Gout is a crystal-associated arthropathy caused by the deposition of monosodium urate crystals and is closely related to purine metabolic disorders and impaired uric acid excretion. It is clinically characterized by hyperuricemia， recurrent joint swelling and pain， and tophus formation. The disease course is divided into three stages： The hyperuricemia stage， acute attack stage， and chronic gouty arthritis stage. Modern medicine has reached a consensus on its pathology， but traditional Chinese medicine （TCM） lacks a systematic stage-specific understanding of gout pathogenesis and its underlying mechanisms， making it difficult to guide precise syndrome differentiation and treatment. By integrating classical TCM theory， clinical practice， and modern medical understanding， and drawing upon descriptions of Bi syndrome caused by endogenous dampness and turbidity in classical texts such as Huangdi Neijing·Ling Shu and Synopsis of the Golden Chamber， our team proposes the pathogenic concept of gout as ''endogenous dampness leading to Bi syndrome'' and the core pathogenesis of ''spleen deficiency with internal retention of dampness-turbidity''. We systematically elucidate the evolution of pathogenesis across different stages and corresponding therapeutic strategies. This study posits that metabolic byproducts such as urate fall under the category of ''endogenous pathogenic dampness-turbidity''. When genetic or dietary factors lead to metabolic abnormalities， it manifests as ''spleen deficiency with impaired transport and transformation''， resulting in ''internal retention of pathogenic dampness-turbidity''. When damp-turbidity stagnates in the blood vessels， serum uric acid levels rise. When it stagnates in the viscera and limbs， monosodium urate crystals deposit in the joints. Triggered by precipitating factors， this leads to gout attacks—the core pathological process of ''endogenous dampness leading to Bi syndrome''. Based on this theory， the stage-specific pathogenic characteristics of gout are proposed： The hyperuricemia stage is characterized by ''spleen deficiency with impaired transport and transformation， internal retention of pathogenic dampness-turbidity''， the acute attack stage is primarily marked by ''dampness-turbidity and static heat obstructing the limbs and joints''， while the chronic stage is defined by ''spleen deficiency with internal retention of pathogenic dampness-turbidity， intermingled with phlegm-stasis binding''. The treatment principle centers on ''strengthening the spleen and draining dampness'' throughout all stages. During the hyperuricemia stage， treatment focuses on ''strengthening the spleen， draining dampness， and eliminating turbidity''. In the acute attack stage， the treatment should "strengthen the spleen， drain dampness， clear heat， eliminate turbidity， alleviate swelling， and relieve pain''. In the chronic stage， the treatments emphasizes to ''strengthen the spleen， drain dampness， transform turbidity， clear heat， resolve phlegm， and activate blood circulation''. This approach has yielded favorable therapeutic outcomes in clinical practice. This theoretical system clarifies the nature of gout as ''spleen deficiency being the root， dampness-turbidity being the secondary manifestation'' and systematically analyzes its pathogenesis evolution process and characteristics. The constructed stage-based treatment protocol has been validated through clinical and basic research， providing systematic theoretical guidance and a practical framework for the precise TCM management of gout， thereby promoting the modernization of TCM pathogenesis theory related to gout.

ObjectiveBased on the clinical characteristics of chronic gouty arthritis （CGA） in both traditional Chinese and western medicine， this study aims to systematically evaluate the clinical concordance of existing CGA animal models， providing recommendations for establishing animal models that align with the pathological characteristics of CGA and the manifestations of traditional Chinese medicine syndromes. MethodsBy comprehensively retrieving Chinese and international databases such as China National Knowledge Infrastructure， Wanfang， VIP Chinese Science and Technology Periodical Database （VIP）， and PubMed， all relevant literature on CGA animal models was collected. Based on the guidelines， the diagnostic criteria of both traditional Chinese and western medicine were summarized and organized. The evaluation indicators for the CGA model were constructed with reference to existing evaluation modes， and the CGA animal models were analyzed to systematically evaluate the clinical concordance of existing models. ResultsThe current methods used to construct CGA animal models mainly include monosodium urate crystal induction， high-protein diet induction （poultry lack urate oxidase）， and high-fat diet combined with urate oxidase inhibitors and joint injection. Based on 11 pieces of included literature， the traditional Chinese and western medicine scoring data of each model were extracted， and the average scoring values of all models were ultimately calculated. The results show that the average clinical concordances of existing CGA animal models in both traditional Chinese and western medicine are 43.33% and 64.44%， respectively. Among them， the model with the highest clinical concordance rate is the one with a high-fat diet combined with potassium oxonate to induce hyperuricemia plus joint injection， achieving 83.33% clinical concordance in western medicine and 60% in traditional Chinese medicine. This model aligns well with the pathogenic characteristics and pathological changes of clinical CGA. ConclusionAlthough current CGA animal models can simulate some pathological characteristics of CGA， they struggle to comprehensively reflect the complex pathological processes of CGA and the characteristics of traditional Chinese medicine syndromes. Therefore， in the future， it is necessary to establish the CGA animal models that incorporate the clinical disease and syndrome characteristics of traditional Chinese and western medicine and formulate the uniform model evaluation criteria， providing more precise tools for CGA mechanism research and the development of traditional Chinese medicine.

