Ivan Cvjetko

Thallium Toxicity in Humans

Thallium Toxicity in Humans Thallium is a naturally occurring trace element, widely distributed in the earths crust, but at very low concentrations. It does not have a known biological use and does not appear to be an essential element for life. It has been considered one of the most toxic heavy metals. Occasionally, there are reports on thallium poisoning as results of suicide or murder attempt or accident. The main threat to humans is through occupational exposure, environmental contamination, and accumulation in food, mainly in vegetables grown on contaminated soil. Increasing use in emerging new technologies and demanding high-tech industry constantly raise concern about exposure risk to all living organisms. Thallium is considered a cumulative poison that can cause adverse health effects and degenerative changes in many organs. The effects are the most severe in the nervous system. The exact mechanism of thallium toxicity still remains unknown, although impaired glutathione metabolism, oxidative stress, and disruption of potassium-regulated homeostasis may play a role. The lack of data about mutagenic, carcinogenic, or teratogenic effects of thallium compounds in humans calls for further research. Toksičnost Talija u Humanoj Populaciji Talij je u prirodi široko rasprostranjen teški metal, prisutan u vrlo niskim koncentracijama pa ga stoga ubrajamo u elemente u tragovima. Budući da organizmima nije potreban ni u jednoj razvojnoj fazi, ne ubrajamo ga u grupu esencijalnih elemenata. Talij zbog njegovih svojstava ubrajamo među najtoksičnije teške metale. Povremeno se još uvijek pojavljuju slučajevi u kojima je talij upotrijebljen kao sredstvo za pokušaj ubojstva, odnosno samoubojstva, ali i slučajevi nenamjernog, slučajnog trovanja talijem. U današnje vrijeme potencijalna opasnost od trovanja talijem postoji zbog profesionalne izloženosti, izbijanja ekološke katastrofe ili zbog akumulacije u hranidbenim lancima, uglavnom zbog uzgoja hrane na onečišćenom tlu. Sve češća uporaba talija u visokotehnološkoj industriji kao odgovor na zahtjeve moderne tehnologije neprestano povećava rizik od izloženosti svih živih organizama štetnim utjecajima talija u okolišu. Talij ima izuzetno negativan učinak na različite organske sustave, a osobito na živčani sustav. Mehanizmi toksičnosti talija još uvijek nisu u potpunosti razjašnjeni, premda važnu ulogu imaju poremećaji metabolizma glutationa, oksidativni stres i narušavanje homeostaze posredovane ionima kalija. Nedostatak podataka o mutagenim, kancerogenim ili teratogenim učincima talija i njegovih spojeva u ljudi opravdava buduća istraživanja ovog vrlo toksičnog metala.

Mortal hyperkalemia disturbances in rats are NO-system related. The life saving effect of pentadecapeptide BPC 157

We demonstrate the full counteracting ability of stable gastric pentadecapeptide BPC 157 against KCl-overdose (intraperitoneal (i), intragastric (ii), in vitro (iii)), NO-system related. (i) We demonstrated potential (/kg) of: BPC 157 (10ng, 10μg ip, complete counteraction), l-arginine (100mg ip, attenuation) vs. L-NAME (5mg ip, deadly aggravation), given alone and/or combined, before or after intraperitoneal KCl-solution application (9mEq/kg). Therapy was confronted with promptly unrelenting hyperkalemia (>12mmol/L), arrhythmias (and muscular weakness, hypertension, low pressure in lower esophageal and pyloric sphincter) with an ultimate and a regularly inevitable lethal outcome within 30min. Previously, we established BPC 157-NO-system interaction; now, a huge life-saving potential. Given 30min before KCl, all BPC 157 regimens regained sinus rhythm, had less prolongation of QRS, and had no asystolic pause. BPC 157 therapy, given 10min after KCl-application, starts the rescue within 5-10min, completely restoring normal sinus rhythm at 1h. Likewise, other hyperkalemia-disturbances (muscular weakness, hypertension, low sphincteric pressure) were also counteracted. Accordingly with NO-system relation, deadly aggravation by L-NAME: l-arginine brings the values to the control levels while BPC 157 always completely nullified lesions, markedly below those of controls. Combined with l-arginine, BPC 157 exhibited no additive effect. (ii) Intragastric KCl-solution application (27mEq/kg) - (hyperkalemia 7mmol/L): severe stomach mucosal lesions, sphincter failure and peaked T waves were fully counteracted by intragastric BPC 157 (10ng, 10μg) application, given 30min before or 10min after KCl. (iii). In HEK293 cells, hyperkalemic conditions (18.6mM potassium concentrations), BPC 157 directly affects potassium conductance, counteracting the effect on membrane potential and depolarizations caused by hyperkalemic conditions.

