Ki-1⁺ anaplastic large cell lymphoma is a cancer of mature T-cells in which the tumor cells are large, look very abnormal (“anaplastic”), and almost always show strong, uniform staining for the Ki-1 antigen, also called CD30. Doctors diagnose it by seeing “hallmark cells” under the microscope—big cells with kidney- or horseshoe-shaped nuclei—and by confirming the CD30 marker and other features with special tests. Some cases produce an abnormal protein called ALK (anaplastic lymphoma kinase) because the ALK gene has fused with another gene; those are called ALK-positive ALCL. Other cases do not show ALK; those are ALK-negative ALCL. There are also forms limited to the skin (primary cutaneous ALCL) and a form linked to textured breast implants (BIA-ALCL). All are CD30-positive but they behave differently, occur in different age groups, and need different management plans. PMC+3PMC+3ScienceDirect+3
Anaplastic large-cell lymphoma (ALCL) is a T-cell non-Hodgkin lymphoma made of large, abnormal immune cells that strongly express CD30—historically detected by the Ki-1 antibody—hence the term “Ki-1⁺.” Under the microscope, doctors often see “hallmark cells” with kidney- or horseshoe-shaped nuclei. ALCL can be systemic (involving lymph nodes and organs) or primary cutaneous (mainly in the skin). Systemic ALCL is further split into ALK-positive (caused by ALK gene fusions, often in younger people) and ALK-negative. Some ALK-negative cases have DUSP22 rearrangements (once thought favorable) or TP63 rearrangements (usually unfavorable). Strong uniform CD30 staining is a key clue; other T-cell markers may be weak or lost. PET-CT is typically used for staging and response assessment. Haematologica+4PubMed+4PMC+4
CD30 is the same molecule that older papers called Ki-1; so “Ki-1⁺ ALCL” simply means CD30-positive ALCL. The disease sits within the World Health Organization (WHO) family of mature (peripheral) T-cell lymphomas. WHO recognizes systemic ALK-positive ALCL, systemic ALK-negative ALCL, primary cutaneous ALCL, and breast-implant–associated ALCL as distinct entities. PMC+1
Other names
CD30-positive ALCL
ALK-positive ALCL (systemic)
ALK-negative ALCL (systemic)
Primary cutaneous ALCL (pcALCL)
Breast-implant–associated ALCL (BIA-ALCL)
T/null-type ALCL (older term used when T-cell markers are weak or absent)
All of these are part of the CD30/Ki-1⁺ spectrum of ALCL. PMC+1
Types
1) Systemic ALK-positive ALCL
Happens more often in children, teens, and young adults. It is driven by ALK gene fusions—most commonly NPM1-ALK from a t(2;5) translocation—which switch ALK “on” all the time. ALK staining is positive, CD30 is strong, and T-cell markers may be variable. Overall outlook is usually better than for ALK-negative disease when treated with modern therapy. PMC+1
2) Systemic ALK-negative ALCL
Usually affects older adults. It is still CD30-strong, but ALK tests are negative. Inside this group are biologic subtypes with different genetics and outcomes:
DUSP22 (IRF4)-rearranged ALCL: often better outcomes in many cohorts.
TP63-rearranged ALCL: rare but linked to very poor outcomes.
“Triple-negative” (no ALK, no DUSP22, no TP63): intermediate behavior.
These labels come from FISH or next-generation sequencing on the biopsy. PMC+2PMC+2
3) Primary cutaneous ALCL
This form starts in the skin as solitary or localized nodules or plaques. It is CD30-strong and typically ALK-negative. It often behaves indolently compared with systemic forms and is treated locally in many cases. PMC
4) Breast-implant–associated ALCL (BIA-ALCL)
This form arises in the fibrous capsule and fluid around textured breast implants, years after implantation. It is CD30-positive and ALK-negative by definition. Common first signs are persistent breast swelling (late seroma) or a peri-implant mass. Management often centers on complete implant removal with capsulectomy; systemic therapy is used when disease extends beyond the capsule. U.S. Food and Drug Administration+1
Causes
For lymphomas, “cause” usually means a mix of molecular drivers inside the cells and risk factors in the person’s environment or immune system. Not everyone with a risk factor will develop ALCL.
