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Mechanistic Deep Dive
Genetics of PA
- KCNJ5 mutation (40% of APA) â affects K channel, causes Ca influx, autonomous aldosterone
- CACNA1D, ATP1A1, ATP2B3, CTNNB1 â somatic mutations
- Familial:
- Type I (GRA): CYP11B1/2 chimeric gene â ACTH-driven aldosterone â glucocorticoid suppresses
- Type II: unknown
- Type III: KCNJ5 germline
- Type IV: CACNA1H
Genetics of Pheo (2024 â Comprehensive Testing)
- 40% germline mutations
- MEN2 (RET): pheo + medullary thyroid + parathyroid
- VHL: pheo + RCC + hemangioblastoma
- NF1: pheo + neurofibromas, café-au-lait
- SDHB/C/D/A/AF2: paragangliomas, often extra-adrenal, malignant risk (SDHB)
- TMEM127, MAX, FH: less common
- Cascade screening of relatives
Recent Trials & Updates
CORAL (2014)
- N = 947 ARAS + HTN
- Stent + OMT vs OMT alone
- No difference in CV events
- Subgroups (FMD, severe HTN, flash edema) excluded
- Established OMT primary, stent for select
PATHWAY-2 (2015) â Confirmed PA Implication
- Many âresistant HTNâ patients respond to spironolactone â suggest PA-like physiology
ENDOCRINE SOCIETY PA Guideline (2024)
- Lower screening threshold
- ARR + plasma aldo > 10 in some patients
- AVS only for surgical candidates
- C-11 metomidate PET emerging
2024 Update on Pheo Genetics (ENDOCRINE SOCIETY)
- ALL patients should have germline testing
- Tailored surveillance based on mutation
- Family screening cascade
Aprocitentan + PA
- May benefit PA-related resistant HTN
- Endothelin pathway also activated
High-Yield Specialist Points
Adrenal Vein Sampling (AVS) Technical
- Bilateral catheterization
- Cortisol + aldosterone in each adrenal vein + IVC
- Cosyntropin stimulation increases reliability
- Lateralization ratio > 4 (with cosyntropin) or > 2 (without)
- Failure rate 5-30% (operator-dependent)
- Refer to high-volume center
Pheo Crisis Management
- α-blockade (phentolamine IV, phenoxybenzamine PO)
- Nicardipine, nitroprusside for HTN
- Volume resuscitation
- Magnesium sulfate (catecholamine antagonist + α-blocker)
- AVOID metoprolol/atenolol alone
OSA in Resistant HTN
- 70%+ have OSA
- CPAP modest BP effect (~ 2 mmHg)
- Best in patients with elevated nocturnal BP
- Address concomitant obesity
NEW: 11β-HSD2 Imaging
- C-11 metomidate PET binds adrenal cortisol synthesis enzymes
- Distinguishes APA from non-functioning adenoma
- Less invasive than AVS
- Emerging since 2021
Mineralocorticoid Excess Beyond PA
- Apparent mineralocorticoid excess (AME):
- 11β-HSD2 deficiency
- Cortisol acts as mineralocorticoid
- Licorice (glycyrrhizic acid) inhibits 11β-HSD2
- Liddle syndrome:
- SCNN1A/B/G gain-of-function â constitutive ENaC
- Low renin + aldo, hypokalemia + HTN
- Amiloride treatment (not MRA)
- Geller syndrome:
- MR mutation activated by progesterone â severe pregnancy HTN
Acromegaly Workup
- IGF-1 (best screen)
- OGTT growth hormone suppression
- Pituitary MRI
- Treatment: surgery, somatostatin analogs (octreotide), pegvisomant (GH receptor antagonist)
MRI Adrenal Characterization
- T1, T2, in/out-of-phase
- Pheo: T2 bright, no fat
- Adenoma: chemical shift loss of signal
- Carcinoma: T2 bright, necrosis
Pearls
- Primary aldosteronism is the most common endocrine cause and very underdiagnosed
- ARR is screening, not diagnostic â confirmatory testing required
- AVS gold standard for lateralization before surgery
- Pheo workup: plasma free metanephrines first; α-block before β-block
- Genetic testing for ALL pheo patients (2024)
- CORAL trial: OMT primary for ARAS; FMD â angioplasty
- OSA + resistant HTN: very high prevalence; treat with CPAP
- C-11 metomidate PET, lutetium-177 DOTATATE = emerging tools