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PubMed2026

Large-scale AI analysis reveals missed opportunities in albuminuria testing and disease-modifying therapy implementation.

AIMS: Albuminuria is a key diagnostic and prognostic biomarker of chronic kidney disease (CKD), associated with adverse cardiovascular and renal outcomes. Despite guideline recommendations, urine albumin-to-creatinine ratio (UACR) testing is infrequently performed in cardiology. This study assessed the uptake of UACR testing, the estimated prevalence of undiagnosed albuminuria, and the use of disease-modifying therapies in patients with cardio-kidney-metabolic (CKM) disease. METHODS AND RESULTS: We conducted a retrospective cohort study of all adults seen at the cardiology department of a tertiary referral centre between 2019 and 2024. Data were extracted using CTcue, an AI-driven platform. Albuminuria was defined as UACR &#x2265;30 mg/g. A weighted logistic regression model estimated albuminuria prevalence in untested patients. Among 77 351 patients (44.8% female, mean age 64.4 years), only 8.9% had a recorded UACR, of whom 46.4% had albuminuria. Testing rates were low across high-risk groups: 29.9% in diabetes, 21.7% in heart failure, and 13.7% in hypertension. In untested patients, the predicted prevalence of albuminuria was 36.6%, and highest in those with eGFR <30 mL/min/1.73m2 (70.0%), heart failure (47.8%), or diabetes (46.8%). Use of disease-modifying therapies was low, even among patients with confirmed albuminuria. In patients with documented vs. predicted albuminuria, 43.0% vs. 39.1% received renin-angiotensin system inhibitors, 12.8% vs. 5.7% received SGLT2 inhibitors, and <1% in both groups received finerenone. CONCLUSION: Albuminuria is substantially underdetected in cardiology practice, possibly contributing to underuse of effective CKM therapies. Systematic UACR screening with structured treatment protocols may help close this gap and improve outcomes for patients with CKM disease.

Humans↗
PubMed1984

Human apolipoproteins AI, AII, CII and CIII. cDNA sequences and mRNA abundance.

The structure and function of the genes encoding the polypeptide components of plasma lipoproteins are of interest because of the central role they play in the regulation of lipid metabolism. We have now completed our previous studies on the human apoAI gene and furthermore isolated and sequenced cDNA clones for apoAII , CII and CIII. The nucleotide sequences show the signal peptides of apoAII , CII and CIII to be 18, 22 and 20 amino acids in length, respectively, and in addition that prepro apoAII bears a classical propeptide structure of 5 amino acids. The amino acid homology detected between apoCII and pro- apoAI is discussed, as is the gene arrangement of the 5' non-coding region of apoAI mRNA. The relative liver mRNA levels of the 4 apolipoproteins analysed in this study have been estimated and compared with their corresponding plasma products. The data reported here provide an essential basis for further studies of structural and functional alleles of apo AI, AII, CII and CIII genes.

Amino Acid Sequence↗
PubMed1998

E1A represses apolipoprotein AI enhancer activity in liver cells through a pRb- and CBP-independent pathway.

The apolipoprotein AI (apoAI) promoter/enhancer contains multiple cis -acting elements on which a variety of hepatocyte-enriched and ubiquitous transcription factors function synergistically to regulate liver-specific transcription. Adenovirus E1A proteins repress tissue-specific gene expression and disrupt the differentiated state in a variety of cell types. In this study expression of E1A 12Sor 13S in hepatoblastoma HepG2 cells repressed apoAI enhancer activity 8-fold. Deletion mapping analysis showed that inhibition by E1A was mediated by the apoAI promoter site B. E1A selectively inhibited the ability of HNF3beta and HNF3alpha to transactivate reporter genes controlled by the apoAI site B and the HNF3 binding site from the transthyretin promoter. The E1A-mediated repression of HNF3 activity was not reversed by overexpression of HNF3beta nor did E1A alter nuclear HNF3beta protein levels or inhibit HNF3 binding to DNA in mobility shift assays. Overexpression of two cofactors known to interact with E1A, pRb and CBP failed to overcome inhibition of HNF3 activity. Similarly, mutations in E1A that disrupt its interaction with pRb or CBP did not compromise its ability to repress HNF3beta transcriptional activity. These data suggest that E1A inhibits HNF3 activity by inactivating a limiting cofactor(s) distinct from pRb or CBP.

Adenovirus E1A Proteins↗
PubMed1985

Rating AIS severity using emergency department sheets vs. inpatient charts.

