# Infections and AA amyloidosis: An overview

Samuel Deshayes, Achille Aouba, Gilles Grateau, Sophie Georgin-lavialle

► To cite this version:

Samuel Deshayes, Achille Aouba, Gilles Grateau, Sophie Georgin-lavialle. Infections and AA amyloidosis: An overview. International Journal of Clinical Practice, 2021, 75 (6), pp.e13966. 10.1111/ijcp.13966 . inserm-04050338

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# Infections and AA amyloidosis: An overview

Samuel Deshayes<fnref n="1" /> ID

Achille Auoba<fnref n="1" /> ID

Gilles Grateau<fnref n="2" /> ID

Sophie Georgin-Lavialle<fnref n="2" /> ID

## Correspondence

Sophie Georgin-Lavialle, Service de médecine interne, Sorbonne Université, GRC-28 (GRAASU), Centre national de référence des maladies autoinflammatoires et des amyloses inflammatoires (CEREMAIA), hôpital Tenon, AP-HP, 75020 Paris, France.
Email: sophie.georgin-lavialle@aphp.fr

## Abstract

**Background:** Amyloidoses are a heterogeneous group of systemic diseases characterised by extracellular accumulation of insoluble amyloid fibrils derived from unfolded proteins. Inflammatory (AA) amyloidosis can complicate various inflammatory disorders that are associated with a sustained acute phase response and serum amyloid A (SAA) protein overproduction. Chronic infections were the first recognised cause of amyloidoses. However, with the better management of underlying diseases, the frequency of AA amyloidosis is decreasing.

**Purpose:** The aim of this overview was to discuss the several infections associated with AA amyloidosis and the relative frequency of infections as aetiological factors.

**Methods:** A search of the literature was performed using the PubMed database using the MeSH terms "Amyloidosis" and "Infections," from inception to December 31st, 2019. Articles written in other languages than English or French were excluded.

**Results:** The frequency of AA amyloidosis secondary to infections decreased from more than 50% to less than 20% after the 2000s, with a parallel increase in the frequency of AA amyloidosis secondary to inflammatory diseases and to an unknown cause.

**Conclusion:** Whereas new antibiotics have been developed and sanitary conditions are better, infections still represent 5%-30% of the causes of AA amyloidosis, including in developed countries. These data argue for better screening of chronic infections to prevent AA amyloidosis and the development of new strategies to manage recurrent infections.

## 1 | INTRODUCTION

AA amyloidosis is characterised by the deposits of an amorphous substance including fragments of the serum amyloid-associated (SAA) protein. As SAA is an acute-phase reactant, several diseases with long-standing inflammation may be complicated by AA amyloidosis, such as chronic idiopathic inflammatory diseases, autoinflammatory diseases, cancers, and chronic infections.<fnref n="1" />⁻³

The first described cases of amyloidosis were of the AA type, secondary to chronic infections.⁴ However, with the better management of underlying diseases, the frequency of AA amyloidosis is decreasing in favour of AL and ATTR amyloidosis.⁵⁻⁷

The aim of this overview was to discuss the several infections associated with AA amyloidosis and the relative frequency of infections as aetiological factors.

## 2 | METHODS

Material for this narrative review was found by searching the PubMed database using the MeSH terms "Amyloidosis" and "Infections," from inception to December 31st, 2019. Articles were included if they reported patients suffering from AA amyloidosis or presumed reactive amyloidosis and an identified infection or a situation associated with recurrent infections, as well as the

<footnote n="1">¹Service de médecine interne, Normandie University, UNICAEN, CHU de Caen Normandie, Caen, France</footnote>

<footnote n="2">²Sorbonne Université, Service de médecine interne, GRC-28 (GRAASU), Centre national de référence des maladies autoinflammatoires et des amyloses inflammatoires (CEREMAIA), hôpital Tenon, AP-HP, Paris, France</footnote>
main case series with more than 100 patients. Articles written in other languages than English or French were excluded. Relevant articles within the reference lists of the retrieved articles were also included.

# 3 | INFECTIONS ASSOCIATED WITH AA AMYLOIDOSIS

## 3.1 | Mycobacteria

Most cases of AA amyloidosis secondary to infections are, or at least were, secondary to mycobacteria (Figure 1).

