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Fulltext Cerebrospinal fluid rhinorrhoea secondary to amyloidosis of the sphenoid sinus

Ali EA, Philip R, Prepageran N, Peh SC

Med J Malaysia, 2008 Oct;63(4):341-2.
PMID: 19385501 MyJurnal

Amyloidosis of the skull base is a rare entity. A patient with localized amyloidosis of the sphenoid sinus presented at our institution with cerebrospinal fluid rhinorrhoea. Endoscopic excision of the lesion and multilayered obliteration of the sphenoid sinus resolved the symptoms.

Matched MeSH terms: Amyloidosis/complications*; Amyloidosis/surgery
The NLRP3 inflammasome is involved in the neuroprotective mechanism of neural stem cells against microglia-mediated toxicity in SH-SY5Y cells via the attenuation of tau hyperphosphorylation and amyloidogenesis

Chan EWL, Krishnansamy S, Wong C, Gan SY

Neurotoxicology, 2019 01;70:91-98.
PMID: 30408495 DOI: 10.1016/j.neuro.2018.11.001

The cognitive impairment caused by Alzheimer's disease (AD) is associated with beta-amyloid (Aβ) and tau proteins, and is accompanied by inflammation. Recently, a novel inflammasome signaling pathway has been uncovered. Inflammasomes are implicated in the execution of inflammatory responses and pyroptotic death leading to neurodegeneration. Thus, the inflammasome signaling pathway could be a potential therapeutic target for AD. Neural stem cells (NSCs) are multipotent cells that can self-renew and differentiate into distinct neural cells. NSC therapy has been considered to be a promising therapeutic approach in protecting the central nervous system and restoring it following damage. However, the mechanisms involved remain unclear. The aims of this study were to investigate the protective effects of NE4C neural stem cells against microglia-mediated neurotoxicity and to explore molecular mechanisms mediating their actions. NE4C decreased the levels of caspase-1 and IL-1β, and attenuated the level of the NLRP3 inflammasome and its associated protein adapter, apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC) in LPS-stimulated BV2 microglial cells, possibly by regulating the phosphorylation of p38α MAPK. The conditioned media obtained from co-culture of LPS-stimulated BV2 and NE4C cells exhibited protective effects on SH-SY5Y cells against microglia-mediated neurotoxicity; this was associated with an attenuation of tau phosphorylation and amyloidogenesis and accompanied by down-regulation of GSK-3β and p38α MAPK signalling pathways. In conclusion, the present study suggested that NSC therapy could be a potential strategy against microglia-mediated neurotoxicity. NSCs regulate NLRP3 activation and IL-1β secretion, which are critical in the initiation of the inflammatory responses, hence preventing the release of neurotoxic pro-inflammatory factors by microglia. This eventually reduces tau hyperphosphylation and amyloidogenesis, possibly through the regulation of GSK-3β and p38α MAPK signalling pathways, and thus protects SH-SY5Y cells against microglia-mediated neurotoxicity.

Matched MeSH terms: Amyloidosis/metabolism*; Amyloidosis/prevention & control
Fulltext Splenic amyloidosis: a rare cause of spontaneous splenic rupture

Chan RS, Abdul Aziz YF, Chandran P, Ng EK

Singapore Med J, 2011 Nov;52(11):e232-5.
PMID: 22173263

A 62 year-old woman who presented with an atraumatic acute abdomen was discovered to have haemoperitoneum with splenic rupture on urgent computed tomography and was immediately referred for life-saving emergency splenectomy. Histopathological examination revealed secondary splenic amyloidosis. The patient was later found to be suffering from infective endocarditis secondary to her permanent cardiac pacemaker. This report describes a patient who could have suffered from a long-standing infected vegetation on a permanent cardiac pacemaker, which led to splenic amyloidosis and spontaneous splenic rupture.