ALK gene fusions (e.g., NPM1-ALK): Powerful driver in ALK-positive ALCL; keeps growth signals permanently “on.” PMC
Other ALK partners (e.g., TPM3-ALK, ATIC-ALK): Less common fusions that act like NPM1-ALK. Modern Pathology
DUSP22 (IRF4) rearrangement: Defines a molecular subset of ALK-negative ALCL with distinct biology and, in many cohorts, a better prognosis. PMC
TP63 rearrangement: Rare subset with very aggressive behavior; the fusion protein disrupts normal cell-cycle control. PMC+1
Activation of the JAK/STAT pathway: Common downstream signaling route that promotes survival and proliferation in ALCL. PMC
Cytotoxic T-cell program gone awry: Many ALCLs express cytotoxic proteins (TIA-1, granzyme B, perforin), reflecting a misdirected killer T-cell phenotype. ASH Publications
Disrupted T-cell markers: Loss or weak expression of typical T-cell antigens (CD3, etc.) is common and signals abnormal T-cell differentiation. PMC
Immune dysregulation/Immunosuppression: A background of weakened immune surveillance (e.g., post-transplant) can rarely be associated, though ALCL is usually EBV-negative. Faculty Experts – Loma Linda University
Chronic inflammation around textured breast implants: In BIA-ALCL, long-standing inflammation and bacterial biofilm on textured surfaces are suspected triggers. U.S. Food and Drug Administration
Time since implantation (BIA-ALCL): Risk appears to rise with years of exposure after a textured implant. PMC
Host genetic background: Research suggests certain immune-response genes may influence risk, though no routine screening exists. (Inference based on molecular heterogeneity across subtypes.) PMC
Age: ALK-positive disease skews younger; ALK-negative skews older—pointing to different biologic routes to lymphoma. PMC
Sex: Males are more often affected in systemic ALK-positive ALCL. PMC
Cutaneous immune disturbances (pcALCL): Local skin immune pathways may allow a CD30⁺ clone to expand. PMC
Cytokine signaling loops: ALCL cells secrete and respond to growth factors that keep them dividing. PMC
Epigenetic changes: Abnormal DNA methylation or chromatin remodeling helps lock in the malignant program. PMC
Genomic instability beyond the hallmark fusions: Additional mutations accumulate and support progression. PMC
Environmental exposures (general lymphoma risk such as some pesticides/solvents): data are mixed and not specific to ALCL; no single exposure is proven to cause ALCL. (Stated cautiously; evidence is limited for ALCL specifically.) NCBI
Prior chemo/radiation: Increases second-cancer risk overall; ALCL as a specific therapy-related entity is rare. (General oncology principle; not a dominant ALCL pathway.) NCBI
Not EBV-driven in almost all cases: Unlike many T/NK lymphomas, classic systemic ALCL is consistently EBV-negative; EBV-positive examples are exceptional. ScienceDirect+1
Common symptoms and signs
Painless, enlarged lymph nodes in the neck, armpit, or groin. Nodes can feel rubbery and may grow quickly. NCBI
“B” symptoms: fevers without infection, drenching night sweats, and unintentional weight loss. NCBI
Extreme tiredness (fatigue) from inflammation or anemia. NCBI
Skin lumps or plaques (pcALCL): often red-brown nodules that may ulcerate but typically stay near the site. PMC
Breast swelling, tightness, or a late seroma years after a textured implant (BIA-ALCL). U.S. Food and Drug Administration
A palpable breast or chest wall mass near an implant capsule (BIA-ALCL). PMC
Chest pressure, cough, or shortness of breath if nodes enlarge in the chest. NCBI
Abdominal fullness or pain when the liver, spleen, or abdominal nodes are involved. NCBI
Bone pain if lymphoma cells affect bone. NCBI
Itchy skin or rash, sometimes with cutaneous disease or general inflammation. PMC
Frequent infections due to low white blood counts or treatment effects. NCBI
Easy bruising or bleeding if platelets are low. NCBI
Swollen spleen (splenomegaly) felt as fullness below the left ribs. NCBI
Unexplained persistent fever even after antibiotics. NCBI
General feeling of being unwell (malaise), poor appetite, or unintended weight loss. NCBI
Diagnostic tests
Diagnosis hinges on biopsy plus immunohistochemistry/molecular tests. The items below are grouped by how they are done. Not every person needs every test.
