Dr Suldan Abdullahi

06/10/2026

ADA / EASD 2026
What Changes in practice ? Consesus report on treatment of Type 2 Diabetes Mellitus .

05/10/2026

MRCP course

Dr suldan's MRCP COURSE

04/10/2026

Any anaemia gives you two numbers to start with.

MCV and reticulocyte count (corrected one).

Start with the reticulocyte count, not the MCV.

It asks one question: is the marrow responding or not?

High retic means the marrow is working fine and cells are being lost or destroyed somewhere.

Cause: Bleeding or haemolysis.

Nothing wrong with production.

Low retic means the marrow itself has failed to make them.

Now the MCV matters, because it tells you what the marrow was short of.

Low MCV: a building block is missing. Iron, or globin chains in thalassaemia, or the heme ring in sideroblastic anaemia.

High MCV: DNA synthesis failed.

The cytoplasm kept growing while the nucleus could not divide. B12, folate, drugs that block DNA.

Normal MCV: production itself was switched off. Chronic disease, renal failure with no erythropoietin, marrow infiltration, aplasia.

Retic tells you whether the marrow is trying. MCV tells you what it was missing.

03/10/2026

The best way, perhaps the only way, to change others is to become an example.

01/10/2026

🔴 What could change our diabetes practice?

1. 🫘 In CKD, eGFR alone tells only half the story.
Among transplant recipients with diabetes, CKD prevalence rose from 49.5% using reduced eGFR alone to 72.6% when albuminuria was also considered.
💡 Clinical message: Always think eGFR + UACR, not eGFR alone.

2. ⚠️ Normal glucose does NOT exclude dangerous ketosis.
PARTNER cases showed that people with T1D—particularly with SGLT2 inhibitor exposure—may develop clinically silent ketonaemia, especially with reduced insulin delivery, low-carbohydrate intake, illness or pump interruption.
💡 CME Pearl: When the clinical situation suggests ketosis, check ketones—not merely glucose. Continuous ketone monitoring is an emerging safety tool, not yet something required for every patient.

3. 🎯 “Low predicted risk” does not mean “low-risk diabetes.”
In the UK cohort, 11.8% of newly diagnosed T2D occurred despite low predicted risk. These patients were younger and leaner, yet had higher HbA1c, more subsequent insulin initiation and higher severe retinopathy and mortality.
💡 Clinical message: Don't let a reassuring risk score overrule clinical suspicion.

4. 📈 Metabolic trajectory may matter as much as a snapshot.
Longitudinal changes in insulin resistance/sensitivity indices added information for predicting future T2D. Interestingly, TyG and TG/HDL-C contributed particularly through their trajectories over time, rather than a single baseline measurement.
💡 Follow the metabolic movie—not just the photograph.

5. 💊 Don't always wait for monotherapy to fail.
Evidence presented from UKPDS follow-up, combination-treatment trials and VERIFY supports earlier proactive combination therapy for better glycaemic durability rather than therapeutic inertia.
💡 CME Pearl: “Treat-to-failure” is increasingly giving way to “treat-to-preserve.”

6. 👴 But early combination is NOT for everybody.
Frailty, dementia, multimorbidity, CKD/liver disease, polypharmacy, hypoglycaemia risk, adherence and treatment burden may make stepwise intensification—or even de-intensification—more appropriate.
💡 The best regimen is not necessarily the regimen with the most drugs; it is the one matched to the patient.

7. 🧑 Young-onset T2D deserves special cardiometabolic attention.
Compared with later-onset T2D, young-onset patients had persistently higher HbA1c and LDL-C and underwent HbA1c/LDL-C testing less frequently. The LDL-C disparity did not narrow with time.
💡 Don't treat young age as cardiovascular reassurance.

8. 📱 Adolescence → young adulthood is a vulnerable diabetes transition.
Among 1,631 people aged 11–22 years with T1D, only about 22% met both stated CGM targets, and target attainment declined with increasing age; hyperglycaemia was the major barrier.
💡 Technology needs to be accompanied by age-specific behavioural and healthcare support.

9. 🔥 Tirzepatide early in T2D: beyond HbA1c and kilograms.
At 104 weeks in SURPASS-EARLY, HbA1c fell to 5.56% vs 6.35% with intensified conventional care, while weight fell by about 15.8 vs 6.5 kg. OGTT-derived measures also indicated greater improvement in β-cell function and insulin sensitivity.
💡 This raises an important concept: early incretin-based treatment may modify multiple components of the metabolic phenotype—not simply glucose.

10. 💉 Before simply escalating basal insulin, reconsider the strategy.
In SUSTAIN OPTIMIZE, adding semaglutide 2.0 mg weekly while reducing basal insulin produced greater HbA1c reduction, 8-kg weight loss, lower insulin requirement and TIR 81.2% vs 64.3% with titrated glargine alone—roughly 4 extra hours/day in range, without increased TBR.

💡 Sometimes the better intensification is less insulin + an effective complementary therapy, rather than progressively more basal insulin.