Matched MeSH terms: Amyloidosis/diagnosis*; Amyloidosis/etiology
The epidemiology of cutaneous amyloidosis in Jakarta (Indonesia)

Djuanda A, Wiryadi BE, Sularsito SA, Hidayat D

Ann Acad Med Singap, 1988 Oct;17(4):536-40.
PMID: 3265605

An analysis of cutaneous amyloidosis cases during a five year period, from January 1, 1983 to December 31, 1987, showed that of 78 cases suffering from lichen amyloidosis, 9 patients (11.5%) were male and 71 patients (80.5%) female. Macular skin amyloidosis was observed. Sixty patients (76.9%) were found in the age range of 20-50 years. Forty-nine patients (62.8%) suffered from the disease for 2 years or less. Skin changes were mainly located on the shin areas, the posterior part of the lower thighs and posterior part of the forearms. Treatment with strong topical corticosteroids and keratolytic agents (salicylic acid ointment in higher than 3%) proved to be unsatisfactory. The literature mentions higher incidence of lichen amyloidosis in Chinese, Malaysians and Indonesians than in Caucasians.

Matched MeSH terms: Amyloidosis/epidemiology*; Amyloidosis/pathology
Lichen amyloidosis

Dutt AK

Med J Malaya, 1969 Dec;24(2):164-5.
PMID: 4244146
Matched MeSH terms: Amyloidosis*
Fulltext Renal-limited AL amyloidosis - a diagnostic and management dilemma

Fuah KW, Lim CTS

BMC Nephrol, 2018 11 06;19(1):307.
PMID: 30400895 DOI: 10.1186/s12882-018-1118-8

BACKGROUND: Amyloidosis is a disorder caused by extracellular tissue deposition of insoluble fibrils which may result in a wide spectrum of symptoms depending upon their types, sites and amount of deposition. Amyloidosis can be divided into either systemic or localized disease.
CASE PRESENTATION: We present a case of a middle-aged gentleman who presented with persistent nephrotic syndrome with worsening renal function. Repeated renal biopsies showed the presence of renal-limited AL amyloidosis. Systemic amyloidosis workup was unremarkable apart from a slightly raised band of IgG lambda level with no associated immunoparesis. The nephrotic syndrome and renal histology did not improve over a 3-year period despite being given two courses of chemotherapies.
CONCLUSION: We hope that early recognition of this unusual localised presentation of renal- limited AL Amyloidosis and its poor response to conventional treatment can alert the nephrologist to the potential existence of this rare condition.

Matched MeSH terms: Amyloidosis/blood*; Amyloidosis/diagnosis*; Amyloidosis/therapy
Fulltext Autopsy findings in 35 cases of leprosy in Malaysia

Jayalakshmi P, Looi LM, Lim KJ, Rajogopalan K

Int. J. Lepr. Other Mycobact. Dis., 1987 Sep;55(3):510-4.
PMID: 3655465

The findings of autopsies performed on 35 leprosy subjects in the University Hospital, Kuala Lumpur, between January 1981 and December 1985 are presented. This is the first report based on autopsy findings from Malaysia. The patients were elderly subjects with a mean age of 74 years. Sixty-six percent had lepromatous leprosy. None had active skin lesions. The most common cause of death was pyogenic infection, particularly bronchopneumonia. Tuberculosis was noted in 25% of the cases. The other important causes of death included cardiac and renal failure. Renal lesions were evident in 71% of the cases, and the most common pathology was interstitial nephritis. Generalized amyloidosis complicated six (17%) patients.

Matched MeSH terms: Amyloidosis/complications
Primary cardiac amyloidosis

Jeyamalar R, Pathmanathan R, Yap SF, Kannan P

Ann Acad Med Singap, 1991 Nov;20(6):795-7.
PMID: 1803972

Cardiac amyloidosis is an uncommon and often unrecognised cause of cardiac failure. It is an infiltrative disease that may mimic either a restrictive or hypertrophic cardiomyopathy, constrictive pericarditis, coronary artery disease or valvular heart disease. The diagnosis should be suspected in a patient with cardiac failure who has low voltage complexes on the electrocardiogram, in association with increased myocardial mass and echogenicity on the echocardiogram. The definitive diagnosis, however, can only be made by endomyocardial biopsy or biopsy of any involved organ in systemic amyloidosis. Prognosis is poor and treatment ineffective.

