THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED 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 THOS PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.
The patient is a 53 yr old male with 116kg weight born in January 1973. Till the age of 11 he was fit and healthy and practiced yoga, played outdoor games like football. He was allergic to grass and had relief with Avil. At the age of 28 he became obese and had irregular food habits and intake of junk food. He had the problem of thigh itching 9rashes) for which he has taken Tinadrum but there was not much relief. Later on he took another medicine which cured completely. At the age of 30 he got married and at that time also he was fit but little obese. At the age of 31 he was diagnosed with diabetes and was prescribed Metformin. At 39 he was started on Insulin. As a result of his diabetes his right foot thumb amputation was done as the thumb turned black with ketones excess in blood at the age of 40. He had charcot foot and bones of toes were fragile.
At 46 he was on insulin Humalog Mix 75 and 12, morning - 30U
Evening 26U
Janumet BD
Voglistar 0.3 mg BD
From the age of 48 his diet control was fair and complete sugar restricted. He completely stopped bread and small amount of sugar intake showed blisters on hand for which he used Neosporin.
At the age of 51 he got his eyes checked on 17/07/2024 with
Right: Sph - 1.75, cyl -1.25 axis 180
Left: Sph - 0.75, cyl -0.75 axis 160
At 52 he was given left eye injection Razumab 10 mg/mL, 2.3 mg/0.23mL, twice with a gap of three months, due to blood in eyes and hazy vision.
He is a non smoker and non alcoholic compared to his father who was a chain smoker and hardcore alcoholic. His father passed away in 2010.
The patient's current problem is non balance while standing and taking the help of a cane or a stick. He experiences breathlessness while walking. According to his diagnosis, consuming soft drinks, soda and junk oily street food in his twenties was the result of his current problems and diabetes.
[10.39 am, 28/01/2026] PA: Left foot thumb nail is getting affected with Diabetes
[10.39 am, 28/01/2026] PA: Both foot picture. Right Foot thumb toe Amputed
[10:39 am, 28/01/2026] PPM 1: Perfect picture that gives us a good direction on what we need to work on @PPM3
We need to address both the sarcopenia and adiposity here through life style modifications that will be tailored to his daily shared diet plate images that his advocate @PA may have to share himself as well his hourly activities
[10:40 am, 28/01/2026] PPM 1: @PPM4 @PPM3 can you use your computer vision equipped LLM to take a look at and comment on this image?
[10.51 am, 28/01/2026] PPM 3: I will restrict conclusions to what is directly observable and what is strongly supported by clinical literature. I cannot diagnose from an image, but I can outline evidence-based differentials and associated risks.
First: limitations
Only a lateral torso view is visible.
The feet and toes are not visible in this image, so I cannot comment on the toe.
No medical history, labs, or vitals are provided.
Observed physical features
1. Central abdominal adiposity
There is prominent anterior abdominal protrusion consistent with increased visceral and/or subcutaneous abdominal fat. The distribution appears centrally concentrated rather than predominantly gluteofemoral.
2. Increased breast tissue in a male
There appears to be enlargement of the chest area consistent with either pseudogynecomastia (fat deposition) or true gynecomastia (glandular proliferation). The image alone cannot distinguish these.
3. Overall body habitus
The individual appears to have overweight or obesity, likely at least class I by visual estimation. However, BMI cannot be calculated without height and weight.
Differential diagnosis
A. Overweight or Obesity with Central Adiposity
Most likely explanation for the abdominal contour.
Evidence: Central adiposity correlates strongly with metabolic syndrome, insulin resistance, type 2 diabetes, and cardiovascular disease.
Key references:
Després JP. Body fat distribution and risk of cardiovascular disease. Circulation. 2012.
Neeland IJ et al. Visceral and ectopic fat, atherosclerosis, and cardiometabolic disease. JACC. 2019.
B. Metabolic Syndrome
Given central obesity, metabolic syndrome becomes a strong possibility if other criteria are present (hypertension, elevated triglycerides, low HDL, elevated fasting glucose).
Evidence:
Alberti KGMM et al. Harmonizing the metabolic syndrome. Circulation. 2009.
C. Nonalcoholic Fatty Liver Disease
Central obesity is a strong risk factor for NAFLD. The abdominal contour does not suggest ascites (no tense distension or flank fullness visible), so visceral fat is more likely than fluid.
Evidence:
Younossi Z et al. Global epidemiology of NAFLD. Hepatology. 2016.
D. Pseudogynecomastia vs True Gynecomastia
1. Pseudogynecomastia
Common in obesity. Caused by adipose deposition in the chest.
2. True gynecomastia
Glandular proliferation due to hormonal imbalance (increased estrogen to androgen ratio), medications, liver disease, hypogonadism, etc.
Evidence:
Narula HS, Carlson HE. Gynecomastia. Endocrinol Metab Clin North Am. 2007.
Johnson RE, Murad MH. Gynecomastia: pathophysiology and management. Mayo Clin Proc. 2009.