11. 🎯 In DKD, look beyond BMI—visceral adiposity may matter.
In T2D with visceral obesity, >10% reduction in visceral fat area was associated with more albuminuria improvement and slower eGFR decline; the VFA-reduction group had a 2.53-fold higher probability of albuminuria improvement.
💡 Where the fat is—and how it changes—may matter to the kidney. Importantly, this was an association from a prospective cohort, not proof of causality.

12. ⚡ Painful diabetic neuropathy may have a neuromodulation option in selected refractory patients.
With 10-kHz spinal cord stimulation, 93.1% of per-protocol participants achieved ≥50% pain reduction at 6 months versus 0% with conventional medical management; sensory improvement was also demonstrated and persisted through 12 months.
💡 Particularly interesting: the signal was not limited to analgesia—objective sensory-function improvement was also reported.

🔥 TAKE-HOME

Diabetes care in 2026 is moving from “lower the HbA1c” → to “identify the phenotype, protect the organs, preserve function and individualize early.”

The 5 shifts worth remembering:
eGFR → eGFR + UACR | Glucose → Glucose + Ketones | BMI → Adiposity phenotype | Stepwise failure → Timely combination | HbA1c → CGM + organ outcomes + quality of life

Source: Essence of EASD 2026, Milan, Day 2. These are conference-study findings as presented in the uploaded document; several should be viewed as emerging evidence rather than automatic changes to clinical guidelines.

25/09/2026

𝐖𝐇𝐎 𝐌𝐀𝐋𝐀𝐑𝐈𝐀 𝐆𝐔𝐈𝐃𝐄𝐋𝐈𝐍𝐄𝐒 𝟐𝟎𝟐𝟔 — 𝐓𝐎𝐏 𝐂𝐋𝐈𝐍𝐈𝐂𝐀𝐋 𝐏𝐄𝐀𝐑𝐋𝐒

The WHO Guidelines for Malaria, 10 September 2026 replace previous versions and include important updates involving pregnancy/HIV, transmission-blocking primaquine, infants

24/09/2026

🦋 | TOP 12 CLINICAL PEARLS

ATA 2026 Guidelines: Thyroid Disease in Preconception, Pregnancy & Postpartum

1. 🤰 TSH remains the anchor test in pregnancy. Prefer laboratory- and trimester-specific TSH and FT4 ranges. If unavailable, the ATA allows a TSH reference interval of 0.1–4.0 mU/L in the first and second trimesters. TSH generally deserves priority when FT4 interpretation is uncertain.

2. 🔍 Universal screening is still NOT recommended. Every newly pregnant woman should undergo clinical risk assessment; TSH should be offered at pregnancy confirmation to women at increased risk. Risk factors include thyroid disease/antibodies, goitre or symptoms, autoimmune disease, ≥2 miscarriages, infertility, relevant drugs, prior neck irradiation/thyroid surgery and severe iodine insufficiency.

3. 💊 Overt hypothyroidism = LT4, and LT4 alone. New overt hypothyroidism with TSH ≥6 mU/L, or disease persisting on confirmation, should be treated. With TSH 500 μg/day should be avoided.

9. 📉 A low TSH in early pregnancy is not automatically Graves’. hCG physiologically lowers TSH, and TSH

11/09/2026

🔴 TOP 12 CLINICAL UPDATES

Rheumatoid Arthritis in Adults — What Every Physician Should Know

JAMA Review | September 10, 2026

RA is not merely a painful joint disorder—it is a potentially joint-destructive systemic autoimmune disease, and early disease control matters.

1️⃣ Diagnose clinically—classification criteria ≠ diagnostic criteria.
There are no formal diagnostic criteria for RA. Think RA when there is persistent symmetric synovitis, particularly involving the wrists, MCP and PIP joints; DIP joints are typically spared. ACR/EULAR classification criteria support, but do not replace, clinical diagnosis.

2️⃣ The “6-week window” matters.
Aim for recognition and treatment within approximately 6 weeks of symptom onset. Early DMARD initiation reduces inflammation and the risk of irreversible joint destruction.

3️⃣ Negative RF/ACPA does NOT rule out early RA.
At diagnosis, only about 40–60% have RF and/or ACPA. Seronegative inflammatory polyarthritis can therefore still be RA. Conversely, autoantibodies may precede clinical disease by years.

4️⃣ Treat-to-target has a simple “3–6 rule.” 🎯
After starting treatment, aim for ≥50% improvement in disease activity by 3 months and remission by 6 months. Failure to achieve these targets should trigger treatment modification rather than therapeutic inertia.

5️⃣ CDAI is particularly practical for the clinic.
It requires no laboratory test: tender-joint count + swollen-joint count + patient global + physician global assessment. CDAI ≤2.8 = remission; ≤10 = low disease activity. Formal serial assessment is preferable to simply asking whether the patient “feels better.”