Matched MeSH terms: Amyloidosis/diagnosis*
Fulltext The pattern of amyloid deposition in the lung

Looi LM

Malays J Pathol, 1999 Jun;21(1):29-35.
PMID: 10879276

A review of routine histopathological samples and autopsies examined at the Department of Pathology, University of Malaya revealed 15 cases of amyloidosis of the lung. Two were localized depositions limited to the lung while in the remainder, lung involvement was part of the picture of systemic amyloidosis. Both cases of localized amyloidosis presented with symptomatic lung/bronchial masses and a clinical diagnosis of tumour. Histology revealed "amyloidomas" associated with heavy plasma cell and lymphocytic infiltration and the presence of multinucleated giant cells. In both cases, the amyloid deposits were immunopositive for lambda light chains and negative for kappa chains and AA protein. One was a known systemic lupus erythematosus patient with polyclonal hypergammaglobulinaemia. The other patient was found to have plasma cell dyscrasia with monoclonal IgG lambda gammopathy. Both patients did not develop systemic amyloidosis. In contrast, lung involvement in systemic AA amyloidosis was not obvious clinically or macroscopically but was histologically evident in 75% of cases subjected to autopsy. Amyloid was detected mainly in the walls of arterioles and small vessels, and along the alveolar septa. It was less frequently detected in the pleura, along the basement membrane of the bronchial epithelium and around bronchial glands. In one case of systemic AL amyloidosis associated with multiple myeloma, an "amyloidoma" occurred in the subpleural region reminiscent of localized amyloidosis. These cases pose questions on (1) whether localized "tumour-like" amyloidosis is a forme fruste of systemic AL amyloidosis and (2) the differing pattern of tissue deposition of different chemical types of amyloid fibrils, with the suggestion that light chain amyloid has a greater tendency to nodular deposition than AA amyloid.

Matched MeSH terms: Amyloidosis/metabolism*
Histomorphological patterns of renal amyloidosis: a correlation between histology and chemical type of amyloidosis

Looi LM, Cheah PL

Hum Pathol, 1997 Jul;28(7):847-9.
PMID: 9224755

A retrospective study was conducted to investigate whether there was a correlation between the histological pattern of renal amyloidosis, the chemical type of amyloid protein involved and the clinical presentation. Eighteen consecutive cases of systemic amyloidosis that had renal biopsies processed and examined histopathologically at the Department of Pathology, Faculty of Medicine, University of Malaya, Kuala Lumpur were reviewed. The age range of patients was 25 to 64 yrs (mean, 46 yrs). The male:female ratio was 2.6:1. Three patients were Malay, 9 Chinese, 3 Indian, 1 Indonesian, 1 Iban, and 1 Bisaya. According to the predominant site of amyloid deposition, 14 cases showed a glomerular pattern and 4 a vascular pattern. 8 cases were designated as 2 anti-human amyloid-A (AA) amyloidosis on the basis of permanganate-sensitivity and immunoreactivity of deposits with anti-human AA protein antibody. Ten cases contained deposits that were permanganate-resistant and nonimmunoreactive for AA protein and were designated as AL in type. The histomorphologic pattern of renal amyloidosis did not provide a reliable means of differentiating AA from AL amyloidosis. The glomerular pattern tended to present with renal manifestations such as nephrotic syndrome and chronic renal failure, whereas the vascular pattern tended to present with nonrenal manifestations such as diarrhoea. These findings may have a bearing on the pathophysiology of amyloidosis and provide clues to appropriate management.

Matched MeSH terms: Amyloidosis/metabolism; Amyloidosis/pathology*
The pattern of amyloidosis in Malaysia

Looi LM

Malays J Pathol, 1994 Jun;16(1):11-3.
PMID: 16329569

Congo red screening of routine biopsies at the University Hospital Kuala Lumpur revealed the following categories of amyloidosis: systemic AL (5.9%); systemic AA (3.2%); isolated atrial (14%); primary localized cutaneous (7.5%); other primary localized deposits (3.2%); localized intratumour (58%); and dystrophic (8.6%). Unlike in the West, AA amyloidosis in this population was usually secondary to leprosy or tuberculosis. Liver involvement in AL amyloidosis was shown to exhibit a sinusoidal pattern and differed from the vascular pattern of AA amyloidosis. Within the category of AA amyloidosis, there were two patterns of renal involvement--glomerular and vascular, with the glomerular pattern carrying a more ominous clinical picture. Notable among the localized amyloidoses were isolated atrial amyloidosis complicating chronic rheumatic heart disease, intratumour amyloidosis within nasopharyngeal carcinomas and dystrophic amyloidosis which occurred in fibrotic tissues.

