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Fulltext Disseminated histoplasmosis mimicking miliary tuberculosis: a case report

Chan KS, Looi LM, Chan SP

Malays J Pathol, 1993 Dec;15(2):155-8.
PMID: 8065179

A 35-year-old Chinese man who was known to have insulin-dependent diabetes mellitus was admitted for fever and weight loss. During his hospital stay, he fell to his death from his ward at the twelfth floor. The clinical features, radiological findings and gross organ changes at autopsy closely simulated miliary tuberculosis. Histology, however, revealed extensive necrosis of the adrenal glands, lungs, spleen, kidneys and thyroid associated with the presence of Histoplasma capsulatum organisms. This case highlights the similarity both clinically and pathologically between histoplasmosis and tuberculosis and emphasizes the need to be aware of this infection in a nonendemic area among patients with a compromised immune system.

Matched MeSH terms: Diabetes Mellitus, Type 1/immunology*
Fulltext Autoimmune markers in young Malaysian patients with type 1 diabetes mellitus

Nazaimoon WM, Azmi KN, Rasat R, Ismail IS, Singaraveloo M, Wan Mohamad WB, et al.

Med J Malaysia, 2000 Sep;55(3):318-23.
PMID: 11200711

This study determined the prevalence and significance of autoantibodies to GAD65 (GAD Ab), insulin (IAA), tyrosine-like phosphatase (IA2) and islet-cell (ICA) in a group of 213 young Malaysian Type 1 diabetics, diagnosed before the age of 40 years. Venous blood was taken at fasting, and at 6 minutes post-glucagon (1 mg i.v.). IAA was detected in 47.4%, GAD Ab in 33.8%, IA2 in 8.9% and ICA in 1.4% of the subjects. When based on post-glucagon C-peptide level of 600 pmol/L, 172 (80.7%) patients had inadequate pancreatic reserve, while the remainder 41(19.3%) showed normal response. The autoantibodies, either alone or in combination, were detectable in both groups of patients; higher prevalence in those with poor or no beta-cell function (73.3% versus 46.3%, p = 0.0001). Although the prevalence of GAD Ab was highest in newly diagnosed patients (< 5 years), unlike IA2 and ICA, the marker remained detectable in 24-25% of those patients with long-standing disease. Nineteen patients could probably belong to the "latent autoimmune diabetes in adults (LADA)" subset, where pancreatic reserve was adequate but patients had detectable autoantibodies and insulin-requiring. On the other hand, 68 of the 213 patients (32%) were seronegative, but presented with near or total beta-cell destruction. Thus, as has also been suggested by others, there is indeed etiological differences between the Asian and the Caucasian Type 1 diabetics, and, there is also the possibility that other, but unknown autoantigens are involved in causing the pancreatic damage.

Matched MeSH terms: Diabetes Mellitus, Type 1/immunology*
Male and female NOD mice differentially express peroxisome proliferator-activated receptors and pathogenic cytokines

Yaacob NS, Goh KS, Norazmi MN

Exp. Toxicol. Pathol., 2012 Jan;64(1-2):127-31.
PMID: 20674317 DOI: 10.1016/j.etp.2010.07.005

The peroxisome proliferator-activated receptors (PPARs) have been implicated in regulating the immune response. We determined the relative changes in the transcriptional expression of PPAR isoforms (α, γ1 and γ2) and cytokines involved in the pathogenesis of type 1 diabetes (T1D) in the immune cells of 5 weeks, 10 weeks and diabetic male non-obese diabetic (NOD) mice compared to those of female NOD mice from our previous studies, "normalized" against their respective non-obese diabetic resistant (NOR) mice controls. Overall PPARα was significantly more elevated in the macrophages of female NOD mice of all age groups whereas PPARγ, particularly the PPARγ2 isoform was more depressed in the macrophages and CD4(+) lymphocytes of female NOD mice compared to their male counterparts. The pro-inflammatory cytokines, IL-1 and TNFα, as well as the Th1 cytokines, IL-2 and IFNγ were more elevated in female NOD mice whereas the Th2 cytokine, IL-4, was more depressed in these mice compared to their male counterparts. These findings suggest that the preponderance of T1D in female NOD mice may be influenced by the more pronounced changes in the expression of PPAR isoforms and pathogenic cytokines compared to those in male NOD mice.

Matched MeSH terms: Diabetes Mellitus, Type 1/immunology*
Low prevalence of autoimmune diabetes markers in a mixed ethnic population of Singaporean diabetics

Todd AL, Ng WY, Lui KF, Thai AC

Intern Med J, 2004 Jan-Feb;34(1-2):24-30.
PMID: 14748910 DOI: 10.1111/j.1444-0903.2004.00482.x

BACKGROUND: Circulating antibodies to glutamic acid decarboxylase (GADab) and tyrosine phosphatase-like molecule IA-2 (IA-2ab) are major indicators for auto-immune destruction of pancreatic islet cells. They identify a majority of Caucasians with type 1 diabetes and approximately 50% of Asians, providing evidence of an idiopathic aetiology in the latter. The present study investigated these autoantibodies in a mixed ethnic group.
METHODS: Hospital clinic patients with clinically defined type 1 (n = 93) and type 2 (n = 300) diabetes and representing Singapore's major ethnic groups--Chinese, Indians and Malays--were studied. GADab and IA-2ab frequencies, and association of autoimmunity status with clinical and biochemical profiles were analysed.
RESULTS: Radio-immunoprecipitation assays detected either or both antibodies (seropositivity) in 41.9% of subjects with type 1 diabetes. GADab was detected in 36.6% and IA-2ab in 23.7% of type 1 diabetics. Prevalence of IA-2ab showed a reduction in frequency with disease duration (P = 0.026). In clinical type 2 diabetics, seropositivity was 10.0% with higher frequency in Malays (17.5%) than Chinese (9.7%) and Indians (4.5%). Multivariate analysis revealed that low fasting C-peptide was associated with seropositivity (odds ratio (OR) = 0.15; 95% confidence interval (CI) = 0.04-0.58). A significant relationship (OR = 13.5; 95% CI = 5.0-36.7) between insulin requirement and duration (>5 years) was also revealed. In patients with type 2 diabetes there was a trend of gradual progression to insulin dependency. However, there was considerable variation in body mass index between ethnic subgroups of type 2 diabetics, particularly for Chinese (mean (SD) = 26.0 (4.7)) and Malays (mean (SD) = 29.2 (5.9); P < 0.001).
CONCLUSIONS: Presence of both antibodies in our mixed ethnic group of type 1 diabetes patients was much lower than in Caucasians. Significant numbers of patients were seronegative for antibodies. Influences due to ethnicity and adiposity would require further investigations.