Indeed, before the introduction of efficient tuberculosis therapy, tuberculosis accounted for more than half of the cases of secondary amyloidosis.⁸⁻¹¹ In addition, tuberculosis can be complicated by secondary amyloidosis in 5% of cases.¹² Tuberculosis remains an important cause of AA amyloidosis in endemic countries; therefore, more than one-third of renal amyloidosis in a Turkish study published in 1995 is secondary to tuberculosis.¹³ Nontuberculous mycobacterial infections are exceptionally reported.¹⁴,¹⁵

Similarly, leprosy could be complicated by amyloidosis in 2%-55% of patients, especially in cases of lepromatous leprosy,¹⁶⁻²⁰ but this cause is currently exceptional.

## 3.2 | Bacteria

Before the mid-19th century, syphilis was a classic cause of amyloidosis.⁹,²¹⁻²⁶

Several cases of amyloidosis secondary to Whipple disease have been published, including recently.²⁷⁻³³

More commonly, focal chronic infection with any bacteria can be complicated by amyloidosis, such as chronic osteomyelitis,³⁴⁻³⁸ chronic pyelonephritis, untreated abscess in any location, prosthetic infections or endocarditis.²²⁻²⁴,³⁹⁻⁴⁹

### Review criteria

* Infections associated with AA amyloidosis were reviewed following the retrieval of relevant articles from PubMed.

### Message for the clinic

* The frequency of AA amyloidosis secondary to infections is decreasing.

* However, infections still represent 5%-30% of the causes of AA amyloidosis.

* Better screening of chronic infections and the development of strategies to manage recurrent infections are needed.

More anecdotally, other chronic infections have rarely been associated with secondary amyloidosis, such as Q fever⁵⁰,⁵¹ and brucellosis.⁵²,⁵³

## 3.3 | Parasites

The most frequently reported parasitic cause of AA amyloidosis is schistosomiasis,⁵⁴⁻⁵⁹ but evidence of this remains highly anecdotal.

Other parasitic infections are much less frequently reported, such as echinococcosis,⁵,⁶⁰⁻⁶³ giardiasis,⁶⁴ leishmaniasis,⁶⁵,⁶⁶ malaria,⁶⁷,⁶⁸ and filariasis.⁶⁹

## 3.4 | Viruses

Very few viruses have been associated with AA amyloidosis. Human immunodeficiency virus (HIV) is the most frequently

<figure><img src="image_2.png" /><figcaption>**FIGURE 1** Illustrative cases of pulmonary tuberculosis with bronchiectasis on chest computed tomography scans (A) and lymph node tuberculosis on ¹⁸F-fluorodeoxyglucose coupled with computed tomography scans (B) responsible for AA amyloidosis</figcaption></figure>
reported.⁴²,⁶⁵,⁷⁰⁻⁷⁶ Therefore, amyloidosis can be responsible for up to 10% of kidney diseases in HIV,⁷⁷ but whether this association is secondary to infections induced by immunodeficiency or coinfections or to the virus that is responsible for the chronic inflammation remains to be determined.

Few cases of AA amyloidosis associated with hepatitis B infection have been published.⁷⁸⁻⁸¹ Regarding cases of AA amyloidosis associated with hepatitis C, patients often have coinfections and/or are drug addicts, making it difficult to ascertain the specific role of hepatitis C.⁸²

## 3.5 | Fungi

Regarding fungi, most of the data are related to aspergillosis,⁸³⁻⁸⁸ but several of these amyloidosis cases could be secondary to bronchiectasis induced by aspergillosis rather than aspergillosis itself. AA amyloidosis has also, seldomly, been associated with coccidioidomycosis,⁴⁵ actinomycosis,²¹,⁸⁹,⁹⁰ and mucormycosis.⁹¹

## 3.6 | Other situations associated with recurrent infections

Apart from chronic infections, several situations associated with recurrent infections can also be complicated by AA amyloidosis. Indeed, drug abuse is responsible for recurrent infections, especially in patients with skin infections because of subcutaneous injection (known as "skin popping").⁹²⁻⁹⁸ Therefore, as many as 14% of subcutaneous drug users have reactive amyloidosis,⁹⁹ 100% of cases of renal AA amyloidosis in a hospital from San Francisco

from 1998 to 2013 were secondary to skin popping,⁸² and 30%-50% of renal diseases in heroin abusers were secondary to amyloidosis.⁷⁰,⁹⁵ These patients are also frequently hepatitis C or HIV positive.⁷⁰,⁹⁶,⁹⁷