ObjectiveTo evaluate the therapeutic effect of Huazhuo SanJie Chubi presciption （HSCD） on chronic gouty arthritis （CGA） rats with low-grade inflammation and to explore the underlying mechanism with a focus on macrophage polarization. MethodsThe 41 male 6-week-old SD rats were randomly allocated， using the random number table， to a normal group （n=8） and a model group （n =33）. CGA with low-grade inflammation was induced in the model group by daily gavage of potassium oxonate （250 mg·kg^-1·d^-1） and hypoxanthine （300 mg·kg^-1·d^-1）， combined with intra-articular injection of a monosodium urate （MSU） crystal suspension （50 μL， 25 g·L^-¹） into the left ankle twice weekly. After 4 weeks of modeling， 3 rats were randomly selected from each group for model validation. The remaining successfully modeled rats were randomly divided into a model group， an HSCD group （10.35 g·kg^-1·d^-1， gavage once daily）， an M1 polarization agonist group （L-methionine sulfoximine， 300 mg·kg^-1， subcutaneous injection every other day）， an M1 polarization agonist + HSCD group， an M2 polarization inhibitor group （PD0325901， 10 mg·kg^-1·d^-1， gavage once daily）， and M2 polarization inhibitor + HSCD group. The corresponding drug or drug combination was administered according to group assignment， whereas rats in the normal and model groups received 0.5% carboxymethyl cellulose sodium （CMC-Na） vehicle （10.35 g·kg^-1·d^-1， gavage once daily）. All interventions were continued for four weeks. During the intervention period， except for the normal group， potassium oxonate （250 mg·kg⁻¹） and hypoxanthine （300 mg·kg^-1） were co-administered by gavage every other day to maintain the model. At the end of treatment， serum uric acid （SUA）， ankle joint diameter and joint swelling index were measured. The levels of high-sensitivity C-reactive protein （hs-CRP）， interleukin-1β （IL-1β）， interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， chemokine C-C motif ligand 2 （CCL2）， S100 calcium-binding protein A8/A9 （S100A8/A9）， interleukin-10 （IL-10） and arginase-1 （Arg-1） in serum and joint fluid were determined by enzyme-linked immunosorbent assay （ELISA）. High-frequency ultrasound was used to assess MSU deposition in the ankle joint. Hematoxylin-eosin （HE） staining was performed to evaluate synovial histopathological changes. Quantitative Real-time PCR and immunofluorescence were used to detect the mRNA and protein expression of the M1 macrophage polarization markers inducible nitric oxide synthase （iNOS） and the M2 macrophage polarization marker scavenger receptor cysteine-rich type 1 protein M130 （CD163） in synovial tissue. ResultsCompared with the normal group， the model group showed significantly elevated SUA level and joint swelling index， and increased levels of pro-inflammatory cytokines， CCL2， and S100A8/A9 in both serum and joint fluid （P<0.05）， accompanied by MSU deposition and synovial inflammation in the ankle joint. The mRNA and protein expression levels of macrophage polarization M1/M2 markers iNOS and CD163 in synovial tissues were also significantly up-regulated （P<0.05）. Compared with model group， rats in HSCD group had significantly lower SUA levels， attenuated joint swelling， reduced serum levels of pro-inflammatory cytokines， and decreased levels of CCL2 and S100A8/A9 in both serum and joint fluid， accompanied with alleviated MSU deposition and synovial inflammation （P<0.05）. HSCD markedly downregulated the mRNA and protein expression of M1 marker iNOS （P<0.05）， whereas it had no significant effect on the expression of M2 marker CD163. Compared with the M1 polarization agonist group， the M1 polarization agonist + HSCD group showed significantly reduced joint swelling， lower serum levels of pro-inflammatory cytokines， and decreased levels of CCL2 and S100A8/A9 in joint fluid （P<0.05）. In addition， synovial inflammatory cell infiltration and angiogenesis were attenuated， and iNOS mRNA and protein expression levels were significantly reduced （P<0.05）. Compared with the M2 polarization inhibitor group， the M2 polarization inhibitor + HSCD group exhibited reduced joint swelling， decreased levels of CCL2 and S100A8/A9 in joint fluid and ameliorated synovial inflammation （P<0.05）， whereas the levels of anti-inflammatory mediators （IL-10， Arg-1） and CD163 mRNA and protein expression were not significantly increased. ConclusionHSCD alleviates low-grade inflammation in CGA rats， at least in part， by inhibiting macrophage polarization toward the M1 phenotype.

