Daniel Repplinger

Can Biochemical Abnormalities Predict Symptomatology in Patients with Primary Hyperparathyroidism

BACKGROUND Primary hyperparathyroidism presents with a myriad of symptoms, which range in severity. The cause of these symptoms is not well understood. We sought to determine if the severity of preoperative biochemical abnormalities (calcium, parathyroid hormone, vitamin D levels) correlated with symptomatology in patients undergoing surgical treatment for primary hyperparathyroidism. STUDY DESIGN Over 15 months, 229 consecutive patients with primary hyperparathyroidism completed a symptom questionnaire before parathyroidectomy. The symptom profiles of patients with significant hypercalcemia at initial presentation (≥11.2 mg/dL) and those with baseline calcium levels (<11.2 mg/dL) were compared. The patients were also categorized based on parathyroid hormone (< or ≥130 pg/mL) and vitamin D (< or ≥30 ng/mL) and analyzed in a similar manner. RESULTS Seventy-eight patients (34%) had a baseline calcium ≥11.2 mg/dL, but compared with patients with calcium <11.2 mg/dL, only the incidence of nephrolithiasis was more common in those patients with significant hypercalcemia (18% vs 9%, p = 0.04). Conversely, depression, bone or joint pain, and constipation were all significantly more common in patients with calcium <11.2mg/dL (p = 0.006, 0.001, and 0.031, respectively). Patients analyzed based on parathyroid hormone and vitamin D levels showed no significant difference in symptom presentation. CONCLUSIONS These data indicate that the degree of parathyroid hormone elevation and the presence of vitamin D deficiency do not correlate with the presence of symptoms in patients with primary hyperparathyroidism. Significant hypercalcemia was associated with nephrolithiasis, but interestingly, patients with milder hypercalcemia had significantly more depression, bone or joint pain, and constipation, suggesting that these symptoms are likely not mediated by hypercalcemia.

Neurocognitive dysfunction: a predictor of parathyroid hyperplasia.

BACKGROUND To determine whether a symptomatic presentation was associated with parathyroid hyperplasia, we retrospectively examined pre-operative symptom profiles of patients who underwent parathyroidectomy. METHODS From October 2007 to July 2008, 111 patients with primary hyperparathyroidism completed a preoperative symptom questionnaire prior to parathyroidectomy. The symptom profiles of patients with and without hyperplasia were compared. RESULTS Neurocognitive symptoms occurred in 51.4% of patients. Patients with 1 neurocognitive symptom had a 25% risk of parathyroid hyperplasia. Additional neurocognitive symptoms increased the risk of hyperplasia linearly, with hyperplasia occurring in 38% of patients reporting 2 neurocognitive symptoms (P < .001) and 61% of patients reporting 3 or more of these symptoms (P < .001). A negative sestamibi scan was associated with a 33% risk of hyperplasia. Coupled with at least 1 neurocognitive symptom, the risk of hyperplasia was 53.3% (P < .001). Of patients with 3 or more neurocognitive symptoms and a negative localizing scan, 100% were found to have parathyroid hyperplasia (P < .001). CONCLUSION The presence of neurocognitive dysfunction in a patient with hyperparathyroidism may be used as a predictor of hyperplastic disease. Three or more of these symptoms, coupled with a negative sestamibi scan, was 100% predictive of parathyroid hyperplasia in our cohort.

Lack of significant bleeding despite large acute rivaroxaban overdose confirmed with whole blood concentrations.

Abstract Background: Since intentional overdose with rivaroxaban is expected to lead to significant coagulopathy and bleeding, prophylactic reversal has been suggested. We report a single massive ingestion confirmed by a blood concentration that was managed with expectant therapy alone. Case report: A 71-year-old man with atrial fibrillation, aortic valve replacement, and congestive heart failure presented to the emergency department after an intentional ingestion of 97 (1940 mg total) rivaroxaban tablets in a suicide attempt. Initial laboratories revealed: PT, 60.2 s; INR 7.2; aPTT, 55.7 s; BUN 28 mg/dL; and creatinine 1.2 mg/dL. A whole-blood rivaroxaban concentration obtained on hospital-day three was 160 ng/mL. The patient was admitted for continued observation and the coagulation markers trended downward with no major bleeding events. No reversal agents or blood products were given during his hospitalization. Conclusion: In the setting of a single, acute rivaroxaban overdose, with normal renal function, and no active bleeding, conservative therapy alone may be sufficient.

Electrophysiologic similarities of overdose between digoxin and bufadienolides found in a Chinese aphrodisiac

Classically derived from toad venom, bufadienolides are a group of cardioactive steroids with properties similar to digoxin. Some traditional Chinese medications, including several aphrodisiacs, contain bufadienolides. Owing to their physiologic similarities to digoxin, bufadienolides have been shown to produce a toxic profile similar to that of digoxin and there have been multiple case reports of the use of these aphrodisiacs resulting in death. This report will describe a case that illustrates the electrophysiologic similarities between bufadienolide toxicity and digoxin toxicity as well as the treatment of bufadienolide toxicity.

Troponin elevations and organophosphate poisoning: Direct cardiac injury or demand ischemia?

We have read with interest the study by Y.S. Cha and colleagues investigating organophosphate (OP) poisoning and myocardial injury. 1 The authors conclude that OP poisoning can cause direct myocardial injury during the acute phase of poisoning as well as that trending serum troponin I concentration may be needed in severe OP poisoning. However, these data presented from this retrospective study raise some questions as to the author ’ s interpretation. Based on 34% of their subjects having elevated troponin I concentration, the authors conclude that severe OP poisoning can cause direct myocardial injury. The highest troponin I level reached was 2.33 ng/ml and the mean elevation was only 0.305 ng/ml. These seemingly trivial elevations make it diffi cult to determine the relationship of OP poisoning as a cause of direct myocardial injury. Rather, these elevations could be related to demand ischemia and “ troponin leak ” in severely poisoned patients. Furthermore, were there any overt signs of cardiac injury or clinical signifi cance to this troponin elevation? Only 26% of these patients with elevated troponins experienced hypotension, and there was no statistical difference in B-type natriuretic peptide (BNP) concentrations, suggesting that the patients did not have acute heart failure. The patients found to have troponin I elevations were different in a number of pertinent demographic variables. Namely, those patients with troponin I elevations were older, had a lower initial Glasgow Coma Scale (GCS), higher Namba classifi cation, a higher incidence of mechanical ventilation, and higher rates of pneumonia. These patient discrepancies would simply indicate that a more severely ill patient population is more likely to have elevations in troponin I. Multiple studies have demonstrated elevated troponin I levels in critically ill patients without acute coronary syndromes (ACS), suggesting that sepsis and other systemic infl ammatory response syndrome (SIRS)-related disease processes account for these elevations. 2 – 4 Here, the authors found no statistical signifi cance in the difference between the two groups with respect to sepsis; however, they did not discuss how they controlled for this specifi c variable. Also, only 18.2% of patients had troponin I elevations on initial presentation suggesting that other confounding variables while in hospital may have attributed to the remainder of troponin I elevations. Moreover, previous studies have shown that mechanical ventilation alone increases mortality in critically ill patients with suggested myocardial injury. 5

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