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👉The changes in calcium and phosphate that result from renal hyperparathyroidism may increase calcification of the arteries leading to heart attacks and strokes.

👉Learn more at https://www.atherosclerosis-journal.com/article/S0021-9150(18)31349-2/fulltext

👉CheckYourCalcium (realízate un calcio total en sangre).

👉Para más información: http://www.hiperparatiroidismo.info

#CheckYourCalcium #Arrangoiz #ParathyroidExpert #ParathyroidSurgeon #Hiperparatiroidism #Hipercalcemia #CheckYourCalcium #HeadandNeckSurgeon #MountSinaiMedicalCenter #MSMC #Miami #Mexico #Hyperparathyroidism

• Focused parathyroidectomy:
  • Is the preferred approach in patients who have a solitary lesion:
    • That is imaged conclusively by:
      • Ultrasound, sestamibi, or other appropriate imaging modalities
• If the surgeon is not attempting to visualize all four glands:
  • The use of IOPTH:
    • To determine whether all hyperfunctioning tissue has been removed and to document an appropriate drop in PTH levels after the removal of the suspected gland:
      • Is the standard of care
• The most common criterion used:
  • Is a 50% or greater reduction in the PTH level from the baseline 10 minute after parathyroidectomy
• The best clinical marker of single-gland disease:
  • Is concordant preoperative imaging:
    • In combination with an appropriate correction of IOPTH levels
• Previous neck surgery or lack of concordant imaging on two types of studies:
  • Is not a contraindication to attempting focused parathyroidectomy
• Patients suspected of having multigland disease are managed by four-gland exploration via a smaller incision

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👉Per American Association of Endocrine Surgeons (AAES) Guidelines, parathyroidectomy is recommended for all patients under 50 with a diagnosis of primary hyperparathyroidism, regardless of the presence of symptoms or physical findings – Dr. Rodrigo Arrangoiz

👉https://jamanetwork.com/journals/jamasurgery/fullarticle/2542667

👉For more information: http://www.hiperparatiroidismo.info

#Arrangoiz #ParathyroidExpert #ParathyroidSurgeon #Hyperparathyroidism #Hipercalcemia #HeadandNeckSurgeon #MountSInaiMedicalCenter #MSMC #Miami #Mexico #Hiperparatiroidismo #ExpertoenParatiroides #CirujanodeParatiroides

• Exposure of the Prevertebral Fascia:
  • The first step in identifying the superior gland:
    • Is to locate the inferior thyroid artery (ITA)
  • The ITA is a crucial reference point for the location of the superior parathyroid gland:
    • The superior parathyroid gland is usually found in an area 1 cm cranial to the ITA
  • Once the ITA has been identified, blunt dissection cranial to the artery and directly posterior is performed down to the shiny prevertebral fascia
  • The prevertebral fascia defines the posterior extent of the dissection, and the most posterior location possible for a superior parathyroid gland
• Visual:
  • Although it is tempting to dive straight in and attempt to dissect the first piece of tissue that resembles parathyroid tissue, considerable time and effort can be saved by slowly and deliberately confirming the key landmarks and looking for some of the morphological features described in section “Pearls for Identification of Parathyroid Glands” (published in a previous Blog)
  • The identification of a parathyroid gland begins withcareful visual inspection:
    • Start by looking for a gland or fat pad in a 1 to 2-cm area cranial to the ITA on the posterior surface of the thyroid lobe (Figure 1)
• Digital
  • The superior glands can be found in a number of positions in association with structures from the fourth branchial arch, including:
    • Retropharyngeal
    • Retroesophageal
    • Para-esophageal
    • Adjacent the hyoid bone
  • Further, when a superior gland enlarges:
    • It tends to do so in a posterior and caudal direction and can pass behind the ITA to lie below the inferior gland
  • After careful visual inspection in the area 1 cm cranial tothe ITA, these potential positions are digitally palpatedfor using five maneuvers (Fig. 1.4):
    • The index finger is introduced into the space previously created above the ITA and directly down to the prevertebral fascia / retroesophageal space and then swept along the esophagus to feel in the retroesophageal / retropharyngeal positions
    • The finger is then swung caudally until the finger lies vertically with the tip below the ITA
    • The tissue over the tip of the finger is gently balloted, feeling for an enlarged superior gland to contact the tip of the posterior index finger
    • The finger is then swung back to a horizontal position
    • The finger is withdrawn slowly while the tip remain in contact with the esophagus and trachea, deliberately feeling for the trachea-esophageal groove