ObjectiveThis paper aims to observe the effect of Huazhuo Sanjie Chubi prescription （HSCD） on the gouty bone erosion model rats and investigate its action mechanism. MethodsThirty-six two-month-old male SD rats were randomly divided into the blank group with nine rats and the modeling group with 27 rats. The rats in the modeling group were administered hypoxanthine solution at 300 mg·kg^-1·d^-1 and potassium oxonate solution at 250 mg·kg^-1·d^-1， combined with intra-articular injection of 200 μL monosodium urate （MSU） crystal suspension at 25 g·L^-1 into the right ankle joint （joint injection once every three days）， so as to induce the gouty bone erosion model. After four weeks of modeling， three rats were selected from these two groups to validate the model. The modeled 24 rats were randomly divided into the model group， HSCD group （10.35 g·kg^-1·d^-1）， allopurinol group （20 mg·kg^-1·d^-1）， and inhibitor group （LY294002， 10 mg·kg^-1·d^-1）， with six rats per group. Except for the blank group， rats in all other groups continued to receive hypoxanthine solution at 300 mg·kg^-1 and potassium oxonate solution at 250 mg·kg^-1 via gavage concurrently with administration to maintain modeling intervention. The rats in the HSCD group and allopurinol group received administration by gavage at the above doses. The rats in the inhibitor group received an intraperitoneal injection at the above dose. The rats in the blank group and model group received saline （10.35 g·kg^-1·d^-1） by gavage for four consecutive weeks. After administration， ankle joint swelling of the rats in all groups was observed， and the diameters were measured. Bone volume fraction （BV/TV） and bone surface area to bone volume （BS/BV） were observed and quantitatively analyzed by Micro-CT. Histopathological changes in the ankle joint were observed by hematoxylin-eosin （HE） staining and safranin O-fast green staining. The uric acid in the rats' serum was determined by enzyme colorimetry. The levels of inflammatory factors， including tumor necrosis factor-α （TNF-α）， interleukin （IL）-1β， and IL-6 were measured by enzyme-linked immunosorbent assay （ELISA）. The protein expressions of receptor activator of nuclear factor-κB ligand （RANKL） and phosphorylated （p）-phosphatidylinositol-3-kinase （PI3K） in ankle joint tissues of rats were detected by immunofluorescence staining. The mRNA levels of the proteins related to the bone erosion， including RANKL， tartrate-resistant acid phosphatase （TRAP）， cathepsin K （CTSK）， and matrix metalloproteinase-9 （MMP-9） in the ankle joint tissues of rats were determined by real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. The expressions of the proteins related to the bone erosion， including RANKL， CTSK， TRAP， MMP-9， and the proteins related to the PI3K/protein kinase B （Akt） signaling pathway， including PI3K， Akt， mammalian target of rapamycin （mTOR）， p-PI3K， phosphorylated protein kinase B （p-Akt）， and phosphorylated mammalian target of rapamycin （p-mTOR）， were detected by Western blot. ResultsCompared with the blank group， the modeling group showed marked ankle swelling and increased diameter. Micro-CT revealed an uneven articular surface and honeycomb-like bone erosion in the ankle joint. Quantitative analysis showed decreased BV/TV and increased BS/BV （P<0.05）. HE staining revealed a narrowed joint space， rough and discontinuous cartilage surfaces， reduced and unevenly distributed chondrocytes， partial hypertrophy， and blurred tidemarks， confirming successful model establishment. After four weeks of intervention， compared with those in the blank group， the rats in the model group exhibited severe ankle swelling and increased diameters （P<0.05）. Micro‑CT showed that the ankle joint surface was irregular， and bone erosion exhibited a honeycomb‑like morphology. The microstructural parameters of the bone revealed a decreased BV/TV and an increased BS/BV （P<0.05）. Histopathological examination revealed a narrowed joint space and severe articular cartilage destruction. The levels of uric acid in the serum and inflammatory factors （IL-1β， IL-6， and TNF-α） were increased （P<0.05）. The mRNA and protein levels of the proteins related to bone erosion in joint tissue， including RANKL， CTSK， TRAP， and MMP-9， were upregulated （P<0.05）. The ratios of p-PI3K/PI3K， p-Akt/Akt， and p-mTOR/mTOR in the proteins related to the PI3K/Akt signaling pathway were increased （P<0.05）. RANKL and p-PI3K protein fluorescence intensities were elevated （P<0.05）. Compared with those in