Matched MeSH terms: Amyloidosis/etiology; Amyloidosis/epidemiology; Amyloidosis/pathology*
Isolated atrial amyloidosis: a clinicopathologic study indicating increased prevalence in chronic heart disease

Looi LM

Hum Pathol, 1993 Jun;24(6):602-7.
PMID: 8505038

Congo red screening of 211 consecutive cardiac biopsy specimens obtained during cardiac surgery from 167 patients revealed 26 (16%) instances of isolated atrial amyloidosis (IAA). The ages of IAA-positive patients ranged from 25 to 52 years (mean age, 39 years). Twenty-three (88%) IAA-positive biopsy specimens were from patients with chronic rheumatic heart disease (CRHD) while three (12%) were from patients with an atrial septal defect (ASD). The prevalence of IAA in the CRHD patients was 23%, appreciably higher than that in the ASD patients (15%) and in other patients with atrial biopsies. The prevalence of IAA in both CRHD and ASD patients was significantly higher (P < .001) than in controls. Controls consisted of 247 healthy adults who were autopsied after traumatic deaths, with an age range of 18 to 89 years (mean age, 38 years). Only seven (3%) control subjects were IAA positive; all were over 40 years of age. Isolated atrial amyloidosis deposits were permanganate resistant and immunohistochemically positive for human amyloid P (AP) protein and negative for human amyloid-associated (AA) protein and immunoglobulin light chains. They were observed as fine congophilic and birefringent deposits in intramyocardial vessel walls, along the myocardial sarcolemma, and in the subendocardium. There was associated myocyte hypertrophy but no atrophy. Electron microscopy demonstrated typical nonbranching amyloid fibrils. It is postulated that stretching of the atria in chronic heart disease results in a raised prevalence of IAA. Recent reports that IAA contains atrial natriuretic peptide, a polypeptide hormone product of atrial myocytes, supports this view.

Matched MeSH terms: Amyloidosis/etiology; Amyloidosis/epidemiology*; Amyloidosis/pathology
Fulltext Fibrillary deposits: amyloids and tactoids

Looi LM

Malays J Pathol, 1995 Jun;17(1):1-10.
PMID: 8906998

Two forms of abnormal fibrillary protein deposition are considered: amyloidosis and fibrillary (immunotactoid) glomerulonephritis. Amyloid is characterised by an antiparallel, beta-pleated configuration which imparts to it a unique apple-green birefringence after Congo red staining. Inspite of its fairly constant physical properties, the chemical composition of amyloid fibrils is amazingly diverse, encomposing AA protein, light chain fragments, transthyretin, procalcitonin, islet amyloid polypeptide, atrial natriuretic peptides, beta-amyloid protein, beta-2-microglobulin, cystatin C, gelsolin, apolipoprotein A1, lyzozyme and their mutant variants. Amyloid P component and heparan sulphate proteoglycan are ubiquitous non-fibrillary amyloid components which have significant roles in the amyloidogenetic process, as do also precursor fibril proteins. Different amyloid fibril proteins relate to different amyloidosis syndromes and different histological patterns, and provide the basis for new diagnostic approaches to this disorder. Glomerular deposits in fibrillary glomerulonephritis (FGN), although often mistaken for amyloid, differ from it in its negative Congophilia, wider fibril width and highly organised, microtubular-tactoidal appearance ultrastructurally. FGN is essentially a primary glomerulopathy resulting in progressive renal failure. Despite certain differences, intriguing similarities between both entities of fibrillary deposition pose a challenge to researchers as to the mechanisms of abnormal protein crystallization and fibril formation in tissues.

