Too young for an acquired cardiomyopathy? Cobalt metallosis as a cardiac amyloidosis mimicker.

Metallosis with subsequent cardiac involvement is a possible long-term complication of hip arthroplasty. We report the case of a young female referred to our centre for the suspicion of cardiac amyloidosis presenting with low electrocardiogram voltage, left ventricular hypertrophy, pericardial effusion, and global and longitudinal systolic impairment with apical sparing pattern. Her medical history was remarkable for arthroplasty in the context of congenital hip dysplasia. Two years prior to presentation, she underwent revision surgery for prosthesis malfunction, and tissue metallosis was initially documented. At the current presentation, cobalt metallosis was confirmed, as the circulating cobalt and chromium levels were severely elevated. The accurate diagnosis prompted the removal of the cobalt source with extensive tissue debridement and the use of chelating agents. Reversal of the cardiac abnormalities occurred as the circulating cobalt levels returned to normal.

Toxic-Induced Nonthyroidal Illness Syndrome Induced by Acute Low-Dose Pesticides Exposure-Preliminary In Vivo Study.

BACKGROUND AND OBJECTIVES: Conditions such as trauma, burns, sepsis, or acute intoxications have considerable consequences on the endocrine status, causing "sick euthyroid syndrome". Organophosphate exposure may induce an increase in acetylcholine levels, thus altering the thyroid's hormonal status. The present study aims to identify the effects of acetylcholinesterase inhibition on thyroid hormones. MATERIAL AND METHODS: A prospective experimental study was conducted on twenty Wistar rats. Blood samples were drawn to set baseline values for thyroid-stimulating hormone (TSH), triiodothyronine (T3), and thyroxine (T4). Chlorpyrifos 0.1 mg/kg was administered by oral gavage to induce acetyl-cholinesterase inhibition. After exhibiting cholinergic symptoms, blood samples were collected to assess levels of cholinesterase and thyroid hormones using ELISA. RESULTS: Butyrylcholinesterase levels confirmed major inhibition immediately after intoxication compared to the baseline, certifying the intoxication. A significant increase in T4 levels was noted (p = 0.01) both at 2 h and 48 h after administration of organophosphate in sample rats. Similarly, T3 almost doubled its value 2 h after poisoning (4.2 ng/mL versus 2.5 ng/mL at baseline). Surprisingly, TSH displayed acute elevation with an afterward slow descending trend at 48 h (p = 0.1), reaching baseline value. CONCLUSIONS: This study demonstrated that cholinesterase inhibition caused major alterations in thyroid hormone levels, which may be characterized by a transient hypothyroidism status with an impact on survival prognosis.