the model group， the above indicators in all other administration groups showed varying degrees of improvement. The HSCD group and inhibitor groups exhibited more significant effects in reducing ankle swelling， improving bone erosion， bone microstructure （significant decrease in BV/TV and increase in BS/BV）， and the pathology of cartilage erosion， lowering inflammatory factor levels， downregulating the proteins related to the bone erosion， and suppressing activation of the PI3K/Akt/mTOR pathway （P<0.05）. The uric acid levels in rats' serum were reduced in both HSCD and allopurinol groups （P<0.05）. Compared with those in the HSCD group， the rats in the allopurinol group had larger ankle diameters （P<0.05）， more severe bone erosion and bone microstructure damage （P<0.05）， worse improvement of the pathology of cartilage erosion， higher levels of IL-6 and TNF-α （P<0.05）， elevated expressions of the proteins related to the bone erosion， higher expression ratio of proteins related to the PI3K/Akt signaling pathway （P<0.05）， and higher fluorescence intensities of RANKL and p-PI3K proteins （P<0.05）. The inhibitor group achieved comparable results to the HSCD group in improvements of bone microstructure and the reduction of IL-1β and IL-6， stronger suppression of TNF-α and PI3K/Akt/mTOR signaling pathway activation （P<0.05）， but weaker effects on cartilage repair and serum uric acid reduction （P<0.05）. ConclusionHSCD effectively reduces uric acid levels in serum， suppresses inflammatory factor secretion， and downregulates the expressions of proteins related to bone erosion， including RANKL， CTSK， TRAP， and MMP-9 in the joint tissues. Its action mechanism of improving gouty bone erosion may be associated with inhibition of the PI3K/Akt signaling pathway.

The patient, a 28-year-old male, had experienced splenomegaly for four years with lymphadenopathy for more than two months and presented to the First Affiliated Hospital of the Naval Medical University on October 16th, 2024. On July 31, 2024, he noticed right upper quadrant pain, and an enhanced abdominal CT performed in an external facility revealed splenomegaly with a rounded nodular lesion at the splenic hilum, suggestive of an accessory spleen; in addition to retroperitoneal lymphadenopathy, while tumor marker levels were unremarkable. A complete blood count on August 22nd, 2024, demonstrated leukopenia (2.22×10 9/L), hemoglobin level of 144 g/L, and thrombocytopenia (60×10 9/L). To further elucidate the diagnosis, the patient visit our hematology clinic on August 26th, 2024. His physical examination was normal in general condition, except for a firm palpable spleen 10 cm below the left costal margin, and ultrasonography revealed right thyroid nodule and hepatosplenomegaly. Because of hepatosplenomegaly and retroperitoneal lymphadenopathy, a PET-CT scan was performed. The scan confirmed marked hepatosplenomegaly, multiple enlarged lymph nodes in the retroperitoneal and mesenteric regions with increased metabolic activity, and evidence of elevated bone metabolic activity in the proximal limbs and axial skeleton. Given the possibility of a hematologic lymphoproliferative disorder, a bone marrow biopsy was recommended. On September 12th, 2024, the patient underwent a bone marrow biopsy for evaluations of cell morphology, initial lymphoma immunophenotyping, cytogenetic analysis, and lymphoma-related FISH testing. Flow cytometry, cytogenetic analysis, and FISH results on September 14th, 2024, were unremarkable, manual microscopy of bone marrow morphological evaluation revealed a small population of poorly differentiated lymphocytes; additionally, AI-assisted automated cell scan identified a subset of abnormal cells suspected to be ′Gaucher cells′. Bone marrow pathology indicated a histiocytic neoplasm accompanied by stage 2 myelofibrosis (MF), with tumor cells comprising approximately 70% of the nucleated cells in the marrow, suggesting immunohistochemistry for confirmation. On October 16th, immunohistochemical analysis confirmed the presence of a histiocytic proliferative disorder suspecting Gaucher disease. After admission, the patient initiated enzyme replacement therapy, receiving an initial intravenous dose of 60 U/kg in a weekly basis. On October 31st, 2024, based on enzyme activity assays, genetic testing, and other results, adult Gaucher disease was finally diagnosed. The patient was scheduled for follow-up with stable vital signs, and reduced size of the spleen compared with previous assessments.