A) Physical-exam–based
Full lymph node and organ exam: doctor checks node areas and feels for enlarged liver/spleen; documents size, tenderness, and whether nodes are fixed or mobile. This directs which site to biopsy first. NCBI
Skin examination: looks for solitary or clustered nodules/plaques that suggest primary cutaneous ALCL. PMC
Breast and chest wall exam in people with implants: checks for swelling, capsular contracture, or a palpable mass suggesting BIA-ALCL. PMC
Performance status assessment (e.g., ECOG): simple bedside scale that predicts tolerance of therapy and helps plan treatment. NCBI
B) “Manual” bedside tests and measurements
Node mapping and serial measurements with a tape measure or calipers to track growth or response between visits. NCBI
Spleen percussion and palpation to estimate enlargement when imaging is not immediately available. NCBI
Breast seroma aspiration under sterile technique (when clearly indicated and safe): fluid is sent for cytology and CD30/ALK testing if BIA-ALCL is suspected. PMC
C) Laboratory & Pathology
Excisional or core-needle biopsy of a node or mass (the key test): pathologist looks for “hallmark” cells and patterns of growth. Wikipedia
Immunohistochemistry (IHC) panel on the biopsy: strong, uniform CD30 positivity is required; ALK staining distinguishes ALK⁺ vs ALK⁻; EMA and cytotoxic markers (TIA-1, granzyme B, perforin) often support the diagnosis; T-cell antigens may be weak or lost. Haematologica+1
FISH/NGS for gene rearrangements: tests for ALK fusions (e.g., NPM1-ALK) and for DUSP22 or TP63 in ALK-negative ALCL, which carry important prognostic information. Modern Pathology+2PMC+2
Flow cytometry on tissue or fluid: defines the cell as T-cell lineage and shows CD30 and other markers; helpful in effusion cytology for BIA-ALCL. PMC
T-cell receptor (TCR) gene rearrangement testing: shows a clonal T-cell population, supporting lymphoma rather than reactive inflammation. ASH Publications
Complete blood count (CBC) and chemistry (LDH, liver tests): not diagnostic by themselves, but LDH and cytopenias help with staging and prognosis. NCBI
Ki-67 proliferation index on the biopsy: estimates how fast cells are dividing; ALCL often shows a high index. PMC
Rule-out EBV (EBER in situ hybridization): classic systemic ALCL should be EBV-negative; a positive result suggests a different entity. ScienceDirect
D) Electrodiagnostic
Electrocardiogram (ECG): not for diagnosing lymphoma itself, but recorded before anthracycline-based chemotherapy to make sure the heart rhythm is safe and to establish a baseline. NCBI
Baseline cardiac assessment for therapy (ECG ± additional tests as indicated): supports safer planning when cardiotoxic drugs are considered. NCBI
E) Imaging
PET-CT (FDG-PET): maps active disease throughout the body for staging and later to measure response after treatment. NCBI
Contrast-enhanced CT of neck/chest/abdomen/pelvis: shows size and distribution of nodes and organ involvement. NCBI
Targeted imaging for special sites:
• Breast ultrasound and MRI to detect peri-implant fluid or capsular masses in suspected BIA-ALCL;
• Ultrasound-guided aspiration of a peri-implant fluid pocket for cytology and CD30 testing. PMC
Non-pharmacological treatments
These are supportive therapies that work alongside anti-cancer drugs to improve safety, strength, and quality of life. None cure lymphoma on their own.