Another situation frequently associated with infections, especially decubitus ulcers and urinary tract infections, is paraplegia.²³,¹⁰⁰⁻¹⁰² Amyloidosis can be found in more than 20% of paraplegic patients at autopsy.¹⁰³,¹⁰⁴

Several diseases predispose patients to recurrent pulmonary infections. Amongst them, bronchiectasis, because of any cause, is the leading cause and represents a substantial percentage of causes of AA amyloidosis,¹⁰⁵,¹⁰⁶ up to 40% of AA amyloidosis in hemodialysis patients in a case series.¹⁰⁷ Regarding other causes, some genetic diseases responsible for recurrent pulmonary infections can be complicated by AA amyloidosis, in part because of secondary bronchiectasis. Therefore, more than 50 cases of AA amyloidosis associated with cystic fibrosis have been reported.¹⁰⁸⁻¹¹⁵ Amyloidosis was found in 0.5% of patients with cystic fibrosis in an Italian study in 1985,¹¹⁶ accounting for approximately one-quarter of the causes of kidney diseases¹¹² and for 1.3% of the causes of death in cystic fibrosis in Italy.¹¹⁷ Kartagener syndrome has also been associated with AA amyloidosis.¹¹⁸⁻¹²⁰

Similarly, several primary immunodeficiencies have been associated with AA amyloidosis, including common variable immunodeficiency,¹²¹⁻¹³⁰ X-linked agammaglobulinemia,¹³¹⁻¹³⁴ cyclic neutropenia,¹³⁵ chronic granulomatous disease,⁸⁴,¹³⁶,¹³⁷ hyperimmunoglobulin E syndrome,¹³⁸ and leucocyte adhesion deficiency.¹³⁹

We can also mention recurrent skin infections³⁹,⁴⁵,¹⁴⁰⁻¹⁴⁵ and recurrent exacerbation of chronic pulmonary obstructive disease.¹⁴⁶⁻¹⁴⁸

<table><caption>TABLE 1 Frequencies of different causes of secondary amyloidosis in the main case series from the literature with more than 100 patients</caption><thead><tr><th>First author [Ref.]</th><th>Country</th><th>Sample size</th><th>Period</th><th>Infections</th><th>Inflammatory diseases</th><th>Hereditary fevers</th><th>Cancers</th><th>Unknown</th><th>Unspecified miscellaneous</th></tr></thead><tbody><tr><td>Auerbach<sup>9</sup></td><td>USA</td><td>379</td><td>Unknown</td><td>379 (100%)</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td></tr><tr><td>Brownstein<sup>45</sup></td><td>USA</td><td>100</td><td>1945-1968</td><td>63 (63%)</td><td>19 (19%)</td><td>0</td><td>18 (18%)</td><td>0</td><td>0</td></tr><tr><td>Rizvi<sup>10</sup></td><td>India</td><td>198</td><td>Unknown</td><td>178 (90%)</td><td>16 (8%)</td><td>0</td><td>4 (2%)</td><td>0</td><td>0</td></tr><tr><td>Chugh<sup>11</sup></td><td>India</td><td>203</td><td>1957-1979</td><td>182 (90%)</td><td>13 (6%)</td><td>NA</td><td>NA</td><td>NA</td><td>8 (4%)</td></tr><tr><td>Tuglular<sup>148</sup></td><td>Turkey</td><td>287</td><td>Unknown</td><td>53 (19%)</td><td>30 (10%)</td><td>183 (64%)</td><td>0</td><td>21 (7%)</td><td>0</td></tr><tr><td>Ensari<sup>149</sup></td><td>Turkey</td><td>101</td><td>Unknown</td><td>12 (12%)</td><td>8 (8%)</td><td>81 (80%)</td><td>0</td><td>0</td><td>0</td></tr><tr><td>Bergesio<sup>150</sup></td><td>Italy</td><td>104</td><td>1995-2000</td><td>16 (15%)</td><td>58 (56%)</td><td>4 (4%)</td><td>3 (3%)</td><td>23 (22%)</td><td>0</td></tr><tr><td>Lachmann<sup>151</sup></td><td>England</td><td>374</td><td>1990-2005</td><td>56 (15%)</td><td>245 (65%)</td><td>32 (9%)</td><td>11 (3%)</td><td>23 (6%)</td><td>7 (2%)</td></tr><tr><td>Ahbap<sup>147</sup></td><td>Turkey</td><td>121</td><td>2001-2013</td><td>38 (31%)</td><td>10 (8%)</td><td>45 (37%)</td><td>NA</td><td>24 (20%)</td><td>4 (4%)</td></tr><tr><td>Lane<sup>43</sup></td><td>England</td><td>635</td><td>1990-2016</td><td>123 (19%)</td><td>330 (52%)</td><td>57 (9%)</td><td>4 (1%)</td><td>121 (19%)</td><td>0</td></tr><tr><td>Palladini<sup>142</sup></td><td>Italy</td><td>200</td><td>1991-2015</td><td>20 (10%)</td><td>87 (44%)</td><td>16 (8%)</td><td>8 (4%)</td><td>64 (32%)</td><td>5 (2%)</td></tr><tr><td>Okuda<sup>44</sup></td><td>Japan</td><td>199</td><td>2012-2014</td><td>9 (5%)</td><td>164 (82%)</td><td>4 (2%)</td><td>22 (11%)</td><td>0</td><td>0</td></tr></tbody></table>