To determine whether sufficiently accurate estimates of injury severity can be based on limited data as would be available from an Emergency Department (ED) Sheet, Abbreviated Injury Severity (AIS) scores were derived for 166 trauma patients using two different sources of data--the ED sheet and inpatient medical chart. These severity scores were compared by type of person assigning the scores and by external cause of the injury. Results indicate that in general, the ED sheet is not a suitable alternative to the complete inpatient chart when coding severity for individuals who sustain injuries severe enough to result in hospital admission.

Diagnosis-Related Groups↗
PubMed2001

Clinical and biochemical outcome of hepatorenal transplantation for hereditary systemic amyloidosis associated with apolipoprotein AI Gly26Arg.

BACKGROUND: Treatment of systemic amyloidosis comprises measures to support failing organ function coupled with attempts to reduce the supply of the respective amyloid fibril precursor protein. Orthotopic hepatic transplantation is effective in familial amyloid polyneuropathy associated with variant transthyretin, because this protein is produced almost exclusively in the liver. Hepatic transplantation has not been performed in hereditary apolipoprotein AI (apoAI) amyloidosis, and the liver's contribution to plasma apoAI levels has not been determined in vivo. METHODS: A 57-year-old Irish man with hereditary systemic amyloidosis associated with apoAI Gly26Arg, which had led to end-stage renal failure and progressive liver dysfunction, underwent hepatorenal transplantation. His outcome was followed clinically and his amyloid deposits were monitored with serum amyloid P component scintigraphy. The proportion of variant apoAI in the plasma was estimated by quantitative isoelectric focusing before and after liver transplantation. RESULTS: Plasma levels of variant apoAI decreased by 50% after liver transplantation, and the patient was asymptomatic 2 years after surgery. Subclinical amyloid deposits that were present in his spleen and heart preoperatively have regressed and stabilized respectively. CONCLUSIONS: Orthotopic liver transplantation substantially reduces the supply of the amyloid fibril precursor protein in hereditary apoAI amyloidosis, and the excellent outcome in this patient probably reflects the balance between deposition and turnover of amyloid having been altered in favor of the latter. These findings support the use of liver transplantation in patients with hereditary apoAI amyloidosis who develop hepatic dysfunction.

Amino Acid Substitution↗
PubMed2005

ATP-binding cassette transporter AI and its role in HDL formation.

PURPOSE OF REVIEW: ATP-binding cassette transporter AI (ABCA1)-mediated assembly of phospholipid and free cholesterol with apoA-I plays an important role in HDL biogenesis. This review focuses on recent progress in ABCA1-mediated HDL formation and regulation of ABCA1 expression. RECENT FINDINGS: Studies of hepatic ABCA1 overexpression suggest that the liver is a major site for HDL formation. Lipidation of apoA-I by ABCA1 increases its potential for reverse cholesterol transport based on the following findings: (1) apoA-I/lipid complexes formed by ABCA1 are better acceptors of cellular lipid via non-ABCA1-mediated efflux pathways than lipid-free apoA-I in vitro and (2) lipidation of apoA-I prevents it from rapidly associating with plasma HDL in vivo, resulting in more available nascent pre-beta HDL for cellular lipid efflux. Several novel regulatory mechanisms for ABCA1 at the post-transcriptional level have been identified recently. Interaction of apoA-I with ABCA1 prevents phosphorylation of a sequence rich in proline, glutamic acid, serine and threonine in a cytoplasmic domain of ABCA1, resulting in less degradation by calpain proteolysis and increased surface expression of ABCA1. In addition, destabilization and decreased cellular surface expression of ABCA1 protein by unsaturated fatty acids have been identified. SUMMARY: Initial lipidation of apoA-I by hepatic ABCA1 is critical for plasma HDL formation because it enables pre-beta HDL to function more efficiently as a cholesterol acceptor for other pathways of cholesterol efflux in the reverse cholesterol transport pathway and prevents apoA-I from rapidly associating with preexisting plasma HDL particles, resulting in greater availability of pre-beta HDL particles for cholesterol efflux.

ATP Binding Cassette Transporter 1↗
PubMed2006

Which AIS based scoring system is the best predictor of outcome in orthopaedic blunt trauma patients?

