication was discontinued and kidney function improved towards the patient’s baseline indicating that this may be the possible cause of his AIN. Proximal tubular cell uptake of amino acids increasing transcription of nuclear factor-kappaB is a proposed mechanism of AIN from this compound.


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 232-232 ◽  
Author(s):  
Olga Wachowski ◽  
Martin Zimmermann ◽  
Birgit Burkhardt ◽  
Olaf Determann ◽  
Ulrike Meyer ◽  
...  

Abstract We evaluated the rate and type of second malignant neoplasms (SMN) after BFM treatment of children with Non-Hodgkin lymphoma (NHL). Between January 1981 and February 2003 2451 patients (pts) &lt;15 years (y) of age at diagnosis were enrolled into the subsequent trials NHL-BFM 81, 83, 86, 90, and 95. Pts with lymphoblastic lymphoma (LBL) (n=547) or non-anaplastic peripheral T-cell lymphoma (n=97) received acute lymphoblastic leukemia (ALL)-type therapy including cumulative doses of cyclophosphamide (max. 3g/m2), daunorubicine/doxorubicin (max. 280mg/m2), but, except few pts, no etoposide. Prophylactic cranial radiotherapy (CRT) was given in stage III/IV (omitted in NHL-BFM95). Pts with mature B-cell neoplasms (n=1597), or anaplastic large cell lymphoma (n=210) received B-type therapy, consisting of 2–8, 5-day courses including cumulative doses of cyclophosphamide (max. 7g/m2), ifosfamide (max. 8g/m2), doxorubicine max. 150mg/m2 (in trial 81 max. 200mg/m2), and etoposide (max. 1.4g/m2). CRT was omitted since trial NHL-BFM86. With a median follow-up of 6.9 (range 0.2–22.6) years the probability of survival at 15 y was 83+1%. By June 2005, 47 SMN were documented, including 16 acute myeloid leukemias/myelodysplastic syndromes (AML/MDS), 11 NHL, 2 ALL, 1 Hodgkin’s lymphoma, 7 brain tumors, and 10 other SMN. All SMN occurred in first remission after a median time of 2.9 (range: 0.4–12.3) years from diagnosis of NHL. The cumulative incidence of SMN at 15 y was 4.0% (95% confidence interval [CI]: 1.9%–6.1%) for the total group. The cumulative incidence of SMN was significantly higher among pts with LBL receiving ALL-type therapy (6.3% at 15 y [95%CI: 2.4%–10.3%] (13 AML/MDS, 2 NHL, 3 brain tumors, and 3 other SMN), as compared to pts with other NHL-entities receiving B-type therapy (3.4% at 15 y [95% CI: 0.5–6.4%] (3 AML/MDS, 9 NHL, 2 ALL, 1 Hodgkin’s lymphoma, 4 brain tumors, and 7 other SMN), p=0.002. There was no significant difference of cumulative incidence of SMN in pts who received CRT compared to pts not receiving CRT. However, 5 of 7 pts, who developed brain tumor, received CRT of 12–24 Gy. Also, there was no significant correlation between the incidence of SMN and the cumulative doses of drugs, except for anthracyclines. For pts receiving a cumulative dose of anthracyclines of &gt;160mg/m2 (almost exclusively pts with LBL receiving ALL-type therapy) the cumulative risk for SMN at 15 y was 6.5% (95% CI: 1.5-11.5%), as compared to 2.0% (95% CI: 1.1–2.9%) for pts with lower doses, p=0.007. Exposure to etoposide was not a risk factor for secondary AML/MDS (11 of 16 pts with sec. AML/MDS did not receive etoposide). In a Cox regression analysis only diagnosis of LBL remained a significant risk factor for SMN (RR 2.5, 95% CI 1.4–4.4). Our analysis revealed a cumulative risk for SMN of 4% at 15 y after successful treatment of childhood NHL. The cumulative incidence of SMN was significantly higher in LBL-pts than in other pts. AML/MDS were the most frequent SMN following LBL while second lymphoid malignancies were the most frequent SMN following non-LBL.


Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 230-230
Author(s):  
Catherine M. Bollard ◽  
Maja Stanojevic ◽  
Ann M. Leen ◽  
Teresita Lopez ◽  
Andrea N. Sheehan ◽  
...  

