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Diabetes Care 24:1503-1504, 2001
© 2001 by the American Diabetes Association, Inc.


Letters: Observations
Letter

Is There a Predisposition to Intestinal Parasitosis in Diabetic Patients?

Yasar Nazligul, MD1, Tevfik Sabuncu, MD2 and Hatice Ozbilge, MD3

1 Department of Internal Medicine, the
2 Department of Endocrinology and Metabolism, and the
3 Department of Clinical Microbiology and Parasitology, University of Harran, Faculty of Medicine, Research Hospital, Sanliurfa, Turkey

Although intestinal parasites usually create benign diseases, sometimes they may cause complications with high mortality and morbidity (1,2). It is known that diabetic patients are more susceptible to bacterial infections. Decreased arterial perfusion, neuropathy, and suppressed immune response in diabetes aggravate the frequency and severity of infectious diseases (3). Lymphocyte and polymorphonuclear leukocyte functions are altered (4). The most prominent alteration is the phagocytic functions of polymorphonuclear leukocytes (5,6). It has also been reported that candidal infections occur more frequently in diabetic patients than in nondiabetic control subjects (7,8). Is a similar kind of predisposition present against parasitic infections, particularly against the intestinal parasites in diabetic patients? There is no adequate study about this subject. Therefore, we assessed whether there is a predisposition against intestinal parasites in the diabetic population by comparing their prevalence in diabetic and nondiabetic individuals living in the Sanliurfa province, which lies in southeast Anatolia. Here, intestinal parasites are very common because of the hot climate, agricultural usage of sewage, and inadequate purified drinking water.

A total of 200 diabetic (16 type 1 and 184 type 2) and 1,024 nondiabetic individuals who were consecutively recruited to endocrinology and internal medicine outpatient clinics were included in the present study. The diabetic group comprised 72 male and 128 female patients (mean age 45.2 years, range 15–79). Of the 200 diabetic patients, 26 were on insulin therapy, 106 were on oral antidiabetic agents, 21 were on diet alone, and 47 were not on therapy. The nondiabetic group comprised 344 male and 680 female patients (mean age 40.0 years, range 15–74). Fresh stool samples were examined macroscopically, followed by microscopic examination by native, lugol, and flotation methods under 10x and 40x magnification. The differences between the categorical variables under consideration were analyzed by {chi}2 test. P < 0.05 was considered statistically significant.

Intestinal parasitosis was diagnosed in 94 of 200 patients (47%) in the diabetic group (61 women and 33 men). The distribution of the parasites found was: 57.5% Ascaris lumbricoides, 14.2% Trichuris trichura, 13.3% Entamoeba histolytica, 11.7% Giardia intestinalis, and 3.3% tenias (T. saginata or Hymenolepis nana). In 15 patients, two or more kinds of parasites were found. There were no statistically significant differences with regard to incidences of intestinal parasites between male and female patients (45.8 and 47.6%, respectively) and between therapy groups. In the control subject group, 380 of 680 women (55.9%) and 184 of 344 men (53.4%) had intestinal parasites, and 72 people had more than one kind of parasite. The prevalence of the parasites did not show significant differences between sex parasites. Ascaris lumbricoides was the most common intestinal parasite in both groups (P < 0.05). Intestinal parasite prevalence in the diabetic group was found to be significantly lower than in the control subject group (47 vs. 55%, P < 0.05).

It has been reported that certain medications and diabetes affect immune mechanisms in AIDS-infected patients. The patient’s immune status is relevant in determining which parasitic infections need to be considered. In patients infected with HIV, specific protozoan diseases may develop opportunistically (9). Patients with hypogammaglobulinemia or cystic fibrosis may develop refractory giardiasis. In patients developing symptoms of enterocolitis while receiving glucocorticoids, the possibility of an exacerbation of unsuspected strongyloidiasis or amebic colitis should be considered (10). Although several defects in the immune system have been reported in diabetic patients (3,4), there are insufficient data in the literature about concordance of diabetes and intestinal parasitic diseases. In a study by Abaza et al. (11), the frequency of opportunistic intestinal parasites was explored in four groups with immunocomprimised hosts and was found in 31.7% of patients under corticosteroid therapy, in 28.8% of patients suffering renal failure, in 25.7% of patients with malign neoplasm, and in 8% of diabetic patients. In our study, no significant predisposition to intestinal parasitosis was observed in diabetic patients. Moreover, diabetic patients had less intestinal parasites compared with the general population in our endemic region. Because of similar frequencies of parasites in all groups, the lower prevalence of intestinal parasitic disease in diabetic patients did not depend on the antidiabetic agents used (i.e., insulin, oral antidiabetic agents, diet alone, or no treatment). This low frequency of parasites in diabetic patients may be a result of the fact that, because of their illness, they undergo physical examinations and laboratory tests more frequently than the general population in our region. The greater number of physician visits incurred by diabetic patients may cause this lower frequency of parasitosis.

FOOTNOTES

Address correspondence to Dr. Tevfik Sabuncu, Bahcelievler, Cengiz Topel Cad., Rahmet Apt. D:10, Sanliurfa 63100, Turkey. E-mail: sabuncut{at}ixir.com.

References

  1. Owen RL: Parasitic diseases. In Gastrointestinal Disease. Sleisinger MH, Fordtran JS, Eds. Philadelphia, PA, W.B. Saunders, 1993, p. 1190–1224
  2. Ochoa B: Surgical complications of ascariasis. World J Surg 15:222–227, 1991[Medline]
  3. Bessman AN, Sapico FL: Infections in the diabetic patient: the role of immune dysfunction and pathogen virulence factors. J Diabetes Complications 6:258–262, 1992[Medline]
  4. Moutschen MP, Scheen AJ, Lefebvre PJ: Impaired immune responses in diabetes mellitus: analysis of the factors and mechanisms involved: relevance to the increased susceptibility of diabetic patients to specific infections. Diabete Metab 18:187–201, 1992[Medline]
  5. Delamaire M, Maugendre D, Moreno M, Le Goff MC, Allannic H, Genetet B: Impaired leucocyte functions in diabetic patients. Diabet Med 14:29–34, 1997[Medline]
  6. Balasoiu D, van Kessel KC, van Kats-Renaud HJ, Collet TJ, Hoepelman AI: Granulocyte function in women with diabetes and asymptomatic bacteriuria. Diabetes Care 20:392–395, 1997[Abstract]
  7. Schiefer HG: Mycoses of the urogenital tract. Mycoses 40(Suppl. 2):33–36, 1997
  8. Atkinson JC, O’Connell A, Aframian D: Oral manifestations of primary immunological diseases. J Am Dent Assoc 131:345–356, 2000[Abstract/Free Full Text]
  9. Amenta M, Dalle Nogare ER, Colomba C, Prestileo TS, Di Lorenzo F, Fundaro S, Colomba A, Ferrieri A: Intestinal protozoa in HIV-infected patients: effect of rifaximin in Cryptosporidium parvum and Blastocystis hominis infections. J Chemother 11:391–395, 1999[Medline]
  10. Weller PF: Approach to the patient with parasitic infection. In Harrison’s Principles of Internal Medicine. Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, Kasper DL, Hauser SL, Longo DL, Eds. Colombus, OH, McGraw-Hill, 1998, p. 1163–1165
  11. Abaza SM, Makhlouf LM, el-Shewy KA, el-Moamly AA: Intestinal opportunistic parasites among different groups of immunocompromised hosts. J Egypt Soc Parasitol 25:713–727, 1995[Medline]

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