• Abdominal bloating or distention
• Abdominal or pelvic pain
• Early satiety or loss of appetite
• Increased urinary frequency or urgency
• Changes in bowel habit
• Fatigue
• Unexplained weight loss
• Post-menopausal bleeding

Symptoms are more likely to be associated with ovarian cancer if they are in a post-menopausal female and/or if they are new, severe, unusual, recurrent or persistent, e.g. occurring 12 or more days per month. New symptoms suggestive of irritable bowel syndrome, e.g. changes in bowel habit, in females aged > 50 years are unusual; consider the possibility of ovarian cancer in these patients (among other potential diagnoses such as bowel cancer).

Kamini is an opioid-containing herbal medicine that may contain high levels of hazardous substances, including lead and mercury. Despite being illegal to import, supply or possess without a prescription, Kamini is increasingly seen in New Zealand within specific groups, mostly within the Indian community and followers of Ayurvedic or Unani medicine. It is claimed to have wide ranging benefits for men’s health, including improved sexual function and overall vitality.

With the recent cluster of lead notifications suspected to be due to Kamini consumption, this is a timely reminder that use of traditional herbal medicines is not without potential harm and that people can be exposed to a range of contaminants. If patients are using herbal medicines/remedies such as Kamini, assess whether they have any abnormal symptoms or signs. Ask them if they experience any problems when they miss a dose or try to stop. Local Community Alcohol and Drug Services can provide assistance with patients experiencing difficulties.

Molnupiravir (Lagevrio), a COVID-19 antiviral, is no longer available in New Zealand. Supplies of molnupiravir expired on 31^st January, 2024, and based on clinical advice, Pharmac is not planning to source additional stock. Pharmacies should return any remaining molnupiravir stock to the wholesaler.

In the first half of 2023, the COVID-19 Therapeutics Technical Advisory Group recommended that funding of molnupiravir be removed based on evidence that it had not shown benefit in preventing hospitalisation or death in people at higher risk of severe symptoms with COVID-19 (see Bulletin 70). In July, 2023, following a consultation process (as reported in Bulletin 72), Pharmac revised the access criteria for funded treatment with molnupiravir to certain groups who were unable to take other funded antivirals (see Bulletin 80 for further details).

Nirmatrelvir with ritonavir (Paxlovid) and remdesivir (Veklury) are still available for people with COVID-19 who are at higher risk of severe disease and meet eligibility criteria. A COVID-19 antiviral access criteria assessment tool is available here.

The currently funded brand of ciprofloxacin (Cipflox) is being discontinued by the supplier; all strengths, i.e. 250 mg, 500 mg and 750 mg, are now out of stock. A replacement brand for the 500 mg tablets is available (Ciprofloxacin – Torrent; as reported in Bulletin 89) and Pharmac has announced that an alternative brand of the 250 mg ciprofloxacin tablets has now been listed on the Pharmaceutical Schedule (stock is expected to become available over the next few weeks). The Ciprofloxacin – Torrent brand of 250 mg and 500 mg ciprofloxacin tablets does not have Medsafe approval, so will need to be prescribed for supply under Section 29 of the Medicines Act 1981. Currently, there is no alternative brand to replace the 750 mg ciprofloxacin tablets.

Pharmac has announced that testosterone transdermal gel (Testogel) will be funded from 1^st April, 2024. As mentioned in Bulletin 87, Testogel will be fully funded without restriction. Testosterone is currently approved for testosterone replacement in people with primary and secondary hypogonadism and for testosterone-based gender affirming hormone therapy, and is available in three formulations: injections, patches and capsules. The availability of testosterone gel will provide people who take testosterone with another option if other testosterone formulations are not suitable or appropriate.

