Patient Summary - Viacheslav Kim

Goals for This Visit

Establish baseline primary care in the U.S.
Review my chronic breathing/chest symptoms after an old injury
Evaluate chronic musculoskeletal issues
Assess intermittent elevated blood pressure and cardiovascular risk given family history
Follow up on prior liver enzyme / fatty liver history
Discuss chronic skin and scalp issues

1. Breathing / Right Chest Symptoms

Intermittent difficulty taking a full breath; restriction/tightness in right chest / lower rib / diaphragm area since teenage years
Traumatic chest injury at age ~14 during martial arts → diagnosed traumatic pleuritis with fluid accumulation → drainage by thoracic surgery
Was told the injury/procedure might lead to future chest wall or diaphragm issues
Continues to feel restricted with deep inhalation; frequent need to stretch or reposition for relief
Stretching/movement sometimes causes popping sensations with temporary relief
Osteopathic provider noted possible asymmetry or inward displacement of a rib/chest wall structure on the right side
March 2026 chest X-ray: small right pleural effusion identified — provider suspects possible relation to old traumatic injury; referred to UWMC Pulmonary Medicine for follow-up

2. Musculoskeletal / Spine / Foot Issues

Flat feet since childhood; more recently developed plantar fasciitis
Chronic back tightness/discomfort with frequent need to stretch/mobilize; popping sensations with temporary relief
History of manual therapy / osteopathic treatment

Bicycle accident at age ~17 (mountain terrain)

Impact to head, left shoulder/arm, left hip/thigh
Brief loss of consciousness / concussion; no full imaging or formal treatment at the time
Later developed pain/spasm around left shoulder blade / left shoulder; at one point left shoulder seemed to roll forward (improved since)
Ongoing discomfort/tension in left thigh/hip area

Prior spine imaging findings

Old compression injury/deformity in the spine
Multiple disc protrusions in cervical, thoracic, and lumbar spine

Childhood fracture history

Approximately 12 fractures (arms/legs/extremities) by 9th grade
Attributed at the time to rapid growth and poor coordination

3. Blood Pressure / Cardiovascular Concerns

Intermittent elevated BP, sometimes ~140/100
Aerobic exercise (especially running) improves both BP and pulse
Intermittent discomfort/poking sensations in chest/heart area
Strong family history of hypertension and heart disease (see Family History below)

4. Liver History

At age ~24: fatty liver / hepatic steatosis with elevated ALT/AST
Hepatitis A, B, and C testing reportedly negative (Hep C re-confirmed nonreactive March 2026)
March 2026 labs: ALT 36, AST 23 — both within normal limits (improved from prior)

5. Skin / Scalp Issues

Chronic small bumps/pimples on backs of upper arms since adolescence (consistent with keratosis pilaris)
Chronic scalp scaling/flaking
Prior scalp culture positive for Staphylococcus aureus

6. Other History

Previously had tinnitus — now much less noticeable or possibly resolved
Sedentary work with prolonged sitting; may be worsening musculoskeletal symptoms

Recent Results (March 23, 2026 — UW Medicine)

PCP: Harrison Strom Dellinger, ARNP — UW Medicine Primary Care, Family Medicine at South Lake Union
View original lab report (PDF)

Chest X-ray (2 views)

Finding: Small right pleural effusion. Lungs clear. No pneumothorax. Heart and mediastinum unremarkable. Bones: no acute or suspicious abnormality.

Provider note: “I am seeing a small right pleural effusion or area near the lung that is filled with liquid. I do wonder if this is a change from the traumatic injury you had when you were younger. Lets plan to follow up with pulmonology.”

Referred to: UWMC Pulmonary Medicine (206-598-4615)

Screening

Test	Result
Hepatitis C Antibody	Nonreactive	✓
HIV Antigen and Antibody	Nonreactive	✓

CBC

Test	Value	Ref Range
WBC	5.98	4.3 – 10.0 10*3/uL
RBC	5.52	4.40 – 5.60 10*6/uL
Hemoglobin	16.9	13.0 – 18.0 g/dL
Hematocrit	51 (H)	38.0 – 50.0 %	↑
MCV	92	81 – 98 fL
MCH	30.6	27.3 – 33.6 pg
MCHC	33.4	32.2 – 36.5 g/dL
Platelet Count	232	150 – 400 10*3/uL
RDW-CV	11.6	11.0 – 14.5 %

