Πρὸς τὸν Φυσικόν

REPRODUCTIVE

• Recurrent pregnancy loss — 5 in the 5–8 week window

  Active

  Oct 2022, May 2023, April 2024 (Aurora — IUP 6w1d, fetal brady 86 bpm; HCG 20→28→96→2013→17; progesterone 14.5 at 3w6d), Aug 2024, Feb 2025. The narrow, consistent window points to thrombotic, immunologic, or endocrine — not tubal or ovulatory. Fibrinogen 583 mg/dL Oct 2024. APS panel largely negative. Genetic thrombophilia never tested. No POC ever sent for chromosomal analysis. Aurora GI symptoms likely unrecognized MCAS flare. Left salpingectomy with pathology-confirmed deep infiltrating endometriosis; one tube remaining.

  “Nobody has put MCAS, coagulation, reproductive immunology, and endometriosis in the same conversation. That's what I'm asking for.”

  Bachmann office visit — Aug 8, 2024 (3rd loss, no RPL workup ordered)

INFLAMMATORY / MCAS

• Severe MCAS flare — August 2025

  Safety concern

  Tue Aug 5: urticaria post hazelnut + interview, on cetirizine 20 BID, famotidine 20 BID, quercetin 500 BID. Diphenhydramine accidentally dosed at 62.5 mg (liquid confusion, brain fog). Spread face/torso Wed. Pinpoint cherry-red dots on legs/arms Thu. Sat: pressed a drinking glass against her own skin and photographed non-blanching petechiae — performed her own diascopy at home because no physician was available. Six days breakthrough on max antihistamines. Used 2-year-expired montelukast (2021 Rx) because no current provider would prescribe it.

  “Liang-Hai told me to go to urgent care. Twice. I went to my Thursday follow-up with Lear instead.”

• Iatrogenic flare exacerbation

  Safety concern

  Dr. Brian Lear (NW Washington Family Medicine), mid-flare follow-up: instructed her to stop antihistamines with active visible petechiae — direct contradiction of standard MCAS management. Charted her as 'doing well.' Earlier Aug 2024: Dr. Brian Bachmann (same practice) charted he did not believe she had MCAS — cited absence of bone marrow biopsy and normal tryptase, despite histamine 171 with tryptase 4 (histamine:tryptase dissociation makes tryptase alone unreliable here). Logged MCAS as 'unclear diagnosis' based on 'patient stating Singulair made things better.' Seven providers denied montelukast despite a written advocacy letter and photographic evidence.

  Bachmann office visit — Aug 8, 2024 (MCAS framed as patient self-report)
• Persistent inflammation, no muscle workup

  Diagnostic gap

  CRP 13.68 mg/L March 2019 — 4.5× ULN, 'high' CV risk category — drawn two weeks into montelukast at Swedish Bainbridge. No CK ordered alongside. No inflammatory myopathy screen. In a patient with congenital hypotonia, exercise intolerance, fatigable weakness, that CRP should have triggered muscle enzymes. It didn't. No CK in 29 years. Not pediatrics, not adult medicine, not any of the eight providers.

CARDIAC

• Tachycardia progression + undisclosed pain episode

  Active gap — partially undisclosed

  Oct–Dec 2025: resting HR changed dramatically over ~3 weeks. HR 164 walking to the bathroom. Zio: 34% sinus tach burden, max 184 bpm at 11:24 PM in bed, structurally normal heart. No PCP to report to. ~Dec 27: episode with spiky pain per pulse at ~213 bpm. Deo has the Zio, the bathroom HR, the general trajectory. The Dec 27 pain episode and the 213 bpm threshold have not been disclosed to Deo.

  “That one stayed in the box longer than it should have.”