Corticosteroids. The association between high-dose glucocorticoids (corticosteroids) and new-onset diabetes (or worsening of existing diabetes) is well established. The extent of hyperglycaemia depends on multiple factors, including baseline HbA_1c level, the dose and duration of treatment and the presence of co-morbidities. If a patient experiences hyperglycaemia with a corticosteroid, and the dose cannot be reduced or withdrawn, it may be appropriate to add metformin (if not already prescribed) with or without a sulfonylurea (e.g. gliclazide, glipizide) to their regimen. In some cases, escalation to other glucose-lowering treatments, including insulin (short-acting) may be required. People with type 1 diabetes may require an increase in their insulin dose. When corticosteroid treatment ceases (with dose tapering), re-assess the need for the sulfonylurea or insulin, if added (or dose increased), as ongoing use may result in hypoglycaemia.

Antipsychotics. The use of antipsychotic medicines can directly influence pancreatic beta cell activity, impairing insulin sensitivity and secretion, and in some cases resulting in apoptosis (cell death). Antipsychotics are also associated with weight gain which, in turn, increases the risk of type 2 diabetes; this is most apparent in antipsychotics which strongly block muscarinic M3 and histamine H1 receptors, e.g. olanzapine, clozapine and chlorpromazine. Haloperidol and quetiapine are also reported to be associated with hyperglycaemia. Ziprasidone, aripiprazole and amisulpride are associated with the least amount of hyperglycaemia and weight gain and may be the most appropriate choices for patients at higher risk. Read more about antipsychotics here.

Thiazide diuretics. Hypokalaemia, dyslipidaemia and increased blood glucose levels are associated with the use of thiazide diuretics, e.g. bendroflumethiazide, chlorthalidone, indapamide. Thiazide diuretic-induced diabetes is possibly due to hypokalaemia, which can in turn decrease insulin secretion and sensitivity in a dose-dependent manner. High doses of thiazides should be avoided in people with diabetes. Regular electrolyte monitoring is recommended for patients taking thiazide diuretics. If hypokalaemia is detected, advise the patient to increase dietary intake of potassium or consider potassium supplementation. Other antihypertensive options may be more appropriate, read more here.

Statins. New-onset diabetes occurs in approximately one in ten patients taking a statin. Statins may contribute to diabetes by decreasing insulin sensitivity and impairing insulin secretion. However, the benefits of statin treatment for cardiovascular disease likely outweighs the potential risk of hyperglycaemia in many cases. People most at risk of developing diabetes while taking a statin are those who already have risk factors such as impaired fasting glucose, elevated HbA_1c, or increased BMI. Higher potency statins such as rosuvastatin are associated with a greater risk than lower potency statins such as pravastatin. Read more here.

Beta blockers. Non-vasodilating beta blockers, e.g. atenolol, metoprolol, are more likely to be associated with diabetes (and weight gain and dyslipidaemia) compared with vasodilating beta blockers, e.g. carvedilol. Carvedilol is therefore usually the preferred beta blocker for people with cardiovascular disease, e.g. heart failure, and co-morbid insulin resistance or type 2 diabetes, as there is some evidence that it improves insulin sensitivity and does not adversely affect glycaemic control. Read more about beta blockers here: and look out for an update of this article coming soon.

• Inform the patient (and/or family/whānau) when harm or a near-miss occurs as a direct result of medical care. Information should be delivered as soon as practical in an honest and transparent manner.
  • Harm is defined as: “An outcome that negatively affects a patient’s health or quality of life. Sometimes, it could result in death. Harm may or may not relate to the risks discussed during the informed consent process.”
  • Near-miss is defined as: “A situation where something occurred during the patient’s treatment that could have, but did not, result in harm to the patient. A near-miss can be the result of an error or a deviation from normal practice.”
• Where possible, review what led to the harm and implement measures to prevent a similar incident from occurring
• When disclosing harm:
  • Ensure that a senior clinician is present (ideally this should be the doctor who has lead responsibility for the patient’s care). If the relevant clinician is not available, consider the impact of delaying disclosure against the benefits of timely communication.
  • Consider the patient’s and family/whānau’s needs for information and further support, e.g. interpreter, social worker, Māori health provider
  • Document details of the harm in the patient records and any disclosures that have been made. This includes the nature of harm, contributing factors, subsequent action(s) taken, details of the disclosure (what was discussed, who was present and what was the patient’s reaction) and any follow-up or ongoing care required.
  • Consider whether any third parties should also be informed of the harm and complete relevant documentation
  • Ensure the patient and/or family/whānau are aware of available complaints processes