Matched MeSH terms: Diabetes Mellitus, Type 1/immunology*
Allicin has significant effect on autoimmune anti-islet cell antibodies in type 1 diabetic rats

Osman M, Adnan A, Salmah Bakar N, Alashkham F

Pol J Pathol, 2012 Dec;63(4):248-54.
PMID: 23359194 DOI: 10.5114/pjp.2012.32772

The research purpose was to experimentally investigate the effect of allicin administration on the levels of main type 1 diabetes (IDDM) autoantibodies which are anti-islet cell antibodies (ICA) with an attempt to find a relation between this immunological effect and histological and/or biochemical findings. We have evaluated, with the help of ELISA kits, the levels of ICA and serum insulin in male Sprague-Dawley rats with Streptozotocin-induced IDDM in addition to pancreatic histological findings. The four groups (6 rats each) under study received or not different intraperitoneal doses of allicin for a period of 30 days. Daily intraperitoneal administration of allicin (either at as low dose of 8 mg/kg or high dose of 16 mg/kg) for up to 30 days to type 1 diabetic rats effectively reduces levels of anti-islet cell antibodies and in addition, reduced the level of insulin due to damaged Langerhans islet cell was significantly increased in the serum due to a repairing tissue process in pancreatic tissues. These experimental results suggest that allicin treatment has a therapeutic protective effect against autoimmune reactions occurring in IDDM. The data may provide new strategies for using allicin to be recommended as an excellent candidate in the clinical management, control, and prevention of IDDM.

Matched MeSH terms: Diabetes Mellitus, Type 1/immunology
The expression of cytokine genes in the peritoneal macrophages and splenic CD4- and CD8-positive lymphocytes of the nonobese diabetic mice

Yaacob NS, Kaderi MA, Norazmi MN

J Clin Immunol, 2004 Mar;24(2):177-84.
PMID: 15024185 DOI: 10.1023/B:JOCI.0000019783.61674.1d

Type 1 diabetes is an autoimmune disease that results from the destruction of the insulin-producing pancreatic beta islet cells, probably via the influence of cytokines. However, direct correlation between the expression of selected cytokines by various immune cells at different time points during the progression of the disease has not yet been clearly demonstrated. In this study, we showed that the mRNA expression of the pro-inflammatory cytokines, TNF-alpha, IL-1 beta, IL-6, and GM-CSF, were increased while the anti-inflammatory cytokine, TGF-beta, decreased in the peritoneal macrophages of nonobese diabetic (NOD) mice. IL-6 expression however decreased when the mice became diabetic. Surprisingly the expression of IFN-gamma and IL-2 by splenic CD4+ cells were lower in 5-week-old NOD mice as compared to the nonobese diabetic resistant (NOR) control mice, but their expression was higher in older NOD mice. The expression of IL-4 and IL-10 decreased in splenic CD4-positive lymphocytes. Splenic CD8-positive lymphocytes expressed increased levels of IFN-gamma and IL-10 but the latter decreased sharply when diabetes occurred. The relevance of these findings to the pathogenesis of type 1 diabetes is discussed.

Matched MeSH terms: Diabetes Mellitus, Type 1/immunology*
Differential transcriptional expression of PPARalpha, PPARgamma1, and PPARgamma2 in the peritoneal macrophages and T-cell subsets of non-obese diabetic mice

Yaacob NS, Kaderi MA, Norazmi MN

J Clin Immunol, 2009 Sep;29(5):595-602.
PMID: 19472040 DOI: 10.1007/s10875-009-9300-1

BACKGROUND: The peroxisome proliferator-activated receptors (PPARs) have been implicated in immune regulation. We determined the transcriptional expression of the three isoforms, PPARalpha, PPARgamma1, and PPARgamma2 in the peritoneal macrophages, CD4- and CD8-positive lymphocytes in non-obese diabetic (NOD) mice at 5 and 10 weeks of age as well as at diabetic stage.
RESULTS: Compared to the non-obese diabetic resistant (NOR) mice, the peritoneal macrophages of NOD mice expressed increased levels of PPARalpha but reduced levels of PPARgamma2, while PPARgamma1 expression was unchanged in all age groups. CD4-positive lymphocytes expressed low levels of PPARalpha in diabetic NOD mice and greatly reduced expression of PPARgamma2 in all age groups. Unlike peritoneal macrophages and CD4-positive cells, the CD8-positive cells expressed low levels of PPARgamma1 in diabetic NOD mice but no difference in PPARalpha and PPARgamma2 expression was observed compared to NOR mice.
CONCLUSION: The current findings may suggest an important regulatory role of PPARs in the pathogenesis of autoimmune diabetes.

Matched MeSH terms: Diabetes Mellitus, Type 1/immunology