Cancer-specific nutrition counseling – Purpose: protect weight, strength, and treatment tolerance. Mechanism: individualized calorie/protein plans (often 1.0–1.5 g/kg/day protein) plus oral nutrition supplements when needed; prevents or treats malnutrition and cachexia. Clinical Nutrition Journal+1
Food-safety education – Purpose: cut infection risk during chemotherapy-related neutropenia. Mechanism: avoid raw/undercooked meats, eggs, seafood; wash/peel produce; reheat deli meats; safe handling. CDC+1
Exercise (aerobic + resistance, tailored) – Purpose: maintain muscle, reduce fatigue, improve mood and function. Mechanism: counters catabolism and deconditioning common in lymphoma therapy. (Aligned with cachexia guidelines promoting multimodal care.) PMC
Oral care protocol – Purpose: lower mucositis and infection. Mechanism: daily soft brushing, alcohol-free rinses, prompt dental issues management. (Standard supportive oncology practice echoed in guidelines.) IDSA
Antiemetic planning session – Purpose: prevent nausea/vomiting from CHOP/A+CHP. Mechanism: classify emetic risk (anthracycline/cyclophosphamide = high) and pre-set prophylaxis per ASCO. ASCO Publications+1
Fertility preservation counseling (pre-treatment) – Purpose: protect future fertility. Mechanism: timely referral for sperm banking or oocyte/embryo cryopreservation when feasible before chemotherapy. (Standard oncology care; included here as supportive best practice.) PubMed
Vaccination planning – Purpose: reduce vaccine-preventable infections. Mechanism: give inactivated vaccines when possible; hold live vaccines during intensive immunosuppression; follow CDC/ACIP and ASCO guidance. CDC+1
Central-line education – Purpose: prevent catheter infections. Mechanism: teach sterile dressing care, prompt fever reporting, and flush protocols. (Aligned with neutropenia/IDSA principles.) IDSA
Sleep hygiene program – Purpose: improve sleep and energy. Mechanism: consistent schedule, morning light, limit naps; aids fatigue control during therapy. (Supportive care standard.) PMC
Psychosocial support & counseling – Purpose: ease anxiety, depression, coping stress. Mechanism: cognitive-behavioral tools, support groups, caregiver training. (Integrated in cancer guidelines). PMC
Physical therapy – Purpose: maintain mobility and prevent deconditioning and neuropathy-related balance issues. Mechanism: progressive, supervised strengthening and gait work. (BV neuropathy awareness). PMC
Occupational therapy & energy conservation – Purpose: protect independence in daily life. Mechanism: task simplification, adaptive tools, pacing. (Supportive oncology practice). PMC
Smoking cessation counseling – Purpose: enhance treatment tolerance and wound healing; cut infection risk. Mechanism: behavioral support + pharmacotherapy per local protocols. IDSA
Alcohol-risk minimization – Purpose: protect liver during chemotherapy. Mechanism: brief intervention to reduce/avoid alcohol, especially with doxorubicin/cyclophosphamide. ASCO Publications
Sun/skin care (for cutaneous ALCL) – Purpose: protect skin lesions/fields and reduce infection. Mechanism: wound care guidance, sun protection, gentle cleansers. PMC
Early palliative-care referral (needs-based) – Purpose: symptom relief (pain, itch, fatigue), better quality of life, decision support. Mechanism: parallel supportive team care. PMC
Infection-prevention plan for neutropenia – Purpose: reduce ER visits and severe sepsis. Mechanism: teach fever ≥38.0 °C triggers; low threshold for evaluation; outpatient low-risk pathways per ASCO/IDSA. PubMed
Medication reconciliation & cardioprotection steps – Purpose: reduce drug-drug interactions and protect heart with anthracyclines. Mechanism: review QT risks, baseline ECHO/ECG as indicated. PubMed
Financial counseling/navigation – Purpose: improve adherence and access to high-cost agents (e.g., brentuximab). Mechanism: link to assistance programs; optimize schedule. The Lancet
Survivorship plan – Purpose: structured follow-up after remission. Mechanism: late-effect screening (neuropathy, cardiac), vaccination catch-up, return-to-work guidance. CDC
Drug treatments
(Each item: long but concise plain description; class; usual dosing/time; purpose; mechanism; major side effects.)
Doses are typical references—final dosing/timing must follow the treating team’s protocol and patient factors.