Objective To investigate the relationship between frailty and readmission during vulnerable periods in elderly patients with chronic heart failure.Methods Using convenience sampling method,290 elderly patients with chronic heart failure admitted to Department of Cardiovascular,the People's Hospital of Guangxi Zhuang Autonomous Region from December 2022 to August 2023 were selected as the research subjects.They were followed up for three months and surveyed using general information questionnaire,frailty scale,and Barthel index.Results Spearman correlation analysis showed a positive correlation between readmission during the vulnerable period and frailty(r=0.266,P＜0.05).The readmission rate during the vulnerable period was 28.6％,and the results of multivariate Logistic regression analysis showed that frailty(OR=2.561,95％CI:1.409-4.654),age(OR=1.113,95％CI:1.067-1.161),and renal dysfunction(OR=2.903,95％CI:1.559-5.406)were independent risk factors for unplanned readmission during the vulnerable period in elderly patients with chronic heart failure.Conclusion There is a positive correlation between frailty and readmission during the vulnerable period in elderly patients with chronic heart failure.Frailty,age,and renal dysfunction are independent risk factors for decompensated admission events in vulnerable elderly patients with chronic heart failure.

Purpose Exploring the clinical indications of coronary artery magnetic resonance imaging(CMRA)from the perspectives of diagnostic efficacy and image quality,providing reference for the clinical application of this technology.Materials and Methods From May 2021 to March 2024,a prospective study was conducted on 110 patients who planned to undergo coronary angiography(CAG)at the First Affiliated Hospital of Henan University of Traditional Chinese Medicine.3.0T whole heart CMRA examination was performed within one week before CAG surgery,and relevant data was collected and recorded.The diagnostic efficacy of CMRA was evaluated comprehensively,the correlation between CMRA image quality and diagnostic efficacy were analyzed,and the relationship between patient factors and CMRA image quality was verified.Results Based on multi-level evaluation,CMRA had a higher diagnostic accuracy for significant coronary artery stenosis(area under the curve>0.811).The diagnostic results of CMRA were affected by image quality.When the image quality was medium or poor,the diagnostic results of CMRA and CAG were prone to inconsistency,while when the image quality was excellent or good,the diagnostic results were mostly consistent.Conclusion CMRA has similar diagnostic efficacy to CAG and high clinical application potential.The quality of CMRA images can easily affect diagnostic efficiency,and image quality should be evaluated before clinical diagnosis.

Objective To investigate the relationship between frailty and readmission during vulnerable periods in elderly patients with chronic heart failure.Methods Using convenience sampling method,290 elderly patients with chronic heart failure admitted to Department of Cardiovascular,the People's Hospital of Guangxi Zhuang Autonomous Region from December 2022 to August 2023 were selected as the research subjects.They were followed up for three months and surveyed using general information questionnaire,frailty scale,and Barthel index.Results Spearman correlation analysis showed a positive correlation between readmission during the vulnerable period and frailty(r=0.266,P＜0.05).The readmission rate during the vulnerable period was 28.6％,and the results of multivariate Logistic regression analysis showed that frailty(OR=2.561,95％CI:1.409-4.654),age(OR=1.113,95％CI:1.067-1.161),and renal dysfunction(OR=2.903,95％CI:1.559-5.406)were independent risk factors for unplanned readmission during the vulnerable period in elderly patients with chronic heart failure.Conclusion There is a positive correlation between frailty and readmission during the vulnerable period in elderly patients with chronic heart failure.Frailty,age,and renal dysfunction are independent risk factors for decompensated admission events in vulnerable elderly patients with chronic heart failure.