Without palpation (firm subareolar gland vs soft diffuse fat), distinction cannot be made.
E. Cushing syndrome (low probability based on image alone)
Central obesity with possible truncal fat distribution can be seen in Cushing syndrome. However, I do not see clear dorsocervical fat pad, facial rounding, or striae. No evidence here strongly suggests it. This remains low probability unless clinical features support it.
Evidence:
Nieman LK et al. The diagnosis of Cushing’s syndrome. Endocrine Reviews. 2008.
F. Ascites (unlikely from this image)
Ascites typically produces tense abdominal distension with flank fullness and often skin tautness. This image appears more consistent with adipose tissue.
Prognosis scenarios
1. If this is uncomplicated obesity
Short term: Increased risk of insulin resistance and metabolic syndrome.
Medium to long term: Increased risk of type 2 diabetes, coronary artery disease, stroke, obstructive sleep apnea, osteoarthritis.
Evidence:
Prospective Studies Collaboration. Body-mass index and cause-specific mortality. Lancet. 2009.
Prognosis improves significantly with:
5 to 10 percent weight reduction
Increased physical activity
Dietary modification
Evidence:
Knowler WC et al. Diabetes Prevention Program. NEJM. 2002.
2. If metabolic syndrome is present
Higher 10-year cardiovascular risk and increased all-cause mortality compared to metabolically healthy individuals.
3. If true gynecomastia due to endocrine disorder
Prognosis depends on cause.
Medication-induced: often reversible
Hypogonadism: treatable
Liver disease related: depends on liver pathology
Rarely malignancy
Regarding the toe
The toe is not visible in this image. I cannot provide any medical assessment of it. If you want an evaluation, provide a clear image of the toe and describe symptoms (pain, swelling, redness, deformity, ulceration, numbness, duration).
Objective next steps if this were a clinical scenario
1. Measure:
BMI
Waist circumference
Blood pressure
2. Labs:
Fasting glucose or HbA1c
Lipid panel
Liver function tests
Possibly testosterone, LH, FSH if gynecomastia suspected
3. Physical exam:
Palpate breast tissue
Assess for hepatomegaly
Look for signs of endocrine disorders
Summary of most likely interpretation
Most consistent with central obesity with possible pseudogynecomastia. This pattern is strongly associated with increased cardiometabolic risk. There is no visible evidence in the image of acute illness.
Confidence score: 0.83
Guesses made:
I assumed the abdominal prominence is adipose rather than ascites based on visual contour.
I assumed male sex based on chest morphology.
I assumed no additional symptoms since none were provided.
I inferred cardiometabolic risk based on body habitus without lab confirmation.
[10:53 am, 28/01/2026] PPM 1: Yes inferring cardio metabolic risk from the overall phenotype is very simple for physicians that would happen at the blink of an eye.
I shall tag again the toe image for the LLM to take another look
[10:54 am, 28/01/2026] PPM 1: 👆@PPM3 please ask the LLM to provide his differential diagnosis from this toe image.
[10.56 am, 28/01/2026] PA:
[11.16 am, 28/01/2026] PA: Presently taking one plate of
home grown organic salad, boiled egg, fruits, steamed vegetables (three type of Capsicum, broccoli beans, mushroom, carrot, sweet corn etc.)
Before lunch, Since last one month
[11.20 am, 28/01/2026] PA: Sample lunch
Daal Chawal, steamed / fried brinjal, Green Salad
home grown organic carrot, peas, cauliflower - Mix Veg
1 or 2 bajara, besan roti
[11:26 am, 28/01/2026] PA: To fight with constipation patient takes half spoon of Triphla / panchskar
everyday at the night.
[11:27 am, 28/01/2026] PPM 3: I did give it both the images, let me specifically asked about the toe
[11:29 am, 28/01/2026] PA: Patient is also suffering with foot drop and lazy tow
Left leg thumb does not move or almost dead. Having very less reaction (Muscle Weak)
[11:32 am, 28/01/2026] PPM 3: I will integrate image findings with the documented history and provide a structured differential diagnosis supported by evidence.
Key objective data
Age 53
Height 6 ft 2 in
Weight 116 kg
BMI approximately 32.8 kg per m2, which is Class I obesity
Type 2 diabetes diagnosed at age 31
Insulin dependent since age 39
Right great toe amputation in 2013 due to gangrene
Charcot foot in 2014
Ongoing insulin plus oral therapy
Intravitreal ranibizumab injection for diabetic retinopathy in 2025
Current symptoms: imbalance, breathlessness on walking
Image of toe
The remaining toe shows: Markedly thickened nail
Yellow-brown discoloration
Nail plate hypertrophy
Possible subungual debris
This morphology is highly consistent with onychomycosis in a diabetic patient.
Differential diagnosis for the toe
1. Onychomycosis
Most likely.
Evidence:
Thickened, discolored, dystrophic nails are classic findings.