Read the full statement here

• Dysmenorrhoea generally involves pelvic or lower abdomen pain (cramping) that occurs before or during menstruation. It typically lasts 8 to 72 hours and may be associated with other symptoms such as bloating, nausea, vomiting, diarrhoea, fatigue and insomnia.
• Dysmenorrhoea can be described as primary (idiopathic) or secondary (resulting from the presence of pelvic pathology, e.g. endometriosis). Primary dysmenorrhoea typically develops within 6 – 12 months of menarche, while secondary dysmenorrhoea can develop at any time, in relation to the causative condition.
  • Risk factors for primary dysmenorrhoea include younger age (< 30 years), menarche occurring before age 12 years, longer or heavier menstrual bleeding, low or high body mass index (< 20 or > 30 kg/m²), nulliparity, smoking, premenstrual symptoms, previous pelvic inflammatory disease, psychological disorders or previous sexual assault. Pain sensitisation (due to the presence of other chronic pain conditions) may also be contributory. Protective factors for primary dysmenorrhoea include use of an oral contraceptive pill, increasing age, increasing parity and exercise.
  • Symptoms suggestive of secondary dysmenorrhoea include worsening pelvic pain, painful intercourse, vaginal discharge, abnormal bleeding or insufficient response to first-line treatment options, i.e. NSAIDs, combined oral contraceptives (see below)
• Dysmenorrhoea is a clinical diagnosis based on symptoms and medical history. Consider the possibility of pregnancy or infection in patients who are sexually active.
  • N.B. A pelvic examination and referral for an ultrasound may be required in patients who present with symptoms and signs suggestive of secondary dysmenorrhoea
• Do not delay initiating treatment when distinguishing between primary or secondary dysmenorrhoea, or investigating potential secondary causes, as standard treatment is often effective for both conditions
• A NSAID (e.g. ibuprofen, naproxen) is usually first-line for managing patients with dysmenorrhoea. Patients should begin use one to two days before menses and continue treatment until two to three days after menstruation has started. A loading dose on the first day of treatment is associated with lower reported pain scores compared to conventional NSAID dosing (see NZF for specific NSAID dosing regimens). Patients who experience adverse gastrointestinal effects should be advised to take the NSAID with food, or consider adding a proton pump inhibitor (e.g. omeprazole). A COX-2 inhibitor, e.g. celecoxib, may be better tolerated.
• Continuous use of a combined oral contraceptive is also an effective treatment option for patients with dysmenorrhoea who are not planning pregnancy. Combined oral contraceptives inhibit ovulation and endometrial thickening; this reduces prostaglandin, progesterone and vasopressin production, which in turn limits uterine motility and cramping.
  • Progesterone-only contraceptives that inhibit ovulation (e.g. oral desogestrel; not funded, depot medroxyprogesterone acetate; Depo-Provera, levonorgestrel intrauterine system; Mirena) have also been used for dysmenorrhoea
• In New Zealand, tranexamic acid can be considered in patients who experience menorrhagia (heavy menstrual bleeding) associated with dysmenorrhoea
• Regular exercise (e.g. 45 – 60 minutes at least three times per week) is associated with a clinically significant decrease in dysmenorrhoea symptoms. This effect is likely due to increased local blood flow, a release of endorphins and a general decrease in the patient’s stress and anxiety levels.
• There is some evidence suggesting the application of heat packs is comparable to ibuprofen in the management of dysmenorrhoea and may be more effective than paracetamol. This effect is also likely due to increases local blood flow and tissue oxygenation.
• High frequency transcutaneous electrical nerve stimulation (TENS) and physiotherapy may also provide symptom relief for some patients with dysmenorrhoea
• Patients with suspected primary dysmenorrhoea who do not have adequate symptom control after three to six months of pharmacological treatment should be referred to a gynaecologist for further investigations and treatment, e.g. surgical intervention