\documentclass[10pt]{article}

\usepackage{fullpage}
\usepackage{setspace}
\usepackage{parskip}
\usepackage{titlesec}
\usepackage[section]{placeins}
\usepackage{xcolor}
\usepackage{breakcites}
\usepackage{lineno}
\usepackage{hyphenat}





\PassOptionsToPackage{hyphens}{url}
\usepackage[colorlinks = true,
            linkcolor = blue,
            urlcolor  = blue,
            citecolor = blue,
            anchorcolor = blue]{hyperref}
\usepackage{etoolbox}
\makeatletter
\patchcmd\@combinedblfloats{\box\@outputbox}{\unvbox\@outputbox}{}{%
  \errmessage{\noexpand\@combinedblfloats could not be patched}%
}%
\makeatother


\usepackage{natbib}




\renewenvironment{abstract}
  {{\bfseries\noindent{\abstractname}\par\nobreak}\footnotesize}
  {\bigskip}

\titlespacing{\section}{0pt}{*3}{*1}
\titlespacing{\subsection}{0pt}{*2}{*0.5}
\titlespacing{\subsubsection}{0pt}{*1.5}{0pt}


\usepackage{authblk}


\usepackage{graphicx}
\usepackage[space]{grffile}
\usepackage{latexsym}
\usepackage{textcomp}
\usepackage{longtable}
\usepackage{tabulary}
\usepackage{booktabs,array,multirow}
\usepackage{amsfonts,amsmath,amssymb}
\providecommand\citet{\cite}
\providecommand\citep{\cite}
\providecommand\citealt{\cite}
% You can conditionalize code for latexml or normal latex using this.
\newif\iflatexml\latexmlfalse
\providecommand{\tightlist}{\setlength{\itemsep}{0pt}\setlength{\parskip}{0pt}}%

\AtBeginDocument{\DeclareGraphicsExtensions{.pdf,.PDF,.eps,.EPS,.png,.PNG,.tif,.TIF,.jpg,.JPG,.jpeg,.JPEG}}

\usepackage[utf8]{inputenc}
\usepackage[ngerman,greek,english]{babel}



\usepackage{float}








\begin{document}

\title{Epidemiology of monoclonal gammopathy in Morocco- A hospital-based study
Running Head: Monoclonal gammopathy}



\author[1]{Zhor  Ouzzif}%
\author[1]{KAMAL DOGHMI}%
\author[1]{nezha messaoudi}%
\author[1]{Sanae  Bouhsain}%
\author[1]{SAMIRA EL MACHTANI IDRISSI}%
\author[1]{Asmâa Biaz}%
\author[1]{Achraf  Rachid}%
\author[1]{Abdellah  Dami}%
\author[1]{Ahmed BEZZA}%
\author[2]{AISSAM EL MAATAOUI}%
\affil[1]{Hopital Militaire d'Instruction Mohammed V}%
\affil[2]{Universite Ibn Zohr}%


\vspace{-1em}



  
  \date{May 26, 2024}


\begingroup
\let\center\flushleft
\let\endcenter\endflushleft
\maketitle
\endgroup





\selectlanguage{english}
\begin{abstract}
Introduction: Monoclonal gammopathies are a group of disorders
associated with monoclonal proliferation of plasma cells that produces a
monoclonal protein. To describe the epidemiological and immunochemical
characteristics of monoclonal gammopathies diagnosed during a
nineteen-year period in a Moroccan teaching hospital was the main
objective of this study. Methods: This study was performed from January
2000 to August 2019. It was a retrospective study that included of 545
Moroccan patients with monoclonal gammopathy. Results: The patients who
participated in the study, 374 (68.6\%) were male and 171(31.4\%) were
female, with a mean \selectlanguage{ngerman}±SD age of 62.24±13.14 years. The most frequent
reasons for admission were bone pain (41,60\%), renal failure (19.08\%),
alteration of the general condition (12.21\%) and anemia (10.69). Plasma
cell proliferative disorders in our study were as follow, multiple
myeloma (MM) (45.65\%), Monoclonal gammopathies of undetermined
significance (MGUS) (39.05\%), Waldenstrom's macroglobulinemia(5.58\%),
Lymphoma (2.27\%+1.2\%), Chronic Lymphocytic Leukemia (2.48\%), Plasma
cell leukemia (1.86\%), Plasmacytoma (0.62\%), POEMS syndrome (0.41\%),
and Amyloidosis (0.84\%). The most frequent isotypes in MM were the IgG\selectlanguage{greek}κ
\selectlanguage{english}(62) 36.5\%, IgG\selectlanguage{greek}λ\selectlanguage{english}(52)30.6\%, IgA\selectlanguage{greek}κ\selectlanguage{english}(27)15.9\% and the IgA\selectlanguage{greek}λ \selectlanguage{english}(19)11.2\%. It
is also worthy of note, that Free light chain MM represents 20\% of all
cases of MM. Conclusions: This is the largest Moroccan cohort, it
included 545 patients. The results of this study point to the need for
an early diagnosis of monoclonal gammopathies in the Moroccan population%
\end{abstract}%