Diabetes is a strong risk factor due to impaired immunity and microvascular compromise.
Evidence source: Gupta AK et al. Onychomycosis in diabetic patients. Journal of the American Academy of Dermatology. 1998.
Dogra S et al. Onychomycosis and diabetes mellitus. Mycoses. 2012.
Clinical importance:
Onychomycosis in diabetics increases risk of ulceration and secondary bacterial infection.
2. Diabetic neuropathic nail dystrophy
Chronic neuropathy and microvascular disease can cause nail thickening and deformity independent of fungal infection.
Evidence: Boulton AJM. Diabetic neuropathy and foot complications. NEJM. 2005.
3. Psoriatic nail dystrophy
Can cause thickened and dystrophic nails. However, no visible pitting or other psoriatic features are apparent. Lower probability.
4. Chronic ischemic changes from peripheral arterial disease
Diabetes predisposes to PAD. Chronic ischemia can alter nail growth and thickness. However, no visible necrosis in current image.
Evidence: American Diabetes Association. Peripheral arterial disease in people with diabetes. Diabetes Care. 2003.
Most probable diagnosis for the toe: Onychomycosis on background of diabetic neuropathy and prior Charcot foot.
Systemic differential diagnosis based on full history
The patient has long-standing, insulin-dependent type 2 diabetes with:
Prior gangrene requiring amputation
Charcot neuroarthropathy
Proliferative diabetic retinopathy requiring anti-VEGF injection
Balance problems
Breathlessness
This pattern suggests advanced microvascular and possibly macrovascular diabetic complications.
A. Advanced Diabetic Peripheral Neuropathy
Explains imbalance and prior Charcot foot.
Evidence: Peripheral neuropathy increases fall risk and postural instability.
Richardson JK et al. The relationship between neuropathy and falls in diabetes. Diabetes Care. 1992.
B. Charcot Neuroarthropathy
Already documented in 2014
Caused by neuropathy leading to bone fragmentation and deformity.
Evidence: Rogers LC et al. The Charcot foot in diabetes. Diabetes Care. 2011.
Prognosis: progressive deformity if not offloaded; high risk of recurrent ulceration.
C. Diabetic Retinopathy
Intravitreal ranibizumab indicates likely proliferative or clinically significant macular edema
Evidence: DRCR Network. Ranibizumab for diabetic macular edema. NEJM. 2010.
Prognosis: With treatment, vision stabilization is common; untreated, high risk of vision loss.
D. Peripheral Arterial Disease
History of gangrene and amputation strongly suggests vascular compromise.
Evidence: Jude EB et al. Peripheral arterial disease in diabetes. Diabetic Medicine. 2010.
Prognosis: Elevated risk of future amputation and cardiovascular mortality.
E. Cardiovascular Disease
Given long-standing diabetes, obesity, and breathlessness, differential includes:
1. Coronary artery disease
2. Diabetic cardiomyopathy
3. Heart failure
Evidence: Diabetes approximately doubles to quadruples cardiovascular risk.
Emerging Risk Factors Collaboration. Diabetes and cardiovascular disease. Lancet. 2010.
Breathlessness on exertion may represent heart failure or deconditioning. Requires echocardiography and stress testing.
F. Autonomic Neuropathy
May contribute to imbalance and exercise intolerance.
Evidence: Vinik AI et al. Diabetic autonomic neuropathy. Diabetes Care. 2003.
Overall staging impression
This case represents advanced, long-duration type 2 diabetes with:
Microvascular complications: retinopathy, neuropathy
Neuroarthropathy
Prior limb loss
Likely macrovascular disease risk
Prognosis
Without aggressive multidisciplinary management:
High 10-year risk of cardiovascular events
High risk of further foot ulceration and amputation
Progressive visual impairment possible
With optimized care (HbA1c control, statin, ACE inhibitor, SGLT2 inhibitor or GLP1 agonist if eligible, podiatry surveillance, cardiac evaluation):
Significant reduction in cardiovascular and renal risk is evidence-based.
Example evidence: Zinman B et al. Empagliflozin cardiovascular outcomes. NEJM. 2015.
Marso SP et al. Liraglutide cardiovascular outcomes. NEJM. 2016.
Critical next evaluations
1. HbA1c
2. Urine albumin to creatinine ratio
3. ABI and vascular imaging
4. Echocardiogram
5. Nerve conduction studies
6. Fungal culture or KOH prep of nail
Most likely integrated diagnosis
Long-standing poorly controlled type 2 diabetes with:
Severe peripheral neuropathy
Charcot neuroarthropathy
Diabetic retinopathy
Prior diabetic foot gangrene
Onychomycosis on neuropathic foot
Possible underlying cardiovascular disease
Confidence score: 0.89
Guesses made:
Assumed onychomycosis without lab confirmation.
Inferred likely peripheral arterial disease from prior gangrene.
Inferred possible cardiovascular disease based on breathlessness and risk profile.
Assumed retinopathy severity based on anti-VEGF injection history.