Axillary artery dissection after scapular fracture.

Blunt shoulder trauma rarely causes damage to either arteries or nerves. Neurovascular structures are covered by muscles and protected by the surrounding bones deep in the axilla. We report a case of a 34-year-old male motorbike driver referred to us 5 hours after injury. Standard X-ray of the left shoulder revealed multipart fracture of the left scapula, and angiography showed that the first segment of the left axillary artery was dissected proximal to the minor pectoral muscle. Urgent diagnosis using imaging techniques and restoration of blood flow using open or endovascular repair are crucial for optimal outcome. Damage to the nerves predicts the final functional outcome regardless of prompt revascularization.

Re: Aortoduodenal Fistula Three Years After Aortobifemoral Bypass: Case Report and Literature Review

Marolt et al. have presented a very interesting case of aortoduodenal fi stula and its successful treatment1. I have read the article with great interest since it is one of the worst complications that vascular surgeon may face. We had a case of infected abscess and leakage in the thoracic aorta successfully treated with endovascular graft (TEVAR). Our approach for abdominal aorta is graft removal and axillobifemoral bypass. I completely agree with the authors that it is necessary to cover duodenal lesion with omental fl ap, although we do not perform excision of the duodenal/intestinal wall. So far, we had no thrombosis of the axillofemoral bypass and it is remarkable to see suffi cient infl ow of the blood through narrow bypass (usually PTFE 6 mm) to both legs. In order to prevent thrombosis, we always perform distal anastomosis above deep femoral artery or directly to the bifurcation of the common femoral artery. Outfl ow through deep femoral artery is usually able to keep the fl ow through axillofemoral bypass running. If not, bypass distal to the occlusion of the superfi cial artery (or popliteal artery) should be performed. Th e European Society for Vascular Surgery (ESVS) has issued clinical practice guidelines for the management of abdominal aortic aneurysms2. Unstable patients might benefi t from stent graft (Level 4, Recommendation C); stable patients with aortoenteric fi stula should receive staged procedure with extra-anatomic bypass fi rst (Level 2c, Recommendation B); and fi nally stable patients without aortoenteric fi stula (patients that do not have direct communication between proximal anastomosis and bowel but infected paraanastomotic sinus) should receive in situ revascularization using autogenous superfi cial femoral vein or aortoiliac allograft (Level 2c, Recommendation C)2.

Porcelain aorta and peripheral arterial disease in a patient with Fahr disease

Fahr disease is an idiopathic nonarteriosclerotic symmetrical calcification of cerebral vessels. This disease has been recognized as a histopathologic entity, and dozens of typical cases have been reported. Patients typically present with numerous neurologic and psychiatric symptoms. A 49-year-old woman, with no history of cardiovascular disease, was referred to our hospital due to intermittent claudication. She also complained of headache and occasional forgetfulness. Blood levels of glucose, lipids, iron, calcium, ferritin, alkaline phosphatase, thyroid hormones, and parathormone were within normal limits. A general workup quickly revealed heavy calcifications of blood vessels, mainly the aorta and the arteries arising from the aortic arch. Dense calcifications were seen on plain X-ray images (A). Multislice computed tomography imaging showed dense calcifications and narrowing of the complete aorta down to the common iliac arteries (B and C). Brain computed tomography imaging showed extensive bilateral and symmetrical parenchymal calcification mostly in the basal ganglia and nucleus dentate, characteristic for Fahr disease (D). Angiography and percutaneous transluminal angioplasty of the infrarenal aorta were performed through the common femoral artery. With additional walking exercise, the patient’s walking distance at the 1-year follow-up increased from 100 to 250 meters.