Matched MeSH terms: Amyloidosis/etiology; Amyloidosis/pathology*
Morphologic differences in the pattern of liver infiltration between systemic AL and AA amyloidosis

Looi LM, Sumithran E

Hum Pathol, 1988 Jun;19(6):732-5.
PMID: 2454214

Biopsy and necropsy tissue from 31 unselected patients with systemic amyloidosis, in which there was histologic evidence of liver involvement, were reviewed with reference to the location and pattern of amyloid deposition in the liver. Amyloidosis was classified into AA and AL types on the basis of immunohistochemistry and permanganate reaction of the amyloid deposits. Nineteen were categorized as AA (secondary) and 12 as AL (primary) amyloidosis. Deposition of AA amyloid was limited to the walls of vessels in the portal tract, constituting a "vascular" pattern. In AL amyloidosis, the deposits exhibited a "sinusoidal" pattern in that they were seen along hepatic sinusoids as well as in vessel walls. This difference was statistically significant (P less than .001). The histologic pattern of liver infiltration offers a valuable clue in the classification of systemic amyloidosis and provides information that may be useful in the selection of patients for therapy.

Matched MeSH terms: Amyloidosis/classification; Amyloidosis/metabolism; Amyloidosis/pathology*
Intratumour amyloidosis in Malaysians: an immunohistochemical study

Looi LM

Ann Acad Med Singap, 1986 Jan;15(1):52-6.
PMID: 3010797

Congo red screening of tumour material examined at the Department of Pathology, University of Malaya revealed intratumour deposits of amyloid in 12% of nasopharyngeal carcinomas, 66% of basal cell carcinomas, 100% of medullary carcinomas of the thyroid, 56% of islet cell tumours of the pancreas, 1 out of 16 carcinoids and 1 out of 100 thyroid adenomas. All the deposits were permanganate resistant and did not contain AA protein, indicating that what was encountered was not secondary amyloid. The deposits showed variable staining for immunoglobulin light chains and amyloid P component with a standard peroxidase antiperoxidase method. The possibility that intratumour amyloid has a neoplastic origin is discussed.

Matched MeSH terms: Amyloidosis/complications; Amyloidosis/metabolism; Amyloidosis/pathology*
Microscopical atrial amyloidosis in chronic heart disease

Looi LM

Histopathology, 1981 Nov;5(6):615-22.
PMID: 7319480

Nineteen out of 121 consecutive cardiac biopsies from 107 patients were found to contain amyloid deposits on routine Congo red screening. Seventeen were left atrial appendages removed during mitral valvotomy for chronic rheumatic mitral valve disease while the remaining two were right atrial appendages excised during surgical repair of atrial septal defects. The distribution of amyloid deposits within the atria and their tinctorial characteristics are described. The high prevalence of atrial amyloidosis observed could not be attributed to generalized or senile amyloidosis. The possibility that this is a distinctive localized form of amyloidosis secondary to chronic heart disease is discussed.

Matched MeSH terms: Amyloidosis/etiology*; Amyloidosis/epidemiology; Amyloidosis/pathology
Localized amyloidosis in basal cell carcinoma. A pathologic study

Looi LM

Cancer, 1983 Nov 15;52(10):1833-6.
PMID: 6627203

Congo-red screening demonstrated intratumor deposits of amyloid in 35 of 53 unselected cases of basal cell carcinoma. Male subjects had a higher amyloid positivity rate than female subjects. The amyloid deposits were permanganate-resistant and located in the stroma between clumps of tumor cells, as well as abutting the advancing front of the neoplasm. Solar elastosis was often observed in the overlying and adjacent subepidermis. The relationship between amyloid positivity and the different histological subtypes of basal cell carcinoma, tumor ulceration, and density of the lymphoplasmacytic stromal infiltrate were also studied. The possibility that amyloid originates from the tumor cells and is a result of tumor apoptosis (degeneration) is discussed.

