Chloroform causes hepatic and renal toxicity in a number of species. In vitro studies have indicated that chloroform can be metabolized by P450 enzymes in the kidney to nephrotoxic intermediate, although direct in vivo evidence for the role of renal P450 in the nephrotoxicity has not been reported. This study was to determine whether chloroform renal toxicity persists in a mouse model with a liver-specific deletion of the P450 reductase (Cpr) gene (liver-Cpr-null). Chloroform-induced renal toxicity and chloroform tissue levels were compared between the liver-Cpr-null and wild-type mice at 24 h following differing doses of chloroform. At a chloroform dose of 150 mg/kg, the levels of blood urea nitrogen (BUN) were five times higher in the exposed group than in the vehicle-treated one for the liver-Cpr-null mice, but they were only slightly higher in the exposed group than in the vehicle-treated group for the wild-type mice. Severe lesions were found in the kidney of the liver-Cpr-null mice, while only mild lesions were found in the wild-type mice. At a chloroform dose of 300 mg/kg, severe kidney lesions were observed in both strains, yet the BUN levels were still higher in the liver-Cpr-null than in the wild-type mice. Higher chloroform levels were found in the tissues of the liver-Cpr-null mice. These findings indicated that loss of hepatic P450-dependent chloroform metabolism does not protect against chloroform-induced renal toxicity, suggesting that renal P450 enzymes play an essential role in chloroform renal toxicity.
Background
While SARS-COV-2 virus infection was reported to cause subacute thyroiditis, the mRNA vaccine for SARS-COV-2 was suspected to induce thyroiditis with thyrotoxicosis.
Case Report
We describe three patients without a history of thyroid disease who presented with symptomatic, biochemical, and radiological evidence of thyroiditis with thyrotoxicosis, 10-20 days after receiving either the Pfizer Bio-NTech or the Moderna COVID-19 mRNA vaccine. All presented with thyrotoxicosis, but with negative thyroid stimulating immunoglobulins for Graves’ disease and no autonomous nodules. Two patients underwent thyroid uptake and scan which confirmed thyroiditis. One patient had significantly increased erythrocyte sedimentation rate (ESR) and Interleukin-6 (IL-6). All had improvement in symptoms with non-steroidal anti-inflammatory drugs (NSAIDs), with one patient eventually requiring steroids for symptom control.
Discussion
The mRNA vaccine for SARS-COV-2 was associated with thyroiditis and presented with thyrotoxicosis. Elevated proinflammatory markers and cytokines after vaccines may play a major role.
Conclusion
Our case series report highlights a possible relationship between the COVID-19 mRNA vaccine and thyroiditis with thyrotoxicosis, which previously not recognized by health providers.
The early symptoms of pancreatic cancer are often very vague. They may precede the diagnosis by years and go unrecognized. This makes pancreatic cancer one of the cancers with the worst survival rates. The progression rate of the early phase might be slower than previously thought. Here, we report a case where symptoms, including thromboembolism and new-onset diabetes mellitus, preceded the diagnosis of pancreatic cancer by 6 years or longer. The awareness of the early symptoms of pancreatic cancer is required for being vigilant and further diagnostic tests. A simple clinical model utilizing certain risk factors and symptoms for pancreatic cancer will help stratify the patients for further screening tests.
Hürthle cell carcinoma (HCC) is a variant of a follicular carcinoma with a tendency to higher frequency of metastases and a lower survival rate. However, intracavitary cardiac metastases from thyroid HCC are extremely rare. We describe the case of a 57-year-old female with thyroid HCC, 5 years after total thyroidectomy, who presented with dyspnea associated with hypoxia and hypotension. The computed tomography angiogram showed extensive pulmonary embolism and a 6-cm right atrial mass while the lower-extremity deep vein thrombosis studies were negative. This patient received a cardiac thrombectomy using cardiopulmonary bypass support. However, intraoperatively, we found out that the mass was from the mediastinum, directly extending into the heart and clearly unresectable since it effaced at least 1/3 of the right atrial wall. The core biopsy of the mass confirmed that it was metastatic poorly differentiated HCC of thyroidal origin. The patient eventually died of respiratory failure due to a massive pulmonary embolism. For cancer patients with unexplained dyspnea, cardiac metastases should be considered regardless of anticoagulation prophylaxis, especially when there is no deep vein thrombosis in the lower limbs. Early recognition of intracavitary cardiac metastases may help in providing prompt treatment and improving the prognosis.
The older age is associated with shorter OS, while disease burden affects OS and PFS in patients with metastatic thyroid cancer. The method of preparation for RAI therapy does not affect the outcome.
Cystic lesions of the pancreas are more frequently recognized due to the widespread use of improved imaging techniques. There are a variety of pancreatic cystic lesions with different clinical presentations and malignant potentials, and their management depends on the type of the cysts. Although the early recognition of a cystic neoplasm with malignant potential provides an opportunity of early surgical treatment, the precise diagnosis of the cystic neoplasm can be a challenge, largely due to the lack of reliable biomarkers of malignant transformation. We report a case of a large, multicystic neoplasm within the body and tail of the pancreas complicated by elevated erythropoietin, which is likely related to the malignant transformation of the pancreatic neoplasm.
Cardiac troponin I (cTnI), a sensitive and specific marker for myocardial injury, has been utilized for the diagnosis of an acute myocardial infarction. However, a variety of clinical scenarios without evidence of acute coronary syndrome (ACS), such as pulmonary embolism, sepsis, renal failure or stress-induced cardiomyopathy may also cause the elevation of cTnI. We described a 55-year-old Hispanic male with abnormal elevations of cTnI without objective evidence of myocardial infarction damage. We hypothesized that his long-term chronic alcoholic intoxication is causing the myocardial injury, responsive for cTnI elevation. We proposed that alcohol-induced early myocardial damage, independent of alcoholic cardiomyopathy, might be related to alcohol-induced cTnI elevation in this patient. This is the first report suggesting that the abnormal elevations of cTnI can be seen in patients with chronic alcoholism without objective evidence of myocardial infarction.
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