05-07-2025
THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DEIDENTIFIED HEALTH DATA SHARED AFTER TAKING HIS SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR PATIENT'S PROBLEMS THROUGH SERIES OF INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THOSE PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.
[05-07-2025 19:59] PPM 1: Elder of four brothers
Two younger brothers have died because of chronic hemolytic anemia
No other family Members are affected
At age 7 he had received blood transfusion but didn't get transfused ever after that especially as one of his brothers was thought to have died due to transfusion.
[05-07-2025 20:01] PPM 1: @Meta AI what is the epidemiological prevalence of HbE beta Thalasemia in India and what are the illness outcomes in this disease.
Please substantiate your answer with perplexity styled references
[05-07-2025 20:01] Meta AI: HbE beta thalassemia is a compound heterozygous state involving hemoglobin E (HbE) and beta thalassemia, resulting in varying degrees of anemia and other complications. Unfortunately, specific epidemiological prevalence data for HbE beta thalassemia in India is limited. However, here's what we know about thalassemia prevalence in India¹ ²:
- Prevalence of Beta Thalassemia Carriers: The average prevalence of beta thalassemia carriers in India is 3-4%, translating to around 35-45 million carriers in the country.
- Regional Variations: Certain ethnic groups and tribal communities have a higher prevalence (4-17%). Regions with high consanguinity rates also show a concerning prevalence.
- Tribal Groups: Around 8% of India's population consists of tribal groups, who are particularly affected by thalassemia.
Illness Outcomes:
- Anemia: HbE beta thalassemia patients often experience moderate to severe anemia, requiring regular blood transfusions.
- Complications: These can include iron overload, organ damage, growth and development issues, and increased risk of infections.
- Variability: The severity of the disease can vary significantly depending on the specific mutations involved and individual factors.
Management and Control:
- Early Diagnosis: Prenatal diagnosis and screening for carriers can help prevent the birth of affected children.
- Blood Transfusions: Regular transfusions are crucial for managing anemia.
- Iron Chelation: Therapy to remove excess iron and prevent organ damage.
- Supportive Care: Addressing related complications and improving quality of life.³
For more specific information on HbE beta thalassemia prevalence in India, further research or consultation with medical experts familiar with the region's epidemiological data might be necessary.
[05-07-2025 20:01] Meta AI: https://www.researchgate.net/profile/Kavitha-Menon/publication/358418116_Prevalence_and_Management_of_b-Thalassemia_in_India/links/6450a821809a535021410a87/Prevalence-and-Management-of-b-Thalassemia-in-India.pdf?origin=publication_detail
[05-07-2025 20:01] Meta AI: https://www.sciencedirect.com/science/article/pii/S2468124517300748
[05-07-2025 22:07] PPM 3: ### Case Report: Chronic Hemolytic Anemia with Hepatosplenomegaly and Jaundice in a 21‑Year‑Old Male
#### Clinical Presentation
A 21‑year‑old man presented for evaluation of longstanding anemia, intermittent jaundice, and abdominal fullness. He reports chronic pallor since early childhood, occasional scleral icterus, and fullness in his left upper quadrant. He has never required regular transfusions—only a single packed‑cell transfusion at age 7, after which his family declined further transfusions due to a sibling’s adverse outcome.
#### Past Medical History
* *Anemia history:* Chronic hemolytic anemia noted since infancy, managed conservatively.
* *Transfusions:* One event at age 7; none thereafter.
* *Symptoms:* Fatigue on exertion, mild jaundice during intercurrent illnesses; no history of bone pain crises or severe infections.
#### Family History
* *Siblings:* Eldest of four brothers. Two younger brothers died in early childhood from presumed chronic hemolytic anemia.
* *Parents & Others:* No one else tested or known to carry thalassemia traits.
#### Physical Examination
* *General:* Moderately pale, evident icterus; afebrile, pulse 84/min, BP 110/70 mmHg.
* *Abdomen:* Liver palpable 4 cm below right costal margin; spleen palpable 6 cm below left costal margin.
* *Other systems:* No frontal bossing or long‑bone deformities; normal cardiac and pulmonary exam.
#### Key Investigations
1. *Complete Blood Count:*
* Hb 6.4 g/dL
* Hct 29.0%
* MCV 61.8 fL, MCH 17.2 pg, MCHC 27.8 g/dL
* RDW 28%
* WBC 9.2 × 10³/µL, Plt 210 × 10³/µL
2. *Red‑cell Indices & Peripheral Smear:*
* Marked microcytosis, target cells, polychromasia.
3. *HPLC (β‑Thal Short Programme):*
* HbF 42.0%
* HbA₂+E 54.8%
* HbA₀ 3.0%
* No other variants detected
4. *Iron Studies:*
* Serum ferritin (pending)
5. *Impression:*
* HPLC profile and chronic hemolysis are consistent with *HbE/β‑thalassemia*—likely a non–transfusion‑dependent phenotype given his long transfusion‐free interval.
---
### Treatment Decision Tree
┌─────────────────────────────┐
│ Confirm Diagnosis │
│ • Review HPLC profile │
│ • Offer β‑globin mutation │
│ analysis (optional) │
└─────────────┬───────────────┘
│
┌─────────────────┴────────────────┐
│ Assess Clinical Severity │
│ • Hb level & symptoms │
│ • Growth, organomegaly │
│ • Iron status (ferritin) │
└─────────────┬───────────────────┘
│
┌─────────────────────────┴─────────────────────────┐
│ Is patient symptomatic or Hb < 7 g/dL? │
└───────────────┬───────────────────┬──────────────┘
│ │
┌─────────────────────────┴───────────┐ ┌────┴───────────────────┐
│ No (Hb ≥7 g/dL & mild) → │ │ Yes → │
│ Conservative / NTDT management │ │ Transfusion‐dependent │
│ • Folate supplementation │ │ management │
│ • Monitor Hb & growth every 3–6 mo │ │ • Regular PRBC every │
│ • Treat infections promptly │ │ 3–4 wk (maintain Hb │
│ • Annual ferritin check │ │ ≥9–10 g/dL) │
└───────────┬─────────────────────────┘ └─────────┬────────────────┘
│ │
│ ┌──────────┴───────────┐
│ │ Manage Iron Overload │
│ │ • If ferritin >1000 │
│ │ ng/mL or ≥10 PRBC │
│ │ → Start chelation │
└───────────────────────────────┴──────────────────────┘
│
┌──────────────────────┴─────────────────────┐
│ Consider Curative Therapy │
│ • HLA‑matched sibling HSCT if available │
│ • If no matched donor: evaluate trials / │
│ gene therapy options │
└──────────────────────┬─────────────────────┘
│
┌──────────────────────┴─────────────────────┐
│ Genetic Counseling & Family Screening │
│ • Test parents/siblings │
│ • Prenatal diagnosis for future pregnancies │
└─────────────────────────────────────────────┘
*Notes for this Patient:*
* *Likely NTDT phenotype*: He has maintained reasonable health with only one transfusion in 14 years.
* *Next steps*:
* Check baseline ferritin to screen for subclinical iron overload from hemolysis.
* Continue folate and monitor Hb every 3–6 months.
* Initiate transfusions only if Hb falls below 7 g/dL or if symptomatic.
* Counsel family on genetic risks; offer carrier testing to parents/siblings.
* Evaluate HSCT candidacy if he develops worsening anemia or iron overload despite supportive care.
[05-07-2025 22:08] PPM 4: Sir do have pajr link? This case seems very sensitive due to earlier mortalities.
[05-07-2025 22:10] PPM 3: 1. What is the current reason for admission?
2. Was any genetic testing done for either the current patient or his siblings?
[05-07-2025 22:12] PPM 3: https://diagnostics.mapmygenome.in/beta-thalassemia
[05-07-2025 22.20] PPM 4: Sir, if this is a diagnosed case of thalassemia then usually due to cost limitations doctors only refer to HPLC. Genetic tests are very expensive and not availed via Ayushman Bharat. I'm sceptical whether it would be done or not.
[05-07-2025 22:24] PPM 4: We would need to have sufficient reason to refer genetic tests-
1. Any syndromic manifestation
2. We would have to dig up the research papers with association of thalassemia's to other genetic conditions (like any other mutation apart from the thalassemia mutation)
[06-07-2025 16.00] PPM 5: 
[06-07-2025 16:02] PPM 1: My hunch: He has come all the way 2000 kms because he has seen his brothers die and he doesn't want the same end.
Nothing done yet as they are from low resource settings.
The genetic tests and therapeutic solutions would cost a bomb
[06-07-2025 16:12] PPM 1: OMG! Thrombocytopenia appears to be a new development! Now where do we place this? It reminds me another of our 21M patients who actually also had a genome testing detailed here and who's just been started on iv rituximab!
[06-07-2025 19:51] PPM 3: Updated summary from AI.
Based on the updated clinical notes, laboratory reports (LFT and hemogram), and transcript commentary, here’s a revised and consolidated case summary in the format you requested:
---
Case Report: Chronic Hemolytic Anemia with New-Onset Thrombocytopenia in a 21-Year-Old Male from West Bengal
Clinical Presentation
A 21-year-old male from West Bengal presented with a long-standing history of anemia, intermittent jaundice, and splenomegaly. He reported one transfusion in childhood (at age 7), but has remained transfusion-free since then due to family concerns after a sibling died during transfusion. His two younger brothers reportedly died from undiagnosed chronic hemolytic anemia. He has traveled over 2000 km seeking diagnosis and management after becoming alarmed about his prognosis.
Past Medical and Family History
Transfusion history: One PRBC transfusion at age 7. No transfusions since.
Family history: Two younger brothers died of presumed chronic hemolytic anemia. No extended family history of similar illness.
No known genetic testing done due to financial constraints.
No documented treatment for iron overload, folate supplementation, or chelation.