\sloppy


\textbf{Title:} Epidemiology of monoclonal gammopathy in Morocco- A
hospital-based study

Running Head: Monoclonal gammopathy

\textbf{Authors:}

Z. OUZZIF1, K. DOGHMI1, N. MESSAOUDI1, S. BOUHSAIN1, S. EL MACHTANI1, A.
BIAZ1, A. RACHID1, A. DAMI1, A. BEZZA1, A. EL MAATAOUI
\textsuperscript{2**}

1. The Military Hospital Instruction Mohamed V / Mohamed V University,
Faculty of Medicine and Pharmacy, Rabat, Morocco.

2. Ibn Zohr University, Agadir teaching hospital, Faculty of Medicine
and Pharmacy, Clinical Chemistry Department-Agadir, Morocco.

\textbf{Authors e-mails:}

Zohra OUZZIF zahra\_ouzzif@yahoo.com

Kamal DOGHMI kdoghmi@gmail.com

Nezha MESSAOUDI messaoudi.nezha@yahoo.fr

Sanae BOUHSAIN bouhsainsanae1@yahoo.fr

Samira EL MACHTANI elmachtaniidrissi@yahoo.com

Asmae BIAZ biazasmaa@yahoo.fr

Achraf RACHID rachid.achraf1@gmail.com

Abdallah DAMI abdami@yahoo.fr

Ahmed BEZZA ahmedbezza239@gmail.com

Aissam EL MAATAOUI a.elmaataoui@uiz.ac.ma

\textbf{**Corresponding author}

AISSAM EL MAATAOUI PharmD PhD

E-mail~: a.elmaataoui@uiz.ac.ma

Address: Clinical chemistry department,

Faculty of medicine and pharmacy, Agadir --Morocco

\textbf{Ethics approval}

The local ethics committee in Mohamed V university, faculty of medicine
and pharmacy Rabat approved this study.

Patients were recruited and enrolled at Mohamed V teaching hospital in
rabat. Written informed consent procedures, conforms to the ethical
guidelines of the declaration of Helsinki and was approved by the ethics
committee in Mohamed V university, faculty of medicine and pharmacy,
Rabat-Morocco.

\textbf{ABSTRACT}

\textbf{Introduction:} Monoclonal gammopathies are a group of disorders
associated with monoclonal proliferation of plasma cells that produces a
monoclonal protein. To describe the epidemiological and immunochemical
characteristics of monoclonal gammopathies diagnosed during a
nineteen-year period in a Moroccan teaching hospital was the main
objective of this study.

\textbf{Methods} : This study was performed from January 2000 to August
2019. It was a retrospective study that included of 545 Moroccan
patients with monoclonal gammopathy.

\textbf{Results:} The patients who participated in the study, 374
(68.6\%) were male and 171(31.4\%) were female, with a mean \selectlanguage{ngerman}±SD age of
62.24±13.14 years. The most frequent reasons for admission were bone
pain (41,60\%), renal failure (19.08\%), alteration of the general
condition (12.21\%) and anemia (10.69). Plasma cell proliferative
disorders in our study were as follow, multiple myeloma (MM) (45.65\%),
Monoclonal gammopathies of undetermined significance (MGUS) (39.05\%),
Waldenstrom's macroglobulinemia(5.58\%), Lymphoma (2.27\%+1.2\%),
Chronic Lymphocytic Leukemia (2.48\%), Plasma cell leukemia (1.86\%),
Plasmacytoma (0.62\%), POEMS syndrome (0.41\%), and Amyloidosis
(0.84\%). The most frequent isotypes in MM were the IgG\selectlanguage{greek}κ \selectlanguage{english}(62) 36.5\%,
IgG\selectlanguage{greek}λ\selectlanguage{english}(52)30.6\%, IgA\selectlanguage{greek}κ\selectlanguage{english}(27)15.9\% and the IgA\selectlanguage{greek}λ \selectlanguage{english}(19)11.2\%. It is also
worthy of note, that Free light chain MM represents 20\% of all cases of
MM.