BACKGROUND: Abbreviated Injury Scale (AIS)-based systems-the Injury Severity Score (ISS), New Injury Severity Score (NISS), and AISmax-are used to assess trauma patients. The merits of each in predicting outcome are controversial. METHODS: A large prospective database was used to assess their predictive capacity using receiver operator characteristic curves. RESULTS: In all, 10,062 adult, blunt-trauma patients met the inclusion criteria. All systems were significant outcome predictors for sepsis, multiple organ failure (MOF), length of hospital stay, length of intensive care unit (ICU) admission and mortality (p < 0.0001). NISS was a significantly better predictor than the ISS for mortality (p < 0.0001). NISS was equivalent to the AISmax for mortality prediction and superior in patients with orthopaedic injuries. NISS was significantly better for sepsis, MOF, ICU stay, and total hospital stay (p < 0.0001). CONCLUSIONS: NISS is superior or equivalent to the ISS and AISmax for prediction of all investigated outcomes in a population of blunt trauma patients. As NISS is easier to calculate, its use is recommended to stratify patients for clinical and research purposes.

Abbreviated Injury Scale↗
PubMed2025

Alzheimer's subtypes A supervised, unsupervised, multimodal, multilayered embedded recursive (SUMMER) AI study.

Since Alzheimer's disease (AD) is a heterogeneous disease, different subtypes may have distinct biological, genetic, and clinical characteristics, requiring tailored interventions. While several proposed subtypes of AD exist, there is still no clear consensus on a definitive classification. By leveraging complementary AI approaches, including supervised and unsupervised learning, within a recursive pipeline (SUMMER) that integrates multimodal datasets encompassing MRI measurements, phenotypes, and genetic data, our goal was to generate robust scientific evidence for identifying AD subtypes. Data was downloaded from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database and included neuroimaging data (MRI), genetics (SNPs), clinical diagnosis, and demographics. 1133 European American participants' images, aged 55-95, were included in this study. The analysis was multi-fold, where the first step involved applying an unsupervised application to a subset of the MRI sample (AD + cognitively normal (CN) aged matched groups, 100 men aged 68-85 years, and 76 women aged 68-85 years). The MRI brain gray matter was segmented into 44 regions of interest (ROIs) according to a standard atlas, and 618 features were extracted, including ROI voxel intensity measurements such as minimum, maximum, and histogram variables. Results identified a cluster of subtype AD men and a cluster of subtype AD women that were distinct from the rest of their respective samples. In the next step, the integrity of the identified subtype AD clusters was investigated using the XGBoost supervised machine learning application with genetic features (SNPs, N=36,724) and labels: the identified subtype AD cluster vs. the rest of the sample, stratified by sex. A significant AD subtype men model (accuracy=0.85, F1=0.72, AUC=0.83) and a significant women AD subtype model (accuracy=0.81, F1=0.81, AUC=0.81) were built, confirming the homogeneity of the isolated AD subtype clusters. Discriminative biomarkers were extracted from the significant models, including selected ROIs and SNPs. Finally, the subtype models were tested on an unseen subset of ADNI data. The genetic-based models identified clusters of AD subtype participants consisting of 34% of the men AD group and 47% of the women AD group. Phenotypic analysis indicates that lower body weight was associated with the women's AD subtype. Complex diseases like AD demand a sophisticated, multimodal approach for precise diagnosis. Effectively identifying disease subtypes enhances the potential for personalized treatment, ultimately improving patient outcomes.

Journal Article↗
PubMed2004

Combining FDI and AI approaches within causal-model-based diagnosis.

This paper presents a model-based diagnostic method designed in the context of process supervision. It has been inspired by both artificial intelligence and control theory. AI contributes tools for qualitative modeling, including causal modeling, whose aim is to split a complex process into elementary submodels. Control theory, within the framework of fault detection and isolation (FDI), provides numerical models for generating and testing residuals, and for taking into account inaccuracies in the model, unknown disturbances and noise. Consistency-based reasoning provides a logical foundation for diagnostic reasoning and clarifies fundamental assumptions, such as single fault and exoneration. The diagnostic method presented in the paper benefits from the advantages of all these approaches. Causal modeling enables the method to focus on sufficient relations for fault isolation, which avoids combinatorial explosion. Moreover, it allows the model to be modified easily without changing any aspect of the diagnostic algorithm. The numerical submodels that are used to detect inconsistency benefit from the precise quantitative analysis of the FDI approach. The FDI models are studied in order to link this method with DX component-oriented reasoning. The recursive on-line use of this algorithm is explained and the concept of local exoneration is introduced.

Algorithms↗
PubMed2006

Associations between apolipoprotein B, apolipoprotein AI, the apolipoprotein B/AI ratio and coronary heart disease: a literature-based meta-analysis of prospective studies.