• Prolonged QTc — no follow-up

  Diagnostic gap

  QTc 480 ms on a June 2021 EKG. Borderline prolonged. No repeat. No medication interaction review (MCAS protocol meds affect QT). No cardiology referral. Four years in the chart untouched. In the context of 34% sinus tach burden and a 213 bpm pain episode, it matters now. Coordinate with Deo — he may not know it exists in the pre-2023 chart.

NEUROMUSCULAR

• Congenital hypotonia — unresolved

  Foundational

  Didn't walk until ~age 2–2.5. PT age 2–12 for hypotonia and motor delays. Developed her own sign language until age 5 (language delay). Muscle biopsy recommended; mother declined. Hyperreflexia documented on exam. Never reassessed in adult medicine. No adult provider asked about childhood motor delays or connected them to current presentation. Physical signs persist: big toe never touches the ground, asymmetric shoe wear, compensatory postural lump on the back — none documented by any prior provider. POTS, fatigue, exercise intolerance, fatigable weakness may all trace back to an undiagnosed congenital neuromuscular condition present for 29 years without formal characterization.

• Fatigable weakness pattern

  Uncharacterized

  Reproducible: strength adequate first few reps, fails around the 5th, recovers with rest. Present since childhood. Not deconditioning — a fatigable weakness signature consistent with NMJ pathology or metabolic myopathy. Never characterized. No repetitive nerve stimulation, no single-fiber EMG. Never connected to the childhood hypotonia. Pyridostigmine bromide is listed as an allergy in the chart, but the nature of the reaction was never investigated — if it was cholinergic rather than hypersensitivity, that itself is NMJ information.

PSYCHIATRIC / ENDOCRINE

• PMDD with cyclic suicidal ideation

  Active

  Cycle days 25–30: predictable biochemically mediated crash — SI, loss of function, dissociation, brain fog, severe GI cramping. Mira: progesterone drops sharply >50 → <2 on those exact days. Likely driven by allopregnanolone at GABA receptors — neurosteroid disorder, not thought disorder. Resolves when hormones shift. Formally untreated for years. After starting the H1/H2/quercetin protocol, the progesterone curve changed for the first time in her documented history — gentle taper instead of cliff drop — zero PMDD symptoms.

  “If this holds, one protocol treats MCAS, PMDD, and the SI together. That's the outcome measure. That's the win condition.”

CARE HISTORY

• 30-month primary care gap

  Foundational

  Eight providers across the odyssey. Most recent termination: prior PCP said 'nothing you could have done' and then sent a non-compliance termination letter. The list of alternative clinics included two that had already rejected her. 40 cold calls, 40 nos. Seven specifically denied montelukast despite a written advocacy letter and photographic evidence. One charted MCAS as a self-diagnosis. The practice before that folded when the founder withdrew. The one before that (Swedish Bainbridge) closed. Every care relationship she invested in was removed by a system failure she did not cause. Consequences: expired meds without supervision, deferred screening, unmonitored cardiac progression, flares managed alone at home.

• Uncharacterized peripheral edema

  Diagnostic gap

  Bilateral dependent foot erythema with heat exposure, present for years. Observed by nurses. Dismissed or undocumented by physicians. Never characterized as vascular, mast-cell mediator, autonomic, or venous insufficiency. With POTS, MCAS, and fibrinogen 583, persistent bilateral lower-extremity findings are not cosmetic. Never photographed by a provider, never measured, never on a problem list, never worked up.

• Exercise capacity mischaracterized

  Reframe required

  Prior athletic performance — including half-marathon completion — was achieved by overriding autonomic dysfunction, not by cardiovascular reconditioning. Pushed through tach, dizziness, exercise intolerance on pain tolerance, not by training the system into a healthier resting state. Prior performance cannot be used as fitness evidence for labor risk assessment. Pain tolerance is a labor asset; it is not cardiac safety data. The CHOP Modified Dallas Protocol now in progress is designed to generate actual reconditioning data — sequential longitudinal autonomic improvement tracked via the Dragon's Path companion app, physician-ready reports for the September 2026 reestablishment.