Note: Values are displayed as absolute numbers (%). Some of these data are rederived from available percentages.

Abbreviations: NA, not available; USA, United States of America.
## 4 | FREQUENCY OF INFECTIONS AS AN AETIOLOGICAL FACTOR IN AA AMYLOIDOSIS

The frequency of infections as an aetiological factor of AA amyloidosis varies over time (better management of chronic infections with the advent of antibiotics and better sanitary conditions) and according to the country (developing vs developed countries) and the method of recruitment (autopsy series, positive renal biopsy or any type of tissue).

In addition, several limitations must be taken into account to analyse these data: (1) the diagnosis of some infections, such as Whipple disease or even tuberculosis, is probably more accurate currently than before; (2) similarly, the diagnosis of amyloidosis, and, a fortiori, the typing of amyloidosis in old articles is questionable, as many papers have diagnosed AA amyloidosis by treatment with KMnO₄; (3) as patients for whom no underlying disease could be found were diagnosed with primary amyloidosis, it is impossible to determine whether these patients had AL amyloidosis or AA amyloidosis without an identified known cause, and this may account, at least in part, in the increase in the frequency of AA amyloidosis of unknown cause currently; (4) causes of AA amyloidosis may be entangled and/or associated, either several associated infections or infectious and noninfectious causes. Typically, subcutaneous drug users are at increased risk of associated HIV, hepatitis C or tuberculosis infections or endocarditis⁷⁰,⁹⁶; (5) some countries may have an overrepresentation of a specific aetiology, such as familial Mediterranean fever in Mediterranean countries or tuberculosis in endemic countries; (6) some rare associations with only a few cases described may be doubtful and be only a coincidental association,³ although from a pathophysiological point of view, any disease responsible, directly or indirectly, for a chronic or recurrent increase in SAA levels may theoretically cause AA amyloidosis.

With these limitations in mind, the respective frequencies of causes of reactive amyloidosis in the main case series and the respective frequencies of infectious causes in the main case series with more than 100 patients are depicted in Tables 1 and 2, respectively, and Figure 2.⁹⁻¹¹,⁴³⁻⁴⁵,¹⁴²,¹⁴⁷⁻¹⁵¹ Therefore, the frequency of AA amyloidosis secondary to infections decreased from more than 50% to less than 20% after the 2000s, with a parallel increase in the frequency of AA amyloidosis secondary to inflammatory diseases and to an unknown cause.

Several cases of nephrotic syndrome disappeared under appropriate treatment of the causal infection, but relapse can occur with reinfection.⁴,³⁴,⁵⁴,¹⁰⁰,¹⁰⁶,¹⁵²⁻¹⁵⁵ In rare cases, a decrease or even the disappearance of amyloid deposits on repeated biopsies has been shown.¹¹,⁵⁵,⁶⁹,¹⁵⁴⁻¹⁵⁶

Of note, it could be possible that some factors favour the development of AA amyloidosis in patients exposed to infections, such as diet and physical activity¹⁸ or genetic cofactors, including variants in the SAA gene.¹⁵⁷