OBJECTIVES: To assess associations of circulating levels of apolipoprotein (apo) AI, apoB and the apoB/AI ratio (apoB/A) with risk of incident coronary heart disease (CHD). DESIGN: Literature-based meta-analysis of prospective studies. DATA SOURCES: Prospective studies in essentially general populations that reported on associations between apoAI, apoB or apoB/A and first incident CHD outcomes. Studies were identified by computer-based searches and by manual searches of the relevant literature. RESULTS: Data from 23 relevant studies were identified. For apoAI, with 6333 CHD cases in 21 studies, comparison of individuals in the bottom third with those in the top third of baseline values yielded a combined relative risk of 1.62 (95% confidence interval: 1.43-1.83), i.e. an inverse association. For apoB, a combined analysis of 6320 CHD cases from 19 studies gave a relative risk of 1.99 (1.65-2.39) for a comparison of individuals in the top third versus those in the bottom third of baseline values. For apoB/A, with 3730 CHD cases from seven studies, a comparison of individuals in the top third versus the bottom third of baseline values gave a combined relative risk of 1.86 (1.55-2.22). These associations were somewhat stronger following correction for within-person variations in apolipoprotein levels. There was evidence of heterogeneity amongst the published studies, but it was only partly explained by available study-level characteristics. CONCLUSIONS: The present quantitative review suggests the existence of moderately strong associations between baseline levels of each of apoAI, apoB, and apoB/A and risk of CHD. More detailed analysis, perhaps based on individual participant data from prospective studies, could help to overcome several limitations in the present review and to clarify any relevance of these apolipoproteins to disease prediction and aetiology.

Apolipoprotein A-I↗
PubMed1986

DNA polymorphisms around the apo AI gene in normal and hyperlipidaemic individuals selected for a twin study.

We have investigated the allele frequencies, in a Norwegian population, of two restriction fragment length polymorphisms (RFLPs) in the apolipoprotein (apo) AI-CIII-AIV gene region. The study group consisted of clinically well twins and their unrelated spouses. In the normotriglyceridaemic individuals tested, the frequency of the rare allele (S2) of the RFLP detected using the restriction enzyme Sst I was 0.17; for the RFLP detected with the enzyme Xmn I, the rare allele (X2) frequency was 0.06. The frequency of the S2 allele was lower in individuals with serum triglyceride levels above 1.7 mmol l-1, but this was not statistically significant. Conversely, the frequency of the X2 allele was higher in individuals with raised serum triglyceride levels, but similarly, did not reach statistical significance. Taken together with the data from our previous study on UK individuals, these results support the suggestion that inherited variations in this apolipoprotein gene cluster are involved in the determination of serum triglyceride levels.

Alleles↗
PubMed1994

Associations of genotypes at the apolipoprotein AI-CIII-AIV, apolipoprotein B and lipoprotein lipase gene loci with coronary atherosclerosis and high density lipoprotein subclasses.

Association studies were carried out in a sample of 86 patients from Sweden who had survived a myocardial infarction (MI) at a young age and 93 age-matched healthy individuals, to compare the impact of polymorphisms at the apolipoprotein (apo) AI-CIII-AIV gene cluster on among-individual differences in plasma lipid and lipoprotein traits, the five high density lipoprotein (HDL) subclasses (2b to 3c), lipoprotein lipase (LPL) activity and presence and progression of atherosclerosis. Individuals were genotyped for four polymorphisms; 5'apoAI (G/A-75), 3'apoAI (PstI; P +/-), apoCIII (C/T1100) and apoCIII (PvuII; V +/-), using PCR-based techniques. Allele frequencies were similar in healthy individuals and patients (frequencies of alleles in combined population: 5'apoAI-A-75 = 0.14, 3'apoAI-P- = 0.05, apoCIII-T1100 = 0.27 and apoCIII-V- = 0.18). In the healthy individuals, levels of low density lipoprotein (LDL) triglycerides were significantly associated with genotypes of the apoCIII-PvuII polymorphism (p = 0.02), but no other associations were found between lipids or HDL subclasses and single polymorphisms in the apoAI-CIII-AIV gene cluster. Levels of triglycerides and very low density lipoprotein (VLDL) triglycerides were significantly higher in the presence of the haplotype defined by the presence of apoCIII-T1100 and common alleles of the other three polymorphisms, explaining 5.8% and 7.8% (p = 0.03 and 0.01), respectively, of sample variance. In the patients, no associations were found between lipids or HDL subclasses and variation at the apoAI-CIII-AIV gene cluster. Associations were also examined between levels of HDL subclasses and variation at the apoE (common isoforms), apoB (signal peptide and XbaI polymorphisms) and lipoprotein lipase (PvuII, HindIII and Serine447/Stop polymorphisms) gene loci. In the patient group only, levels of protein in HDL2b, HDL2a and HDL3b subclasses were significantly associated with genotypes of the LPL-HindIII polymorphism (22.1, 19.3 and 11.4%, respectively, of sample variance; p < 0.05). Finally, associations were examined between genotypes at the apoAI-CIII-AIV gene cluster and the extent of coronary atherosclerosis. Global severity of atherosclerosis at the first angiography was weakly associated with genotypes of the apoCIII-C/T1100 polymorphism, presence of the T1100 allele being associated with 53% lower median score (1.6 vs 0.75; p = 0.09).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1982