A+CHP (Brentuximab vedotin + cyclophosphamide + doxorubicin + prednisone) – Front-line standard for CD30⁺ PTCL including ALCL. Brentuximab vedotin (BV) is an anti-CD30 antibody–drug conjugate that delivers MMAE into CD30⁺ cells. In ECHELON-2, A+CHP improved PFS and OS over CHOP. Typical schedule: BV 1.8 mg/kg day 1 + cyclophosphamide 750 mg/m² + doxorubicin 50 mg/m² day 1, prednisone days 1–5; q3 weeks × 6 cycles. Main risks: peripheral neuropathy, neutropenia, GI upset. PubMed+2The Lancet+2
CHOP (cyclophosphamide, doxorubicin, vincristine, prednisone) – Historic standard. Purpose: induce remission when BV is unavailable/contraindicated. Mechanism: multi-agent cytotoxic chemotherapy. Risks: myelosuppression, alopecia, neuropathy, cardiotoxicity (doxorubicin). The Lancet
CHOEP (CHOP + etoposide) – In some centers for young/fit ALK⁺ patients. Rationale: higher dose intensity; data mixed in PTCL. Side effects: more myelosuppression. PubMed
Brentuximab vedotin (single-agent) – For relapsed/refractory (R/R) systemic or cutaneous ALCL. Dosing 1.8 mg/kg q3 weeks. Purpose: target CD30 cells. Key toxicity: dose-related neuropathy; usually improves with dose holds/reduction. PMC
Crizotinib (ALK inhibitor) – For R/R ALK-positive systemic ALCL, FDA-approved in children and young adults (≥1 year). Dosing varies by weight/surface area. Side effects: transaminitis, visual disturbances, edema. PubMed+1
Pralatrexate (antifolate) – Approved for R/R PTCL (includes ALCL). Typical: 30 mg/m² weekly ×6, then 1-week rest (7-week cycle) with folate/B12 support. Side effects: mucositis, cytopenias. PMC+1
Belinostat (HDAC inhibitor) – Approved for R/R PTCL. Dose: 1,000 mg/m² IV days 1–5 q21 days. Side effects: cytopenias, fatigue, nausea. PubMed+1
Gemcitabine – Often in salvage regimens (GDP, GemOx) to debulk disease pre-transplant. Risks: myelosuppression, rash. ASH Publications
Ifosfamide – Component of ICE salvage; cytotoxic alkylator. Risks: myelosuppression, encephalopathy, hemorrhagic cystitis (needs mesna and hydration). ASH Publications
Carboplatin – Part of ICE or GDP. Risks: cytopenias, renal function monitoring. ASH Publications
Etoposide – In CHOEP/ICE; topoisomerase-2 inhibitor. Risks: neutropenia, mucositis; secondary leukemia (rare). ASH Publications
Cisplatin – In DHAP/GDP. Side effects: nephrotoxicity, ototoxicity, nausea (needs strong antiemetics). ASCO Publications
High-dose cytarabine (Ara-C) – In DHAP salvage. Risks: myelosuppression, neuro/ocular toxicity (steroid eye drops). ASH Publications
Bendamustine – Active in some R/R PTCL series; convenient dosing. Risks: cytopenias, rash. ASH Publications
Lenalidomide (immunomodulator) – Off-label option in selected R/R PTCL; monitor for cytopenias, thrombosis (consider anticoagulation if risk). ASH Publications
Alemtuzumab (anti-CD52) – Selected refractory T-cell lymphomas; infection risk can be high, requiring prophylaxis. Use is specialized. Oxford Academic
Everolimus (mTOR inhibitor) – Investigational/salvage use in T-cell lymphomas; can stabilize disease in small studies. Side effects: stomatitis, hyperglycemia. PMC
Pembrolizumab / Nivolumab (PD-1 inhibitors) – Limited data in PTCL; considered in trials or selected cases; immune-related adverse events possible. Spandidos Publications
Corticosteroids (e.g., dexamethasone) – Cytotoxic to lymphoma cells; useful for symptom control and as part of many regimens; side effects: hyperglycemia, mood, infection risk. PubMed
Supportive growth-factor strategy (see “booster” drugs below) – Not anti-lymphoma, but prevents febrile neutropenia so curative chemo can continue on time. PubMed
Dietary molecular supplements
Evidence for supplements is limited in cancer; major societies emphasize nutrition counseling + adequate protein/energy first. Use supplements only with your oncology team’s approval.