[11:35 am, 28/01/2026] PPM 3: This additional information materially shifts the neurologic differential and worsens prognosis.
Key new findings
Foot drop
Great toe weakness or near paralysis
Marked motor deficit in left lower limb
This changes the prior assessment in the following ways:
1. Neuropathy is no longer purely sensory
Previously, I emphasized diabetic peripheral neuropathy primarily in a sensory context. Foot drop indicates significant motor involvement. That substantially narrows the differential.
Revised differential for foot drop in this patient
A. Common peroneal nerve palsy
Most likely focal cause.
Mechanism: Compression at fibular head or ischemic mononeuropathy in diabetes.
Evidence: Peroneal neuropathy is the most common compressive neuropathy in the lower limb and frequently causes foot drop.
Stewart JD. Foot drop: where, why and what to do? Practical Neurology. 2008.
Diabetes predisposes to mononeuropathies due to microvascular ischemia.
Dyck PJ et al. Diabetic neuropathies. NEJM. 1999.
B. Diabetic lumbosacral radiculoplexus neuropathy
Also called diabetic amyotrophy.
More severe condition involving asymmetric proximal and distal weakness.
Evidence: Dyck PJ et al. Diabetic lumbosacral radiculoplexus neuropathy. Annals of Neurology. 2001.
C. L5 radiculopathy
Compression from lumbar disc disease can cause foot drop and great toe weakness.
Evidence: Wilbourn AJ. Electrodiagnostic approach to foot drop. Neurologic Clinics. 1999.
D. Advanced motor-predominant diabetic neuropathy
Long-standing diabetes can cause distal symmetric sensorimotor polyneuropathy, but complete foot drop is less typical unless severe.
Clinical implication
This is now a high-risk neurologic complication, not just balance impairment from sensory neuropathy.
Prognostic change
Without motor involvement: Risk was mainly ulceration and falls.
With motor foot drop:
Much higher fall risk
Rapid progression to deformity
Increased plantar pressure abnormalities
Markedly increased ulcer risk
Potential need for ankle foot orthosis
Risk of permanent deficit if untreated
If peroneal neuropathy: Prognosis can be partially reversible if due to compression.
If radiculoplexus neuropathy: Often painful and may partially recover over months, but residual weakness common.
If L5 radiculopathy: Prognosis depends on structural lesion.
What this changes in the big picture
1. Stronger indication for:
Nerve conduction studies
EMG
Lumbar spine MRI
Vascular assessment
2. Significantly elevated amputation risk due to:
Motor deficit
Prior amputation
Charcot history
Nail pathology
Likely neuropathy
3. Cardiovascular risk assessment remains urgent but neurologic evaluation becomes time sensitive.
Revised overall staging
This is now advanced complicated diabetes with:
Severe sensorimotor neuropathy
Focal motor neuropathy or radiculopathy
Charcot neuroarthropathy
Prior limb loss
Diabetic retinopathy
High risk of further limb loss
Short summary of change
The case shifts from predominantly sensory diabetic neuropathy with structural foot complications to a severe motor neuropathic or focal nerve pathology with immediate functional and limb preservation implications. Urgency and amputation risk increase substantially.
Confidence score: 0.92
Guesses made:
Assumed unilateral involvement based on description.
Assumed no acute trauma history.
Assumed weakness is neurologic rather than mechanical tendon rupture.
[11:37 am, 28/01/2026] PA: Ok. Noted
[11:40 am, 28/01/2026] PPM 3: @PPM1 Sir
[11:45 am, 28/01/2026] PPM 3: Please note that any of the AI generated responses are to be reviewed by one of the doctors in the group before acting on it.
[11:52 am, 28/01/2026] PPM 1: Well identified problem requirements although in the realm of solution offerings a long way to go for science (that the LLM can't help) 👏
Patient has to remove hard skin / Dead skin after 15 to 20 days
[3:30 pm, 28/01/2026] PA: With the aim to lose weight.
Should patient go for bariatric surgery or not?
Whether it is advisable or not?
However, patient have started yoga since last one month but could not lose weight.
[3:35 pm, 28/01/2026] PPM 3: GPT 5.2 @PPM 1 Sir
---
I will answer this in a decision-analysis framework based on established bariatric guidelines and outcome data.
Patient profile summary
Age 53
BMI approximately 32.8 kg per m2
Long-standing type 2 diabetes, insulin dependent
Microvascular complications: neuropathy, Charcot foot, retinopathy requiring anti-VEGF
Prior amputation
Motor neuropathy with foot drop
Breathlessness on exertion
Question: Is bariatric surgery advisable?
1. Guideline eligibility
Current international guidelines (ASMBS and ADA) recommend metabolic surgery for:
BMI 40 or greater regardless of comorbidities
BMI 35 or greater with obesity-related comorbidities
BMI 30 to 34.9 with inadequately controlled type 2 diabetes despite optimal medical therapy
Reference: Rubino F et al. Metabolic surgery in the treatment algorithm for type 2 diabetes. Diabetes Care. 2016.
