Probal Moulik

Once weekly thyroxine treatment as a strategy to treat non-compliance.

Hypothyroidism is a common disorder, which is mainly treated in primary rather than secondary care. Once daily thyroxine replacement restores euthyroidism in most patients; some patients, however, remain hypothyroid despite adequate thyroxine replacement. Non-compliance is the most common cause of lack of response to thyroxine treatment. We describe two cases of primary hypothyroidism in which daily thyroxine treatment did not restore biochemical euthyroidism but once weekly thyroxine treatment was successful. In addition we review the evidence and discuss the differential diagnosis of lack of response to thyroxine treatment. Once weekly thyroxine treatment can be a safe, well-tolerated, and effective therapy for patients with non-compliance.

Impact of practice size on delivery of diabetes care before and after the Quality and Outcomes Framework implementation

General practice characteristics are important for healthcare providers to maximise outcomes. Although different aspects of general practice characteristics have been studied previously, the impact of practice size on the delivery of care has been sparsely studied, particularly in relation to diabetes care. This brief report presents a longitudinal study in Shropshire (66 practices, 16,858 patients with diabetes) to assess the impact of practice size on diabetes care before and after implementation of the Quality and Outcomes Framework (QOF). Achievement of glycaemic control targets was better before the QOF for larger as compared to smaller practices (P=0.02 and P=0.003 for haemoglobin A1c [HbA1c]<or=7.4% and 10% respectively). This difference disappeared following QOF implementation. Repeated measures analysis showed significant improvement in achieving glycaemic control targets following QOF implementation in both large and small practices (P<0.001 for HbA1c<or=7.4% and 10%). The study failed to reveal an impact of practice size on achieving the HbA1c target<or=7.4% (P=0.1) by this analysis. However, it did show an impact on reaching the target of HbA1c<10% (P=0.04) in favour of smaller practices. There was a significant difference in favour of smaller practices for achievement of prescription of angiotensin-converting enzyme inhibitors (P=0.001).

Evaluation of glargine group-start sessions in patients with type 2 diabetes as a strategy to deliver the service.

Improving glycaemic control in patients with type 2 diabetes reduces microvascular complications. The national service framework for diabetes and the new general medical service contract have been aiming to direct more focus on improving HbA1c. These measures have resulted in increasing number of patients being initiated on insulin therapy, which increases the workload of diabetes specialist nurses (DSNs). Initiating insulin on a one‐to‐one basis is time consuming. As a result DSN‐led insulin group‐start sessions were introduced. To evaluate DSN‐led glargine group‐start and self‐titration as a strategy of providing service. We assessed the impact of this method on the use of DSNs time, HbA1c and on patients’ satisfaction. A prospective audit in a district general hospital. Groups of 5–7 patients received two 2‐h sessions at weeks 0 and 2. During these sessions, patients were initiated on insulin glargine and received an educational package and a self‐titration protocol. DSNs did not see patients after week 2. Patients were able to phone the DSNs for advice till the end of the titration period. Patients completed Diabetes Treatment Satisfaction Questionnaire (DTSQ) at baseline, week 2 and 12 months. Weight and HbA1c were assessed at base line and 12 months later. Twenty‐nine consecutive patients were included. Baseline HbA1c improved at 6 months and remained stable at 12 months (medians 10.0, 8.7 and 8.9 respectively, p < 0.001). DTSQ score improved between week 0 and 2 and this was maintained at 12 months (medians 26, 35 and 34 respectively, p < 0.001). After week 2, the DSNs spent a median of 21 min advising patients by phone during the titration period. Weight did not increase significantly. In our centre, DSN‐led insulin group‐start sessions and self‐titration improved glycaemic control. Patients were satisfied with this method of starting insulin. This was achieved with minimal DSNs time and input and proved to be effective, yet less time consuming.