\textbf{Conclusions:} This is the largest Moroccan cohort, it included
545 patients. The results of this study point to the need for an early
diagnosis of monoclonal gammopathies in the Moroccan population

\textbf{Key words}

Epidemiology, monoclonal gammopathy, Morocco, Monoclonal protein.

\textbf{INTRODUCTION}

Monoclonal gammopathies (MG) represent a group of pathologies
characterized by the clonal proliferation of plasma cells that produce a
paraprotein or monoclonal protein (M-protein). The generalization of the
screening of the MG by serum protein electrophoresis, which represents a
heterogeneous group of diseases, and especially the evolution of imaging
and radiology techniques, have made possible to diagnose MG frequently
and at early stages. The most important risk factors are age, gender and
black race. Several studies have reported a mean age of patients at the
time of diagnosis of monoclonal gammopathy of 68 years, most patients
(99\%) were over 40 years old at the time of
diagnosis\textsuperscript{1,2}. Regarding gender, monoclonal
gammopathies affect men more than women. In a retrospective study, the
age-adjusted incidence of monoclonal gammopathies was 10.3 and 8.6 per
100,000 in men and women, respectively \textsuperscript{3} . Finally,
for the black race, in a study found that the prevalence of monoclonal
gammopathies of undetermined significance (MGUS) in men from Ghana
(5.84\% (95\% CI, 4.27-7.40)) was significantly higher than the
prevalence in white men from Olmsted in the USA (2.97\%, (95\% CI,
2.59-3.34))\textsuperscript{4,5} .

Monoclonal gammopathy of undetermined signification (MGUS), is defined
by the production of monoclonal protein without any systemic effect. It
represents the early stage of the multiple myeloma (malignant stage).
MGUS accounts for 3\% of MG in patients over 50 years of
age\textsuperscript{6} . In general, MGUS will progress to hematologic
malignancies including multiple myeloma or MM, which progresses at a
rate of 1\% per year \textsuperscript{7} .

MM represents 10\% of hematologic malignancies in general, the median
age at diagnosis is estimated to be 70 years, and it affects more men (7
per 100,000) than women (4.5 per 100,000), blacks more than whites,
thus, the highest prevalence rate is observed in African Americans,
particularly in those aged 80-84 years and older \textsuperscript{6} .
Furthermore, the most frequently observed primary immunoglobulin heavy
chain (IgH) translocation was t(11;14), found in 16\% of patients in the
absence of trisomies, and in 3\% in the presence of
trisomies\textsuperscript{8} . Nevertheless, the following cytogenetic
abnormalities, t(4;14), t(14;16), t(14;20), del(17p), gain 1q, or p53
mutation are associated with high risk MM \textsuperscript{8} .

To describe the epidemiological and immunochemical characteristics of
monoclonal gammopathies diagnosed during a nineteen-year period in a
Moroccan teaching hospital was the main objective of this study.

\textbf{MATERIALS AND METHODS}

\textbf{Patient selection}

The study was carried out over a period of 19 years, between January
2000 and August 2019. A retrospective study that included of 545
Moroccan patients with monoclonal gammopathy detected through a serum
electrophoresis, urine and serum immunofixations. Urine immunofixation
is important in defining the nature of the band and in distinguishing
between Bence Jones protein and an intact monoclonal protein originating
from the serum. The patients who had monoclonal protein were included.
But, only 484 patients were selected, they have had complete medical
records at the clinical departments.