Abstract EBV-associated Hodgkin’s Lymphoma (HL) and some non-Hodgkins lymphoma (NHL) have type II viral latency expressing the subdominant EBV antigens EBNA1, LMP1 and LMP2. These antigens may serve as targets for immunotherapy approaches and in previous studies, we used polyclonal EBV-specific CTL in patients with relapsed EBV +ve HL obtaining 2 complete and 1 partial response in 11 patients. Analyses of EBV-CTL lines showed that small populations of T cells reactive against the tumor-associated antigen LMP2 were present in the majority of the infused lines, with some expansion in the peripheral blood following infusion. We therefore hypothesized that CTL enriched for effector cells specifically targeting LMP antigens would have greater efficacy in these patients. LMP-CTL were generated using dendritic cells for initial stimulations then EBV-transformed lymphoblastoid cell lines (LCL) both of which had been genetically modified to overexpress either LMP2 alone or inactive LMP1 (ΔLMP1) and LMP2 by transduction with an Ad5f35LMP2 (n=16) or Ad5f35ΔLMP1-I-LMP2 (n=14) vector respectively. All LMP-CTL lines were polyclonal comprising CD4+ (mean 17±18%; range 1–92%) and CD8+ (mean 74 ± 25%; range 1–99%) T-cells. Flow cytometric analysis of memory markers revealed mixed populations of CD45RA- CD62L- T-cells (45±15%; range 31–63%) and CD45RA- CD62L+ T-cells (34±5%; range 28–41%). The CTL lines had specificity for CD4+ and CD8+ restricted LMP2 epitopes alone (n=19; mean 1; range 0–7) or both LMP1 and LMP2 epitopes (n=13; mean 2; range 0–6) per CTL line, as determined using overlapping LMP1 and LMP2 peptide pools in ELISPOT assays. Twenty-four patients with EBV+ Hodgkin’s Lymphoma and non-Hodgkin Lymphoma have been treated on dose escalation studies. 16 with LMP2 CTLs and 8 with LMP1/2 CTLs. No immediate toxicity was observed. After CTL infusion, increased numbers of LMP-specific T cells were detected in the blood of 15/22 evaluable patients, (range 2 to 70 fold) persisting for up to 3 months. Additionally, two patients had lymph node biopsies 3–6 months post CTL, which showed selective accumulation of LMP2-multimer positive cells in lymph nodes. 12/13 high-risk and/or multiply relapsed patients who received LMP-CTL as adjuvant treatment after chemotherapy remain in remission for a median of 2years (range &gt;3months to &gt;5years) after CTL. 11 patients had detectable disease at the time of CTL, 2 of these had progressive disease by 8 weeks and 9 had clinical responses. The median duration of the clinical responses is 1 year with one stable disease (&gt;12months), one partial response (36 months) and 7 complete responses (range 9 months to &gt;4.5 years). One of the complete responders was biopsied 7 weeks after receiving CTL, which were predominantly CD4+ (92%). Increased CD4+ T cells were seen compared to pre-CTL biopsy specimens and imaging studies confirmed remission. In conclusion, immunotherapy with CTL targeting LMP antigens is well tolerated in patients with EBV+ lymphoma and infused LMP-CTL can accumulate at tumor sites and induce complete and sustained clinical responses.


1988 ◽  
Vol 102 (5) ◽  
pp. 468-470 ◽  
Author(s):  
R. C. Bickerton ◽  
M. J. Brockbank

AbstractNon-Hodgkin's lymphoma of the larynx is uncommon and when it occurs presents as a non-ulcerating supraglottic mass with a predilection for the ventricle. No case of the lymphoplasmacytic variety occurring in the larynx has been reported in the literature to date. We present such a case with distant leisons in the soft palate and nasal cavity, mimicking nasal polyps.


2014 ◽  
Vol 3 (2) ◽  
Author(s):  
Dian Rahma Kasir ◽  
Irza Wahid ◽  
Hafni Bachtiar