Comprehensive Metabolic Panel

Test	Value	Ref Range
Sodium	141	135 – 145 meq/L
Potassium	3.7	3.6 – 5.2 meq/L	lower end
Chloride	101	98 – 108 meq/L
CO2, Total	28	22 – 32 meq/L
Anion Gap	12	4 – 12
Glucose	90	62 – 125 mg/dL
BUN	12	8 – 21 mg/dL
Creatinine	0.95	0.51 – 1.18 mg/dL
Total Protein	8.3 (H)	6.0 – 8.2 g/dL	↑
Albumin	5.2	3.5 – 5.2 g/dL
Total Bilirubin	0.5	0.2 – 1.3 mg/dL
Calcium	9.5	8.9 – 10.2 mg/dL
AST	23	9 – 38 U/L
Alk Phos	52	36 – 122 U/L
ALT	36	10 – 64 U/L
eGFR (CKD-EPI 2021)	>60	>59 mL/min/1.73m²

Thyroid

Test	Value	Ref Range
TSH	3.086	0.400 – 5.000 u[IU]/mL

Lipid Panel

Test	Value	Ref Range
Total Cholesterol	190	<210 mg/dL
Triglycerides	149	0 – 175 mg/dL	upper end
HDL Cholesterol	40	>39 mg/dL	borderline low
Non-HDL Cholesterol	150	<190 mg/dL
LDL Cholesterol (calc.)	125	<160 mg/dL	may be above target given family hx
Cholesterol/HDL Ratio	4.8		>4.0 = elevated risk
TG/HDL Ratio (calculated)	3.7		>3.5 = insulin resistance marker

Additional Labs

Test	Value	Ref Range
Uric Acid	6.8	3.9 – 7.6 mg/dL	at crystallization threshold (6.8)
Apolipoprotein B	137	63 – 152 mg/dL	>130 per some CV guidelines
Ferritin	267 (H)	20 – 230 ng/mL	↑

Summary of notable findings

Right pleural effusion — possibly related to old traumatic chest injury at age 14; pulmonology referral initiated
Hematocrit 51, Total Protein 8.3, Ferritin 267 — all three elevated simultaneously. This pattern can reflect mild dehydration at the time of fasting blood draw (hemoconcentration raises all three proportionally). May be worth rechecking after adequate hydration to distinguish from other causes.
Ferritin 267 (above range) — genomic data shows all three HFE hemochromatosis mutations (C282Y, H63D, S65C) are absent, making genetic hemochromatosis unlikely. In HFE-negative men, elevated ferritin is most commonly associated with metabolic/inflammatory causes. Transferrin saturation could help clarify.
Lipid pattern: ApoB 137, TG 149, HDL 40, TG/HDL ratio 3.7 — these form a consistent pattern. ApoB at 137 is within the lab reference range but exceeds the ESC/EAS threshold of 130 mg/dL for risk-enhancing classification. A TG/HDL ratio >3.5 is a recognized surrogate marker for insulin resistance. The combination of elevated triglycerides, borderline-low HDL, and high ApoB is sometimes called atherogenic dyslipidemia.
Uric acid 6.8 — within lab reference range, but 6.8 mg/dL is the concentration at which urate crystals begin to form. Given the family history of gout with tophi and the ABCG2 homozygous genotype (see genomic appendix), this may be worth monitoring over time.
ALT 36, AST 23 — both normal; improvement from prior elevated liver enzymes at age 24
Hep C, HIV — both nonreactive
TSH 3.086 — within normal range. Genomic data shows a homozygous thyroid cancer risk variant (see genomic appendix) that may be relevant to thyroid monitoring decisions.
Glucose 90, kidney function, electrolytes — all normal

Tests not yet performed that may be relevant

These were not part of the initial panel but may provide additional context given the results above.

Serum 25(OH)D — not tested; patient lives in Seattle (47.6°N, limited UVB October–March) and carries vitamin D pathway risk genotypes (see genomic appendix)
Fasting insulin / HOMA-IR — could help clarify the insulin resistance question raised by the TG/HDL ratio of 3.7
HbA1c — metabolic screening; complements the fasting glucose of 90
hs-CRP — cardiovascular risk stratification; could also help contextualize the ferritin elevation (inflammation vs. iron stores)
Transferrin saturation — to clarify ferritin elevation in the absence of HFE mutations
Full thyroid panel (FT4, FT3, TPO/TgAb) — if thyroid warrants further evaluation given the genomic finding

Family History

Father (deceased)

Significant heart disease
Hypertension
Gout with tophi
Cardiac disease was a major factor

Paternal relatives

Multiple family members with high blood pressure
Multiple cardiac events/deaths

Current Supplements

Supplement	Notes
Creatine	May affect serum creatinine lab values
Fiber (psyllium + ground flaxseed)
B vitamins
TMG (trimethylglycine)	Methyl donor
GlyNAC (glycine + N-acetylcysteine)	Glutathione precursor

Pharmacogenomic Profile

These findings may be relevant if medications in these categories are considered.