The development of non-insulin-dependent diabetes after total body irradiation and bone marrow transplantation in adolescence: a case report and literature review

Abstract:  A 6‐yr‐old‐child received total body irradiation (TBI) and bone marrow transplantation (BMT) for relapsed acute lymphocytic leukemia. Nine years later, he developed diabetes mellitus (DM). He was started on basal bolus insulin therapy. Islet cell and anti‐GAD antibodies were negative. Insulin and C‐peptide levels were elevated consistent with insulin resistance (IR), even though his body mass index (BMI) was only 19.5. Hepatocyte nuclear factor (HNF‐1α) mutation was not detected. Insulin was stopped and hemoglobin Alc (HbA1c) stabilized at 6.5% on gliclazide 40 mg/day. TBI has rarely been associated with IR and the development of diabetes. These patients can be managed with oral hypoglycemic agents and do not necessarily require insulin. Patients who received BMT and TBI may require long‐term monitoring of glucose and lipid metabolism.

Severe hypomagnesaemia due to lansoprazole

A 71-year-old woman, who had been taking lansoprazole for 18 months for dyspepsia, presented with vomiting, thought to be due to gallstones, and was found to have severe hypomagnesaemia. She was treated with intravenous and then oral magnesium, and discharged, but was soon readmitted with symptoms due to hypomagnesaemia, and again treated with magnesium supplementation. No other recognised cause for hypomagnesaemia was found. Because of recent reports of hypomagnesaemia due to other proton pump inhibitors, lansoprazole was changed to ranitidine. Her symptoms resolved and the serum magnesium returned to normal. Oral magnesium supplementation was stopped with no return of symptoms or hypomagnesaemia. Such an association must be borne in mind with suggestive symptoms in patients on long term proton pump inhibitors; their cessation or change to H2 receptor antagonists is likely to correct the situation rapidly.

A case of multi-organ failure

Colchicine is a commonly used drug in the treatment of gout. Gastrointestinal side effects such as nausea, vomiting and diarrhoea are commonly associated with colchicine but more severe adverse effects are uncommon. We report a case of colchicine toxicity, which resulted in multi-organ failure, bone marrow suppression and death. This clinical message highlights the important lessons learnt from this case and summarises the clinical features and management of colchicine toxicity. Colchicine is a commonly used drug in the treatment of gout. Gastrointestinal side effects such as nausea, vomiting and diarrhoea are commonly associated with colchicine but more severe adverse effects are uncommon. We report a case of colchicine toxicity, which resulted in multi-organ failure, bone marrow suppression and death. A 65-year-old patient was admitted to hospital with 12 days history of watery diarrhoea and vomiting. Two days prior to onset of diarrhoea, he was started on colchicine by his general practitioner for the treatment of an attack of suspected acute gouty affecting the left big toe. He consumed 1.5 mg of colchicine a day for 2 weeks prior to admission. The patient was known to have gout for the last 5 years and had previous attacks of gout affecting the toes. There was no significant past medical history, apart from gout, or family history of note. He was not taking any regular medications prior to his current illness. The patient denied any alcohol intake on admission. However, later during the admission his daughter revealed a history of moderately excessive alcohol intake of 30 units a week approximately. On admission, he was drowsy but responsive with a Glasgow coma scale of 15/15. Clinical examination revealed a blood pressure of 110/70 and heart rate of 110 beats/ min and tachypnoea. Jugular venous pressure was low. There was no evidence of jaundice, clubbing, cyanosis, oedema or lymphadenopathy. There was no evidence of chronic gouty arthropathy or tophi. Abdominal, cardiac and respiratory examination revealed no further abnormalities. Chest and abdominal X-rays were unremarkable. An electrocardiograph showed sinus tachycardia. Urinalysis showed evidence of microscopic haematuria and proteinuria. Initial investigations showed evidence of acute renal failure, leucopenia, neutropenia, thrombocytopenia, hypocalcaemia, hyperphosphataemia, metabolic acidosis and abnormal clotting. These results are summarised in Table 1. There were no previous blood test results recorded for this patient to compare with prior to this admission. Colchicine was stopped and the patient was resuscitated with intravenous fluids. Broad-spectrum antibiotics (imipenem, ciprofloxacin and fluconazole) and granulocyte colony-stimulating factor (GCSF) were started for neutropenia. Further investigations were carried out. Urinary total protein was 0.98 g/l, no urinary free light chains, lactate 7.5 mmol/l [normal range (NR) 0.3–1.3] and troponin T 0.5 lg/l (NR < 0.01). D-dimer levels were raised and fibrinogen levels were normal throughout the admission. Blood film did not show any evidence of haemolysis. Anti-nuclear, antismooth muscle, anti-mitochondria, anti-glomerular basement membrane and anti-neutrophil cytoplasmic antibodies were negative. There was no growth on urine, blood or stool cultures. Hepatitis B surface antigen and hepatitis C antibody were both negative. Abdominal/renal ultrasound was unremarkable and kidney size was 10 cm bilaterally. The patient’s clinical condition continued to deteriorate despite some improvement in renal function with hydration. He received intravenous fluids replacement guided by central venous pressure monitoring, electrolytes supplements, antibiotics, GCSF and platelet, blood and fresh frozen plasma (FFP) transfusions (see Figure 1). He developed abdominal distension secondary to intestinal pseudoobstruction. On day 5, he had upper gastrointestinal bleeding and endoscopy showed severe oesophageal ulceration that was treated with intravenous omeprazole infusion. The patient then started to develop respiratory distress and hypoxia with inspiratory crackles on examination. Chest X-ray (CXR) was unremarkable. He was transferred to the intensive care unit where he received continuous positive airway pressure respiratory support and also inotropic support for hypotension. On day 7 the patient developed asystole and died. Post-mortem examination showed the presence of complicated atheroma in the aorta and the left descending coronary artery was reduced to 20% of normal. There was also evidence of pulmonary oedema and bilateral pleural effusions. Gastrointestinal system examination revealed fatty liver and oesophageal ulceration.