AbstrakAwal abad ke-2l masyarakat Indonesia mengalami transisi epidemiologi penyakit. Perubahan pola penyakit ini dapat dilihat dari peningkatan insiden penyakit kanker sebagai penyebab kematian di Indonesia dalam 10 tahun terakhir, yaitu dari urutan ke-12 menjadi urutan ke-6. Di Indonesia, limfoma non Hodgkin (LNH) menduduki urutan keenam keganansan yang sering terjadi. Berdasarkan penelitian yang dilakukan oleh Olivia Putri Perdana di bagian patologi anatomi Fakultas Kedokteran Universitas Andalas didapatkan data bahwa pada januari 1997-desember 2001 terdapat 70 (81,39%) penderita limfoma maligna non Hodgkin dari keseluruhan penderita limfoma maligna. Penelitian ini bertujuan untuk mengetahui hubungan kadar laktat dehidrogenase (LDH) dengan stadium pada penderita limfoma maligna non Hodgkin. Penelitian ini adalah penelitian analitik dengan pendekatan cross sectional dengan menggunakan data yang bersumber dari rekam medik pasien. Populasi dari penelitian ini adalah data rekam medik seluruh penderita limfoma maligna non hodgkin yang berobat ke RSUP Dr. M. Djamil Padang yaitu 317 data rekam medik, tetapi yang memenuhi syarat untuk menjadi sampel hanya 40 data. Analisis statistik yang digunakan adalah uji T. Hasil uji statistik menunjukkan adanya hubungan kadar laktat dehidrogenase dengan stadium pada penderita limfoma non Hodgkin (P = 0,001). Diketahui nilai laktat dehidrogenase pada stadium III-IV lebih tinggi daripada nilai laktat dehidrogenase pada stadium I-II.Kata kunci: Laktat dehidrogenase, Limfoma maligna non Hodgkin, Stadium AbstractEarly 21th century, Indonesian society in transition epidemiology of the disease. Changing patterns of disease can be seen from the increased incidence of cancer as a cause of death in Indonesia in the last 10 years, ie from 12th to 6th order. In Indonesia, non-Hodgkin's lymphoma (NHL) ranks sixt frequent in all of cancer. Based on research conducted by Olivia Putri Perdana in anatomic pathology at the Faculty of Medicine, University of Andalas that the data obtained during the January 1997 - December 2001 there were 70 (81.39%) patients with non -Hodgkin's malignant lymphoma of the overall malignant lymphoma patients.This study aims to determine the relationship of levels of lactate dehydrogenase (LDH) with stage of non -Hodgkin's malignant lymphoma patients.This research is a cross sectional analytic approach using data derived from patient medical records. The population is the entire medical record malignant non Hodgkin lymphoma patients who went to DR. M. Djamil Padang hospital, they are 317 medical records, but are eligible to be sampled only 40 data. Statistical analysis used is the T test.Statistical test results show that there is relationship between lactate dehydrogenase levels with stage in non -Hodgkin's lymphoma patients (P = 0.001). Known value of lactate dehydrogenase in stage III - IV is higher than the value of lactate dehidrodenase in stage I - II.Keywords: Lactate dehydrogenase, malignant non-Hodgkin's lymphoma, Stage


1995 ◽  
Vol 81 (2) ◽  
pp. 91-95 ◽  
Author(s):  
Monica Mangiagalli ◽  
Isabella Miccolis ◽  
Pierfranco Maffé ◽  
Enrico Maria Pogliani ◽  
Gianmarco Corneo

Aims and background The study assessed the role and potential benefit of rhG-CSF in reducing the frequency, duration and severity of neutropenia following cytotoxic chemotherapy according to the E-SHAP protocol and, at the same time in improving the response rate. Methods Twenty patients with resistant/relapsed intermediate or high-grade non-Hodgkin's lymphoma were treated with the E-SHAP regimen (etoposide + methyl prednisolone + high dose cytosine arabinoside and cisplatin), and in 15 of them, we administered rhG-CSF between chemotherapeutic courses. Results The 15 patients who received G-CSF after E-SHAP were neutropenic for a short time and experienced no febrile episodes or infective complications. In contrast, in the group (5 patients) who did not receive G-CSF, the WBC nadir was lower and the number of days with a neutrophil count below 1.0 × 109/L was longer, with a greater risk of inferctious complications. Of the 15 patients, only one had a delay in chemotherapy administration, and the RDI was 95% in the 65% of patients who received G-CSF. Of 5 patients treated with chemotherapy alone, 4 had a delay and the RDI was over 95% in only one patient. We obtained a good overall response rate (70%) in the group who received G-CSF. In the historical group of 5 non-Hodgkin lymphoma patients, we observed only 1 partial response and 4 had progression of disease. Conclusions Administration of G-CSF is associated with an acceleration of neutrophil recovery, indicating its potential to reduce the risk of infection. The use of G-CSF permitted us to administer intensive chemotherapy without delay and according to standard dosage, with an improved response rate.


2010 ◽  
Vol 3 (4) ◽  
pp. 338-340
Author(s):  
S. Jorge ◽  
J. A. Lopes ◽  
S. Goncalves ◽  
G. Esteves ◽  
J. Alves do Carmo

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