Matched MeSH terms: Amyloidosis/pathology*
Dystrophic amyloidosis: a local complication of tissue damage with heterogeneous distribution

Looi LM

Histopathology, 1991 Aug;19(2):169-72.
PMID: 1757071

Seventeen consecutive patients with dystrophic amyloidosis are reported here (eight Chinese, three Indian, three Iban, two Malay and one Caucasian). Ten were females and seven males, with ages ranging from 12 to 80 years (mean of 48 years). Five instances of dystrophic amyloidosis occurred in areas of tissue damage in the cardiovascular system, including fibrotic cardiac valves and an atheromatous plaque. Three occurred in osteoarthritic joint tissue. Of note were three occurrences in endometriotic cyst walls, four in the fibrotic walls of epidermal cysts, one in a hernial sac and one at the edge of a skin ulcer. All deposits were congophilic and exhibited green-birefringence and permanganate-resistance. Immunohistochemistry did not reveal reactivity for AA protein or immunoglobulin lambda or kappa light-chains. AP protein was detected in 35% of cases. Our results show that, besides the usual sites of osteoarthritic joints and damaged heart valves, dystrophic amyloidosis can complicate other areas of chronic tissue damage and fibrosis such as walls of cysts and ulcers. While the pathogenesis and biochemical nature remain unresolved, immunohistochemistry indicates that neither AA nor AL proteins are present in the deposits, and suggests that a different amyloid protein is involved.

Matched MeSH terms: Amyloidosis/pathology*
The pattern of amyloidosis in a Malaysian patient population

Looi LM

Histopathology, 1991 Feb;18(2):133-41.
PMID: 1901294

Congo red screening of 27,052 routine biopsy specimens from 22,827 patients over a 5 1/2-year period in the Department of Pathology, University of Malaya detected 186 cases of amyloidosis. The categories of amyloidosis encountered and their prevalences in relation to each other were: systemic AL (5.9%); systemic AA (3.2%); isolated atrial (14%); primary localized cutaneous (7.5%); other primary localized deposits (3.2%); localized intratumour (58%); and dystrophic (8.6%). A third of patients with systemic AL amyloidosis had coexistent immunocyte abnormality. The commonest underlying pathology for systemic AA amyloidosis was leprosy. Notable among the types of localized amyloidosis revealed by this study were isolated atrial amyloidosis, which appeared to complicate chronic rheumatic heart disease, and intratumour amyloidosis complicating nasopharyngeal carcinoma. Other tumours in which amyloid deposits were observed included basal cell carcinoma, islet cell tumour and medullary carcinoma of the thyroid. Dystrophic amyloidosis was observed in fibrotic tissues, such as damaged cardiac valves and osteoarthritic joints. Heredofamilial amyloidosis, senile systemic amyloidosis and degenerative cerebral amyloidosis were notably absent from this study.

Matched MeSH terms: Amyloidosis/metabolism*; Amyloidosis/epidemiology; Amyloidosis/pathology*
Histomorphological variations in systemic AA amyloidosis: clues of AA protein polymorphism

Looi LM

Histopathology, 1989 Feb;14(2):111-20.
PMID: 2707747

The histological location of amyloid within various organs in 25 cases of systemic AA amyloidosis was studied with a view to determine whether different morphological patterns exist in this category of amyloidosis. Although morphological variations due to progressive severity of disease were observed, there were appreciable variations in the patterns of amyloid deposition in the kidney and spleen that could not be simply explained on those grounds. Eleven (61%) of 18 kidneys examined showed severe glomerular involvement with mild degrees of vascular deposition while the remaining seven showed predominantly vascular involvement. The glomerular pattern appeared to be more ominous, being significantly associated with severe proteinuria or chronic renal failure. In nine (69%) of 13 spleens examined, amyloid was confined to the walls of small and medium-sized arteries while in the remaining four, vascular involvement was less severe and amyloid was deposited mainly along the reticulin of the white pulp. Possible explanations for these different patterns included resorption and redistribution of amyloid within the body during the course of the disease, and variation in tissue deposition as a manifestation of polymorphism of amyloid proteins. The latter appeared more feasible in view of the recent demonstration of SAA polymorphism and AA heterogeneity in man.

Matched MeSH terms: Amyloidosis/metabolism; Amyloidosis/pathology*

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