Dissociation of apolipoprotein AI from apoprotein-lipid complexes and from high-density lipoproteins. A fluorescence study.

The dissociation of the apoprotein AI (apoAI) from the apoAI-dimyristoylglycerophosphocholine complex and from human high-density lipoproteins (HDL), was induced by incubation with guanidinium hydrochloride at concentrations between 0 M and 7 M. The kinetics and extent of denaturation were followed by monitoring both the fluidity of the lipid phase by fluorescence polarization measurements and the protein conformation by measuring the tryptophanyl fluorescence emission. The association with lipids protects apoAI against denaturation both in HDL and in the apoAI-phospholipid complex. The results of the kinetic and end-point measurements suggest that the denaturing effect of guanidine hydrochloride on the apoAI-lipid complex and on HDL is a two-step process. It involves the dissociation of the apoAI-phospholipid bond, as evidenced by fluidity measurements: this effect is maximal between 3 M and 4 M guanidine hydrochloride. The conformational change of the apoAI protein into a randomly coiled structure with the tryptophanyl residues exposed to the solvent is maximal between 4 M and 6 M guanidine hydrochloride. HDL and the apoAI-phospholipid complex have a closely similar behaviour towards denaturation by guanidine hydrochloride indicating that the phospholipid-apoAI association in HDL is primarily responsible for the stability of the lipoprotein molecule.

Apolipoprotein A-I↗
PubMed1996

Branched synthetic constructs that mimic the physico-chemical properties of apolipoprotein AI in reconstituted high-density lipoproteins.

Amphipathic helical repeats are considered as the structural units of numerous apolipoproteins and have been described as being responsible for the interaction of apolipoproteins with phospholipids in high-density lipoproteins (HDL). Furthermore, apolipoproteins, and especially apolipoprotein AI (apoAI), are involved in various biological functions of these circulating particles in plasma. Studies with synthetic peptides corresponding to domains of the apoAI sequence have however shown that short 39-residue fragments do not interact strongly enough with phospholipids to generate particles that correctly mimic the physico-chemical properties of HDL reconstituted with native apoAI [Vanloo, B., Demoor, L., Boutillon, C., Lins, L., Baert, J., Fruchart, J. C., Tartar, A. & Rosseneu, M. (1995) Association of synthetic peptide fragments of human apolipoprotein A-I with phospholipids, J. Lipid Res. 36, 1686-1696.]. Here we show that synthetic branched multimeric peptides, often used as carriers for the design of synthetic vaccines (multiple-antigen peptides), can be used to mimic the physiochemical properties of apoAI in HDL. This type of molecule is obtained by using a small core matrix of Lys residues bearing radially branched synthetic peptides as dendritic arms. We compared the lipid-binding capacities and the structural properties of a linear peptide corresponding to residues 145-183 of apoAI [apoAI-(145-183)-peptide] with those of two multimeric peptides consisting respectively of three [trimeric apoAI-(145-183)] and four copies [tetrameric apoAI-(145-183)] of the selected sequence, branched on a covalent core matrix. This paper provides evidence for the increased abilities of the multimeric peptides to associate with phospholipids compared with the short linear peptides. Moreover, the trimeric apoAI-(145-183) peptide was most efficient in mimicking the physico-chemical and structural properties of native apoAI in reconstituted HDL. As tools adequate to unravel the structure/function relationship of separate apolipoprotein domains are still missing, these multimeric peptides might constitute an alternative approach to linear peptides which are poor mimetics and to protein mutants which are difficult to produce and only provide information about the total sequence.

Amino Acid Sequence↗
PubMed1997

Role of the carboxy-terminal domain of human apolipoprotein AI in high-density-lipoprotein metabolism--a study based on deletion and substitution variants in transgenic mice.