High-protein oral nutrition supplements (ONS) – Helps reach 1.0–1.5 g/kg/day protein targets; supports lean mass and intake on low-appetite days. Mechanism: compact calories/protein. Clinical Nutrition Journal+1
Whey protein isolate – Quickly absorbed protein that can aid meeting daily targets; do not exceed renal limits. Mechanism: essential amino acids for muscle synthesis. Frontiers
Omega-3 fatty acids (EPA/DHA) – Mixed data; ASCO makes no firm recommendation; may help some with appetite/weight as part of multimodal care. Mechanism: anti-inflammatory lipid mediators. eguideline.guidelinecentral.com+1
Vitamin D (if deficient) – Correct deficiency per labs to support bone/muscle health; avoid mega-doses. Mechanism: endocrine/metabolic support. Clinical Nutrition Journal
Oral rehydration/electrolyte solutions – Maintain hydration during treatment; mechanism: replace fluids and electrolytes lost to nausea/diarrhea. ASCO Publications
Soluble fiber (e.g., psyllium) – May help diarrhea/constipation balance; start low and titrate. Mechanism: stool-bulking and water-binding. Clinical Nutrition Journal
Vitamin B-complex & folate per protocol – Required with pralatrexate to reduce mucositis/toxicity; dosing per regimen. PMC
Oral glutamine – Evidence inconsistent; discuss with team, especially if mucositis risk; not routine. ASCO Publications
Micronutrient repletion (iron, B12) only if deficient – Correct documented deficits to treat anemia/fatigue; avoid empiric high-dose supplements. Clinical Nutrition Journal
Vitamin C/E or herbals: avoid high doses – No proven benefit; potential drug interactions and bleeding risk; discuss all products with your oncologist. eguideline.guidelinecentral.com
Immunity-booster / regenerative / stem-cell–related drugs
These do not treat ALCL directly but reduce complications and help you stay on curative therapy.
Filgrastim (G-CSF) – Daily injections after chemo to shorten neutropenia; lowers febrile neutropenia risk. Mechanism: stimulates neutrophil production. Common effects: bone pain. PubMed
Pegfilgrastim (long-acting G-CSF) – Single shot each cycle; same purpose as above with convenience. PubMed
Epoetin alfa / darbepoetin – For selected chemotherapy-induced anemia after careful risk-benefit discussion; improves transfusion needs; not for curative intent unless criteria met. Mechanism: RBC production. Clinical Nutrition Journal
Romiplostim or Eltrombopag (TPO-receptor agonists) – Off-label in refractory chemo-induced thrombocytopenia to support dosing; used case-by-case. Mechanism: platelet production. Clinical Nutrition Journal
IVIG (immunoglobulin) in hypogammaglobulinemia – For recurrent serious infections with proven low IgG; replaces antibodies. IDSA
Palifermin (keratinocyte growth factor) – Can reduce severe oral mucositis in high-dose chemo/HSCT settings. Mechanism: epithelial protection/regeneration. PMC
Surgery-related procedures
Excisional lymph-node (or mass) biopsy – Removes a whole node/mass for accurate diagnosis with full immunohistochemistry and genetics. Why: needle cores may miss patterns; full tissue is best. PubMed
Central venous catheter/port placement – A small device under skin for safe chemo delivery and blood draws. Why: protects veins and simplifies multi-cycle treatment. IDSA
Complete implant removal + total capsulectomy (for BIA-ALCL) – Surgery removes the implant and surrounding capsule fluid/tissue; often curative for localized disease. Why: eliminates the disease site and reduces relapse. PMC
Autologous hematopoietic stem-cell transplantation (auto-HSCT) – Patient’s own stem cells collected, high-dose chemo given, then reinfused. Why: consolidation in first remission (selected PTCL/ALCL) to lower relapse risk. Haematologica+1
Allogeneic stem-cell transplantation (allo-HSCT) – Donor stem cells given after conditioning. Why: graft-versus-lymphoma effect can cure some R/R cases but with higher non-relapse mortality; reserved for fit patients with aggressive disease. JAMA Network+1
Prevention & safety tips
Know fever rules (≥38.0 °C): call urgently—this can be life-saving. PubMed
Vaccines: keep inactivated shots up to date; avoid live vaccines during intense chemo; plan boosters post-therapy. CDC
Food safety: avoid raw/undercooked foods; wash produce; reheat deli meats; safe water. CDC
Antiemetic plan each cycle to keep nausea controlled and nutrition adequate. ASCO Publications
Oral hygiene daily to lower mucositis/infection. IDSA
Exercise + PT to maintain strength and balance (especially if neuropathy). PMC
Sun/skin care if you have cutaneous ALCL. PMC
Avoid elective textured breast implants; discuss risks if considering implants. U.S. Food and Drug Administration
Adhere to growth-factor use if your team recommends it to prevent neutropenia. PubMed
Medication review every visit for interactions (including supplements/herbals). eguideline.guidelinecentral.com
When to see a doctor urgently
Call now if you have fever ≥38.0 °C, shaking chills, shortness of breath, chest pain, confusion, rapid bleeding/bruising, severe dehydration, uncontrolled vomiting/diarrhea, sudden leg swelling, new severe headache, or rapidly enlarging lymph-node masses. These can signal febrile neutropenia, blood clots, or disease flare that need immediate care. PubMed
Foods: what to eat & what to avoid
Eat more of:
Well-cooked lean proteins (fish, chicken, eggs fully cooked).