<table><caption>TABLE 2 Specific infectious causes responsible for secondary amyloidosis in the main case series from the literature</caption><thead><tr><th>First author [Ref.]</th><th>Mycobacteria (tuberculosis)</th><th>Bacteria</th><th>Fungi</th><th>Lung infections</th><th>Bone infections</th><th>Skin infections</th><th>Urinary infections</th><th>Paraplegia</th><th>Drug abuse</th><th>Cystic fibrosis</th><th>Other chronic or recurrent infections</th></tr></thead><tbody><tr><td>Auerbach<sup>9</sup></td><td>374 (374)</td><td>1</td><td>0</td><td>4</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td></tr><tr><td>Brownstein<sup>45</sup></td><td>27 (24)</td><td>0</td><td>1</td><td>6</td><td>2</td><td>3</td><td>23</td><td>0</td><td>0</td><td>0</td><td>1</td></tr><tr><td>Rizvi<sup>10</sup></td><td>152 (150)</td><td>0</td><td>0</td><td>26</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td></tr><tr><td>Chugh<sup>11</sup></td><td>125 (120)</td><td>NA</td><td>NA</td><td>49</td><td>8</td><td>NA</td><td>NA</td><td>NA</td><td>NA</td><td>NA</td><td>NA</td></tr><tr><td>Tuglular<sup>148</sup></td><td>28 (28)</td><td>0</td><td>0</td><td>18</td><td>7</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td></tr><tr><td>Ensari<sup>149</sup></td><td>8 (8)</td><td>0</td><td>0</td><td>4</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td></tr><tr><td>Bergesio<sup>150</sup></td><td>6 (6)</td><td>0</td><td>0</td><td>4</td><td>2</td><td>0</td><td>2</td><td>0</td><td>0</td><td>2</td><td>0</td></tr><tr><td>Lachmann<sup>151</sup></td><td>3 (3)</td><td>NA</td><td>NA</td><td>20</td><td>5</td><td>NA</td><td>NA</td><td>8</td><td>13</td><td>NA</td><td>7</td></tr><tr><td>Ahbab<sup>147</sup></td><td>30 (30)</td><td>NA</td><td>NA</td><td>8</td><td>NA</td><td>NA</td><td>NA</td><td>NA</td><td>NA</td><td>NA</td><td>NA</td></tr><tr><td>Lane<sup>43</sup></td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td><td>51</td><td>0</td><td>72</td></tr><tr><td>Palladini<sup>142</sup></td><td>0</td><td>0</td><td>0</td><td>4</td><td>0</td><td>0</td><td>8</td><td>0</td><td>0</td><td>8</td><td>0</td></tr><tr><td>Okuda<sup>44</sup></td><td>6 (2)</td><td>NA</td><td>NA</td><td>NA</td><td>2</td><td>NA</td><td>NA</td><td>NA</td><td>NA</td><td>NA</td><td>1</td></tr></tbody></table>

Note: Values are displayed as absolute numbers. Some of these data are rederived from available percentages.

Abbreviation: NA, not available.
<figure><img src="image_3.png" /><figcaption>FIGURE 2 Respective frequencies of causes of inflammatory amyloidosis in the main case series from the literature with more than 100 patients before (A) and after (B) the 2000s and respective frequencies of infections (C)</figcaption></figure>

5 | CONCLUSION

Whereas new antibiotics have been developed and sanitary condi-
tions are better, infections still represent 5%-30% of the causes of
AA amyloidosis, including in developed countries. These data argue
for better screening of chronic infections to prevent AA amyloi-
dosis and the development of new strategies to manage recurrent
infections.

DISCLOSURE

The authors have no conflict of interest to declare.

DATA AVAILABILITY STATEMENT

Data sharing not applicable to this article as no datasets were gener-
ated or analysed during the current study.

ORCID

Samuel Deshayes ID https://orcid.org/0000-0001-8887-3233

Achille Aouba ID https://orcid.org/0000-0003-1726-3811

Gilles Grateau ID https://orcid.org/0000-0002-8767-7385

Sophie Georgin-Lavialle ID https://orcid.

org/0000-0001-6668-8854

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**How to cite this article:** Deshayes S, Aouba A, Grateau G, Georgin-Lavialle S. Infections and AA amyloidosis: An overview. *Int J Clin Pract*. 2021;75:e13966. https://doi.org/10.1111/ijcp.13966