Key Investigations
1. Hemogram and Peripheral Smear
Parameter Result Normal Range Interpretation
Hemoglobin 7.9 g/dL 13–17 g/dL Anemia
RBC Count 4.21 M/µL 4.5–5.5 M/µL ↓
MCV 61.1 fL 83–101 fL Microcytosis
MCH 18.8 pg 27–32 pg Hypochromia
RDW-CV 31.0% 11.6–14.0% Anisocytosis
Platelet Count 68,000/µL 150,000–410,000/µL Thrombocytopenia
Total WBC 16,800/µL 4,000–10,000/µL Leukocytosis
Peripheral Smear: Microcytic hypochromic anemia with anisopoikilocytosis, tear-drop cells, pencil forms, target cells. No hemoparasites.
2. Liver Function Test
Parameter Result Normal Range Interpretation
Total Bilirubin 4.65 mg/dL 0–1 mg/dL Markedly Elevated
Direct Bilirubin 0.61 mg/dL 0–0.2 mg/dL Mildly elevated (unconjugated hyperbilirubinemia)
SGOT / SGPT 23 / 13 IU/L Normal Normal
Alkaline Phosphatase 148 IU/L 53–280 IU/L Normal
Albumin / Globulin Normal Preserved synthetic function
Interpretation: Unconjugated hyperbilirubinemia likely due to ongoing hemolysis. No overt hepatic dysfunction.
3. HPLC Report (from earlier submission)
HbF: 42.0%
HbA2 + E: 54.8%
HbA: 3.0%
→ Consistent with HbE/β-thalassemia, likely compound heterozygote.
---
Updated Working Diagnosis
1. HbE/β-Thalassemia (non-transfusion dependent variant)
2. New-onset thrombocytopenia — unexplained, possibly immune-mediated or hypersplenism-related
3. Chronic hemolysis with secondary unconjugated hyperbilirubinemia
4. Anemia of moderate severity — transfusion threshold may soon be reached
---
Discussion
1. Diagnosis of HbE/β-Thalassemia
The HPLC pattern and clinical picture are diagnostic of HbE/β-thalassemia.
Genetic confirmation is currently unaffordable for the family, but could inform prognosis and eligibility for curative therapies (e.g., HSCT, gene therapy).
2. New-Onset Thrombocytopenia
Platelet count of 68,000/μL is a new development and concerning.
Differential considerations:
Hypersplenism (splenic pooling from chronic enlargement)
Autoimmune thrombocytopenia (ITP-like) — consider testing for ANA, Coombs, anti-platelet antibodies if accessible
Early marrow suppression or infiltration — requires follow-up
3. Family Context and Psychosocial Burden
The patient is deeply concerned about replicating the course of his deceased siblings.
He’s seeking help despite minimal resources — pointing toward the importance of low-cost, high-yield interventions like folate supplementation, periodic monitoring, and rational transfusion decisions.
---
Management and Treatment Tree (Adapted)
Domain Action Points
Transfusion Need Hb 7.9 g/dL: borderline — start close monitoring, consider transfusion if Hb drops below 7 or symptoms develop
Iron Monitoring Check serum ferritin, transferrin saturation if accessible; dietary education
Folate Supplementation Start empirically (e.g., folic acid 5 mg OD)
Thrombocytopenia Re-check platelets, confirm with peripheral smear → if persistent and symptomatic, investigate for immune or marrow causes
Bone Marrow Biopsy Consider if platelets continue to decline or pancytopenia develops
Splenectomy? Not currently indicated, but hypersplenism must be monitored
Genetic Counseling Strongly advised for surviving family; explore NGO, institutional subsidies for testing
HSCT Refer if matched sibling donor and funding possible — may be curative
---
Conclusion
This 21-year-old man likely has HbE/β-thalassemia with NTDT phenotype, complicated now by new thrombocytopenia. His history, hemogram, and bilirubin trends point to ongoing hemolysis with relative stability but risk of worsening. He has come seeking proactive care due to fear from family losses. Given financial constraints, a low-cost, stepwise plan focused on folate, monitoring, counseling, and optional transfusion support should be initiated. Genetic work-up and consideration for curative options may follow based on clinical evolution and resource availability.
---
[06-07-2025 19:53] PPM 4: Does he have hypersplenism?
[06-07-2025 19:55] PPM 4: If it's chronic hemolytic anaemia, over functioning of the spleen can lead to thrombocytopenia too as far as I remember from paediatrics. But never read such a thing in adults (yet to come to this part of adult medicine in textbooks)
[06-07-2025 19:59] PPM 4: Another research theme for Jeevan Yapan:
Impact of previous mortalities or comorbidities in relatives or close family members on their own health problems decision-making. The need to consider the patient’s voice in EMR to see what factors influenced them to make a particular treatment decision.
[06-07-2025 20:01] PPM 3: Pallis, M., & Sinclair, J. H. (2007). Hypersplenism. Blood, 110(11), 3011.
[06-07-2025 20:03] PPM 4: @Meta AI what are the hemogram and lab findings of multiple myeloma on peripheral smear?
(Sorry @PPM1sir I don't remember therefore asking AI 😅😂)
[06-07-2025 20:03] Meta AI: No worries, let's dive into the lab findings for multiple myeloma! 🎉
Peripheral Smear:
- Rouleaux formation: Stacking of RBCs, resembling a roll of coins, due to increased serum proteins (paraproteins).
- Normocytic normochromic anemia: Commonly seen in multiple myeloma patients.
- Leukoerythroblastosis: Presence of immature white blood cells and nucleated RBCs, indicating bone marrow infiltration.
- Plasma cells: May be seen in the peripheral blood, but not always present.
Hemogram:
- Anemia: Low hemoglobin levels, often normocytic normochromic.
- Leukopenia or leukocytosis: Variable white blood cell count.
- Thrombocytopenia: Low platelet count due to bone marrow infiltration or suppression.
Other Lab Findings:
- Serum protein electrophoresis (SPEP): Monoclonal spike (M-protein) in the gamma region.
- Urine protein electrophoresis (UPEP): Bence Jones proteins (light chains) in the urine.
- Serum free light chain (FLC) assay: Abnormal kappa/lambda ratio.
- Bone marrow biopsy: Increased plasma cells (>10%), often with atypical morphology.
- Cytogenetic analysis: Abnormalities like del(13q), t(11;14), or t(4;14) may be present.
Additional Tests:
- Imaging studies: X-rays, CT, MRI, or PET scans to assess bone lesions.
- Serum beta-2 microglobulin: Elevated levels correlate with disease severity.
These findings can help diagnose and monitor multiple myeloma. Hope that helps!
[06-07-2025 20:04] PPM 4: @Meta AI are there studies with thalassemia co-existing with multiple myeloma or residual disease?
[06-07-2025 20:04] Meta AI: There have been reported cases of thalassemia co-existing with multiple myeloma. One notable case study published in 2024 documented a 45-year-old Asian male patient with concurrent multiple myeloma, immune thrombocytopenic purpura, and thalassemia trait. This patient presented with severe thrombocytopenia, back pain, and bleeding manifestations. Laboratory findings and bone marrow biopsy revealed 90% plasma cell involvement and KRAS/BRCA2 mutations. Management focused on controlling immune thrombocytopenic purpura with corticosteroids, rituximab, and romiplostim ¹.
Another case report, MM-145, described a patient with beta-thalassemia (non-transfusion-dependent thalassemia) who developed active multiple myeloma, highlighting the rare coexistence of these two conditions. The relationship between thalassemia and malignancies, including multiple myeloma, requires further research to understand potential correlations and implications for patient management ².
Key Findings:
- Coexistence of Thalassemia and Multiple Myeloma: Rare cases have been reported, emphasizing the need for comprehensive diagnostic approaches.
- Management Challenges: Treatment strategies must address both conditions, considering potential interactions and complications.
- Research Directions: Further studies are necessary to elucidate the relationship between thalassemia and multiple myeloma, informing optimal management strategies.
Minimal Residual Disease (MRD) in Multiple Myeloma:
MRD assessment has become increasingly important in multiple myeloma management, providing insights into treatment response and disease prognosis. Techniques like next-generation flow cytometry and sequencing enable sensitive detection of residual disease. Sustained MRD negativity has been associated with improved outcomes, and research continues to explore its role in guiding treatment decisions ³ ⁴.
[06-07-2025 20:04] Meta AI: https://magazine.sciencepod.net/coexisting-thalassemia-immune-thrombocytopenic-purpura-and-multiple-myeloma-with-osteopenia-complex-hematologic-case-in-an-adult-asian-male-patient/
[06-07-2025 20:04] Meta AI: https://ashpublications.org/hematology/article/2021/1/37/483004/Minimal-residual-disease-in-multiple-myeloma-why
[06-07-2025 20:04] Meta AI: https://ashpublications.org/thehematologist/article/doi/10.1182/hem.V22.1.202511/535036/Minimal-Residual-Disease-as-a-Primary-Endpoint-in
[06-07-2025 20:04] Meta AI: https://www.sciencedirect.com/science/article/pii/S2152265024016471
[06-07-2025 20:10] PPM 4: @PPM1Sir are there any complaints of recent bleeding? Or is this thrombocytopenia a recent development?
[06-07-2025 20:11] PPM 4: Given the size of the spleen in the PaJR link, thrombocytopenia is just due to overfunctioning spleen.
[06-07-2025 20:16] PPM 3: Perplexity -
# Co-reported Thalassemia and Plasma-Cell Dyscrasias
*Take-home message:* The coexistence of thalassemia (α- or β-chain defects) with plasma-cell disorders is extremely uncommon; evidence is limited to scattered case reports, small case series and one focused review. Publications nonetheless confirm that every stage of the plasma-cell spectrum—monoclonal gammopathy of undetermined significance (MGUS), smoldering myeloma and overt multiple myeloma (MM)—has been documented in patients carrying thalassemic mutations.