American Diabetes Association Standards of Care.
With BMI 32.8 and insulin-dependent diabetes with complications, this patient meets criteria under the third category if diabetes remains inadequately controlled.
So from a guideline standpoint: eligible.
2. Expected metabolic benefit
Bariatric surgery in patients with BMI 30 to 35 and type 2 diabetes:
Significant HbA1c reduction
Reduced insulin requirement
Partial or complete remission in some patients
Cardiovascular risk reduction
Key trials:
STAMPEDE trial: Schauer PR et al. Bariatric surgery versus intensive medical therapy. NEJM. 2012, 2017 follow-up.
Demonstrated superior glycemic control compared to medical therapy alone.
However, remission rates are lower in:
Long duration diabetes
Insulin dependence
Presence of complications
Your diabetes duration is over 20 years and insulin dependent. That predicts lower remission probability.
3. Impact on existing complications
Important: Bariatric surgery does not reverse:
Established neuropathy
Charcot deformity
Foot drop
Established retinopathy
It may slow progression if glucose control improves.
Some studies show early worsening of retinopathy after rapid glycemic improvement.
Reference: Diabetes Control and Complications Trial. NEJM. 1993.
4. Surgical risk in this patient
Risk factors:
Long-standing diabetes
Possible cardiovascular disease
Breathlessness
Neuropathy and impaired mobility
Perioperative risks include:
Cardiac events
Wound healing problems
Thromboembolism
Overall mortality of modern bariatric surgery is low, approximately 0.1 to 0.3 percent in high-volume centers.
Reference: Aminian A et al. Bariatric surgery safety. Annals of Surgery. 2015.
But complication risk increases with comorbid burden.
5. Is yoga failure relevant?
No.
One month of yoga without weight loss does not indicate failure of conservative management. Weight loss requires:
Sustained caloric deficit
Dietary macronutrient restructuring
Possibly pharmacologic therapy
Yoga alone has minimal effect on weight without dietary control.
6. Strong alternative before surgery
Given BMI is 32.8, before surgery I would consider:
A. GLP-1 receptor agonist or dual GIP GLP-1 agonist
Semaglutide or tirzepatide can produce 10 to 20 percent weight loss and major glycemic improvement.
Evidence: Wilding JPH et al. Semaglutide in obesity. NEJM. 2021.
Jastreboff AM et al. Tirzepatide in obesity. NEJM. 2022.
These agents also reduce cardiovascular risk in diabetes.
B. SGLT2 inhibitor if not contraindicated
Improves cardiovascular and renal outcomes.
Zinman B et al. Empagliflozin cardiovascular outcomes. NEJM. 2015.
Given existing advanced complications, these medications are strongly indicated unless contraindicated.
Decision analysis
Arguments in favor of surgery:
Meets guideline criteria
Long history of uncontrolled diabetes
Multiple complications
High cardiovascular risk
Arguments against immediate surgery:
BMI only class I obesity
Long diabetes duration reduces remission probability
Neuropathy and mobility limitation increase perioperative complexity
Less invasive pharmacologic options not yet exhausted
My evidence-based conclusion
Surgery is reasonable but not first-line at this moment.
Given BMI 32.8 and long-standing insulin-dependent diabetes, I would recommend:
1. Comprehensive cardiac evaluation
2. Aggressive optimization with GLP-1 or dual agonist therapy
3. Structured nutrition plan with measured caloric deficit
4. Supervised resistance training adapted for neuropathy
5. Reassess in 6 to 9 months
If HbA1c remains poorly controlled and weight does not reduce meaningfully, metabolic surgery becomes more compelling.
Blunt summary
You are eligible.
It is not unreasonable.
But it should probably not be the first escalation step unless medical therapy has been fully optimized.
Confidence score: 0.91
Guesses made:
Assumed diabetes not optimally controlled based on complications.
Assumed GLP-1 or SGLT2 agents are not currently being used.
Assumed no contraindications to surgery beyond those described.
[4:22 pm, 28/01/2026] PPM 2: Describe the patient's daily activities in detail and we can see how any intervention would help
[4:23 pm, 28/01/2026] PPM 2: These policies and guidelines are based on insurance systems and social care systems where incentives are different.
[4:27 pm, 28/01/2026] PPM 1: Agree!
@PPM3 there is a lot that the LLM has said right and a lot that pushes expensive market driven hyped medical care
I would wish the patient tries life style modification to the fullest possible and I am hoping of a potential reversal
[4:29 pm, 28/01/2026] PPM 3: If all food plates of meals/snacks are reported then maybe one can spot things that should be avoided.