\textbf{Methods}

Blood samples were collected using serum dry tubes, the samples left to
clot for one hour before centrifugation at 1000 RPM for 15 minutes.
Total protein (g/L), C-reactive protein~\selectlanguage{english}CRP" \selectlanguage{english}(mg/l), Calcium (mg/l),
creatinine (mg/l), urea(g/l) were measured with Dimension Rxl Siemens
analyzer\selectlanguage{ngerman}®. The \selectlanguage{greek}β\selectlanguage{english}\textsubscript{2}-microglobulin and the immunoglobulins
(IgA, IgG and IgM) was measured with an immunonephelometer analyzers
from Dade Behring BN II \selectlanguage{ngerman}®. The Sedimentation rate was measured at the
first hour (mm) (SRFH). Hemoglobin (Hb) (g/dl) was measured with the
Beckman Coulter hematology analyzers (reference values: In woman Hb \selectlanguage{english}<12
g/dl, in men Hb<\selectlanguage{english}13 g/dl). Urine immunofixation was performed in urine
samples collected for 24 hours.

Protein electrophoresis was performed on all samples with capillary
electrophoresis system from Sebia\selectlanguage{ngerman}®. Immunofixation was performed in the
following situations when an abnormal serum protein electrophoresis was
defined by the presence of a quantifiable Monoclonal spike,
hypogammaglobulinemia and a fuzzy band. Furthermore, when we have an
increased numbers of abnormal, atypical or immature plasma cells in the
bone marrow, hypercalcemia, histological proof of plasmacytoma and high
SRFH.

Serum and urine immunofixation were performed on Hydrasys Sebia®.
Patient records have been reviewed for clinical history and the
monoclonal protein type. The diagnosis of monoclonal gammopathies is
based on the presence of an increase in the number of plasma cells
and/or immature and dystrophic plasma cells in the marrow, the presence
of histological evidence of plasmacytoma, the presence of monoclonal
protein in the serum and urine and/or bone lesions.

\textbf{Statistical analysis}

The statistical analysis was carried out by a software SPSS 13.0 of IBM
for windows. the continuous parameters, the results were expressed by
the Mean ± standard deviation (SD).

\textbf{RESULTS}

The baseline characteristics of the study participants are as follow.
The study included 374 (68.6\%) men and 171 (31.4\%) women, the mean ±SD
ages were 62.24±13.14 years. The mean ±SD years age for the MM, MGUS,
WM, LLMM, KLMM and the POEMS (Polyneuropathy, organomegaly,
endocrinopathy, monoclonal gammopathy, and skin changes syndrome) were
respectively of 61.70± 11.66, 63.64± 13.66, 61.71± 13.35, 60.57± 10.90,
56.50± 12.83 and 45.50 ± 2.12. regarding ethnic origin, all patients
were of Caucasian origin, from the twelve regions of the Kingdom of
Morocco. The most frequent reasons for admission were the bone pain
(41,60\%), the renal failure (19.08\%), the alteration of the general
condition (12.21\%) and anaemia (10.69) (Table1). Plasma cell
proliferative disorders in our study were as follow, MM (45.65\%),
Monoclonal gammopathies of undetermined significance (MGUS) (39.05\%),
Waldenstrom's macroglobulinemia(5.58\%), Lymphoma (2.27\%+1.2\%),
Chronic Lymphocytic Leukaemia (2.48\%), Plasma cell leukaemia (1.86\%),
Plasmacytoma (0.62\%), POEMS syndrome (0.41\%), and Amyloidosis (0.84\%)
(Table 2).

The estimated glomerular filtration rate (eGFR) in patients with MM was
low compared to other monoclonal gammopathies, but the lowest eGFR were
in patients with Free light chain MM, with more cases with kappa versus
lambda light chain myeloma myeloma. The frequency of hypercalcemia was
very high in patients with multiple myeloma and plasma cell leukaemia
compared to other gammopathies. The kappa/Lambda ratio was highly
elevated in patients with MM, plasma cell leukaemia, and plasmacytoma in
comparison to the other MG. Even in patients with MGUS, the kappa/Lambda
ratio was elevated.

The total protein level is highly increased in patients diagnosed with
MM and WM and low in patients diagnosed with light chain MM. Low albumin
concentration was found in patients with MM and plasma cell leukaemia.
The SRFH was very high in patients with WM and MM. Furthermore,
monoclonal protein levels were higher in patients with MM (38.21±23.83),
MW (33.31±20.65) and MGUS (11.76±6.96).