## 1. Published clinical evidence
| Year | First author (country) | Thalassemia genotype | Plasma-cell disorder | Salient points |
|------|-----------------------|----------------------|----------------------|----------------|
| 1977 | Fabris (Italy) | β-thal trait | Active MM | First description of the association[1] |
| 1986 | Dash (India) | β-thal trait | Smoldering MM (IgG-κ) | Non-responder to melphalan/prednisone; outlined “altered immunity” hypothesis[2] |
| 2004 | Elhajj (Lebanon) | Hb H disease (α-thal) | Active MM | Lytic lesions, responded to thalidomide/melphalan[3] |
| 2009 | Saroha (India) | β-thal trait | Active MM | Pseudo-Gaucher histiocytes obscured plasma cells; diagnostic pitfall[4] |
| 2013 | Alavi (Iran) | β-thal major/intermedia | Series review | One MM case among other hematologic malignancies[5] |
| 2017 | Halawi (Global review) | Various | Literature review | <20 malignant plasma-cell cases in 50 yrs; postulated iron/virus interplay[6] |
| 2020 | Prominent pseudo-Gaucher cells case (USA) | β-thal intermedia | Plasma-cell myeloma | Extensive histiocytosis; highlighted marrow “masking”[7] |
| 2021 | PB2544 abstract (Europe) | β-thal intermedia | MGUS ➔ MM | MGUS evolved to treatable MM; underscores need for surveillance[8] |
| 2024 | Zhang (China) | Heterozygous β-thal mutation | MM treated with ASCT | Autologous transplant feasible; iron overload monitored[9] |
| 2024 | Chambi-Torres (USA) | β-thal trait | Active MM + ITP | 90% marrow plasma cells; KRAS/BRCA2 mutations; case emphasised therapeutic sequencing[10] |
| 2024 | ScienceDirect case report | β-thal (NTDT) | Active MM | Acute renal failure at presentation[11] |
NTDT = non-transfusion-dependent thalassemia.
## 2. Key clinical lessons
1. *Rarity and spectrum* – < 30 well-documented cases have been published over five decades, spanning MGUS, smoldering myeloma and overt MM[6].
2. *Diagnostic pitfalls* –
- Severe microcytosis and transfusion-induced iron overload may mask the typical normocytic anemia of myeloma.
- Marrow aspirates can contain sheets of pseudo-Gaucher histiocytes generated by the high cell-turnover state of thalassemia; these cells may conceal neoplastic plasma cells[4][7].
3. *Pathophysiologic hypotheses* – chronic antigenic stimulation from repeated transfusions, viral infections and iron-mediated oxidative DNA damage have been proposed, but no causal link is proven[5][6].
4. *Treatment considerations* –
- Standard triplet induction regimens were used in most reports; thalassemia per se did not preclude bortezomib- or lenalidomide-based therapy[10].
- Successful high-dose melphalan/ASCT has been reported in a heterozygous β-thal carrier, provided iron status and organ function are carefully assessed[9].
- Persistent microcytosis or ongoing transfusion can complicate minimal residual disease (MRD) assessment that relies on flow cytometry of small marrow samples; molecular techniques (NGS, ASO-PCR) may be preferable, though no dedicated studies are yet available.
## 3. Residual / precursor disease data
- *MGUS and smoldering myeloma:* at least three thalassemia patients have been reported with MGUS that remained stable or progressed to MM over 2–5 years[2][8][12].
- *Monitoring:* authors recommend applying standard International Myeloma Working Group risk-stratification (M-protein, BM plasma-cell % and FLC ratio) but adding ferritin, liver iron and transfusion burden to the follow-up protocol[6].
- *Minimal residual disease after therapy:* no prospective MRD study has been undertaken in thalassemia; evidence is limited to the single post-ASCT case which achieved MRD negativity by flow at day +100[9].
## 4. Practical implications for clinicians
1. Maintain *high suspicion* when a thalassemia patient develops back pain, rising serum protein or unexplained cytopenias; order serum/urine electrophoresis and marrow biopsy early.
2. *Differentiate anemia etiologies*: iron studies, RBC indices and hemolysis markers help parse thalassemia-related anemia from myeloma-related marrow failure.
3. *Screen for iron overload* before high-dose chemotherapy or ASCT; cardiac and hepatic MRI T2* are advisable.
4. When anticoagulation or anti-platelet therapy is needed, remember the *additive bleeding risk* if immune thrombocytopenia coexists, as in one recent case[10].
### Bottom line
Although exceedingly rare, thalassemia and plasma-cell dyscrasias can coexist at any disease stage. Published experience—currently limited to single-patient reports—shows that standard myeloma therapeutics, including autologous transplant, remain feasible with appropriate attention to iron load and marrow diagnostic challenges. Continued case documentation and prospective registries are required to clarify true incidence, pathogenesis and optimal MRD monitoring strategies in this double hematologic context.
[1] https://www.ectrx.org/detail/supplement/2024/22/1/0/80/0
[2] https://www.jstage.jst.go.jp/article/internalmedicine1962/25/1/25_1_57/_pdf/-char/en
[3] https://pubmed.ncbi.nlm.nih.gov/15008270/
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC2803944/
[5] https://pmc.ncbi.nlm.nih.gov/articles/PMC3698402/
[6] https://onlinelibrary.wiley.com/doi/full/10.1002/ajh.24681
[7] https://pubmed.ncbi.nlm.nih.gov/33301039/
[8] https://pmc.ncbi.nlm.nih.gov/articles/PMC10429570/
[9] https://pubmed.ncbi.nlm.nih.gov/38284377/
[10] https://www.cureus.com/articles/311415-coexisting-thalassemia-immune-thrombocytopenic-purpura-and-multiple-myeloma-with-osteopenia-complex-hematologic-case-in-an-adult-asian-male-patient.pdf
[11] https://www.sciencedirect.com/science/article/abs/pii/S2152265024016471
[12] https://medcraveonline.com/PPIJ/paraspinal-extramedullary-hematopoiesis-in-alpha-thalassemia-with-concurrent-monoclonal-gammopathy-of-undetermined-significance-an-uncommon-case-report.html
[13] https://pmc.ncbi.nlm.nih.gov/articles/PMC11706632/
[14] https://www.sciencedirect.com/science/article/abs/pii/S0268960X19300165
[15] https://healthtree.org/myeloma/community/articles/about-anemia-in-multiple-myeloma
[16] https://pubmed.ncbi.nlm.nih.gov/3086604/
[17] https://www.bloodcancercure.com/cancer-types/thalassemia/
[18] https://myelomabeacon.org/forum/thalassemia-and-multiple-myeloma-t4185.html
[19] https://www.sciencedirect.com/science/article/pii/S2152265024016471
[20] https://imagebank.hematology.org/image/64199/pseudogaucher-cells-in-beta-thalassemia
[21] https://ashpublications.org/blood/article-pdf/99/6/1883/1681329/1883.pdf
[22] https://www.tandfonline.com/doi/pdf/10.1081/HEM-120028892
[23] https://pmc.ncbi.nlm.nih.gov/articles/PMC9387011/
[24] https://thalassemia.ucsf.edu/thalassemia-information/what-is-thalassemia/hemoglobin-h-disease/treatment-guidelines
[25] https://pmc.ncbi.nlm.nih.gov/articles/PMC6757179/
[26] https://en.wikipedia.org/wiki/Multiple_myeloma
[27] https://www.learnhaem.com/courses/frcpath-morph/lessons/thal-haemoglobinopathies/topic/haemoglobin-h-hbh-disease/
[28] https://www.tandfonline.com/doi/pdf/10.1080/10245330701393675
[29] https://www.nature.com/articles/s41598-020-77450-y
[30] https://www.mdpi.com/2039-4365/12/3/12
[31] https://www.mdpi.com/2079-9721/11/4/161
[32] https://thalassemia.ucsf.edu/sites/g/files/tkssra7596/f/HbH_english.pdf
[33] https://www.hoacny.com/patient-resources/blood-disorders/what-thalassemias/signs-symptoms-and-complications-thalassemias
[34] https://www.sciencedirect.com/topics/nursing-and-health-professions/hemoglobin-h-disease
[35] https://www.sciencedirect.com/science/article/abs/pii/0002934379904133
[36] https://onlinelibrary.wiley.com/doi/pdf/10.1002/(SICI)1096-8652(199903)60:3%3C250::AID-AJH21%3E3.0.CO;2-K
[37] https://www.mayoclinic.org/diseases-conditions/mgus/symptoms-causes/syc-20352362
[38] https://ashpublications.org/blood/article/144/Supplement%201/1916/533032/MGUS-Prevalence-in-Special-Populations-Insights
[39] https://pressbooks.openeducationalberta.ca/mlsci/chapter/hypochromic-microcytic-anemias-thalassemias/
[40] https://www.osmosis.org/learn/Monoclonal_gammopathy_of_undetermined_significance
[41] https://www.sciencedirect.com/science/article/abs/pii/S0268960X21000758
[42] https://www.sciencedirect.com/science/article/abs/pii/S0006497124046639
[43] https://pmc.ncbi.nlm.nih.gov/articles/PMC5997745/
[44] https://my.clevelandclinic.org/health/diseases/23911-smoldering-multiple-myeloma
[45] https://www.ncbi.nlm.nih.gov/books/NBK585137/
[46] https://www.mdpi.com/2072-6694/13/13/3319
[47] https://www.unboundmedicine.com/washingtonmanual/view/Washington-Manual-of-Medical-Therapeutics/602488/all/Monoclonal_Gammopathy_of_Unknown_Significance?q=Amyloidosis
[48] https://www.mdpi.com/2075-4418/14/17/1907
[06-07-2025 20:28] PPM 1: One of our Web 1.0 era students currently is an oncologist and works only with MM patients
[06-07-2025 20:30] PPM 1: In this patient hypersplenism is the likely cause for his thrombocytopenia although that's what we had thought for the other 21M too which later turned out to be immune mediated
[06-07-2025 20:36] PPM 3: What is the cost for the test?
[06-07-2025 20:39] PPM 1: Which test?
[06-07-2025 21:31] PPM 3: Genetic test would give us more insight, right?
