These data indicate that curcumin has nephroprotective properties against cisplatin-induced kidney damage in rats and this effect is associated with its anti-inflammatory and anti-apoptosis profiles, in addition to its antioxidant. Hence, curcumin may be useful for preventing kidney damage against cisplatin administration.

Cisplatin is a platinum-based drug that is usually used for the treatment of many carcinomas. However, it comes with several devastating side effects, including nephrotoxicity. Cisplatin toxicity is a very complex process, which is exacerbated by the accumulation of cisplatin in renal tubular cells via passive diffusion and transporter-mediated processes. Once cisplatin enters these cells, it induces the formation of reactive oxygen species that cause cellular damage, including DNA damage, inflammation, and eventually cell death. On a small scale, these damages can be mitigated by cellular antioxidant defense mechanism. However, on a large scale, such as in chemotherapy, this defense mechanism may fail, resulting in nephrotoxicity. The current article reviews the molecular mechanisms underlying cisplatin-induced nephrotoxicity and possible renoprotective strategies to determine novel therapeutic interventions for alleviating this toxicity.

Background: Nephrotoxicity is a limiting factor of the platinum-based chemotherapeutic drug cisplatin. One third of patient treated with cisplatin eventually develop acute nephrotoxicity due to accumulation of cisplatin in renal tubular cell which causes oxidative stress and DNA damage. Curcumin is the active ingredient of Curcuma longa, which is reported to exhibit anti-inflammatory property and nephroprotective property, despite its low bioavailability. To increase its bioavailability, nanocurcumin can be used instead. This study aims to know the difference between administration of curcumin and nanocurcumin on cisplatin induced acute nephrotoxicity. Methods: Nanocurcumin and curcumin were used in this study on rat model of AKI which induced by cisplatin (n=25) and observe the expression of Nrf2 and Keap1, Oct2 and Ctr1, Kim-1 and Ngal, and curcumin concentration in kidney tissues of rats. Rats were divided into five groups randomly: (1) Control, (2) Cisplatin (7mg/kgBW single dose), (3) Cisplatin + Curcumin (7mg/kgBW single dose + 100mg/kg/day), (4) Cisplatin + 50mg Nanocurcumin (7mg/kgBW single dose + 50mg/kg/day), ( 5) Cisplatin + 100mg Nanocurcumin (7mg/kgBW single dose + 100mg/kg/day). qRT-PCR was then conducted to calculate the relative expression of the genes. LCMS/MS was used to analyze curcumin and nanocurcumin concentration in kidney tissues. Results: There was no significant difference between groups in expression of Nrf2 and Keap1 gene, although there is an increase in Keap1 expression in rats treated with 100mg nanocurcumin. There was also no significant difference in expression of Oct2 and Ctr1 gene, although administration of 100mg Nanocurcumin increases Oct2 gene expression. Kidney damage markers (Kim-1 and Ngal) were also not significantly different between groups, although rats treated with 100mg of Nanocurcumin express lower level of Kim-1 and Ngal. We also found that nanocurcumin 100 mg has a highest concentration accumulation in the kidney tissues compared to that of other groups. Conclusion: Our conclusion is that nanocurcumin have better nephroprotective effect compared to curcumin shown by increase in Keap1 and Oct2 with decreased Kim-1 and Ngal expression in rats treated with 100 mg nanocurcumin at least in part due to increase concentration of 100 mg nanocurcumin in kidney tissues.

Gastrin is an important hormone in the gastrointestinal system that promotes gastric acid secretion. Gastrin hormone is produced by the G-cells in the antrum of the stomach. Besides stimulating gastric acid secretion, gastrin also induces the proliferation of the gut epithelial cells, tissue remodelling, and angiogenesis. Gastrin levels higher than 100-150 pg/ml are known as hypergastrinemia. Hypergastrinemia may cause the hypersecretion of stomach acid, which, if not treated properly, may leads to refractory peptic ulcer, severe gastroesophageal reflux disease (GERD), diarrhea, or death due to complications of refractory peptic ulcer. This case presented a 12 years old boy with a chief complaint of severe epigastric pain in the past month, accompanied by nausea, especially during supine position. The patient had a previous history of esophagitis. He showed no significant changes upon empirical PPI treatment. However, slight improvements were observed after the administration of Helicobacter pylori treatment. The gastrin level in this patient was 198 pg/mL. Upon discharge, the patient was still given PPI treatment. During the follow-up visitation, patient complaints had improved significantly, and the patient was planned to undergo routine evaluations of gastrin.

Autoimmune hepatitis (AIH) is a condition caused by self-perpetuating immune response towards hepatocytes in liver. In children, AIH may progressed more rapidly compared to adults. Thus, early diagnosis and prompt treatment are the key for successful management of AIH. Five main characteristics of AIH include female predominance, increased IgG or hypergammaglobulinemia, circulatory autoantibody seropositivity, and hepatitis interface from the histological finding. Liver biopsy is needed to evaluate the degree of damage and to confirm the diagnosis. The standard regiment for AIH include prednisone (or prednisolone) and azathioprine. Other alternative treatments available for non-responder, such as mycophenolate mofetil, tacrolimus, cyclosporine, budesonide, rituximab, and infliximab. AIH treatment is recommended to be taken minimally for 2-3 years before attempting treatment termination.