Statin considerations — dual transporter variants

Two transporter gene variants (SLCO1B1 *1/*5 and ABCG2 Q141K homozygous) may affect how several statins are metabolized. Per CPIC 2022 guidelines, some statins carry higher myopathy risk in this genotype profile:

Statin	Consideration	CPIC 2022
Pravastatin	Least affected by these transporters	Strong
Fluvastatin	Least affected by these transporters	Strong
Rosuvastatin	ABCG2 variant may approximately double blood levels; ≤10 mg suggested	Moderate
Atorvastatin	Moderate SLCO1B1 sensitivity; ≤40 mg suggested	Moderate
Pitavastatin	Limited by SLCO1B1; ≤2 mg suggested	Moderate
Simvastatin	Highest myopathy risk with SLCO1B1 *5; ≤20 mg or consider alternatives	Strong

Warfarin sensitivity

VKORC1 −1639 A/A (rs9923231 T/T) + CYP4F2 *1/*3 (rs2108622 C/T)

This genotype is associated with significantly lower warfarin requirements (~3–4.4 mg/day vs. 5–7 mg standard). If warfarin is ever considered, the IWPC pharmacogenetic dosing algorithm may be helpful. CPIC Strong, 2017.

Clopidogrel — intermediate metabolizer

CYP2C19 *1/*2 (rs4244285 G/A)

This genotype reduces active metabolite formation by ~30%. CPIC 2022 guidelines note that prasugrel or ticagrelor may be more effective alternatives for ACS/PCI indications. Standard PPI dosing is unaffected.

CYP3A5 expressor

rs776746 T/C • *1/*3

If tacrolimus is ever needed, this genotype is associated with faster metabolism and potentially higher starting doses. CPIC Strong, 2015.

CYP2D6 — normal metabolizer

rs1065852 G/A • *1/*10 (AS 1.25)

Reclassified as normal metabolizer per 2019 CPIC consensus. Standard dosing expected for codeine, tramadol, beta-blockers, SSRIs.

Cardiovascular Genomic Context

These variants provide background context for the family history and blood pressure findings.

Uric acid / gout risk Elevated risk

ABCG2 Q141K homozygous (rs2231142 T/T) — this is the primary renal/intestinal urate transporter. Homozygous carriers have substantially reduced urate excretion, with published gout odds ratios of 3.1–4.3×.
GCKR P446L homozygous (rs1260326 C/C) — may increase uric acid production via hepatic de novo lipogenesis.
Combined with father's gout with tophi, this may warrant baseline uric acid screening. ABCG2 Q141K may also reduce allopurinol efficacy (DPWG) and increase rosuvastatin blood levels.

Blood pressure context

AGT M235T (rs699 het) — modestly associated with higher angiotensinogen levels (hypertension OR 1.08 in meta-analysis of 45,267). May suggest RAAS pathway involvement.
ADRB2 Gln27Gln (rs1042714 C/C hom) — associated with exaggerated sympathetic activity, but exercise training specifically normalizes this in Gln27 carriers. Consistent with the blood pressure improvement I notice with running.
NOS3 Glu298 (rs1799983 G/G) — wild-type. Normal endothelial nitric oxide production.

Lipid and cardiovascular protective findings Favorable

APOE ε3/ε3 — neutral cardiovascular risk, no ε4 allele.
PON1 192R/R (rs662 C/C hom) — highest paraoxonase enzymatic activity; associated with protection against LDL oxidation.
IL-6 −174 G/G (rs1800795) — reference genotype associated with lower IL-6 and CRP levels. No IL-6-driven inflammatory risk.
LIPC −514 C/T (rs1800588 het) — associated with modestly higher HDL, particularly with exercise.
TRIB1 T/T (rs2954029) — reference/favorable genotype for lipids.
Factor V Leiden (rs6025) and Prothrombin G20210A (rs1799963) — both absent.