[06-07-2025 21:34] PPM 1: 👆@PPM3 @Meta AI what is usefulness or utility of further genetic testing in chronic Thalasemia HbE who may not be able to afford HSCT?
[06-07-2025 21:34] Meta AI: For patients with chronic Thalassemia HbE who may not be able to afford Hematopoietic Stem Cell Transplantation (HSCT), further genetic testing can still provide valuable insights and potential benefits:
Usefulness of Genetic Testing:
1. Predictive value: Identifying specific genetic mutations can help predict disease severity, complications, and potential response to treatment.
2. Personalized management: Knowing the exact genetic mutations can guide personalized treatment strategies, such as tailored transfusion regimens or iron chelation therapy.
3. Family planning: Genetic testing can help identify carriers in the family, enabling informed reproductive choices and reducing the risk of having affected children.
4. Research opportunities: Participating in genetic studies can contribute to a better understanding of the disease and potentially lead to new treatment options.
5. Risk assessment: Genetic testing can help assess the risk of developing complications, such as iron overload or organ damage, allowing for early interventions.
Potential Benefits in the Context of Affordability:
1. Optimized resource allocation: By understanding the disease's genetic basis, healthcare providers can prioritize resources and focus on managing the most critical aspects of the disease.
2. Targeted interventions: Genetic testing can help identify potential targets for therapy, enabling more effective use of available treatments.
3. Informed decision-making: Patients and families can make informed decisions about their care, taking into account the genetic characteristics of the disease.
Considerations:
1. Cost-effectiveness: The cost of genetic testing should be weighed against the potential benefits and the patient's financial situation.
2. Access to testing: Availability and accessibility of genetic testing facilities and expertise may vary.
3. Counseling and support: Genetic testing should be accompanied by appropriate counseling and support to help patients and families understand the results and implications.
In summary, genetic testing can provide valuable information for patients with chronic Thalassemia HbE, even if HSCT is not feasible. By understanding the genetic basis of the disease, patients and healthcare providers can make informed decisions, optimize management, and potentially improve outcomes.
[06-07-2025 21:37] PPM 1: @Meta AI please provide specific examples of how an understanding of the genetic basis of the HbE disease in a specific individual patient, healthcare providers can make informed decision, optimize management, and potentially improve outcomes for that individual patient who can't afford HSCT
[06-07-2025 21:37] Meta AI: Here are some specific examples of how understanding the genetic basis of HbE disease in an individual patient can inform decision-making, optimize management, and improve outcomes:
Example 1: Tailored Transfusion Regimen
- Genetic finding: A patient with HbE beta thalassemia has a mutation that results in a more severe reduction in beta-globin chain production.
- Informed decision: Based on this genetic information, the healthcare provider may decide to implement a more aggressive transfusion regimen to maintain a higher hemoglobin level, reducing the risk of complications like anemia and organ damage.
- Optimized management: Regular transfusions can help alleviate anemia, reduce iron overload, and prevent organ damage.
Example 2: Iron Chelation Therapy
- Genetic finding: A patient with HbE beta thalassemia has a mutation that increases the risk of iron overload due to increased intestinal absorption.
- Informed decision: The healthcare provider may initiate iron chelation therapy earlier and more aggressively to prevent iron overload and related complications like cardiac and liver damage.
- Optimized management: Iron chelation therapy can help remove excess iron, reducing the risk of organ damage and improving patient outcomes.
Example 3: Monitoring for Complications
- Genetic finding: A patient with HbE beta thalassemia has a mutation that increases the risk of developing splenomegaly.
- Informed decision: The healthcare provider may schedule regular monitoring for splenomegaly and related complications, enabling early intervention if necessary.
- Optimized management: Early detection and management of splenomegaly can prevent complications like hypersplenism and improve patient outcomes.
Example 4: Family Planning and Genetic Counseling
- Genetic finding: A patient with HbE beta thalassemia has a specific mutation that can be passed on to offspring.
- Informed decision: The patient and their family can make informed reproductive choices, such as prenatal testing or preimplantation genetic diagnosis, to reduce the risk of having affected children.
- Optimized management: Genetic counseling can help families understand the risks and options, enabling them to make informed decisions about family planning.
These examples illustrate how understanding the genetic basis of HbE disease in an individual patient can inform decision-making, optimize management, and improve outcomes, even in the absence of HSCT.
[06-07-2025 21:40] PPM 1: @Meta AI I feel most of the examples that you have cited are pretty speculative unless you can substantiate each with real patient data where these currently hypothetical outcomes based on logic have actually been proven to be true
[06-07-2025 21:40] Meta AI: You're right to question the speculative nature of these examples. While genetic testing can provide valuable insights, its practical applications in managing HbE beta thalassemia are still being explored. Let's examine the potential benefits and limitations:
Practical Applications:
- Family Planning and Genetic Counseling: Genetic testing can identify carriers of HbE beta thalassemia, enabling informed reproductive choices, such as prenatal testing or preimplantation genetic diagnosis. Studies have shown that preimplantation genetic testing (PGT) can be effective in preventing the transmission of beta-thalassemia. For instance, a study published in the Journal of Assisted Reproduction and Genetics found that PGT resulted in 11 healthy live births from 112 embryos tested in couples carrying alpha- and beta-thalassemia mutations.¹
- Personalized Management: Understanding the genetic basis of HbE beta thalassemia can help healthcare providers tailor treatment strategies to individual patients. However, more research is needed to determine the most effective ways to apply genetic information in clinical practice.
Limitations:
- Complexity of Genotype-Phenotype Correlations: The relationship between genetic mutations and disease severity is complex, making it challenging to predict outcomes based solely on genetic information.
- Limited Evidence: More studies are needed to substantiate the hypothetical benefits of genetic testing in managing HbE beta thalassemia.
In conclusion, while genetic testing holds promise for improving the management of HbE beta thalassemia, further research is necessary to fully realize its potential benefits.
[06-07-2025 21:41] Meta AI: https://www.southcarolinablues.com/web/public/brands/medicalpolicy/external-policies/genetic-testing-for-alpha--and-beta-thalassemia/
[06-07-2025 21:42] PPM 1: @Meta AI that's better. We need to own up to the current vast swathes of unknown in healthcare instead of trying to play up the limited knowns until we can really collect patient data at a granular level
[06-07-2025 21:42] Meta AI: I appreciate your emphasis on acknowledging the unknowns in healthcare. You're right; it's essential to be transparent about the limitations of our current understanding and the need for further research. By doing so, we can:
1. Set realistic expectations: Patients and families can better understand the complexities of their condition and the uncertainties surrounding treatment.
2. Foster collaboration: Researchers, clinicians, and patients can work together to collect more data, share knowledge, and advance our understanding of conditions like HbE beta thalassemia.
3. Prioritize research: By acknowledging the gaps in our knowledge, we can focus on investigating the most critical questions and areas where more research is needed.
Granular patient data can indeed help us better understand the intricacies of conditions like HbE beta thalassemia. This can lead to more effective treatment strategies, improved patient outcomes, and enhanced quality of life.
Let's continue to prioritize transparency, collaboration, and research to advance our understanding of complex conditions and improve patient care.
[06-07-2025 21:47] PPM 1 Yesterday's bedside clinical examination of this 21M long distance patient with chronic congenital hemolysis and an enlarged spleen
Dynamic UDLC ontology here https://pajrcasereporter.blogspot.com/2025/07/21m-chronic-hemolytic-anemia.html?m=1
[07-07-2025 12:14] PPM 1: [06/07, 20:07] PPM 3: Here is an GPT comparison, can you @ PPM1Sir and @PPM6 give feedback on whether it got it right?
Here's a clear comparison between the current case (21M with chronic hemolytic anemia) and the earlier case (Evans syndrome + 10q deletion + growth/puberty delay):
---
🧾 Comparison Table: Two Patient Profiles
Feature Current Case (21M, Chronic Hemolytic Anemia) Earlier Case (Evans Syndrome + 10q deletion)
Age/Gender 21-year-old male Pediatric/Adolescent (likely <18)
Genetic Diagnosis No genetic testing done yet Known 10q deletion (genetically confirmed)
Main Hematologic Issue Chronic hemolytic anemia, thrombocytopenia, leukocytosis Evans syndrome (autoimmune hemolytic anemia + thrombocytopenia ± neutropenia)
Family History 2 younger brothers died from similar anemia Not mentioned, but likely sporadic
Transfusion History One transfusion at age 7; none after that (fear of risk) Recurrent flares requiring therapy
Thrombocytopenia Present (new finding, 68,000/μL) Integral part of Evans syndrome (autoimmune)
Leukocytosis Present (16,800) Not noted in Evans syndrome case
Growth & Puberty Issues Not reported Short stature, delayed puberty (requires GH/sex hormone therapy)
Genetic Counseling Need Suspected; still pending Already done (implications of 10q deletion explained)
Management Discussion No current treatment; family from low-resource setting Management plan locally vs. tertiary (NIMHANS) thoroughly discussed
Current Risk Concern Progressive cytopenias, possible hypersplenism, unexplored cause Flare-ups, endocrine delay, possible GH resistance
Specialist Involvement Hematology planned, needs genetic input Hematology, endocrinology, and genetics already coordinated
---
🧠 Key Differences in Diagnosis & Management
🔬 Etiology
Current case likely involves a hereditary red cell disorder (e.g., thalassemia, hereditary spherocytosis), not autoimmune.
Evans syndrome case is autoimmune and systemic (overlaps with immune cytopenias, autoimmunity, and genetic syndromes).
🧪 Investigations
Current case: Needs genetic/hemoglobinopathy workup (e.g., HPLC, osmotic fragility, EMA test).
Evans case: Already worked up genetically; immune workup and endocrine evaluations underway.
💉 Treatment Complexity
Current case: May need transfusions, splenectomy, chelation (if iron overload), and genetic confirmation.
Evans case: Requires immunosuppression (steroids, IVIG, rituximab), GH, and sex hormone therapy.