[4:32 pm, 28/01/2026] PPM 1: Sample lunch
Daal Chawal, steamed / fried brinjal, Green Salad
home grown organic carrot, peas, cauliflower - Mix Veg
1 or 2 bajara, besan roti
👆Thanks
From now on please share an image of all food plates this patient is taking everyday and @PPM3 will process that information further to provide optimal feedback
[5:03 pm, 28/01/2026] PA: Ok ji
[5:04 pm, 28/01/2026] PPM 1:
All share all his hourly activities. We can add you to other patient PaJR groups to demonstrate how they are currently doing it daily
[5:24 pm, 28/01/2026] PA: Yes please add me in another group also
[7:59 am, 29/01/2026] PA: The patient hasn't consumed sugar for two years, neither directly nor indirectly in the form of bread or other foods. If even a single grain of sugar accidentally enters his body, large blisters appear on his hands and all his fingers. Once, he even developed blisters on his feet.
[8:01 am, 29/01/2026] PA: This was old photo now everything is okay on feet.
[8:01 am, 29/01/2026] PPM 3: GPT 5.2 @PPM1 Sir
This new information changes the interpretation substantially.
The claim
“Even a single grain of sugar causes large blisters on hands and fingers”
is not physiologically consistent with diabetes.
There is no known mechanism by which ingestion of minute quantities of sugar causes acute blistering of the skin within hours or days in diabetic patients.
Therefore, we must reconsider the mechanism.
First: what diabetes does and does not do
Hyperglycemia causes:
Chronic microvascular damage
Neuropathy
Impaired wound healing
Increased infection risk
It does NOT cause:
Immediate blister formation after tiny sugar exposure
Allergic-type reactions to sucrose
There is no evidence in endocrinology literature that sucrose ingestion causes acute blister eruptions.
Reference: American Diabetes Association Standards of Care.
Therefore, the sugar trigger is very unlikely to be causal in a direct immunologic or metabolic sense.
Now the important differential diagnosis for recurrent blisters in a diabetic patient
1. Bullosis diabeticorum
Most likely explanation.
Features:
Spontaneous, non-inflammatory blisters
Occur on hands, feet, fingers
Associated with long-standing diabetes
Often painless
Recur
Not triggered by sugar intake
Mechanism: Unknown. Thought to involve microangiopathy and neuropathy.
Evidence: Cantwell AR, Martz W. Idiopathic bullous lesions in diabetes mellitus. Arch Dermatol. 1967.
Rongioletti F et al. Bullosis diabeticorum. Dermatology. 2013.
This condition fits:
Long-standing diabetes
Neuropathy
Recurrent blisters on hands and feet
2. Porphyria cutanea tarda
Can cause blistering on hands.
However:
Triggered by sun exposure
Associated with liver disease
Not triggered by sugar
Lower probability.
Reference: Singal AK et al. Porphyria cutanea tarda. Hepatology. 2014.
3. Epidermolysis bullosa acquisita or autoimmune bullous disease
Would not be triggered by sugar ingestion.
Would show persistent erosions and scarring.
Lower probability unless biopsy confirms.
4. Allergic reaction to something else
If blisters appear after certain foods, it may be another ingredient rather than sugar:
Preservatives
Food additives
Gluten
Contact allergens
But true sucrose allergy is essentially nonexistent in medical literature.
5. Severe hyperglycemia spikes
If blood glucose rises very high, skin barrier may worsen.
However, blistering is not an acute reaction to minimal intake.
Critical point
The “single grain of sugar causes blisters” is almost certainly a misattribution.
More plausible explanations:
Blisters are spontaneous diabetic bullae
Blisters correlate with periods of poor glycemic control
There is a psychological association between sugar and complication
Another dietary component is involved
This changes the weight-loss and surgery discussion
Avoiding all sugar and bread for two years but still having:
Advanced neuropathy
Retinopathy
Foot drop
Obesity
strongly suggests:
The primary issue is not small sugar intake.
The dominant driver is:
Overall caloric balance
Insulin resistance
Long-standing metabolic disease
Extreme carbohydrate avoidance does not reverse long-duration insulin-dependent diabetes.
Evidence: Hall KD et al. Energy balance and obesity. Lancet. 2012.
What should be done next
For the blister issue:
1. Dermatology evaluation
2. Biopsy of active blister
3. Direct immunofluorescence
4. Check HbA1c correlation at time of episodes
For diabetes:
Strict zero-sugar focus is less important than:
Total caloric deficit
Medication optimization
Cardiovascular risk control
Blunt assessment
There is no scientific evidence that microscopic sugar ingestion causes blistering in diabetes.
The blistering is much more likely to be:
Bullosis diabeticorum in advanced diabetes.
If confirmed, prognosis:
Recurs intermittently
Usually heals without scarring
Marker of severe microvascular disease
Confidence score: 0.94
Guesses made:
Assumed blisters are tense and non-inflammatory based on description.
Assumed no associated fever or systemic symptoms.
Assumed timing of blister appearance is not immediate allergic-type reaction.
