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Response to Treatment in a sample of Iraqi Patients with Prolactinoma
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Abstract<sec> <title>Background:

Hyperprolactinemia is a common endocrine abnormality caused by physiological factors like pregnancy and lactation, drug-induced factors like antipsychotics, pituitary adenomas that secrete prolactin, or stalk compression or section that reduces dopamine inhibition. Dopamine agonists cure most prolactinomas.

Objectives:

To assess response to treatment in micro versus macroprolactinoma.

Materials and Methods:

A total of 35 patients (20 female and 15 male) with documented hyperprolactinemia (serum prolactin above the assay-specific reference range) due to prolactin-secreting pituitary adenoma attending the national diabetes center in Baghdad from April 2019 to March 2020 were selected. For each patient, we were recorded clinical presentation, drug history, age, body mass index, prolactin, T4, TSH, and pituitary MRI. After at least 6 months of therapy, prolactinoma patients were examined for cabergoline dosage, duration, and clinical, biochemical, and radiological response.

Results:

Cabergoline treatment with a dosage of 0.5–2.5 mg/week and a period of 6–52 months restores gonadal function and libido in most prolactinoma patients, with a stronger but nonsignificant response in micro vs macroprolactinoma (87.5% vs. 57% respectively). Cabergoline normalized menses in all microprolactinoma patients and 87.5% of macropros. Normalization of prolactin levels in 80% of prolactinoma patients, with microprolactinoma responding 95% vs 60%. gender, treatment length, or age did not affect prolactin response. 50% of surgery-radiotherapy patients experienced cabergoline-induced prolactin normalization, compared to 86% of medical therapy-only patients. Cabergoline shrank tumors in 74% of patients (80% in micro vs. 66% in macro), regardless of age, gender, length of treatment, or prior surgery/radiotherapy.

Conclusion:

patients with prolactinoma, cabergoline-induced clinical, biochemical, and radiological improvement in the majority of patients.

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The members of the family of Eentrobacteriaceae harbour a gene cluster called polyketide synthase (pks) island. This cluster is responsible for the synthesis of the genotoxin colibactin that might have an important role in the induction of double-strand DNA breaks, leading to promote human colorectal cancer (CRC). Eleven out of the eighty eight isolates (12.5%) were pks+, distributed as 7 (8%) isolates of E. coli, 2 (2.25%) of K. pneumoniae and 2 (2.25%) of E. aerogenes. The cytotoxic effects of selected pks+ isolates (E. coli and E. aerogenes) on HeLa cells were represented by decreasing cell numbers and enlarged cell nuclei in comparison to the untreated cells. Cyt

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Association of modifiable and non-modifiable risk factors with periodontal disease in Iraqi individuals: a retrospective study
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