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👉Normocalcemic hyperparathyroidism (HPT) is characterized by normal calcium, high PTH levels, and may be a distinct entity that behaves differently than classical HPT.

👉Rodrigo Arrangoiz MS, MD, FACS cirujano de tumores de cabeza y cuello / cirugia endocrina es experto en el manejo del hiperparatiroidismo primario.

👉Introdujo a su país (Mexico) la técnica de exploración bilateral de cuello con valoración de la funcionalidad de las glándulas paratiroides con paratiroidectomia radioguiada:

https://m.youtube.com/watch?v=AgvQmtz1gnA&time_continue=127

👉Su entrenamiento fue el siguiente:

• Cirugia general y gastrointestinal:
• Michigan State University:
• 2004 al 2010• Cirugia oncológica / tumores de cabeza y cuello / cirugia endocrina:
• Fox Chase Cancer Center (Filadelfia):
• 2010 al 2012• Maestria en ciencias (Clinical research for healthprofessionals):
• Drexel University (Filadelfia):
• 2010 al 2012• Cirugia de tumores de cabeza y cuello / cirugiaendocrina
• IFHNOS / Memorial Sloan Kettering Cancer Center:
• 2014 al 2016

#Arrangoiz

#CirugiadeTumoresdeCabezayCuello

#CirugiaEndocrina

#CirugiaOncologica

#HeadandNeckSurgery

#EndocrineSurgery

#SurgicalOncology

#Hyperparathyroidism

#Hiperparatiroidism

#MountSinaiMedicalCenter

#MSMC

#Miami

#Mexico

• Primary hyperparathyroidism (PHPT) is seen in 0.1% to 0.5% of the adult population:
  • It is the most common cause of hypercalcemia (high calcium level) in the general population
  • It is about three times to four times more common in women than men
  • Patients are usually older, with an average age at presentation of 65 years:Most cases are over 45 years
• Learn more at:https://collectedmed.com/index.php/article/article/demo_article_display/7545/83/2/1

#Arrangoiz #ParathyroidSurgeon #ParathyroidExpert #Hyperparathyroidism #PrimaryHyperparathyroidism #CancerSurgeon #EndocrineSurgery #Teacher #Surgeon #HeadandNeckSurgeon #SurgicalOncologist #ParathyroidAdenoma #Hypercalcemia #ElevatedCalciumLevels #Miami #MountSinaiMedicalCenter #MSMC #Mexico #Hialeah

• Primary Hyperparathyroidism (PHPT):
  • Is a common disorder:
    • Affecting 100,000 individuals annually in the United States
  • PHPT occurs in 0.1% to 0.3% of the general population
  • Is more common in women (1:500) than in men (1:2000)
  • Increased PTH production leads to hypercalcemia via:
    • Increased GI absorption of calcium, increased production of vitamin D3, and reduced renal calcium clearance
  • PHPT is characterized by increased parathyroid cell proliferation and PTH secretion:
    • That is independent of calcium levels