Liver & Metabolic Genomic Context

NAFLD genetic risk — low Favorable

PNPLA3 I148M (rs738409) and TM6SF2 (rs58542926) — both absent (reference genotype). These are the two strongest genetic predictors of NAFLD progression and fibrosis risk. Their absence suggests that the prior steatosis at age 24 was likely lifestyle-driven and potentially reversible.

GCKR P446L — metabolic modifier

rs1260326 C/C • homozygous

Associated with increased hepatic glucose uptake, higher triglycerides, and paradoxically lower fasting glucose. May have contributed to prior steatosis. Carriers reportedly respond well to lifestyle intervention.

Obesity-related variants Informational

FTO (rs9939609, rs1558902, rs9930506 — all heterozygous) — each allele raises BMI ~0.3–0.4 kg/m² (obesity OR ~1.2). A meta-analysis of 218,166 individuals found that physical activity attenuates FTO-mediated risk by ~30%.
MC4R (rs17782313 T/C het) — associated with increased appetite drive (obesity OR 1.32). Sedentary work may amplify this effect.
These variants are common and modest in effect, but exercise appears to be an effective countermeasure for both.

Bone Health & Vitamin D Genomic Context

Potentially relevant to the ~12 childhood fractures.

Vitamin D pathway — multiple variants suggest lower levels

CYP2R1 (rs10741657 G/G hom) — the primary hepatic 25-hydroxylase. GG is the GWAS risk genotype, associated with significantly lower 25(OH)D (meta-analysis of 52,417 participants).
CYP24A1 (rs6013897 A/A hom) — increased vitamin D catabolism. Combined with CYP2R1, this creates reduced activation plus increased degradation.
NADSYN1/DHCR7 (rs12785878 T/T hom) — favorable for cutaneous vitamin D synthesis (partially offsetting).
GC (rs7041 het) and VDR FokI (rs2228570 het) — intermediate effects.

The combined genetic profile may predict ~3–5 ng/mL lower 25(OH)D than average, which could contribute to suboptimal bone mineralization during adolescent growth. COL1A1 Sp1 polymorphism (rs1800012) is absent, making collagen-mediated bone quality defects unlikely.

Joint & connective tissue

GDF5 (rs143383 A/A hom) — associated with reduced GDF5 expression and increased osteoarthritis risk.
COL5A1 (rs12722 C/T het) — collagen type V variant; research links it to altered connective tissue properties and tendon/ligament injury susceptibility.

Thyroid Genomic Context

FOXE1/PTCSC2 region — thyroid cancer risk variant Elevated risk

rs965513 G/G • homozygous alt • ClinVar: “Established risk allele” for nonmedullary thyroid cancer

This variant resides in a regulatory region affecting FOXE1 (thyroid transcription factor 2) expression. A meta-analysis of 23 studies (n=163,136) found homozygous carriers have an odds ratio of approximately 2.8 for nonmedullary thyroid cancer. About 11% of the general population carries this homozygous genotype.

Some research also suggests that higher TSH levels within the normal range are independently associated with increased thyroid malignancy risk. The patient’s TSH of 3.086 is within the standard reference range but above the level found in 95% of disease-free individuals (<2.5 per NACB data).

This context may be relevant when considering baseline thyroid evaluation (ultrasound, full thyroid panel including TPO/TgAb) and long-term monitoring frequency.

Blood Work & Genomic Integration

How some of the lab findings connect to the genomic data.

Lipid pattern and insulin resistance context

The combination of TG 149, HDL 40, ApoB 137, and a TG/HDL ratio of 3.7 is consistent with a pattern sometimes called atherogenic dyslipidemia, which is associated with insulin resistance. The GCKR P446L homozygous genotype increases hepatic glucose uptake and de novo lipogenesis, which can elevate triglycerides and drive hepatic VLDL production. The FTO and MC4R heterozygous variants contribute modest metabolic predisposition that is amplified by sedentary occupation.

Fasting insulin and HbA1c could help quantify the degree of insulin resistance suggested by this pattern.

Ferritin in the absence of hemochromatosis

Ferritin at 267 with all three HFE mutations absent (C282Y, H63D, S65C confirmed absent in genomic data) makes genetic hemochromatosis very unlikely. In HFE-negative individuals, elevated ferritin is most commonly seen with metabolic syndrome/insulin resistance (“dysmetabolic hyperferritinemia”), inflammation, or liver disease. Given the TG/HDL ratio of 3.7 and the GCKR genotype, a metabolic cause is plausible. Transferrin saturation and hs-CRP could help differentiate.