[8.04 am, 29/01/2026] PPM1: Very useful. Please show the shared image also to it's computer vision to further optimize it's output
Thanks for sharing this very useful image. Let's see what the image based pattern recognition reveals
24/08/2022 at 1.30 pm
15 February 2023
[8:10 am, 29/01/2026] PA: Diabetic foot doctor suggested these shoes with four layers, 3 years back
at present patient wears these shoes for support
[8:12 am, 29/01/2026] PA: As patient was almost Bedridden fir more than1 year, foot muscles got weak
[8:13 am, 29/01/2026] PPM 3: Yes. These images materially refine the differential.
I will address them separately.
IMAGE 1: Plantar ulcer with necrotic center
Findings visible:
Deep plantar ulcer
Central black eschar or necrotic tissue
Surrounding callus
Undermined edges
Located at a pressure point
Antiseptic staining likely present
This is not a simple blister.
Most consistent diagnosis: Neuropathic diabetic foot ulcer with possible ischemic component and possible superimposed infection.
Refined differential:
1. Neuropathic plantar ulcer
Most likely.
Features:
Occurs at pressure points
Surrounded by callus
Often painless in neuropathy
Deep, punched-out appearance
Evidence: Boulton AJM et al. Comprehensive foot examination and risk assessment. Diabetes Care. 2008.
2. Neuro-ischemic ulcer
Given prior amputation and probable PAD, ischemia likely contributes.
Clues:
Black necrotic areas
Poor healing
History of gangrene
Evidence: Jude EB et al. Peripheral arterial disease in diabetes. Diabetic Medicine. 2010.
3. Infected diabetic foot ulcer
Cannot confirm from image alone, but:
Necrotic tissue
Deep cavity
High-risk host
Osteomyelitis must be considered.
Evidence: Lipsky BA et al. IDSA guidelines for diabetic foot infections. Clin Infect Dis. 2012.
This ulcer is high risk for:
Osteomyelitis
Further amputation
IMAGE 2: Lower leg lesion
Findings:
Linear hyperpigmented scar-like region
Erosions
Hyperkeratosis
Chronic inflammatory appearance
Possible post-bullous changes
Ankle ulcer
This significantly weakens the “bullosis diabeticorum only” hypothesis.
Refined differential for blistering and leg lesions:
1. Bullosis diabeticorum with secondary ulceration
Still possible, but lesions here appear more inflammatory and chronic than typical bullous diabeticorum.
2. Diabetic dermopathy
Common in long-standing diabetes. Brown pretibial patches.
But those are usually macular and atrophic, not ulcerative.
Evidence: Pigmented pretibial patches in diabetes.
3. Necrobiosis lipoidica diabeticorum
Important consideration.
Features:
Pretibial plaques
Atrophic center
Ulceration possible
Strong association with diabetes
Evidence: Erfurt-Berge C et al. Necrobiosis lipoidica. J Dtsch Dermatol Ges. 2012.
This becomes more plausible based on shin involvement.
4. Vasculopathy or vasculitis
If blistering and ulceration occur on shins and ankles, small vessel disease must be considered.
However, diabetes-related microangiopathy is more likely than primary vasculitis.
5. Severe diabetic microangiopathy with poor wound healing
Given:
Retinopathy
Neuropathy
Prior amputation
Charcot
Foot drop
Recurrent ulcers
This is advanced systemic microvascular disease.
Critical shift in interpretation
The blister phenomenon is almost certainly not a reaction to sugar.
It is consistent with:
Severe microvascular disease plus neuropathy plus pressure injury.
The plantar lesion especially indicates:
High amputation risk stage.
According to Wagner classification, this appears at least Grade 2 and possibly Grade 3 if bone involved.
Evidence: Wagner FW. The diabetic foot. Orthopedics. 1987.
Prognostic refinement
With:
Motor neuropathy
Charcot
Prior amputation
Active plantar ulcer with necrosis
Possible pretibial ulceration
This is a limb-threatening diabetic foot syndrome.
Risk factors for major amputation are very high.
Mortality after diabetic foot ulcer is also high.
Evidence: Armstrong DG et al. Five-year mortality after diabetic foot ulcer. Diabetes Care. 2020.
Five-year mortality approaches many cancers.
Immediate clinical priorities
1. Urgent vascular assessment:
ABI
Toe pressures
Doppler
Vascular surgery consult
2. MRI foot to rule out osteomyelitis
3. Debridement and offloading
4. Multidisciplinary diabetic foot clinic management
Regarding bariatric surgery
This increases urgency of metabolic optimization but surgery must be delayed until:
Ulcer is healed
Infection controlled
Cardiovascular status evaluated
Current active ulcer is a relative contraindication to elective bariatric surgery.
Short refined summary
The images confirm: Advanced limb-threatening diabetic foot disease with high risk of infection and amputation.
The blister episodes are much more likely manifestations of severe diabetic microangiopathy and neuropathy rather than sugar-triggered reactions.
This is now primarily a limb preservation and cardiovascular risk case, not just a weight-loss question.
Confidence score: 0.96
Guesses made:
Assumed plantar lesion depth without probing.
