A 40-year-old gravida 1, para 1001 presents with worsening pelvic pain. Her symptoms have been present for over 15 years and are progressing. Most recently, she has daily symptoms described as sharp, stabbing, intermittent pelvic pain. Her menstrual cycle exacerbates the pain. In addition to dysmenorrhea, she reports deep dyspareunia and a history of infertility. She denies any bowel or bladder dysfunction. Menarche was early at age 10. Menses occur every 25 days, with an 8- to 10-day duration with heavy bleeding and dysmenorrhea. Past treatments include combined oral contraceptive pills, gonadotropin-releasing hormone (GnRH) agonist following laparoscopy-proven endometriosis, and she is currently in her fourth year of a levonorgestrel-containing intrauterine device (IUD). She has no significant past medical history. Her past surgical history is significant for operative laparoscopy 12 years ago with excision of endometriosis (pathology confirmed) and adhesiolysis to improve fertility. She is not taking any medications and is allergic to sulfa (rash). She is a non-smoker, drinks alcohol socially. She is happily married and works for a non-profit organization. Her daughter is 10 years old and healthy. Due to her increasing pelvic pain she now requests hysterectomy.

A 32-year-old para 0 presents with persistent pain after laparoscopic assisted vaginal hysterectomy/bilateral salpingo-oophorectomy (LAVH/BSO) for endometriosis. Her surgery was notable for bilateral endometriomas with scarring of the ovaries to each respective ovarian fossa and adhesions of the rectosigmoid colon to the left ovary. She had an uneventful recovery from surgery and was started on estrogen-only therapy for skeletal and cardiovascular protection. Three months following surgery, she reports the onset of an intense intermittent left lower quadrant pain. This began cyclically though it has progressed to pain for at least two weeks of each month. She has no past medical history. Her past surgical history is significant for three laparoscopic endometriosis surgeries, LAVH/BSO. She is taking estradiol (Estrace) 1 mg PO daily. She has no allegies.

Chronic pelvic pain, is defined as any pelvic pain lasting over six months. It can result from a variety of urological, gynaecological or gastrointestinal aetiologies. It tends to affect women of reproductive age and can have a signi?cant impact on women’s health, relationships and quality of life. In a majority of cases no aetiological factors are identifiable and there is no consensus in treating and managing such patients. Treatment can be frustrating and can lead to breakdown of the patient–doctor relationship.

A 28-year-old nulligravid woman presents reporting severe dysmenorrhea, deep dyspareunia, and dyschezia that worsens with menses. She states she has always had painful periods, but they have worsened over the past year. She describes it as sharp, twisting, and feels that something is “stabbing her from the inside out.” She is in a long-term relationship and desires future fertility. She has tried several different combined oral contraceptive pills, which mildly improved her pain. She has also tried non-steroidal anti-inflammatory drugs, medroxyprogesterone acetate, and a gonadotropin-releasing hormone agonist without relief. She states the dyspareunia and constipation have worsened over time. She underwent a diagnostic laparoscopy at age 26 and was told she had stage IV endometriosis. She continues to have debilitating pain that significantly impacts her quality of life. She would like to proceed with fertility-sparing surgical management. She has no other relevant relevant past medical or surgical history. She is currently taking oral contraceptives (ethinyl estradiol/norethindrone) and has no known drug allergies.

The large number of gene–disease associations that have been discovered through the use of high-throughput genomics have revolutionized our understanding of complex disease biology. Genomics holds ample scope from the clinical perspective, particularly with regards to disease risk prediction, improving disease classification, risk stratification and drug selection. Elucidating the functional impact of genomic variants is a critical challenge that should further facilitate the ‘bench to bedside’ translation. Additionally, healthcare systems need to acknowledge the necessity of updating and adapting current practices to ensure direct and cost-effective translation of modern genomics to the clinic.

Uterine and tubal abnormalities alone or in combination with other factors are present in 17%–25% of all couples who seek care for infertility treatment. The prevalence is higher in older women and in those with secondary infertility. Although suspected at the history, it is usually confirmed by ultrasound/ laparoscopy and/or MRI depending on the cause. Multiple pathologies are identified under the umbrella of tubal and uterine factors, some are associated with infertility but very few are proven to be the only cause of infertility. Treatment depends on the condition. It ranges from no intervention to surgery to in vitro fertilisation (IVF). With advances in the technology of IVF, surgery is becoming a lost art, especially for tubal factors. Various surgical techniques have been suggested for uterine factors. Given most tubal and uterine factors have association rather than causation for infertility, the effect of surgery on improving fertility is debatable. We will discuss the causes of uterine and tubal factors, their implications on fertility, diagnostic modalities and treatment options with limitations of the available evidence. A good history and a high index of suspicion along with primary and secondary prevention of tubal and uterine factor infertility are important to prevent long-term implications.

Endometriosis is a chronic oestrogen-dependent condition that affects 10% of women from puberty to menopause. It is characterised by the presence and proliferation of endometrial-like cells outside the uterine cavity, generally within the pelvis. Endometriosis can present as superficial or deep peritoneal lesions, ovarian endometrioma or deep rectovaginal disease. The two hallmark symptoms of endometriosis are pelvic pain and infertility resulting in poor quality of life. There is no correlation between the extent of the disease and severity of symptoms. The true prevalence of the condition is not known, as it requires a laparoscopy to confirm the diagnosis. It is found in up to 30% of women with infertility and in 45% of those with pelvic pain. While there are several theories of pathogenesis, an interplay of genetic, hormonal, environmental and immunological factors is implicated in the development of endometriosis in susceptible women. Symptoms are managed with a combination of hormonal treatment and laparoscopic ablation or excision of lesions for pain and usually assisted reproduction for infertility. Endometriosis is prone to recurrence after treatment, requiring multiple contacts with healthcare and repeat surgery. Management of endometriosis requires an individualised approach based on the woman’s age, predominant symptoms and priorities, which are subject to change over time.

Diverticular disease of the sigmoid colon is one of the most common diseases at sigmoidoscopy/colonoscopy and yet biopsies are not often taken from the colon afflicted by this disease. Indeed, biopsies are often contraindicated in acute diverticulitis because of the risks of perforation. Nevertheless, there is increasing understanding that the disease is associated with luminal mucosal pathology, namely diverticular colitis, which is a close histological mimic of chronic inflammatory bowel disease (IBD). Indeed, there is a close relationship between the diseases and there are occasional cases where diverticular colitis is followed, in due course, by the onset of true chronic IBD, specifically ulcerative colitis. The disease is also associated with characteristic mucosal polypoid change. Often mucosal biopsies show similar inflammatory changes to those seen in classical diverticular colitis but the pathology of mucosal prolapse may also be seen. The latter features may occur in many different situations, although all show the same characteristic morphological appearances. Such situations include stomas, both ileal and colonic, in association with ‘cap polyposis’, in solitary ulcer (mucosal prolapse) syndrome in the rectum, and at the anorectal junction in so-called inflammatory cloacogenic polyp. Several other conditions can produce mimicry of chronic IBD in mucosal biopsies, having in common the ability to produce underlying mass lesions that result in ‘secondary colitis’ in the mucosa. These conditions include endometriosis, pneumatosis coli, primary and secondary tumours, and inevitably, intramural and extramural suppuration associated with diverticular disease itself.