---
🩺 Clinical Implication
Current Case Evans Case
Can be managed locally if stable ✅ Yes, with hematology + supportive care ✅ Yes, with multidisciplinary support
Requires genetic testing for diagnosis ✅ Already done
May benefit from splenectomy ✅ Possibly ❌ Less useful in autoimmune
Immunosuppressants essential ❌ Not currently ✅ Required
Endocrine care needed ❌ No evidence ✅ Required for height/puberty
---
[06/07, 20:36]pm: Key differences are well done but the profiles are mixed up perhaps again due to formatting issues.
However LLMs are trained with current high resource settings evidence that is also miniscule in comparison to the vast swathes of unknown that drives real world medicine and I'm not sure how long it may take to reach health tech singularity even if one can AGI driven reach tech singularity earlier
[06/07, 23:08] PPM6 Med Ed Leads: Based on the clinical comparison provided, here's feedback on its accuracy and key insights for @PPM1 and @PPM6:
---
### *Overall Assessment*
*The comparison is largely accurate and clinically insightful*, but a few nuances warrant refinement for precision.
---
#### *Key Feedback Points*
#### *1. Etiology & Diagnosis*
- ✅ *Current Case (21M):*
- Correctly identifies likely *hereditary hemolytic anemia* (e.g., thalassemia/spherocytosis).
- *Critical gap:* Strongly suggest *genetic testing* (e.g., HS/OSM fragility, G6PD, HPLC, gene panels) given sibling deaths.
- *Thrombocytopenia:* May indicate *hypersplenism* (consider splenic size) or a *combined disorder* (e.g., MYH9-related).
- ✅ *Evans Case:*
- Accurate link between *10q deletion*, Evans syndrome, and endocrine delays.
- *Clarification:* Leukocytosis can occur in Evans during crises/infections (though not classic).
#### *2. Management Differences*
| *Aspect* | *Current Case* | *Evans Case* |
|--------------------------|-------------------------------------------|-----------------------------------------|
| *Transfusions* | Avoided (fear); high risk if hereditary | Recurrent (autoimmune-driven) |
| *Splenectomy* | ✅ High benefit if HS/thalassemia | ❌ Rarely used (autoimmune rebound risk)|
| *Immunosuppression* | ❌ Unlikely to help (unless AIHA overlap) | ✅ Core therapy (steroids/rituximab) |
| *Endocrine Care* | ❌ Not needed yet (monitor growth/iron) | ✅ Essential (GH/sex hormones) |
#### *3. Critical Concerns*
- *Current Case:*
- *Progressive cytopenias + splenomegaly?* Urgently rule out *hypersplenism* or *bone marrow failure*.
- *Genetic counseling:* Vital given sibling mortality (possible *autosomal recessive* disorder).
- *Resource limitations:* Prioritize low-cost tests (peripheral smear, OSM fragility, G6PD).
- *Evans Case:*
- Monitor for *autoimmune endocrinopathies* (thyroid/adrenal) beyond puberty delay.
- Assess *10q deletion size* – larger deletions may involve PTEN (cancer risk).
#### *4. Specialist Input*
- *Current Case:*
- *Genetics:* Expedite testing (targeted panels for hemolytic anemias).
- *Hematology:* Evaluate for splenectomy vs. transfusion/chelation.
- *Evans Case:*
- *Immunology:* Rule out ALPS or CTLA4 haploinsufficiency (overlap with 10q deletion).
- *Endocrinology:* Address GH resistance risk.
---
### *Suggested Refinements*
1. *Current Case Thrombocytopenia:* Specify if *new-onset* or chronic (may suggest evolving pathology).
2. *Evans Leukocytosis:* Note if baseline or crisis-related (infectious/inflammatory workup needed).
3. *Family History:* Current case’s sibling deaths strongly imply *inherited disorder* – emphasize genetic urgency.
4. *Resource Setting:* For current case, highlight *cost-effective diagnostics* (e.g., smear > flow cytometry).
---
### *Clinical Takeaway*
| *Parameter* | Current Case | Evans Case |
|------------------------|---------------------------------------|-------------------------------------|
| *Root Cause* | Hereditary hemolysis ± hypersplenism | Immune dysregulation (10q deletion) |
| *Diagnostic Focus* | Genetics + splenic eval | Autoimmune/endocrine workup |
| *Intervention* | Splenectomy/transfusion | Immunosuppression + hormone Rx |
| *Prognosis* | Guarded (sibling mortality) | Chronic but manageable |
*For @PPM1:* Genetic context is crucial here – consider WES if targeted testing negative.
*For @PPM6:* Monitor current case for iron overload (even without transfusions; chronic hemolysis).
This comparison effectively highlights distinct pathways – *hereditary vs. autoimmune/cytogenetic* – and would benefit from the above refinements. Well-structured! 👏
[06/07, 23:08] PPM6 Med Ed Leads: You've highlighted a critical truth: *LLMs operate within the confines of their training data—which *is skewed toward high-resource settings and documented "knowns"—while *real-world medicine thrives in the unknown*, especially in resource-constrained environments. This gap won’t close until AGI achieves true clinical context-awareness (a distant "health tech singularity").
Below, I’ve reorganized the comparison to avoid formatting mix-ups and added *contextual caveats* reflecting real-world limitations:
---
### 🧾 *Refined Patient Profile Comparison*
| *Feature* | *Current Case (21M, Chronic Hemolytic Anemia)* | *Earlier Case (Evans + 10q Deletion)* |
|---------------------------|--------------------------------------------------------|------------------------------------------------------|
| *Age/Gender* | 21-year-old male | Pediatric/Adolescent (<18) |
| *Key Pathophysiology* | *Hereditary hemolysis* (likely thalassemia/HS) ± hypersplenism | *Immune dysregulation* (autoimmune cytopenias + 10q deletion) |
| *Family History* | *Critical*: 2 siblings died of similar anemia | Not reported (likely sporadic) |
| *Thrombocytopenia* | Present (new; 68K/μL) → ? Hypersplenism or combined defect | Core feature of Evans syndrome |
| *Leukocytosis* | Present (16.8K) → ? Stress response/infection | *Not typical* for Evans (unless crisis/infection) |
| *Genetic Workup* | *Pending* (urgent due to sibling deaths) | Confirmed 10q deletion |
| *Resource Context* | *Low-resource setting*: Avoids transfusions/fears risk | Tertiary care access (NIMHANS) |
---
### 🧠 *Key Differences & LLM Knowledge Gaps*
#### 🔬 *Etiology Uncertainty*
- *Current Case*:
- LLM suggests hereditary hemolysis (statistically probable), but *sibling mortality hints at rarer disorders*:
- Uncommon possibilities: Pyruvate kinase deficiency, Wilson’s disease, or even *atypical Evans* (if autoimmune).
- *Ground reality: In low-resource settings, diagnosis often relies on **peripheral smear + clinical heuristics*—not genetic panels.
- *Evans Case*:
- 10q deletion is a known association, but *deletion size matters* (e.g., PTEN involvement = cancer risk).
- LLMs may overlook that *autoimmune endocrinopathies* (e.g., thyroiditis) can emerge later.
#### 🚑 *Management Nuances*
| *Intervention* | *Current Case (Real-World Constraints)* | *Evans Case (Tertiary Setting)* |
|------------------------|--------------------------------------------------------|------------------------------------------------------|
| *Genetic Testing* | ✅ But: May only afford HPLC/G6PD/osmotic fragility | ✅ Already done (karyotype/array) |
| *Splenectomy* | ✅ High value if HS → but *post-vaccine access barrier* | ❌ Rarely used (risk of fatal sepsis/autoimmune rebound) |
| *Immunosuppression* | ❌ Wasteful if hereditary (unless AIHA co-exists) | ✅ Lifelong steroids/rituximab + infection monitoring |
| *Endocrine Care* | ❌ Not needed yet → but *monitor for iron overload* | ✅ GH/sex hormones + bone density tracking |
---
### ⚠ *Where LLMs Fall Short in Real-World Medicine*
1. *The "Unknown" Gap*:
- LLMs can’t intuit *undiagnosed syndromes* (e.g., if the 21M has a novel hemolytic gene mutation).
- Sibling deaths suggest a *high-stakes, undocumented pattern*—LLMs lack "lived clinical intuition."
2. *Resource-Agnostic Bias*:
- Recommending "genetic testing" is meaningless if unavailable. *Ground alternative*:
- Current case: Trial of *folate + malaria prophylaxis* (if endemic) while saving for splenectomy.
3. *Temporal Dynamics*:
- *Current case’s "new" thrombocytopenia* could signal evolution to *myelodysplasia* or *subclinical hypersplenism—LLMs struggle with *longitudinal context.
4. *Psychosocial Layers*:
- Family’s transfusion fear → rooted in *cultural trauma* (e.g., prior bad outcomes). LLMs miss this.
---
### 🩺 *The Path Forward*
While we await AGI that bridges the "unknown":
- *For the 21M: Prioritize **low-cost diagnostics* (smear, osmotic fragility, LDH/haptoglobin) → splenectomy if HS-like.
- *For Evans case: Screen for **subclinical endocrinopathies* (adrenal/thyroid) and PTEN variants.
- *For LLMs: Use as **hypothesis generators—but **anchor decisions in local reality* (resources/culture/clinical gestalt).
*@: Your insight on genetic urgency is spot-on—this family needs a diagnosis *now, even if via old-school labs.
*@Dr.*: The leukocytosis here may be compensatory (not pathological)—trust your eyes over the algorithm.
The "singularity" won’t replace clinicians navigating the unknown—it’ll just give us better flashlights 🔦. Until then, we bridge the gap together.
[07/07, 10:32]cm: After the Hb electrophoresis confirming HbE further testing appears currently unnecessary.