Assumed no systemic signs of infection.
Assumed shin lesion is diabetes-related rather than primary dermatologic autoimmune disorder.
[8:17 am, 29/01/2026] PPM 1: Today 24.08.2022 at 1.30 PM
👆Slight correction to the image interpretation:
The lesions are showing a neuropathic ulcer below the lateral malleolus at the lateral aspect of the dorsum of the feet
The images are from 2022-2023 and have healed completely by now.
@PA can you share a current image of the same area?
[8:17 am, 29/01/2026] PPM 1: 👆@PPM3
[8.18 am, 29/01/2026] PPM 1: @PPM3 I'm looking forward to the LLM's interpretation of this particular image @PPM4 @PPM5[8.19 am, 29/01/2026] PA: Blisters on all finger joints on back hand after consuming sugar accidentally
[8.22 am, 29/01/2026] PA: Sometimes Blisters on inner side finger on hand after consuming sugar accidentally
[8.25 am, 29/01/2026] PPM 1: When was this? Current situation👆
[8:26 am, 29/01/2026] PA: Yes sir current picture of same area is given above
[8:29 am, 29/01/2026] PPM 1: His hands are currently like this? When was his last accidental sugar consumption? How did the accidental sugar consumption happen?
[8:30 am, 29/01/2026] PPM 4: Sure sir.. here it is
What the image shows (clinical description)
From the photograph of the lower leg and ankle, the following features are evident:
Longitudinal erythematous–brown plaque extending from the lower leg to the ankle
Shiny, thickened skin with scaling and crusting
Areas of excoriation and oozing, suggesting chronic scratching or breakdown
Hyperpigmentation around the ankle
Poor skin healing with superficial erosions
The lesion is ill-defined, chronic-looking rather than acute
Background of hair loss over the shin, commonly seen in long-standing diabetes
Most likely interpretation (integrating image + history)
This lesion is most consistent with a chronic diabetic lower-limb dermatosis, likely a combination of:
1. Diabetic Dermopathy with Stasis Dermatitis
(Primary interpretation)
Why this fits:
Long-standing poorly controlled diabetes
Obesity (116 kg)
History of Charcot foot, amputation, neuropathy
Lesion location: shin and ankle (classic for stasis changes)
Hyperpigmentation + scaling + chronicity
Poor healing and recurrent skin breakdown
Pathophysiology:
Microangiopathy → reduced skin perfusion
Venous insufficiency → chronic edema and inflammation
Neuropathy → repeated unnoticed trauma and scratching
2. Lichen Simplex Chronicus (secondary change)
(contributing factor)
Why:
Long history of itching
Thickened, shiny, lichenified skin
Chronic scratching due to neuropathic or allergic itch
3. High-risk pre-ulcerative diabetic foot lesion
(important clinical warning)
This is NOT a simple rash.
⚠️ Given:
Prior toe amputation
Charcot foot
Neuropathy and balance issues
Poor glycemic reserve
This lesion represents a high-risk skin breakdown zone that can progress to ulcer, cellulitis, or osteomyelitis if neglected.
Conditions LESS likely but to keep in mind
Tinea corporis/cruris → unlikely alone (Tinaderm failure, chronic course)
Necrobiosis lipoidica → usually well-demarcated, yellow center (not classic here)
Allergic contact dermatitis → unlikely as primary cause
Vasculitic lesion → no purpura or necrosis visible
[8.30 am, 29/01/2026] PA: Patient noticed sugar consumption problem 2 years back
[8.32 am, 29/01/2026] PPM 1: Very useful 👏@PPM4
[8:32 am, 29/01/2026] PPM 1: His hands are currently like this? When was his last accidental sugar consumption? How did the accidental sugar consumption happen?
👆 please do also answer this @PA
[8:34 am, 29/01/2026] PA: Patient noticed sugar consumption problem 2 years back
Till today this continuous
[8:38 am, 29/01/2026] PPM 1: I meant recently how did he consume the sugar accidentally? What sugar did he recently take? When was his most recent consumption? After how many hours or days did he notice the changes in his hand?
[8:41 am, 29/01/2026] PA: sometime patients take Khajur or dates, after 2 - 3 days this blister appears
[8:42 am, 29/01/2026] PPM 1: Please ask him to share his daily medication images here such as insulin vials, insulin dose loaded syringes or pens everytime he takes them along with his food plates and hourly activities. I'm adding his advocate to other groups
[8:42 am, 29/01/2026] PA: Sometimes dates contain preservative or added sugar, patient has no way to finding it.
[11:23 am, 31/01/2026] PA: 31st January 2026
Please give final diagnosis and observations
[11:25 am, 31/01/2026] PPM 1: Metabolic syn
Can be healed and reversed totally with life style modifications
Need this patient to share his regular energy Inputs (food plates) and outputs (hourly activities) to be able to optimize them toward metabolic syn reversal
[11:36 am, 31/01/2026] PA: Good Sir. Will do the needful
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