• Atypical presentations of PHPT include a spectrum of disturbances in calcium homeostasis, ranging from:
  • Symptomatic severe hypercalcemia (parathyroid crisis) to normocalcemic PHPT
• Laboratory testing often can distinguish atypical presentations of PHPT from other diseases, such as:
  • Malignancy
  • Familial hypocalciuric hypercalcemia (FHH)
  • Secondary hyperparathyroidism
• In PHPT and FHH:
  • The calcium and PTH levels:
    • Are usually simultaneously elevated
• Nonparathyroid-mediated causes of hypercalcemia, including milk-alkali syndrome, granulomatous disease, and hypervitaminosis D:
  • Are associated with suppressed rather than elevated PTH concentrations
• Malignancy:
  • PHPT and malignancy are the most common causes of hypercalcemia:
    • Accounting for more than 90% of the cases:
      • It is usually not difficult to differentiate between them
  • Malignancy is often evident clinically by the time it causes hypercalcemia:
    • Patients with hypercalcemia of malignancy have higher calcium concentrations and are more symptomatic from hypercalcemia than individuals with PHPT
    • However, it may be difficult to differentiate the two problems clinically when the presentation is less typical:
      • As an example, some patients with occult malignancy may present with mild hypercalcemia
      • Alternatively, patients with hyperparathyroidism can occasionally have acute onset of severe, symptomatic hypercalcemia (parathyroid crisis):
        • In these cases, measurement of intact PTH will usually distinguish the two diseases:
          • Intact PTH concentrations are generally:
            • Undetectable or very low in hypercalcemia of malignancy
            • Elevated or high-normal in PHPT
        • It is uncommon for patients with hypercalcemia of malignancy to have elevated PTH levels:
          • But this finding may occur rarely in individuals with:
            • Hypercalcemia of malignancy and concomitant PHPT or
            • In individuals with PTH-secreting tumors:
              • Which are also rare
    • Patients with parathyroid carcinomas:
      • Have severe hypercalcemia and PTH levels in the hundreds to thousands pg/mL range
• Familial hypocalciuric hypercalcemia (FHH):
  • An autosomal dominant disorder characterized by:
    • Longstanding, mild hypercalcemia:
      • Normal or mildly elevated PTH levels
      • Low urinary calcium excretion:
        • Less than 100 mg/24 hours
  • In most cases, it is due to:
    • An inactivating mutation in the calcium-sensing receptor in the parathyroid glands and the kidneys
  • A family history of hypercalcemia:
    • Especially in young children
    • And the absence of symptoms and signs of hypercalcemia are characteristic of this disorder
  • 15% to 20% of patients with FHH:
    • May have a mildly elevated PTH concentration:
      • In these individuals, it may be difficult to distinguish asymptomatic PHPT from FHH:
        • It is important to make this distinction, however, because FHH is a benign inherited condition:
          • That typically does not require parathyroidectomy and will not be cured by it
  • The major feature that distinguishes FHH from PHPT is:
    • A low urine calcium excretion and calcium/creatinine (Ca/Cr) clearance ratio
  • In contrast, in the absence of hypovitaminosis D, most patients with PHPT have either normal or elevated urinary calcium excretion. Because the calcium-sensing receptor is a cation receptor, urinary magnesium excretion parallels calcium excretion and is therefore low in FHH, in contrast with PHPT. Measurement of urinary magnesium is not, however, recommended in the evaluation of PHPT or FHH.
