Male patient K.N.B., born in 1944, underwent stem cell treatment at EmCell clinic; case record No. 6172.
Diagnosis: Diabetes mellitus type 2, severe form, compensation. Diabetic retinopathy of the 2nd degree, maculodystrophy, diabetic microangiopathy (stage II) and macroangiopathy (stage III) of legs, diabetic foot, unhealed trophic ulcer of left foot, diabetic polyneuropathy. Ischemic heart disease: atherosclerotic cardiosclerosis, circulatory defficiency 0, cerebral atherosclerosis.
On admittance, the patient complained of pain in the left foot, unhealed trophic ulcer on the left sole, vision disturbances.
Diabetes mellitus was revealed 15 years ago. For several years, the patient kept to a diet, following which he started taking peroral sugar-reducing preparations (glibenclamid). On admittance, daily dosage of glibenclamid was 0.005 g. From the beginning of the disease, no thorough glycemic control was carried out. 3 years ago, patient’s condition worsened: as a result of a wound infection on the left great toe and development of gangrene, this toe was amputated. After 18 months, a trophic ulcer appeared on the sole of this foot, the ulcer was not healed during 14 months. Within recent six months, patient has vision disturbances.
Ophthalmologist’s conclusion: Diabetic retinopathy of the 2nd degree, maculodystrophy. During the last year, the patient stayed three times at the departments of surgery and endocrinology of Donetsk Oblast hospital. Treatment procedures included: unloading of the injured extremity by way of special footwear and liners; antibacterial therapy; treatment of wound; preparations for microcirculatory improvment; antiaggregants. The patient received two courses of insulin therapy with daily dosage of up 18 Units. Ulcer surface became clean although the ulcer did not scar.
On admittance to the Cell Therapy Clinic the patient was in the state of carbohydrate metabolism compensation: glycemic profile of 5.8-6.6-7.8 mmole/l; aglucosuria.
Objectively: moves with the crutches; wears orthopedic footwear. Nutrition is satisfactory. Skin and visible mucosa are clean and of usual color. Peripheral lymph nodes are not enlarged. Pulse rate is 76 beats/min, rhythmic. Arterial pressure is 140/90 mm Hg. Cardiac sounds are moderately weak, systolic murmur on the top. Lungs are clear. The abdomen is soft and painless on palpation. Liver at the edge of costal arch; lien not enlarged. Large bowel unremarkable. Stools and diuresis are normal. Some decrease of pulsation on a dorsalis pedis of both feet. Left great toe has been amputated. Trophic ulcer on the left sole. Clinical laboratory tests (average blood counts, chemistry, urinasyses) revealed no pathology. ECG shows A-V block of the 1st degree, diffusive changes and hypoxia of myocardium. In rheovasography, peripheral circulation in the right foot considerably decreased, and moderately decreased in the left foot.
Treatment was carried out with the use of medicinal preparation based on fetal cell suspensions: sample 3038K614; cell count 37.7x106; CFU-GM 22x103; CFU-GEMM 12x103; CD34+ 3.7x106; total volume 4.0 ml. Method of administration was intravenous, dropwise.
The patient well tolerated the procedure and felt improvement from the very first day: quiet and deep sleep at night, improved appetite, increase in mental and physical working capacity, decrease in foot pain. The patient continued taking glibenclamid in daily dosage of 0.005 g. No other preparations were prescribed. The patient was discharged from the clinic with the previously prescribed hypoglycemic therapy and recommendations of thorough glycemic control.
Gradually, in the course of 1 month, the trophic ulcer scared without any additional treatment. After 2 months, with regular control of glycemia and glucosuria, the daily dosage of glibenclamid was decreased to 0.025 g, and after 4 months the level of glycemia was corrected by diet only.