Potential inaccuracy in recording the presence of diabetes in people with amputations of the lower limb in hospitals in England.

To the Editor: We applaud Holman et al [1] for gathering data regarding the incidence of major lower limb amputations in people with diabetes. However, we believe that comparison of areas covered by primary care trusts (PCTs) is not sufficiently accurate because of poor quality data collection in hospitals in England. Data regarding prevalence of diabetes were gleaned from general practice systems, generated during clinical care. Data recording coexistence of diabetes are taken from hospital episode statistics (HES), usually collected by non-clinical coders, after perusal of hospital notes. We have examined the case records of all patients coded as having major lower limb amputations in two hospitals that are the major catchment of our two PCTs, for the same time period. There were 21 patients in Shropshire County PCT (SCPCT), and 15 in Telford and Wrekin PCT (TWPCT), a prevalence of 0.58 and 0.71 amputations per year per 1,000 people with diabetes respectively (as opposed to 0.6–0.9 and >1.2, quoted by Holman et al [1]). However, seven of those patients in SCPCT and one from TWPCT were incorrectly coded as not having diabetes, which would have resulted in a false prevalence of 0.36 for SCPCT and 0.66 for TWPCT. We suspect that similar inaccuracies occur in other hospitals in England. We therefore believe that it is premature to compare areas with small numbers of amputations, such as our PCTs, given that coding for diabetes in relevant patients from HES, as opposed to GP systems, is so inaccurate. Some areas may be unfairly criticised, whilst others become complacent.

A young person with recurrent severe hypokalaemia - familial, iatrogenic or just unknown?

A 26-year-old female presented with 5-year history of episodic muscle weakness, abdominal cramps and facial paraesthesia. She had 2 hospital admissions elsewhere within 6months with severe hypokalaemia (1.9mmol/L). She was started on Lamotrigine for epilepsy 7 years ago and changed to Levetiracetam in October 2010 following further seizures. She is now seizure-free for over 5 years. Her potassium levels before and after Levetiracetam are shown in Table 1.

Bilateral adrenal calcification caused by a previous Streptococus mitis septicaemia

This 23 year old man was noted incidentally to have bilateral adrenal calcification on CT scan of his abdomen for chronic abdominal pain. He had normal growth and milestones with no neonatal events. Aged 10 years he was admitted briefly to a high dependency unit with circulatory shock and hyperthermia, with isolation of Streptococcus mitis from blood culture. One year later he was noted to have bilateral adrenal calcification on abdominal XR, and a short Synacthen (250mcg) test was considered normal (baseline cortisol of 303 nmol/l rising to a peak of 543 nmol/l). Current investigations reveal normal adrenal function including a Short synacthen test; which revealed normal response with normal base line cortisol of 440 nmol/l rising to a peak of 620 nmol/l with normal serum renin and ACTH.