Concentrations of parameters used in the prognostic evaluation of
monoclonal gammopathies ( \selectlanguage{greek}β\selectlanguage{english}\textsubscript{2}- microglobulin, CRP and
LDH) were higher in patients with MM and MGUS respectively. Anaemia was
more profound in patients with multiple myeloma in general (9.76\selectlanguage{ngerman}±2.21),
and in patients with free light chains MM ( LLMM (7.76±1.12), KLMM
(9.07±1.81)), and Waldenstrom's macroglobulinemia (9.29±2.15) (Table 3).

The isotype repartition by Plasma cell proliferative disorders in this
study is given in table 4. The most frequent monoclonal proteins in MM
were the IgG\selectlanguage{greek}κ \selectlanguage{english}(62) 36.5\%, IgG\selectlanguage{greek}λ\selectlanguage{english}(52)30.6\%, IgA\selectlanguage{greek}κ\selectlanguage{english}(27)15.9\% and the IgA\selectlanguage{greek}λ
\selectlanguage{english}(19)11.2\%. It is also worthy of note, that Free light chain MM
represents 20\% of all cases of MM.

For the MGUS, the most frequent isotypes were the IgG\selectlanguage{greek}κ \selectlanguage{english}(87) 46.27\%,
IgG\selectlanguage{greek}λ \selectlanguage{english}(61)32.44\%, IgA\selectlanguage{greek}κ\selectlanguage{english}(4)2.13\%, IGA\selectlanguage{greek}λ \selectlanguage{english}(9)4.78\% , IgM\selectlanguage{greek}λ \selectlanguage{english}(5)2.66\% and
IgM\selectlanguage{greek}κ\selectlanguage{english}(9)4.78\%. Finally, the most frequent isotypes in Waldenstr\selectlanguage{ngerman}öm's
macroglobulinemia were IgM\selectlanguage{greek}κ \selectlanguage{english}(19)70.37\%, IgM\selectlanguage{greek}λ \selectlanguage{english}(7)25.93\%, and an
oligoclonal profil (1)3.70\% (Table 4).

\textbf{DISCUSSION}

The study was carried out over a period of 19 years, between January
2000 and August 2019. The patients who were included in this study were
545 patients. To describe the epidemiological and immunochemical
characteristics of monoclonal gammopathies diagnosed during a
nineteen-year period in a Moroccan teaching hospital was the main
objective of this study. The results of this study point to the need for
an early diagnosis of monoclonal gammopathies in the Moroccan
population. The mean\selectlanguage{ngerman}±SD age at diagnosis of all MG was 62.24±13.14
years, and with a sex ratio male/female of 2.14. Our results are in
agreement with the results of international studies confirming that GM
is age-related and affects men more than women \textsuperscript{1--3} .

Plasma cell proliferative disorders in our study were as follow, MM
45.65\% (n=221), MGUS 39.05\% (n=189), WM 5.58\% (n=27), plasmacytomas
5.58\% (n=27), plasma cell leukaemia 0.62\% (n=3). The most frequent
diagnosis of MG in the European and American studies was
MGUS\textsuperscript{9,10} . In contrast, the most frequent diagnosis of
monoclonal gammopathies in our study and the studies from Maghreb
countries (Algeria and Tunisia) was MM \textsuperscript{11,12} . This is
due to the delay in diagnosis and the lack of serum protein
electrophoresis in most of the hospitals in Maghreb countries. In a
cross-sectional study Gupta et al have reported a low incidence of MGUS
in Indians compared to blacks and whites populations\textsuperscript{13}
. This study included 3429 patients, only 49 (1.43\%) had a diagnosis of
MGUS at the time of diagnosis\textsuperscript{13}.

In this study, the POEMS syndrome was diagnosed only in 2 patients
(0.41\%), POEMS syndrome is relatively rare, in a mayo clinic study only
99 cases were diagnosed \textsuperscript{14} .

The \selectlanguage{greek}κ/λ \selectlanguage{english}ratio was very high in patients with MM (25.04), plasma cell
leukaemia (26.67), MGUS (2.06) and plasmacytoma (19.00). Indeed, in
patient with MM, Belouni et al, Mseddi et al and the Mayo clinic
\textsuperscript{10--12} have found the kappa/Lambda ratio respectively
of 14.9, 14.13 and 16. Nevertheless, normal \selectlanguage{greek}κ/λ \selectlanguage{english}ratio does not exclude
the presence of a monoclonal gammopathy according to Singh et al, and
false negatives rates associated with lambda chain are higher than those
for lesions with kappa chains \textsuperscript{15} .