Vitamin D was not tested

The patient lives in Seattle (47.6°N latitude), where UVB is insufficient for cutaneous vitamin D synthesis roughly October through March. The genomic profile includes CYP2R1 G/G (reduced 25-hydroxylation) and CYP24A1 A/A (increased catabolism), plus GC rs7041 het (reduced vitamin D binding protein), which together may predict lower 25(OH)D levels. Additionally, the GC variant can reduce response to standard supplementation doses. Serum 25(OH)D testing could be informative.

Skin / Scalp Genomic Context

VDR FokI (het) — VDR regulates cathelicidin/LL-37, a key antimicrobial peptide in skin that is bactericidal against S. aureus. Vitamin D status directly affects this pathway.
IL-10 −819 C/T (rs1800871 het) — intermediate anti-inflammatory cytokine capacity. Associated with susceptibility to S. aureus skin infections in some studies.
The vitamin D pathway variants described above may also affect skin antimicrobial defense. Vitamin D optimization could potentially benefit both bone health and skin barrier function.

Methylation Profile

MTHFR Normal

C677T (rs1801133): wild-type — full enzyme activity
A1298C (rs1801131): T/G het — ~85% activity, clinically insignificant alone

COMT Val158Met Intermediate

rs4680: G/A het
Intermediate catecholamine clearance.

MTRR (rs1801394 A/G het) — mildly reduced B12 recycling; clinically insignificant in isolation.

Supplement Genomic Context

For reference — how the current supplement stack relates to the genomic findings.

Supplement	Genomic context
Creatine	Safe with liver history (NHANES n=5,957). Spares ~40% of SAM methylation demand.
Psyllium	Meta-analysis of 28 RCTs: ~13 mg/dL LDL reduction. May be particularly valuable if statin options are limited.
Ground flaxseed	ALA omega-3; some evidence that omega-3 modulates GCKR impact on triglycerides.
B vitamins	MTHFR C677T is wild-type, so standard folic acid is fully metabolized. Standard doses appear adequate.
TMG	Provides methyl groups via BHMT pathway, complementary to folate cycle. Pilot data for hepatoprotective effects.
GlyNAC	NAC reduces ALT in NAFLD per multiple RCTs. Glutathione precursor.
Vitamin D3 (not currently taking)	Given the CYP2R1/CYP24A1 genotype, standard doses (600–1,000 IU) may be insufficient. Higher doses (2,000–4,000 IU/day) are sometimes suggested for this profile, with a target of 40–60 ng/mL.

Possible Considerations for Follow-up

These are not prescriptive — just context that might inform follow-up decisions at your discretion. Several baseline labs have already been completed (see results above).

Already completed (March 2026)

CBC, CMP, lipid panel, ApoB, uric acid, ferritin, TSH, Hep C, HIV
Chest X-ray → pulmonology referral initiated

Not yet tested — potentially informative given results + genomics

Serum 25(OH)D — vitamin D pathway risk genotypes + Seattle latitude + 12 childhood fractures + skin findings
Fasting insulin / HOMA-IR — to quantify insulin resistance suggested by TG/HDL ratio of 3.7
HbA1c — metabolic screening complement to fasting glucose of 90
hs-CRP — cardiovascular risk stratification + may help contextualize ferritin elevation
Transferrin saturation — to clarify ferritin 267 in the absence of HFE mutations
Full thyroid panel (FT4, FT3, TPO/TgAb) — given homozygous thyroid cancer risk variant + TSH 3.086
Thyroid ultrasound — baseline imaging given ~2.8× genetic thyroid cancer risk (if clinically appropriate)
Fasting homocysteine — one-time baseline given mild MTRR variant
Calcium, phosphate, intact PTH — bone mineral metabolism (ALP already drawn: 52, normal)
DEXA scan — 12 childhood fractures + vitamin D pathway variants (if clinically appropriate)
Ambulatory/home BP monitoring — to confirm intermittent readings of ~140/100

Reassuring Findings

APOE ε3/ε3 (no ε4) • PNPLA3 + TM6SF2 reference (low NAFLD-progression risk) • NOS3 Glu298 wild-type (normal eNOS/NO) • MTHFR C677T wild-type • PON1 RR (highest paraoxonase activity) • TRIB1 TT (favorable lipids) • IL-6 −174 GG (no inflammatory risk from this locus) • Factor V Leiden + Prothrombin absent • COL1A1 Sp1 absent • CYP2D6 normal metabolizer • CASR normal