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"Adverse Drug
Event of the month"
Brief History: A 52-year male resident of Nepal, diagnosed as Type 2 Diabetes Mellitus 20 year back, hypertensive, non-smoker and non alcoholic was admitted to the Endocrinology ward with complaints of loss vision of 3 months duration and tingling and numbness of both lower limbs of 3 years duration. The complaints began as difficulty in reading and difficulty in moving around in the evenings, which then progressed to complete loss of vision in both eyes. There was no history of pain in the eyes or sudden deterioration of vision. Tingling and numbness were present in both lower limbs since 3 years and since the past 3 months it had progressively increased and he had difficulty in walking. There was no history of rest pain. His general practitioner prescribed insulin for him after it was found that the Metformin 500 mg BD with Glibenclamide 5 mg BD did not control his hyperglycemia. The details of previous insulin therapy were however not available with the patient at the time of presentation. Clinical Examination: This revealed a moderately built and well-nourished male with a BMI of 17.04. Cardiovascular examination was normal except for the non palpable posterior tibial pulses bilaterally. Neurological examination showed that his vision was limited to hand movements in both eyes and fundus examination showed bilateral retrobulbar neuritis and nonproliferative diabetic retinopathy. Power was grade 5 bilaterally in the upper and lower limbs and knee and ankle jerks were absent bilaterally. Sensory examination showed decreased touch, pain and vibration sensations below the knee joints bilaterally There was bilateral Diabetic foot grade 0 at risk . There were swellings of approximately 4 x 5 cms on the anteromedial aspect of the left and right thigh. The swellings were soft, non-tender, non pulsatile and with restricted mobility. Other system examinations were within normal limits. Investigations: Biochemical investigations and CSF examination were within normal limits. Fasting blood sugar was 174 mg %,and post prandial sugar (2hr) was 226 mg%, while glcosylated hemoglobin (HbA1C) was 8.4. His ECG and 2D Echo showed changes consistent with hypertension. His CSF examination was normal and there were no oligoclonal bands. ANCA was negative, MRI of Brain showed prominence of frontoparietal cortical convexity sulci with lacunae's in subcortical white matter in the frontoparietal region. Nerve conduction studies showed evidence of sensorimotor polyneuropathy affecting the lower limbs. Electromyography studies showed evidence of denervation in distal lower limb consistent with distal axonal neuropathy. Management: He was treated with Inj. Human Neutral Insulin and Inj Human Isophane Insulin in progressively higher doses by dose titration with respect to his blood sugar levels.At time of discharge his blood sugar values were FBS 112mg% and PPBS 128 mg% ..He was also treated with Prednisolone 40 mgs in tapering doses, Enalapril 2.5 mg BD, Amlodipine 5 mg OD and Hydrochlorthiazide 12.5 mg BD. Diagnosis: Type 2 Diabetes Mellitus, bilateral distal symmetric sensory motor neuropathy, bilateral nonproliferative Diabetic Retinopathy with possible retrobulbar neuritis and injection site Lipohypertrophy of both lower limbs. Follow up: Patient was better at the time of discharge and was under glycemic control. He was advised regular follow up and since the lipohypertrophy regressed on its own within duration of 1 week after changing the injection site during the period of hospitalization itself, it was decided to leave the site alone and to reassess it at the next follow up. Patient was subsequently lost to follow up. Discussion: Lipodystrophy occurs in about 30 % of patients who are on insulin and consists of two distinct entities-Lipohypertrophy and Lipoatrophy. Injection site Lipohypertrophy is a non-immunological complication of Insulin therapy[1] whereas lipoatrophy is due to contaminants in the insulin molecule. Lipohypertrophy is a localized overgrowth of subcutaneous tissue in response to the lipogenic and growth promoting effects of high local insulin concentrations. It is more frequent problem in patients taking multiple daily insulin injections who repeatedly inject at the same site, usually the abdomen and also in patients taking purified monocomponent insulins. Injection site lipohypertrophy occurs more often in individuals who have dermal reactions to insulin and in young children. While the lesions are usually limited to injection sites, they may also occur distally. Lipoatrophic lesions occurred in individuals with high levels of circulating anti-insulin antibodies .The edge of these lesions are characterized by deposition of immunological proteins within dermal vessels most commonly Ig M and C3 or fibrin-fibrinogen. Such fatty tumors are fibrous and have decreased vascularity .Patients often continue to select these injection sites due to relative anesthesia. Absorption from hypertrophic sites has been shown to be significantly impaired[2] and causes poor glycemic control. lipohypertophy can be largely avoided by rotating insulin injection sites. If avoidance of affected sites does not result in regression and removal is desirable, Liposuction has been tried as a treatment modality[3]. Some of the other conditions and medications that are associated with lipodystrophy syndromes are Diabetes Mellitus ,HIV positive status (HIV-1 associated adipose redistribution syndrome-HARS), Zidovudine, Stavudine (NRTIs), Protease inhibitors ( Ritonavir, Indinavir) References: 1. KGMM Alberti, Zimmet and De Fronzo RA.International textbook of Diabetes Mellitus.Eds 2nd Edition,John Wiley &Sons, Chichester 23;960-961 2. Young RJ .Diabetic lipohypertrophy delays insulin absorption. Diabetes Care 1984;4:479-480 3. Bodansky HJ Treatment of Insulin lipohypertrophy with liposuction. Diabetes Med 1992;9:395-396. *Departments of Clinical Pharmacology and **Endocrinology Seth GS Medical College & KEM Hospital, Parel, Mumbai 400 012, INDIA |