Cholesterol levels in high-density lipoprotein (HDL) of transgenic mice overexpressing human apolipoprotein AI (apoAI), a des-(190-243)-apoAI deletion mutant or an apoAI-(1-189)-apoAII-(12-77) chimera were 2.8-fold (P<0.001), 1.3-fold (P<0.05) and 2.2-fold (P<0.001) higher than in control mice, respectively. Human apolipoprotein levels in apoAI and in apoAI-(1-189)-apoAII-(12-77) transgenic mice were 5.2-fold and 3.5-fold higher than in des-(190-243)-apoAI transgenic mice, whereas their HDL cholesterol levels were 2.1-fold and 1.6-fold higher. PAGE of HDL isolated by ultracentrifugation revealed that murine HDL migrated as 9.6-nm and 7.2-nm particles. Overexpression of human apoAI and apoAI-(1-189)-apoAII-(12-77) resulted in the production of polydisperse HDL (9.6, 9.2, 8.4 and 7.2 nm) particles, whereas overexpression of des-(190-243)-apoAI primarily resulted in an increase of 7.2-nm particles. The fractional catabolic rates of human apoAI and apoAI-(1-189)-apoAII-(12-77) were very similar, whereas that of des-(190-243)-apoAI was 4.9-fold higher. The endogenous production rates of human apoAI, des-(190-243)-apoAI and apoAI-(1-189)-apoAII-(12-77) in transgenic mice were very similar. It is concluded that deletion of the carboxy-terminal domain of apoAI reduces its lipoprotein association, resulting in the production of small, phospholipid-rich HDL particles that are cleared more rapidly. Substitution of the carboxy-terminal helices of apoAI with helices of apoAII restores lipoprotein association, resulting in the production of HDL, which migrates as human HDL3 and HDL2. Although the carboxy-terminal domain of the chimera contained more than 80% of the amino acid sequence of apoAII, its HDL-distribution profile in transgenic mice was very similar to that of human apoAI. This study demonstrates the importance of the helical structure of apoAI of the carboxy-terminal domain of apoAI, rather than of its exclusive amino acid sequence, in HDL metabolism.

Animals↗
PubMed2006

Organ transplantation in hereditary apolipoprotein AI amyloidosis.

Patients with hereditary apolipoprotein AI (apoAI) amyloidosis often have extensive visceral amyloid deposits, and many develop end-stage renal failure as young adults. Solid organ transplantation to replace failing organ function in systemic amyloidosis is controversial due to the multisystem and progressive nature of the disease and the risk of recurrence of amyloid in the graft. We report the outcome of solid organ transplantation, including dual transplants in 4 cases, among 10 patients with apoAI amyloidosis who were followed for a median (range) of 16 (4-28) and 9 (0.2-27) years from diagnosis of amyloidosis and transplantation, respectively. Eight of 10 patients were alive, seven with a functioning graft at censor. Two patients died, one of disseminated cytomegalovirus infection 2 months after renal transplantation and the other of multisystem failure following severe trauma more than 13 years after renal transplantation. The renal transplant of one patient failed due to recurrence of amyloid after 25 years. Amyloid disease progression was very slow and the natural history of the condition was favorably altered in both cases in which the liver was transplanted. Failing organs in hereditary apoAI amyloidosis should be replaced since graft survival is excellent and confers substantial survival benefit.

Adolescent↗
PubMed2003

Apolipoprotein AI as therapy for atherosclerosis: does the future of preventive cardiology include weekly injections of the HDL protein?

Conventional wisdom suggests that halting or reversing long-term atherosclerosis requires increasing the amount of circulating high-density lipoprotein (HDL) coursing through the vasculature. However, recent evidence seems to indicate that reducing the size of cholesterol-containing lipid plaques might be accomplished by methods that either do not raise or, in fact, lower the amount of circulating HDL. Carriers of apoAI(Milano), a variant of apoprotein AI (a component of HDL), have reduced levels of circulating low-density lipoprotein (LDL). Intriguingly, these individuals have reduced amounts of circulating HDL and total apoAI. Infusions of the ApoAI(Milano) variant given to patients with coronary atherosclerosis appear to lead to disease regression and reduced plaque size. However, larger studies are required to provide definitive proof of apoAI(Milano)'s benefits. What is certain is that attention should be focused on the removal of cholesterol from plaques rather than simply desiring to raise HDL concentrations in patients.

Apolipoprotein A-I↗