Purpose Exploring the clinical indications of coronary artery magnetic resonance imaging(CMRA)from the perspectives of diagnostic efficacy and image quality,providing reference for the clinical application of this technology.Materials and Methods From May 2021 to March 2024,a prospective study was conducted on 110 patients who planned to undergo coronary angiography(CAG)at the First Affiliated Hospital of Henan University of Traditional Chinese Medicine.3.0T whole heart CMRA examination was performed within one week before CAG surgery,and relevant data was collected and recorded.The diagnostic efficacy of CMRA was evaluated comprehensively,the correlation between CMRA image quality and diagnostic efficacy were analyzed,and the relationship between patient factors and CMRA image quality was verified.Results Based on multi-level evaluation,CMRA had a higher diagnostic accuracy for significant coronary artery stenosis(area under the curve>0.811).The diagnostic results of CMRA were affected by image quality.When the image quality was medium or poor,the diagnostic results of CMRA and CAG were prone to inconsistency,while when the image quality was excellent or good,the diagnostic results were mostly consistent.Conclusion CMRA has similar diagnostic efficacy to CAG and high clinical application potential.The quality of CMRA images can easily affect diagnostic efficiency,and image quality should be evaluated before clinical diagnosis.

The patient, a 28-year-old male, had experienced splenomegaly for four years with lymphadenopathy for more than two months and presented to the First Affiliated Hospital of the Naval Medical University on October 16th, 2024. On July 31, 2024, he noticed right upper quadrant pain, and an enhanced abdominal CT performed in an external facility revealed splenomegaly with a rounded nodular lesion at the splenic hilum, suggestive of an accessory spleen; in addition to retroperitoneal lymphadenopathy, while tumor marker levels were unremarkable. A complete blood count on August 22nd, 2024, demonstrated leukopenia (2.22×10 9/L), hemoglobin level of 144 g/L, and thrombocytopenia (60×10 9/L). To further elucidate the diagnosis, the patient visit our hematology clinic on August 26th, 2024. His physical examination was normal in general condition, except for a firm palpable spleen 10 cm below the left costal margin, and ultrasonography revealed right thyroid nodule and hepatosplenomegaly. Because of hepatosplenomegaly and retroperitoneal lymphadenopathy, a PET-CT scan was performed. The scan confirmed marked hepatosplenomegaly, multiple enlarged lymph nodes in the retroperitoneal and mesenteric regions with increased metabolic activity, and evidence of elevated bone metabolic activity in the proximal limbs and axial skeleton. Given the possibility of a hematologic lymphoproliferative disorder, a bone marrow biopsy was recommended. On September 12th, 2024, the patient underwent a bone marrow biopsy for evaluations of cell morphology, initial lymphoma immunophenotyping, cytogenetic analysis, and lymphoma-related FISH testing. Flow cytometry, cytogenetic analysis, and FISH results on September 14th, 2024, were unremarkable, manual microscopy of bone marrow morphological evaluation revealed a small population of poorly differentiated lymphocytes; additionally, AI-assisted automated cell scan identified a subset of abnormal cells suspected to be ′Gaucher cells′. Bone marrow pathology indicated a histiocytic neoplasm accompanied by stage 2 myelofibrosis (MF), with tumor cells comprising approximately 70% of the nucleated cells in the marrow, suggesting immunohistochemistry for confirmation. On October 16th, immunohistochemical analysis confirmed the presence of a histiocytic proliferative disorder suspecting Gaucher disease. After admission, the patient initiated enzyme replacement therapy, receiving an initial intravenous dose of 60 U/kg in a weekly basis. On October 31st, 2024, based on enzyme activity assays, genetic testing, and other results, adult Gaucher disease was finally diagnosed. The patient was scheduled for follow-up with stable vital signs, and reduced size of the spleen compared with previous assessments.