Abstract A 35-year-old male developed Post-Finasteride Syndrome (PFS) following a 9-10 month course of finasteride 1.25mg/day (Proscar, quartered), with symptom onset in June 2012 at age 21. Over the subsequent 13 years, approximately 218 interventions were trialled. Standard blood tests returned normal (thyroid, liver, renal, lipid, HbA1c, cortisol, coeliac, and inflammatory markers). A standard hydrogen and methane lactulose breath test in March 2021 was negative. However, a hydrogen sulphide (H2S) lactulose breath test in October 2025 returned strongly positive, with a peak concentration of 79.7 ppb (normal <25 ppb). The flat hydrogen reading alongside high H2S is consistent with cross-feeding: fermenting bacteria generate hydrogen (or its precursor, formate) that is consumed by sulphate-reducing bacteria to produce H2S. The patient responded powerfully to H. pylori triple therapy (amoxicillin, clarithromycin, lansoprazole) despite repeatedly testing negative for H. pylori. Lansoprazole provided sustained benefit, while esomeprazole and omeprazole did not - suggesting the mechanism of benefit was not stomach acid suppression but rather urease inhibition via biliary excretion. The patient also responded to bismuth (Pepto-Bismol, Devrom) and to co-amoxiclav. Metronidazole and ciprofloxacin provided minor benefits, while secnidazole, paromomycin, nitazoxanide had no effect. Rifaximin and doxycycline worsened symptoms. Faecal microbiota transplant (FMT) worsened symptoms. Colonics had zero effect. These two findings suggest the problem is in the small intestine, not the large intestine, consistent with the SIBO (Small Intestinal Bacterial Overgrowth) breath test result. A stool microbiome analysis showed Ruminococcus gnavus at 2.93% (99th percentile; normal <0.5%) and beta-glucuronidase at 2.94% (99th percentile; normal 0.01-1.00%), while colonic H2S producers were low. This suggests the H2S-producing organisms are located in the small intestine rather than the colon. This case report supports the theory PFS may be sustained by a dual-population community of microbes (some of which are in the small intestine and may be a SIBO): fermenting bacteria (e.g. R. gnavus) that disrupt hormone excretion via beta-glucuronidase and produce formate - a direct precursor to hydrogen - and hydrogen sulphide-producing bacteria (perhaps Bilophila wadsworthia or a non-pylori Helicobacter) that consume the hydrogen and generate H2S, which inhibits mitochondrial function. The first population may contribute primarily to the androgenic symptoms; the second, primarily to the cognitive, fatigue, and neurological symptoms. This case report recommends studies to investigate the link with a larger sample of PFS patients.
Avery X Trace (Thu,) studied this question.