Bal Krishna Subedi

Dr. Bal Krishna Subedi

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Research Focus & Metrics

Academic Career Length

4Years (2023-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 April 2023 in Annals of Medicine & Surgery
Verified
Journal Article
Open access
BSBasudev Subedi
Basudev Subedi
GYGopal Kumar Yadav
Gopal Kumar Yadav
ARAmar Raut
Amar Raut
NJNisha Joshi
Nisha Joshi
BSBal Krishna Subedi
Bal Krishna Subedi
RARamesh Prasad Acharya
Ramesh Prasad Acharya
Background: There are limited literatures studying the pancreatic involvement in organophosphate (OP) poisoning using biochemical means. This study focused on assessing the type of OP poisoning and determining the association of serum amylase levels with the patient’s presentation and outcome. Materials and methods: A cross-sectional study was carried out in the Maharajgunj Medical Campus, Tribhuwan University Teaching Hospital, Kathmandu, Nepal, after ethical approval [Ref: IRB/308 (6-11-E)]. We collected data from 172 participants with OP poisoning over the period of 2 years using nonprobability purposive sampling method. All patients with age group 16–75 years having a history of OP poisoning within the previous 24 h with clinical features and physical evidence of poisoning were included in the study. Those participants with indications of exposure to an entirely different poisons, poisoning with multiple poisons, OP poisoning along with alcohol, chronic alcoholics, comorbid conditions, taking drugs that could affect serum amylase levels (azathioprine, thiazides, furosemide, etc.), and/or treated in other hospitals after poisoning were excluded from the study. Appropriate statistical calculations were made using the statistical package for social sciences (SPSS), version 21. The P-value of less than 0.05 was considered statistically significant. Results: Metacid (53.5%, 92) was the most common OP poison. There were significantly higher mean values of serum amylase levels either within 12 h of exposure (468.60 vs. 135.4 IU/ml, P<0.001) or after 12 h of exposure (152.0 vs. 58.9 IU/ml, P<0.001) in dead participants than alive ones. The participants with initial and after 12 h of exposure-serum amylase level 100 or more IU/ml had more than two-fold and 18-fold higher odds of severe/life-threatening severity (odds ratio=2.40, 95% CI: 1.28–4.52, P=0.007 and odds ratio=18.67, 95% CI: 8.02–43.47, P<0.001) respectively than those with less than 100 IU/ml. Conclusions: The clinical severity of OP poisoning is directly related to serum amylase levels. Importantly, higher mean values of serum amylase levels were depicted in those participants with OP poisoning culminating to death. Thus, serum amylase level could be one of the easy measurable prognostic marker of OP poisonings.

4 April 2025 in Annals of Medicine & Surgery
Verified
Journal Article
Open access
BSBal Krishna Subedi
Bal Krishna Subedi
SMShivani Modi
Shivani Modi
NGNaveen Gautam
Naveen Gautam
AUAnuja Upadhyay
Anuja Upadhyay
PBPaul Baek
Paul Baek
DBDaniel Bitetto
Daniel Bitetto
Introduction and importance: Renal cell carcinoma (RCC) represents 90% of renal malignancies with rising global incidence. While the classic triad includes hematuria, flank pain, and palpable masses, paraneoplastic hypercalcemia occurs in 17% of cases and indicates aggressive disease behavior. This case documents severe hypercalcemia as the initial manifestation of metastatic RCC. Case presentation: A 64-year-old male presented with malaise, bloating, and weight loss. Laboratory evaluation revealed severe hypercalcemia (15.1 mg/dL), suppressed parathyroid hormone (4.2 pg/mL), and elevated parathyroid hormone-related peptide (83 pg/mL). Imaging identified a 5.5 × 5.0 × 5.3 cm left renal mass with metastases to lungs, brain, and possibly bone. Biopsy confirmed metastatic clear-cell RCC. Management comprised aggressive hydration, zoledronic acid, combined immunotherapy (pembrolizumab/lenvatinib), and palliative radiation for cerebral lesions. Clinical discussion: This case illustrates PTHrP-mediated humoral hypercalcemia of malignancy in metastatic RCC. The pathophysiology differs from alternative mechanisms such as calcitriol-mediated hypercalcemia or cytokine-driven osteoclast activation. Diagnostic markers demonstrated a classic humoral pattern with PTHrP elevation (83 pg/mL) and PTH suppression (4.2 pg/mL). The multimodal imaging protocol effectively delineated primary tumor dimensions, vascular invasion, and metastatic burden. Treatment efficacy was objectively measured through serial calcium levels and documented radiographic regression of primary and metastatic lesions. This aligns with recent data on combination immunotherapy (anti-PD-1) with tyrosine kinase inhibition in advanced RCC, supporting current therapeutic paradigms for PTHrP-mediated hypercalcemia in metastatic disease. Conclusion: Prompt recognition of paraneoplastic hypercalcemia in RCC facilitates timely intervention. This case demonstrates the value of comprehensive diagnostic evaluation and multidisciplinary management combining supportive care with targeted immunotherapy. Further prospective studies are needed to optimize therapeutic strategies for patients presenting with metabolic derangements suggestive of underlying malignancy.