Energy-dense sides (rice, potatoes, pasta) to hit calorie goals.
Pasteurized dairy and yogurts.
Peeled or well-washed fruits/veggies; cooked vegetables.
Oral nutrition shakes on low-appetite days. CDC+1
Avoid (or only if made safe):
Raw or undercooked meats/eggs/seafood.
Unpasteurized milk/juices and soft cheeses made from unpasteurized milk.
Unwashed raw produce and salad bars/buffets.
Deli meats/cold cuts unless reheated steaming hot.
Raw sprouts and refrigerated pates. CDC+1
Frequently asked questions
Is ALCL curable?
Yes—many people are cured, especially with A+CHP up front in CD30⁺ disease and appropriate consolidation when indicated. Outcomes vary by subtype (ALK⁺ tends to be better). PubMedWhat is “Ki-1⁺”?
“Ki-1” is the original antibody that recognizes CD30. Ki-1⁺ ALCL means the lymphoma cells express CD30 strongly. PMCHow is staging done?
With PET-CT using Lugano criteria; it guides treatment and follow-up. ASCO PublicationsWhat is the role of brentuximab vedotin?
It is a targeted anti-CD30 drug that, when combined with CHP chemo, improves survival vs CHOP. It is also used alone in relapsed ALCL. Main side effect: neuropathy. PubMed+1If I’m ALK-positive and relapse, are there pills?
Yes—crizotinib (ALK inhibitor) is FDA-approved for children/young adults with R/R ALK⁺ systemic ALCL; adults may access ALK inhibitors via trials/selected use. PubMedDo I need a transplant?
Some patients benefit from auto-HSCT consolidation in first remission; allo-HSCT is reserved for selected relapsed/refractory cases due to higher risks. Decisions are individualized. Haematologica+1What about cutaneous ALCL?
Often indolent; may respond to local therapy or BV if needed; prognosis is generally good. PMCWhat is BIA-ALCL?
A lymphoma that arises around breast implants, especially textured devices. Early surgery (implant removal + capsulectomy) is the main treatment for localized disease. U.S. Food and Drug Administration+1Are “immune-boosting” supplements helpful?
No supplement replaces vaccines, G-CSF, good nutrition, and infection precautions. Discuss any product with your oncologist to avoid interactions. PubMedCan I get vaccines during treatment?
Inactivated vaccines are generally recommended; live vaccines are avoided during intensive chemo and for a period afterward. Timing is coordinated with your team. CDCHow do you prevent nausea?
Teams follow ASCO antiemetic guidelines based on your regimen’s emetic risk to prevent nausea from the start of each cycle. ASCO PublicationsWhat about neuropathy from BV?
Report tingling/numbness early. Dose adjustments or breaks often reverse symptoms over time. PT can help balance/strength. PMCDo DUSP22 or TP63 tests matter?
Yes—they refine prognosis in ALK-negative ALCL and may influence intensity of therapy/monitoring. PMC+1Can diet slow weight loss?
Nutrition counseling plus adequate protein/energy (and ONS if needed) is recommended; no specific supplement reliably reverses cachexia by itself. ASCO PublicationsWhat follow-up do I need after remission?
A survivorship plan covering symptoms, late effects (heart, nerves), vaccinations, and lifestyle helps you stay well. CDC
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
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Last Updated: September 16, 2025.
