Spectrum of Prostate Disorder in Jos, Plateau State of Nigeria

Affi Ayuba¹ , Imoh Lucius¹ , Longwap S.A¹ , Alfred Odo¹ , Solomon Luka Mercy¹ , Anzaku A²

¹Department of Chemical Pathology, University of Jos, Plateau, Nigeria

²Department of Anatomical Pathology, Jos University Teaching Hospital, Jos, Plateau, Nigeria

Corresponding Author Email: ayubaaffi67@gmail.com

DOI : https://doi.org/10.51470/eSL.2025.6.3.34

Abstract

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INTRODUCTION

Acute prostatis is commonly caused by a bacterial  and is usually by uropathogens and can be treated initially by broad spectrum antimicrobials until the results from urine culture are available for a more tailored antibiotic therapy chronic prostatitis-like symptoms in men may have multifactorial causes. About 10% will progress to chronicity [1,2]. Benign prostratic hyperplasia (BPH) is a  to the nonmalignant growth or hyperplasia of postrate tissue and is a non malig of lower urinary tract symptoms (LUTS) in older men. Prevalence has been shown to increase with advancing age. The etiology BPH is influenced by a wide variety of risk factors, in addition to the direct hormonal effects of testosterone on prostrate tissue. Men who are castrated before puberty or who have an androgen-related disorder do not develop BPH.  Some risk factors contribute to the development of BPH[3,4].

The second-leading cause of cancer death in men in the United States and many other westernized countries is CaP; accordingly, judicious screening of healthy men allows for diagnosis sufficiently early that  all options (i.e., treatment or surveillance) are still available in most cases [5]. The prostate-specific antigen (PSA) blood test is the foundation for modern prostate cancer (CaP) screening. Initially it was used in forensic medicine. The subsequent discovery that it could be measured in serum, and that serum levels increase in the setting of prostatic disease, led to its current application as a CaP marker. It is now used to screen for CaP and monitor disease course [6]. A significant predictor of the development of BPH is age over 50% of older men show evidence of BPH and with associated LUTS increasing with age linearly. The aim of study is portray the prevalence of prostate disorder in Jos  secondary diagnostic centre.

Materials and Methods

Study Area

The study center is SKANE RADIO-DIAGNOSTIC CENTRE a secondary  health facility located in Jos, the capital city Plateau State in North-Central Nigeria. SKANE serves as a referral center for Plateau Hospital, OLA hospital and Bingham Teaching Hospital mainly for diagnostic purposes. Plateau state is situated at an elevation of about 1,238 meter  above sea level. The city is geographically located between latitude 9055’N and  longitude 8054E.

Study Design

This study employs a hospital-based cross-sectional descriptive study. The design was chosen to determine the prevalence of Prostate BPH and CaP Specific levels and their distribution across different age categories among male patients who attended Jos University Teaching Hospital during the study period. Each subjects have gone through physical examination including DRE, Ultrasound.

Study Population

The study population consisted of Ninety-Two (92) male patients who attended Skane Radio-Diagnostic Centre. Diseases that form the spectrum are prostitis, BPH and Ca prostate. Serum PSA and USS results, DRE findings obtained from documented hospital records.  BPH and CaP can be diagnosed by ultrasound and prostatis was diagnosed clinically by tenderness of the of the gland.

 DRE Patients with incomplete records, duplicate entries, or inconclusive laboratory results were excluded.

Data Collection

Data were obtained from the hospital’s laboratory information management system and patient records in the Pathology. Relevant variables extracted included Patient age and prostate sizte serum PSA levels (ng/mL). The data collection was carried  out with strict adherence to patient confidentiality.  Prostate  sonography findings of each patient was obtained from hospital records .

RESULTS 

This report presents  is results a comprehensive statistical, clinical and visualization-based analysis of prostate health data. The data set initially contained 92 records; however, one was removed due to inconsistency, resulting in 91 valid entries. This result presents  with prostate size, PSA concentration, prostate volume, Age and BPA for prostatis.

Descriptive Statistics

• Mean: 12.06ng/l
• Min: 0.20
• Max: 105.80

Age:

• Mean: 65.93 years
• Min: 50
• Max: 81

Prostate Volume:

• Mean: 127.71cm³
• Min: 3 cm
• Max: 380cm

The data set represents an older adult male population with diverse prostate conditions. PSA and values show high variability, suggesting both benign and malignant conditions.

Relationship Summary

• PSA Volume: Weak correlation
• Volume vs Age: Weak correlation
• PSA vs Size: Weak correlation
• PSA vs Diagnosis: strong differentiation

Overall Clinical Inferences

1. PSA is a strong indicator of malignancy
2. Prostate size varies independently of PSA and age
3. BHP is the common condition (69%)
4. CAP cases, though fewer, produce very high PSA values (20%)
5. Visualization patterns reveal two populations:
6. Large benign cluster (low-moderate PSA)
7. Small malignant cluster (high PSA)
8. E – Prostatis form in (2%)

Conclusion

This analysis confirms that PSA is the most reliable marker for differentiating prostate pathologies. Prostate volume and age alone are insufficient for predicting disease severity. The diagnostic and PSA patterns align with established clinical knowledge. These findings can guide screening, diagnosis and management of prostate health conditions.

       REFERENCES

1. K. G Naber prostatis: challenges in diagnoses and treatment int. J infect dis IJID 2016; 45(1): 67-68. https://www.ijidonline.com/article/S1201-9712(16)30175-8/fulltext. 
2. Michael Ng; Stephen W. Leslie; Krishna M. Baradhi. Author information and Affiliations. Spectrum of Prostate disorder in an (IDD) Iodine Deficiency disorders region – of set Nigeria. https://www.ncbi.nlm.nih.gov/books/NBK558920.
3. Roehrborn CG. Benign prostatic hyperplasia: an overview. Rev Urol. 2005: 7(9):3-14.
4. Chughtai B, Forde JC, Thomas DD, Laor L, Hossack T, Woo HH, Te AE, Kaplan SA. Benign Prostatic Hyperlasia. Nat Rev Dis Primers.
5. Gacci M, Corona G, Vignozzi L, Salvi M, Serni S, De Nunzio C, Tubaro A, Oelke M, Carini M, Maggi M. Metabolic syndrome and benign prostatic enlargement: a systematic review and meta-analysis. BJU Int. 2015 Jan;115(1):24-31.
6. Abrams P. New words for old: lower urinary tract symptoms for “prostatism”. BMJ. 1994 Apr 09;308(6934):929-30.
7. Stamey TA, Yang N, Hay AR et al. Prostate – specific antigen as a serum marker for adenocarcinoma of the prostate. N Engl Med. 1987;317:909-916. Doi: 10.1056/NEJM198710083171501.
8. Catalona, WJ, Smith DS, Ratliff TL, et al. measurement of prostate- specific antigen in serum as a screening test for prostate cancer. N Engl J Med. 1991;324:1156-1661. Doi:10.1056/NEJM199104253241702.
9. Stephenson AJ, Kattan MW, Eastham JA, et al. Prostate cancer specific mortality after radical prostatectomy for patients treated in the prosate- specific antigen era. J Clin Oncol.
10. Welch HG, Albertsen PC. Prostate cancer diagnosis and treatment after the introduction of prostate – specific antigen screening: 1986-2005. J Natl Cancer Inst. 2009;101:1325-1329. Doi 10.1093/jnci/djp278.