Please ask the LLM to point out to a real patient published trajectory where the management was influenced by further genetic testing once the HPLC Hb electrophoresis showed HbE and HbF as in the report available for the 21M with Thalasemia here: https://pajrcasereporter.blogspot.com/2025/07/21m-chronic-hemolytic-anemia.html?m=1
[07/07, 10:33]cm: Shifting this discussion to the Narketpally syn local CBBLE group
[07/07, 10:55] Kmcq: Where is the electrophoresis report?
Unable to trace it in blog
[07/07, 11:00]cm: Second image below the clinical phenotype
[07/07, 11:23] Kmcq: That is hplc-high precision liquid chromatography report.
Not electrophoresis
[07/07, 11:25] Kmcq: Guys prompted LLM for electrophoresis and it gave its inputs
[07/07, 11:26] Kmcq: @Meta AI what is difference between chromatography(especially HPLC) and Hb Electrophoresis.
Share the miscommunication in discussions above
[07/07, 11:26] Meta AI: Let's break down the differences between chromatography, specifically High-Performance Liquid Chromatography (HPLC), and Hb Electrophoresis.
Key differences:
- Principle: Chromatography separates molecules based on their partition coefficient and adsorption properties, whereas electrophoresis separates charged molecules based on their attraction to oppositely charged electrodes.
- Technique: Chromatography uses pressure to force a sample through a column, while electrophoresis applies an electrical field to separate molecules.
- Types: Chromatography has many types, including HPLC, column, paper, and thin layer chromatography. Electrophoresis has fewer types, such as capillary and gel electrophoresis.
- Cost: Chromatography instrumentation can be expensive, while electrophoresis instrumentation is relatively inexpensive.
- Uses: Chromatography is used for both analytical and preparatory purposes, whereas electrophoresis is primarily used for analytical purposes.
- Separation media: Chromatography uses liquids, solids, and sometimes gases, while electrophoresis uses semi-solid gel media ¹.
HPLC vs Hb Electrophoresis:
- Accuracy: HPLC is considered more accurate and sensitive than Hb electrophoresis, especially for detecting hemoglobin variants.
- Speed: HPLC is generally faster than electrophoresis, with results available in a shorter time frame (around 6.5 minutes).
- Application: HPLC is widely used for thalassemia screening and hemoglobinopathy diagnosis, while electrophoresis is commonly used for hemoglobinopathy screening.
- Detection: HPLC can detect and quantify most hemoglobin variants, including HbA2 and HbF, whereas electrophoresis may not always provide accurate results for certain mutations ² ³.
There doesn't seem to be any miscommunication in the discussions above, but rather a comparison of the two techniques and their applications. However, it's worth noting that some studies suggest HPLC may eventually replace electrophoresis for detecting hemoglobin disorders due to its speed, accuracy, and cost-effectiveness.
When to choose HPLC over Hb Electrophoresis:
- When high accuracy and sensitivity are required for detecting hemoglobin variants.
- For thalassemia screening and hemoglobinopathy diagnosis.
- When working with large sample sizes and high-throughput analysis is necessary.
When to choose Hb Electrophoresis:
- When the primary goal is to separate and identify major hemoglobins.
- For smaller sample sizes or when resources are limited.
- When the cost of instrumentation is a significant factor ² ⁴.
[07/07, 11:33]cm: Excellent inputs 👏👏
Yes lesson learnt around the technical differences between the two.
Speaking from a patient outcomes centered perspective, the Hb analysis be it chromatography or electrophoresis tells us that the patient has a significant beta Thalasemia and HbE and the current debate @PPM3 @PPM6 is around the relevance of further genetic testing in the patient (this is not even his PaJR group).
Let's take this discussion to his PaJR group here👇
https://chat.whatsapp.com/I2VsA4dlCUs4usqGLQvlWh
[07/07, 11:39] Kmcq: Pedigree chart? @PPM7
[07/07, 11:41] Kmcq: Theres a first degree family history and clinical features suggestive in history.
However to document, lets take it that we have advised for HPLC.
The other case?
[07/07, 11:46] Kmcq: Lets begin by asking few questions.
1.What are patients current requirements?
2.How would genetic testing gives us more inputs which may help in patient outcomes other than what we have currently,through HPLC,family history?
[07/07, 11:59]cm: Exactly these are the main questions now in this patient.
1) He needs to know what's going to happen to him due to his Thall E disease. How many more blood transfusion will he need that may actually worsen secondary hemochromatosis and otherwise how many times will he become symptomatic to merit transfusion.
Otherwise if you look at his phenotype he appears to be quite well preserved in terms of muscle mass etc
[07/07, 11:59] Kmcq: Hows his daily functioning?
[07/07, 11:59]cm: This is not his PaJR group.
Let's please take this discussants to his PaJR link shared above
[07-07-2025 12:33] PPM 8: Present complaints?
[07-07-2025 14:40] PPM 1: He's relatively asymptomatic with a Hb of 7.9 and indirect bilirubin of 4.5
My hunch: He has come all the way 2000 kms because he has seen his brothers die and he doesn't want the same end.
Nothing done yet as they are from low resource settings.
The genetic tests and therapeutic solutions would cost a bomb
[07-07-2025 14:44] PPM 8: If he's comfortable in English or Telugu, I can have a call with him once
[07-07-2025 14:44] PPM 1: I'll let him know
[07-07-2025 15:16] PPM 1: What is the available real patient data regarding favorable HSCT outcomes in HbE beta Thalasemia between those who underwent HSCT vs those who didn't? @Meta AI @PPM4
[07-07-2025 15:16] Meta AI: Favorable outcomes of Hematopoietic Stem Cell Transplantation (HSCT) in patients with β-Thalassemia major, which may include HbE beta Thalassemia, are well-documented. Here's a summary of what's known:
HSCT Outcomes:
- Survival Rates: Studies show that HSCT can achieve high overall survival rates, often above 90%, especially in patients without significant iron-related tissue damage.
- Thalassemia-Free Survival: Thalassemia-free survival rates after HSCT are also promising, ranging from 80% to over 90% in some cases.
- Quality of Life: Research indicates that patients who undergo HSCT tend to have better health-related quality of life (HRQoL) compared to those receiving conventional treatment, including improvements in physical and emotional domains.
Comparative Studies:
- A systematic review and meta-analysis of HRQoL in β-Thalassemia patients who underwent HSCT showed that transplanted patients had better scores in physical and emotional function domains compared to those treated conventionally.
- Studies comparing HSCT outcomes between β-Thalassemia patients and other diseases have reported varying results, but HSCT appears to offer benefits for β-Thalassemia patients, particularly in terms of reducing transfusion dependence.
Complications and Considerations:
- Graft-Versus-Host Disease (GVHD): GVHD is a significant complication of HSCT, which can impact HRQoL. Studies have shown that patients without GVHD tend to have better outcomes.
- Age and Risk Factors: Age at transplant and pre-existing organ damage can influence HSCT outcomes. Younger patients and those with fewer risk factors tend to have better results.¹ ²
Real Patient Data:
While specific data on HbE beta Thalassemia patients undergoing HSCT versus those who didn't is limited, the available evidence suggests that HSCT can be an effective treatment option for β-Thalassemia patients, offering improved HRQoL and potential cure. More research is needed to fully understand the benefits and risks of HSCT in HbE beta Thalassemia patients specifically.
[07-07-2025 15:16] Meta AI: https://ashpublications.org/hematology/article/2010/1/456/95968/Hematopoietic-Stem-Cell-Transplantation-in
[07-07-2025 15:16] Meta AI: https://clinical-practice-and-epidemiology-in-mental-health.com/VOLUME/19/ELOCATOR/e174501792301031/FULLTEXT/
[07-07-2025 15:20] PPM 1: @Meta AI not sure if specific data comparing the two intervention groups is unavailable how we can conclude that one group has better outcomes over the other.
Please share what happens to the hemogram of a patient of HbE beta Thalasemia after HSCT on follow up (mention the current available follow up duration with perplexity styled references @PPM6 and what are the changes in their hemogram over time over the duration the data is available
[07-07-2025 15:20] Meta AI: You're right to question the comparison between HSCT and non-HSCT groups in HbE beta Thalassemia patients, given the limited specific data available. The conclusion that HSCT offers better outcomes is largely based on studies in β-Thalassemia major patients, which might not perfectly represent the HbE beta Thalassemia subgroup.
Hemogram Changes After HSCT:
After Hematopoietic Stem Cell Transplantation, patients with HbE beta Thalassemia can experience significant changes in their hemogram. Here's what typically happens:
- Initial Phase: Post-transplant, patients often experience pancytopenia due to conditioning regimens. This phase requires close monitoring and supportive care.
- Engraftment: As the transplanted stem cells engraft, patients start to show signs of hematopoietic recovery, including:
- Neutrophil Recovery: Absolute Neutrophil Count (ANC) increases, typically within 2-4 weeks post-transplant.
- Platelet Recovery: Platelet counts improve, often within 4-6 weeks post-transplant.
- Long-term Outcomes: With successful engraftment, patients can achieve:
- Stable Hemoglobin Levels: Patients may achieve normal or near-normal hemoglobin levels, reducing or eliminating transfusion dependence.
- Improved Red Blood Cell Indices: Mean Corpuscular Volume (MCV) and Mean Corpuscular Hemoglobin (MCH) may normalize or show significant improvement.
Follow-up Duration and Outcomes:
Studies on β-Thalassemia patients, including some with HbE beta Thalassemia, have reported follow-up durations ranging from a few months to several years. A study on HSCT outcomes in Thalassemia major patients reported:
- Short-term Follow-up (1-2 years): Significant improvements in hemoglobin levels, transfusion dependence, and quality of life.
- Long-term Follow-up (5-10 years): Sustained benefits, including stable hemoglobin levels, reduced transfusion dependence, and improved overall survival.¹ ²
Current Research and Limitations:
More research is needed to fully understand the benefits and risks of HSCT in HbE beta Thalassemia patients specifically. Current studies are limited by:
- Small Sample Sizes: Few studies focus exclusively on HbE beta Thalassemia patients.
- Variability in Transplant Protocols: Differences in conditioning regimens, graft sources, and GVHD prophylaxis can impact outcomes.