• Drugs — Two drugs deserve special consideration when evaluating a patient for hyperparathyroidism: thiazide diuretics and lithium.
• Thiazide diuretics, including chlorthalidone, reduce urinary calcium excretion and therefore can cause mild hypercalcemia (up to 11.5 mg/dL [2.9 mmol/L). In addition, some patients with hyperparathyroidism may be prescribed thiazides, which may elevate the serum calcium further and thereby unmask the hyperparathyroidism. Following discontinuation of the drug, these individuals remain hypercalcemic, although perhaps less so, and are found to have surgically proven hyperparathyroidism. Thus, if a patient taking a thiazide is found to be hypercalcemic, the drug should be withdrawn, if possible, and calcium and PTH assessed three months later. Persistent hypercalcemia (with elevated or high-normal PTH) after drug withdrawal suggests that the thiazide has unmasked PHPT.
• Lithium decreases parathyroid gland sensitivity to calcium, shifting the calcium-PTH curve to the right. Lithium may also reduce urinary calcium excretion. Lithium is thought to affect calcium-PTH dynamics through an action downstream of the calcium-sensing receptor, but the exact locus is still unknown. Some patients taking lithium develop hypercalcemia and hypocalciuria, and a subset of these individuals have high serum PTH concentrations. If the lithium can be stopped without exacerbating the psychiatric condition, the hypercalcemia may resolve. Following discontinuation, the serum calcium concentration is more likely to normalize if the duration of lithium use had been relatively short (eg, less than a few years), but less likely if it had been longer (eg, more than 10 years).
• Secondary hyperparathyroidism — Occasionally, patients with PHPT have consistently normal total and ionized calcium concentrations (normocalcemic PHPT). These patients typically come to medical attention in the setting of an evaluation for low bone mineral density (BMD). In these cases, it may be difficult to distinguish secondary hyperparathyroidism from early PHPT because the biochemical findings may be similar.
• Secondary hyperparathyroidism occurs when the parathyroid gland appropriately responds to a reduced level of extracellular calcium. PTH concentrations rise, and calcium is mobilized by increasing intestinal absorption (via increase in calcitriol) and by increasing bone resorption. Thus, it is characterized biochemically by elevated PTH and normal or low serum calcium concentrations.
• Secondary hyperparathyroidism may occur in patients with renal insufficiency or failure and impaired calcitriol (1,25 dihydroxyvitamin D) production, as well as in individuals with inadequate calcium intake or absorption, as can occur with vitamin D deficiency or with gastrointestinal diseases causing malabsorption. Assessment of renal function (serum creatinine), vitamin D status (25-hydroxyvitamin D [25(OH)D]), and calcium sufficiency (urinary calcium excretion) may help differentiate normocalcemic primary and secondary hyperparathyroidism. Further assessment and work-up for specific gastrointestinal disorders is generally undertaken only when the clinical suspicion is high.
• Some patients may have more than one condition leading to increased PTH secretion. Co-existing PHPT and vitamin D deficiency is not uncommon. When this occurs, the serum calcium level in the primary hyperparathyroid patient may be reduced (into the normal range in some cases) due to vitamin D deficiency.

