BackgroundHydrocarbon-induced occupational liver injury is a well-known clinical entity among petroleum industry workers. There are many types of hydrocarbon exposure, with inhalation being the most common. Hydrocarbon-induced occupational liver injury is a rarely suspected and commonly missed etiological agent for liver injury. We report a case of a non-petroleum industry worker with chronic liver disease secondary to hydrocarbon-induced occupational liver injury caused by chronic low-grade hydrocarbon ingestion due to occupational malpractice.Case presentationA 23-year-old Sri Lankan man who was a motor mechanic presented to our hospital with decompensated cirrhosis. He had been chronically exposed to gasoline via inadvertent ingestion due to occupational malpractice. He used to remove gasoline from carburetors by sucking and failed to practice mouth washing thereafter. On evaluation, he had histologically proven established cirrhosis. A comprehensive history and workup ruled out other nonoccupational etiologies for cirrhosis. The patient’s long-term occupational gasoline exposure and clinical course led us to a diagnosis of hydrocarbon-induced occupational liver injury leading to decompensated cirrhosis.ConclusionsHydrocarbon-induced occupational liver injury should be considered as a cause when evaluating a patient with liver injury with possible exposure in relevant occupations.
The piriformis syndrome is an entrapment neuropathy of the sciatic nerve, which before MRI was often misdiagnosed as lumbar radiculopathy. Using MR neurography, Filler et al. [1] showed that among patients with a diagnosis of sciatica in whom standard treatment failed to effect an improvement, up to 68% had the piriformis syndrome. The piriformis muscle arises from the anterior surface of the middle third of the sacrum, between and lateral to the anterior sacral foramina and inserts into the medial aspect of the greater trochanter. Contraction of the piriformis, externally rotates the extended lower limb at the hip joint, and abducts the flexed hip. The piriformis lies on the sciatic nerve as both structures exit the pelvis via the greater sciatic foramen, where it confines the sciatic nerve to a potentially tight compartment.A 63-year-old, well-built male (BMI = 27.58 kg/m 2 ), presented with severe and progressive, bilateral buttock pain radiating to the back of the thighs of 2 years duration. His pain was unbearable at the time of waking; movement reduced the pain, whilst prolonged sitting aggravated it. He had associated anal pain. He was fit and had engaged in contact sports in his youth. There was no history suggestive of either neuromuscular disease or trauma to the buttock or pelvic regions. Abdominal examination was unremarkable;and rectal examination revealed tenderness over the piriformis muscle, which also triggered his buttock pain. Flexible sigmoidoscopy was unremarkable. Pelvic CT showed hypertrophy and herniation of the piriformis muscle between the rectum and sacrum. Pelvic MRI showed evidence of hypertrophy with altered signals in and around the piriformis muscles on both sides, suggesting fluid accumulation; more on the left side ( Figs. 1 and 2). Overall, MRI was suggestive of inflammation of the piriformis muscles. MRI of the lumbo-sacral spine was normal.Oral prednisolone 10 mg 8-hourly, gave dramatic pain relief within 2 days. Symptoms improved for 14 days leaving only mild intermittent buttock pain but recurred after therapy was discontinued. After 1 month, a second Fig. 1 Pre-treatment magnetic resonance image showing altered signal intensity and herniation of both piriformis muscles (solid arrows)
Background: Hepatocellular carcinoma (HCC) is becoming a challenging global health concern with Asian and African countries carrying the highest burden of it. The rising prevalence of non-alcoholic steatohepatitis (NASH) associated HCC is linked with unhealthy dietary patterns and sedentary life styles. In addition, genetic predisposition may play a critical role in developing NASH-related HCC. Previous studies have identified that variants in patatin-like phospholipase domain-containing protein 3 (PNPLA3), transmembrane 6 superfamily member 2 (TM6SF2) and membrane bound O-acyltransferase domain containing 7 (MBOAT7) genes are significantly associated with non-alcoholic fatty liver disease (NAFLD) pathogenicity among different populations. But there are no published reports on their impact on Sri Lankan NASH-HCC patients. Methods: We conducted an exploratory study to evaluate the prevalence of five single nucleotide polymorphisms (SNPs) (PNPLA3 rs738409, PNPLA3rs2281135, PNPLA3 rs2294918, TM6SF2 rs58542926 and MBOAT7 rs641738) as genetic risk factors for NASH-HCC pathogenicity. We genotyped 48 NASH-HCC samples that were collected at a clinical setting and analyzed using statistical modelling to explore the impact of each SNP with tumor prognostic factors. Results: We observed high frequencies in four out of five polymorphisms, namely PNPLA3 rs738409 (0.79, 95%CI 0.650-0.895), PNPLA3 rs2281135 (0.77, 95%CI 0.627-0.880), PNPLA3 rs2294918 (0.9, 95%CI 0.773-0.965) and MBOAT7rs641738 (0.85, 95%CI 0.722-0.939) among Sri Lankan NASH-HCC patients. Our analyses further demonstrated significant associations of PNPLA3variants with a total tumor diameter of NASH-HCC patients while PNPLA3 rs2294918 and MBOAT7 rs641738 had significant associations with single-nodular HCC. Of the five SNPs, we observed a strong correlation between PNPLA3 rs738409 and PNPLA3 rs2294918 through pairwise linkage disequilibrium (LD) analysis. Conclusion: Observed high frequencies of risk alleles among genotyped SNPs warrants the possibility of genetic predisposition as a risk factor for NASH-related HCC in the Sri Lankan setting.
Objectives C-reactive protein (CRP) is a serum marker of systemic inflammation which has been suggested to predict need for emergent surgical intervention in patients with acute renal colic at a value of > 28 mg/l on admission. We aimed to determine if this applied to our patients.
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