Given these limitations, it's essential to interpret current findings with caution and await further research to better understand the role of HSCT in HbE beta Thalassemia patients.³
[07-07-2025 15:21] Meta AI: https://link.springer.com/article/10.1007/s12288-025-02074-z
[07-07-2025 15:21] Meta AI: https://www.sciencedirect.com/science/article/pii/S2666636725005196
[07-07-2025 15:21] Meta AI: https://www.astctjournal.org/article/S1083-8791(19)31462-4/fulltext
[07-07-2025 16:09] PPM 1: 👆@PPM3@PPM4
[08-07-2025 11:06] PPM 1: @PPM5 please send his repeat HPLC for hemoglobinopathy
[08-07-2025 11:35] PPM 5: Sir HPLC is done in biochemistry
[08-07-2025 11:41] PPM 1: And?
[08-07-2025 14:15] PA: স্যার মাথা ব্যাথা সাথে চোখ ব্যাথা টা কমতেছে না
[08-07-2025 16:36] PA: স্যার কি একটা টেস্ট ছিলো সেটা নাকি nalgonda গিয়ে করতে হবে ?
স্যার এখানে করা গেলে খুব ভালো হত স্যার
[08-07-2025 16:42] PPM 1: @PPM5 do they need to go to Nalgonda for this test? Can't we send it otherwise there? If not then send it through our lab to LB Nagar
[08-07-2025 16:47] PPM 5: স্যার আমাদের লোক তো এ ভাষা বলতে পারে না।
এজন্যই বলছিলাম আরকি
টেস্ট করতে শুধু পয়সা লাগে তাহলে পয়সা দেবো আমরা
[08-07-2025 16:56] PPM 5: Thy have to take sir
[08-07-2025 16:57] PPM 5: In LB nagar
Hb Electrophoresis sir
[08-07-2025 16:57] PPM 5: Then Shall I send for Hb Electrophoresis sir
[08-07-2025 19:44] PPM 1: Alright send for that. What's the cost?
@Meta AI for HbE beta Thalasemia which test has better sensitivity and specificity? HPLC or Hb Electrophoresis?
[08-07-2025 19:45] Meta AI: For HbE beta Thalassemia, High-Performance Liquid Chromatography (HPLC) is a more effective diagnostic tool compared to Hb Electrophoresis. Here's why¹ ²:
- Sensitivity and Specificity: HPLC has higher sensitivity and specificity in detecting hemoglobinopathies, including HbE beta Thalassemia. A study found that HPLC identified several types of hemoglobinopathies that would have been missed by conventional CBC-first screening methods.
- Cost-Effectiveness: Conducting HPLC as the first step is cost-effective, with a study showing only a 0.7% increase in cost compared to CBC-first approach. Performing both HPLC and CBC together increases the cost by 47.8%.
- Detection Capabilities: HPLC provides accurate quantitation of hemoglobin concentrations, particularly Hb F and A2, useful for diagnosing beta-thalassemia. It can also detect various hemoglobin variants, such as Hb E, Hb S, and Hb D.
In contrast, Hb Electrophoresis can identify abnormal hemoglobin variants but may not provide the same level of quantitation as HPLC. For beta-thalassemia trait diagnosis, HbA2 level cut-off of 3.5% is considered, which can be accurately measured using HPLC.
As for the cost in India, a study mentioned the cost of CBC as Rs 100 and HPLC as Rs 200. However, these prices may vary depending on the location and laboratory.
Diagnostic Approach:
- HPLC: More sensitive and specific, cost-effective, and provides accurate quantitation of hemoglobin concentrations.
- Hb Electrophoresis: Useful for identifying abnormal hemoglobin variants, but may not provide the same level of quantitation as HPLC.
Keep in mind that the choice of diagnostic approach may depend on the specific laboratory and clinical context.³
[08-07-2025 19:45] Meta AI: https://www.sciencedirect.com/science/article/abs/pii/S0009898101006726
[08-07-2025 19:45] Meta AI: https://ashpublications.org/blood/article/122/21/4709/12411/Thalassemia-and-Hemoglobinopathy-Screening-By-HPLC
[08-07-2025 19:45] Meta AI: https://www.frontiersin.org/journals/hematology/articles/10.3389/frhem.2025.1461498/full
[08-07-2025 20:36] PPM 5: HPLC sample they gave sir
[08-07-2025 20:36] PPM 5: By Thursday evening we will be getting the reports sir
[08-07-2025 20:36] PPM 1: Where? How?
[08-07-2025 20:38] PPM 5: THYROCARE Nalgonda sir
patient’s attender sir
[08-07-2025 20:51] PPM 1: He went and gave it there? Good 👏
[08-07-2025 20:52] PPM 5: Yes sir.
[08-07-2025 21.59] PA: স্যার রাত হলে কাশি আমার বেশি হয়, কিন্তু কালকের তুলনায় বেশি হচ্ছে ঘুমাতে পারছি না
[09-07-2025 03.43] PPM 1: Bed er tolai a mathar deeke bed ta uchu kore shute bola hoyechilo jaate acid ta upore uthe saash nali te giye kashi na kore
[09-07-2025 19.45] PA: স্যার মাথাটা খুব ব্যথা করতেছে
[10-07-2025 12.26] PPM 1: Learning point Thyrocare from Nalgonda does only Hb electrophoresis and not HPLC. The sales person who we interfaced with was misleading.
Either way the test doesnt show any significant change from his previous report
[10-07-2025 14:10] PA: স্যার হাফিজর রহমানের থ্যালাসেমিয়া রিপোর্ট টা কি দিয়েছে ।
[10-07-2025 14:16] PPM 1: 👆@~Apiul Mia ekhane diyeche
[10-07-2025 14:16] PPM 1: Aager moton ache
[10-07-2025 14:17] PA: স্যার দেখা করা যাবে আজকে আপনার সাথে
[10-07-2025 14:19] PPM 1: ICU
[10-07-2025 14:19] PA: ওকে স্যার আসছি
[10-07-2025 20:14] PPM 1: @PPM5 pm me the discharge summary
[11-07-2025 09:06] PA: স্যার হাফিজুর রহমানের থ্যালাসেমিয়া রিপোর্টটা আমাদের দেবে না ।
রিপোর্টটা দিলে পরে দরকার হলে দেখাতে পারতাম ডাক্তারবাবু
[11-07-2025 10:03] PPM 1: @PPM5 please give the patient a copy of their Hemoglobin electrophoresis report ASAP
[11-07-2025 10:49] PPM 5: Okay sir
[11-07-2025 17.02] PPM 1: EMR summary:
Age/Gender: 22 Years/Male
Admission Date: 05/07/2025 04:08 PM
Name of Treating Faculty
[AP]
[SR]
[PGY3]
[PGY2]
[PGY1]
Diagnosis
URTI
HEMOLYTIC ANEAMIA SECONDARY TO THALASSEMIA
JAUNDICE SECONDARY TO THALASEMMIA
K/C/O BETA THALASSEMIA SINCE 15 YEARS
S/P 2 POINT PRBC TRANSFUSION (DONE IN 2010)
Case History and Clinical Findings
C/O COUGH, COLD, FEVER SINCE SEVEN DAYS
HOPI:
PATIENT WAS APPARENTLY ASYMTOMATIC 7 DAYS AGO.THEN DEVELOPED COUGH WHICH
IS INSIDIOUS IN ONSET, GRADUALLY PROGRESSIVE ASSOCIATED WITH SPUTUM 1CU IN
QUANTITY, WHITE IN COLOUR.
H/O FEVER [INCREASED DURING NIGHT] NOT ASSOCIATED WITH CHILLS, RIGOR AND RASH
H/O JAUNDICE PRESENT
NO H/O HEADACHE, GIDDINESS, TINITUS
NO H/O CHEST PAIN/PEDAL EDEMA/ORTHOPNEA/SOB
NO H/O LOOSE STOOLS, BURNONG MICTURITION, VOMTING, NAUSEA, ABDOMINAL PAIN
NO H/O ABDOMINAL PAIN
NO H/O GROWTH RETARDATION
** Tentative Date Page-2
KIMS HOSPITALS
PAST HISTORY:
K/C/O THASLASSEMIA SINCE 15 YEARS [S/P 2 POINT PRBC TRANSFUSION DONE IN 2010]
N/K/C/O DM/EPILERSY/HTN/THYRIOD DISORDERS/CVA/CAD
PERSONAL HISTORY:
SINGLE, STUDENT, APPETITE: NORMAL, DIET: MIXED BOWEL AND BLADDER MOVEMENT: NORMAL, MICTURITION NORMAL, ALCOHOL: TEETOTALER, NO KNOWN ALLERGIES
FAMILY HISTORY: PARENTS MARRIAGE: NON CONSANGUINEOUS MARRIAGE.