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• The renal manifestations implicated with PHPT are:
  • Decreased glomerular filtration rate:
    • Up to 20% of patients with asymptomatic PHPT:
      • Have an estimated glomerular filtration rate (eGFR):
        • Below 60 mL/min/1.73 m²
    • The development of kidney insufficiency in PHPT is related to:
      • The degree and duration of hypercalcemia:
        • Mild hypercalcemia is rarely associated with kidney insufficiency
        • In randomized trials of two to three years duration, there is little evidence that kidney function deteriorates in patients with mild chronic hypercalcemia due to PHPT
  • Hypercalciuria:
    • Hypercalciuria is a contributing factor for stone formation in PHPT
    • Although PTH directly stimulates the distal tubular reabsorption of calcium:
      • This effect is overshadowed by the increase in filtered calcium due to hypercalcemia:
        • Leading to increased urinary calcium excretion in 35% to 40% of patients with PHPT
        • Nephrolithiasis
        • Nephrocalcinosis
        • Impaired urinary concentrating ability sometimes leading to polyuria, polydipsia, nocturia
        • Reduced fractional phosphate reabsorption leading to hypophosphatemia
        • Increased urinary exertion of magnesium
• Nephrolithiasis:
  • Is the universally accepted:
    • Classical kidney manifestation of PHPT
    • It was previously reported in approximately 40% to 80% of patients with PHPT:
      • But now occur only in about 20% to 25% (5% to 55% in some series) of the cases:
        • This wide range likely reflects differences in the methods used for kidney imaging, as well as heterogeneity in PHPT severity
    • Conversely, approximately 5% of patients with nephrolithiasis have hyperparathyroidism
    • Among normocalcemic patients with nephrolithiasis:
      • PHPT should be suspected if the serum calcium concentration is in the high-normal range:
        • Because the hypercalcemia of PHPT may be intermittent and detected only by multiple measurements
    • In one series of 48 patients with nephrolithiasis and PHPT:
      • 30 patients (63%) had serum calcium concentrations between 10.2 and 11 mg/dL
    • The pathophysiology is thought to be related to the filtered load of calcium in the glomerulus:
      • That increases proportionately with the degree of hypercalcemia
    • Most renal stones in patients with PHPT are composed of:
      • Calcium oxalate although slightly alkaline urine may favor the precipitation of calcium phosphate stones
      • Contributing factors for calcium oxalate stone formation in PHPT include:
        • Hypercalciuria
        • Hyperoxaluria
        • Hypocitraturia
        • Hypomagnesuria
        • Dietary risk factors such as a low calcium intake, high oxalate intake, high animal protein intake, high sodium intake, low fluid intake
        • A high serum calcitriol concentration – The high serum calcitriol concentration, caused by PTH stimulation of renal hydroxylation of 25-hydroxyvitamin D (25[OH]D), may contribute to both hypercalciuria and stone formation. Genetic factors such as polymorphisms in calcium-sensing receptor (CaSR) gene have also been described
      • Stone formers are more likely to be hypercalciuric:
        • But less than one-third of the hypercalciuric patients with PHPT actually develop renal stones
      • Hypercalciuria is not a predictor of nephrolithiasis in patients with PHPT and is no longer considered as an indication for surgery:
        • At the present time, it is almost impossible to securely foresee which patients with PHPT will develop nephrolithiasis bases on biochemical analysis of urine
• Nephrocalcinosis:
  • Which refers to renal parenchymal calcification:
    • Is found in less than five percent of patients and is more likely to lead to renal dysfunction
• Subclinical nephrocalcinosis and nephrolithiasis:
  • Are more common in patients with than without hyperparathyroidism
  • In a retrospective review of 271 renal ultrasounds from patients with surgically proven, asymptomatic PHPT:
    • The prevalence of kidney stones on ultrasound performed within six months prior to surgery was significantly higher than in age-matched subjects who had renal ultrasounds for other reasons (7% versus 1.6%)
  • In a cross-sectional analyses of asymptomatic patients with PHPT:
    • Occult urolithiasis or kidney calcifications (nephrolithiasis and / or nephrocalcinosis) were identified in approximately 20% of patients
• Hypertension:
  • The incidence of hypertension is variable:
    • Anywhere between 30% to 50% of patients with PHPT
  • Hypertension appears to be more common in:
    • Older patients and correlates with the magnitude of renal dysfunction
  • In contrast to other symptoms:
    • Is least likely to improve after parathyroidectomy
  • Another plausible explanation of the origin of hypertension in patients with PHPT:
    • Is the synthesis of parathyroid hypertensive factor that triggers an increase in blood pressure
  • The elevated levels of PTH is also linked with the disruption in the renin-angiotensin- aldosterone system

👉Higher rates of hypertension, arrhythmias, left ventricular hypertrophy/dysfunction, and coronary artery disease have been observed in patients with Primary hyperparathyroidism.

👉There is also an increased all-cause and cardiovascular mortality when compared to the general population.

👉Currently, the impact of parathyroidectomy on cardiovascular events and mortality is not well-defined, but some research has suggested a benefit may exist.

👉The Appropriate Diagnosis of Primary Hyperparathyroidism

http://mdpub.net/fulltext/172-1564440673.pdf?1583602321

#Arrangoiz #ParathyroidSurgeon #ParathyroidExpert #CancerSurgeon #EndocrineSurgery #HeadandNeckSurgeon #SurgicalOncologist #MountSinaiMedicalCenter #MSMC #Miami #Mexico