The mean concentrations of monoclonal peak were MM (38.21\selectlanguage{ngerman}±23.83), MW
(33.31±20.65) and MGUS (11.76±6.96), these results are very far from the
means noted in the patients included in the Algerian study of Belouni et
al (22.19±20.19 g/l) \textsuperscript{11} and in the majority of the
other series, this can be explained by the late diagnosis of the
monoclonal gammopathies in our country, and the high frequency of MM in
our study in comparison of the international
studies\textsuperscript{9,10}. Furthermore, Monoclonal protein
concentration was elevated in patients diagnosed with MW or MM compared
to MGUS.

Anaemia was more profound in patients with free light chain MM, LLMM
(7.76±1.12), KLMM (9.07±1.81). This may be explained by the high
frequency of free light chain MM, and the delay in the diagnosis of our
patients with MM.

The isotype repartition by plasma cell proliferative disorders is given
in table 4. The most frequent monoclonal proteins in the group of
patients with MM were the IgG\selectlanguage{greek}κ \selectlanguage{english}(62) 36.5\%, IgG\selectlanguage{greek}λ\selectlanguage{english}(52)30.6\%,
IgA\selectlanguage{greek}κ\selectlanguage{english}(27)15.9\% and the IgA\selectlanguage{greek}λ \selectlanguage{english}(19)11.2\%. Regarding the MGUS group, the
most frequent isotypes were the IgG\selectlanguage{greek}κ \selectlanguage{english}(87) 46.27\%, IgG\selectlanguage{greek}λ \selectlanguage{english}(61)32.44\%,
IgA\selectlanguage{greek}κ\selectlanguage{english}(4)2.13\%, IgA\selectlanguage{greek}λ \selectlanguage{english}(9)4.78\%, IgM\selectlanguage{greek}λ \selectlanguage{english}(5)2.66\% and IgM\selectlanguage{greek}κ\selectlanguage{english}(9)4.78\%. The
same results were reported in the study of Landgren et al, the most
frequent isotypes by race/ethnicity were IgG \%(n) 76.1 (71), IgA 5.2
(5), IgM 2.7 (3) in black, IgG 68.1 (150), IgA 9.7 (12), IgM 15.4 (34)
in whites and IgG 63.1 (29) IgA 16.7(8) IgM 7.4 (6) in Mexican
Americans\textsuperscript{16} .

Finally, the most frequent isotypes in Waldenstr\selectlanguage{ngerman}öm's macroglobulinemia
were IgM\selectlanguage{greek}κ \selectlanguage{english}(19)70.37\%, IgM\selectlanguage{greek}λ \selectlanguage{english}(7)25.93\%. These results are consistent
with the results of studies from the Maghreb countries, in which the
most common isotypes were the Ig G followed by the Ig A and the IgM in
the studies of Mseddi et al in Tunisia, and Belouni et al in
Algeria\textsuperscript{11,12} .

\textbf{Declarations:}

\textbf{Author contribution}

All the authors have seen and approved the final manuscript. All authors
meet the criteria of authorship

Extracted the clinical and lab data: \textbf{KD ,NM ,SB ,SE ,AB ,AR ,AD,
AB, AE} ; Acquisition of data: \textbf{AE} ; Analysis and interpretation
of data: \textbf{AE} ; Drafting of manuscript: AE; Critical revision:

\textbf{ZO, AE}

\textbf{Funding}

The authors declare no competing financial interests

\textbf{Conflict of interest}

\textbf{ZO, KD ,NM ,SB ,SE ,AB ,AR ,AD, AB, AE} declare that they have
no conflict of interest

\textbf{REFERENCES}

1. Mateos MV. How to maintain patients on long-term therapy:
understanding the profile and kinetics of adverse events. \emph{Leuk
Res} . 2012;36 Suppl 1:S35-43. doi:10.1016/S0145-2126(12)70007-3

2. Hideshima T, Mitsiades C, Tonon G, Richardson PG, Anderson KC.
Understanding multiple myeloma pathogenesis in the bone marrow to
identify new therapeutic targets. \emph{Nature Reviews Cancer} .
2007;7(8):585-598. doi:10.1038/nrc2189