10 YEARS BROTHER DIED1 1/2 YEAR BACK,12YEARS BROTHER DIED 8YEARS BACK.
GENERAL EXAMINATION:
PATIENT IS CONSCIOUS, COHERENT, COOPERATIVE
ICTERUS PRESENT, NO PALLOR, CYNOSIS, LYMPHADENOPATHY, CLUBBING OF FINGERS PEDAL EDEMA AND MALNUTRITION
VITALS: BP:140/90MMHG, PR:98BPM, RR:24, TEMP:98 AT RA, GRBS:127
SYSTEMIC EXAMINATION:
CVS: S1S2 HEARD
CNS:NO FOCAL NEUROLOGICAL DEFICIT
RESP: BLAE PRESENT, NVBS
P/A: SOFT NON-TENDER, HEPATOSPLENOMEGALY PRESENT
Investigation
LIVER FUNCTION TEST (LFT) 05-07-2025Total Bilurubin 4.65 mg/dl Direct Bilurubin 0.61 mg/dl
SGOT(AST) 23 IU/L SGPT(ALT) 13 IU/L LALKALINE PHOSPHATASE 148 IU/L TOTAL PROTEINS
7.4 gm/dl ALBUMIN 4.61 gm/dl A/G RATIO 1.65
BLOOD UREA 05-07-2025: 35 mg/dl SERUM CREATININE 05-07-2025: 1.0 mg/dl
SERUM ELECTROLYTES (Na, K, C l) 05-07-2025 SODIUM 135 mmol/L POTASSIUM 3.9 mmol/L
CHLORIDE 98 mmol/L
COMPLETE URINE EXAMINATION (CUE) 05-07-2025 COLOUR Pale Yellow, Appearance
Clear REACTION Acidic SP. GRAVITY 1.010ALBUMIN Trace SUGAR Nil BILE SALTS Nil BILE
PIGMENTS Nil PUS CELLS 3-4EPITHELIAL CELLS 2-3 RED BLOOD CELLS Nil CRYSTALS
Nil CASTS Nil AMORPHOUS DEPOSITS Absent OTHERS Nil
Anti HCV Antibodies - RAPID 05-07-2025: Non-Reactive
HBsAg-RAPID 05-07-2025: Negative
USG OF ABDOMEN DONE ON:5/7/25
IMPRESSIONS: SPLENOMEGALY
COOMBS TEST:
ICT AND DCT: negative
** Tentative Date Page-3
KIMS HOSPITALS
HB ELECTROPHORESIS DONE ON 10/7/25: S/O 1. HOMOZYGOUS HB E DISEASE 2. BETA
THALASSEMIA
Treatment Given (Enter only Generic Name)
TAB: PCM 650MG PO/TID
INJ: NEOMOL 100ML IV /SOS [IF TEMP.>101F]
SYP.ASCORIL DS 10ML PO/TID
Advice at Discharge
TAB FOLVITE 5 MG PO/OD TO BE CONTINUED
TAB PCM 650MG PO/SOS
SYP.LUPITUSS 15ML PO/TID X 3 DAYS
Follow Up
REVIEW GM OPD AFTER 2WEEKS/ SOS
When to Obtain Urgent Care
IN CASE OF ANY EMERGENCY IMMEDIATELY CONTACT YOUR CONSULTANT DOCTOR OR ATTEND EMERGENCY DEPARTMENT.
Preventive Care
AVOID SELF MEDICATION WITHOUT DOCTORS ADVICE, DONOT MISS MEDICATIONS. In case of Emergency or to speak to your treating FACULTY or For Appointments, Please Contact:
For Treatment Enquiries Patient/Attendent Declaration: - The medicines prescribed
and the advice regarding preventive aspects of care, when and how to obtain urgent care have been
explained to me in my own language
SIGNATURE OF PATIENT /ATTENDER:
SIGNATURE OF PG/INTERNEE:
SIGNATURE OF ADMINISTRATOR:
SIGNATURE OF FACULTY:
Discharge Date
Date:11-07-2025
Ward:MMW
Unit:IV
[12-07-2025 09.28] PA: স্যার আমরা যাচ্ছি স্টেশনে
[15-07-2025 12:01] PA: জ্বর মাথা ব্যাথা সর্দি কাশি।
সেদিন থেকে খেয়ে আসছি তো কমছে না স্যার।
আজকে আবার প্রচুর জ্বর আসছে মাথা ব্যথা করতেছে
[15-07-2025 12:02] PPM 1: Eta kar 21M Thalasemia patient er naki 27M headache patient er?
Temperature ta proti 4 ghontai ghontai mepe ekhane janaben
[15-07-2025 12:03] PA: হ্যাঁ স্যার
[15-07-2025 12:22] PPM 1: Kar? 21M er naki 27M er?
[15-07-2025 12:23] PA: থ্যালাসেমিয়া পেশেন্ট।
[15-07-2025 12:23] PPM 1: Temperature ta proti 4 ghontai ghontai mepe ekhane janaben
[15-07-2025 12:55] PA: এখন এরকম, 99.2F
[15-07-2025 13:09] PPM 1: Thik ache aebhabe proti 4 ghonta baade baade janaben
[15-07-2025 13:21] PA: স্যার মাথাব্যথা তো কমতেছে না।
সর্দি কাশি কমতেছে কাশতে কাশতে বুক ব্যাথা করতেছে এখন
[15-07-2025 15.40] PA: 97.4F
[15-07-2025 18:29] PA: স্যার আমার কাশি টা আগের চেয়ে অনেক বেশী হয়েছে।
এখন কাশতে কাশতে বুক খুব ব্যাথা করছে
[15-07-2025 18:42] PA: স্যার কাশতে কাশতে বুক খুব ব্যাথা করতেছে
কাশি টা মিনিটে সাত-আট বার হচ্ছে।
[15-07-2025 18:45] PA: স্যার এই সিরাপ বাবা নিয়ে আসলো এটা খাওয়া যাবে ।
[15-07-2025 18:46] PA: বসে থাকলেও কাশি আসতেছে দাঁড়ায় থাকলেও কাশি আসতেছে শুয়ে থাকলেও আসতেছে
[15-07-2025 18:49] PPM 1: Hain khete paren
[15-07-2025 18:49] PPM 1: Aaste aaste kome jabe
Local daktar ke ekbar dekhiye neben
[15-07-2025 19:31] PA: স্যার আমার কাশি টা আরও অনেক বেশী হলো ।
[15-07-2025 19:37] PA: স্যার কাশি টা খুব বেশি হলো আগের থেকে অনেক বেশী
[15-07-2025 20:45] PPM 1: অনুগ্রহ করে তাঁকে বলুন যেন ২৪ ঘণ্টার কফ একটি বোতলে সংগ্রহ করে এখানে শেয়ার করেন।*
এখন থেকেই শুরু করে আগামীকাল দুপুর ১টা পর্যন্ত যতবার কাশি হবে, ততবার যতটা কফ বেরোবে, সবটুকু ঢাকনাওয়ালা একটি পাত্রে জমা করতে থাকুন। আগামীকাল দুপুরে তার ছবি পাঠান।
ভাল হয় একটি স্বচ্ছ কাঁচের গ্লাস অর্ধেকটা জল দিয়ে ভর্তি করে পাশে থেকে ছবি তোলা।*
স্ফুটুম গ্লাসের ছবি দেখতে এখানে ক্লিক করুন👇*
[15-07-2025 20:54] PA2: স্যার ক্ফ তো বেরোচ্ছে না,
শুকনো কাশ।
[22-07-2025 19:30] PA: জ্বর আর মাথাব্যথা সারতেছে না ।
স্যার এদিকে লোকাল ডাক্তার দেখাচ্ছিলাম।
লোকাল ডাক্তার হাসপাতালে ভর্তি করতে বলল ।
হাসপাতালে কি ভর্তি করব ?
কোন ওষুধ দিল না ।
[22-07-2025 19:33] PPM 1: Hain bhorti kore 4 ghontai ghontai temperature ta mepe janaben
[01-08-2025 16:12] PA: Sir হাসপাতালে ভর্তি হল থ্যালাসেমিয়ার পেশেন্ট টা
[01-08-2025 16:12] PA: আজকে জ্বর আর মাথাব্যথা
[01-08-2025 16:33] PPM 1: 22 July theke 31 July kemon chilen? Ekhane eto din janalen na?
[01-08-2025 16:39] PA: স্যার পেশেন্ট এতদিন ধরে জ্বর মাথা ব্যাথা ছিলই।
জ্বরটা বেশি একটা ছিল না
কিন্তু মাথাব্যথাটা ছিলই টোটো চালাইলে আবার মাথা ব্যথা বেশি করে তাই আজকে প্রচুর মাথা ব্যথা না হাসপাতালে ভর্তি করাইলাম
[02-08-2025 21:05] PPM 1: Update:
[02/08, 19:39] Patient Advocate 27M Abdominal Migraine: স্যার থ্যালাসেমিয়া পেশেন্ট টার রক্ত 7.1 বর্তমান আছে আজকে রিপোর্ট করলো।
হাসপাতালে ডাক্তার বলতেছে ব্লাড ভরতে লাগবে।
ব্লাড কি ভরা যাব
[02/08, 19:52] Patient Advocate 27M Abdominal Migraine: স্যার ব্লাড দেয়া যাবে কি
[02/08, 19:59] Patient Advocate 27M Abdominal Migraine: ডাক্তার বললো ব্লাড দেয়া লাগবে ।
স্যার থ্যালাসেমিয়া পেশেন্ট টা কে ব্লাড দেয়া যাবেনা আপনি বলছিলেন।
কিন্তু এখানে তো ব্লাড দেয়া লাগবে।
[02/08, 19:59] Patient Advocate 27M Abdominal Migraine: স্যার আমরা এখন কি করব
[02/08, 20:32] Patient Advocate 27M Abdominal Migraine: স্যার আমরা এখন ব্লাড দিব ?
[02/08, 21:03]cm: Blood dite habe ki habena sheta nirbhor korche roogir bortoman koshter upor.
Unar bortoman koshto ta ki ektu bistarito janate parle kichu bola jeto
[02-08-2025 21:06] PA: জ্বর ও মাথা ব্যাথা
[02-08-2025 21:07] PPM 1 Koto din dhore
Proti char char ghontai temperature ta jante parle bojha jeto
[02-08-2025 21:09] PA: এটা আজকের করা রিপোর্ট
[02-08-2025 21:24] PPM 1: Aer aageo unar Hb 7-8 er modhyei chilo.
Matha byatha are jorer jonye rokto dewar proyojon aei muhurte amader mone hocchena
Baki unar char char ghonta temperature chart ta dekhte parle aro bojha jeto.
Ebong meningeal signs ache kina shetao clinically examine kore dekha dorkar
[02-08-2025 21:28] PPM 1: Just some mild unconjugated hyperbilirubinemia similar to his previous Lft reports archived in your case report here which were actually higher and double the current bilirubin
[02-08-2025 21:30] PPM 1: Proti char char ghontai janaben. Aekhon jor nei dekha jacche
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