6️⃣ Methotrexate remains the anchor drug. 💊
For most patients without contraindications, methotrexate remains first-line DMARD therapy. EULAR recommends starting 7.5–10 mg once weekly and escalating rapidly toward 20–25 mg/week within 4–8 weeks, with folic acid supplementation. Methotrexate is weekly—not daily.

7️⃣ Steroids are a bridge—not a destination.
EULAR allows short-term low-dose glucocorticoids with initial methotrexate—for example prednisone 5–7.5 mg/day, generally for 6–12 weeks and tapered/discontinued within 3 months. Chronic steroid dependence should prompt reconsideration of disease control.

8️⃣ If methotrexate cannot be used, there are good conventional alternatives.
Consider sulfasalazine 2–4 g/day or leflunomide 20 mg/day. Routine first-line “triple/combination” conventional DMARD therapy is not necessarily superior and may increase toxicity.

9️⃣ Don't wait indefinitely before escalating to biologic therapy.
Persistent disease despite appropriately optimized conventional DMARD treatment warrants a biologic DMARD—TNF inhibitor, IL-6 receptor inhibitor, abatacept or rituximab. Available biologic classes have broadly similar efficacy; many perform better when combined with methotrexate.

🔟 JAK inhibitors need cardiovascular/VTE/malignancy thinking. ⚠️
JAK inhibitors are effective targeted synthetic DMARDs, but patient selection matters. The review recommends considering them particularly when patients are not at high risk of cardiovascular disease, thromboembolism or malignancy.

1️⃣1️⃣ Seropositive RA deserves particular vigilance.
RF and especially ACPA positivity predict greater structural progression. In long-term data summarized in the review, radiographic progression risk was approximately 2.1-fold with RF positivity and 2.5-fold with ACPA positivity.

1️⃣2️⃣ Treating RA well is also preventive medicine. ❤️
With modern escalation strategies, approximately 80% of patients can achieve remission or low disease activity. High disease activity is associated with excess mortality, while patients with low disease activity had mortality similar to the general population in cited registry data. Don't forget smoking cessation and aggressive cardiovascular risk-factor control, including BP and lipid management when indicated.

🧠TAKE-HOME

Suspect early → Start DMARD early → Optimize methotrexate rapidly → Measure disease activity → 50% better by 3 months → Remission by 6 months → Escalate if target missed.

The major paradigm is simple: in RA, pain relief is not the therapeutic endpoint—suppression of inflammation and prevention of irreversible structural damage are.

jamanetwork.com/journals/jama/…

09/09/2026

AI advancement—and the potential danger that comes with it—is growing faster than expected.

The real risk is humans losing control, as AI companies compete to build increasingly independent and self-improving systems.

05/09/2026

📢 A 𝐍𝐞𝐰 𝐖𝐚𝐯𝐞 𝐨𝐟 𝐭𝐡𝐞 𝐌𝐑𝐂𝐏 𝐏𝐚𝐫𝐭 𝟏 𝐂𝐨𝐮𝐫𝐬𝐞 𝐈𝐬 𝐍𝐨𝐰 𝐎𝐩𝐞𝐧

We are pleased to announce a new wave of the 𝐌𝐑𝐂𝐏 𝐏𝐚𝐫𝐭 𝟏 𝐇𝐢𝐠𝐡-𝐘𝐢𝐞𝐥𝐝 𝐈𝐧𝐭𝐞𝐧𝐬𝐢𝐯𝐞 𝐂𝐨𝐮𝐫𝐬𝐞.

The course brings together a structured set of resources designed to help you prepare for MRCP Part 1 with a focus on 𝐮𝐧𝐝𝐞𝐫𝐬𝐭𝐚𝐧𝐝𝐢𝐧𝐠 𝐭𝐡𝐞 𝐥𝐨𝐠𝐢𝐜 𝐛𝐞𝐡𝐢𝐧𝐝 𝐭𝐡𝐞 𝐪𝐮𝐞𝐬𝐭𝐢𝐨𝐧𝐬 — 𝐧𝐨𝐭 𝐬𝐢𝐦𝐩𝐥𝐲 𝐦𝐞𝐦𝐨𝐫𝐢𝐳𝐢𝐧𝐠 𝐟𝐚𝐜𝐭𝐬.

The course includes:

✅ High-yield notes
✅ Recorded teaching sessions
✅ Live interactive sessions
✅ Question solving & clinical reasoning
✅ System-based preparation
✅ Exam-focused revision

Whether you are starting your preparation or looking for a more structured way to revise, this new wave is now open for registration.

𝐈𝐟 𝐲𝐨𝐮’𝐫𝐞 𝐩𝐫𝐞𝐩𝐚𝐫𝐢𝐧𝐠 𝐟𝐨𝐫 𝐌𝐑𝐂𝐏 𝐏𝐚𝐫𝐭 𝟏, 𝐲𝐨𝐮’𝐫𝐞 𝐰𝐞𝐥𝐜𝐨𝐦𝐞 𝐭𝐨 𝐣𝐨𝐢𝐧.

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