3. Ogmundsd\selectlanguage{ngerman}óttir HM, Haraldsdóttir V, M Jóhannesson G, et al. Monoclonal
gammopathy in Iceland: a population-based registry and
follow-up.\emph{Br J Haematol} . 2002;118(1):166-173.
doi:10.1046/j.1365-2141.2002.03589.x

4. Landgren O, Gridley G, Turesson I, et al. Risk of monoclonal
gammopathy of undetermined significance (MGUS) and subsequent multiple
myeloma among African American and white veterans in the United
States.\emph{Blood} . 2006;107(3):904-906.
doi:10.1182/blood-2005-08-3449

5. Landgren O, Katzmann JA, Hsing AW, et al. Prevalence of monoclonal
gammopathy of undetermined significance among men in Ghana. \emph{Mayo
Clin Proc} . 2007;82(12):1468-1473. doi:10.1016/S0025-6196(11)61089-6

6. Kyle RA, Therneau TM, Rajkumar SV, et al. Prevalence of Monoclonal
Gammopathy of Undetermined Significance. \emph{New England Journal of
Medicine} . 2006;354(13):1362-1369. doi:10.1056/nejmoa054494

7. Blessum C, Jeppsson JO, Aguzzi F, Bernon H, Bienvenu J. {[}Capillary
electrophoresis: principles and practice in clinical
laboratory{]}.\emph{Ann Biol Clin (Paris)} . 1999;57(6):643-657.

8. Abdallah N, Rajkumar SV, Greipp P, et al. Cytogenetic abnormalities
in multiple myeloma: association with disease characteristics and
treatment response. \emph{Blood Cancer Journal 2020 10:8} .
2020;10(8):1-9. doi:10.1038/s41408-020-00348-5

9. Decaux O, Rodon P, Ruelland A, Estepa L, Leblay R, Grosbois B.
Épidémiologie descriptive des gammapathies monoclonales. Expérience d'un
centre hospitalier général et d'un service de médecine interne de centre
hospitalier et universitaire. \emph{Revue de Medecine Interne} .
2007;28(10):670-676. doi:10.1016/j.revmed.2007.04.011

10. Katzmann JA, Kyle RA, Benson J, et al. Screening panels for
detection of monoclonal gammopathies. \emph{Clinical Chemistry} .
2009;55(8):1517-1522. doi:10.1373/clinchem.2009.126664

11. Belouni R, Allam I, Cherguelaine K, et al. Epidemiological and
immunochemical parameters of monoclonal plasma cell dyscrasias of 2121
cases in Algeria. \emph{Current Research in Translational Medicine} .
2020;68(2):67-70. doi:10.1016/j.retram.2019.11.003

12. Mseddi-Hdiji S, Haddouk S, Ben Ayed M, et al. Gammapathies
monoclonales en Tunisie: Analyse épidé miologique, immunochimique et
étiologique d'une série de 288 cas. \emph{Pathologie Biologie} .
2005;53(1):19-25. doi:10.1016/j.patbio.2004.01.014

13. R G, M D, L K, et al. Prevalence of Monoclonal Gammopathy of
Undetermined Significance in India-A Hospital-based Study.\emph{Clinical
lymphoma, myeloma \& leukemia} . 2018;18(9):e345-e350.
doi:10.1016/J.CLML.2018.06.005

14. Dispenzieri A, Kyle RA, Lacy MQ, et al. POEMS syndrome: definitions
and long-term outcome. \emph{Blood} . 2003;101(7):2496-2506.
doi:10.1182/blood-2002-07-2299

15. Singh G. Serum and Urine Protein Electrophoresis and Serum-Free
Light Chain Assays in the Diagnosis and Monitoring of Monoclonal
Gammopathies. \emph{The journal of applied laboratory medicine} .
2020;5(6):1358-1371. doi:10.1093/JALM/JFAA153

16. O L, BI G, JA K, et al. Racial disparities in the prevalence of
monoclonal gammopathies: a population-based study of 12,482 persons from
the National Health and Nutritional Examination Survey. \emph{Leukemia}
. 2014;28(7):1537-1542. doi:10.1038/LEU.2014.34

\textbf{Hosted file}

\verb`Tables.docx`  available at \url{https://authorea.com/users/517082/articles/591738-epidemiology-of-monoclonal-gammopathy-in-morocco-a-hospital-based-study-running-head-monoclonal-gammopathy}

\selectlanguage{english}
\FloatBarrier
\end{document}

