Teebi (1990) reported two brothers, born to first-cousin parents, with Robinow syndrome. Their paternal uncle also married a first cousin and had three similarly affected children (2 boys, 1 girl). The two affected brothers had short stature, mesomelic and acromelic brachymelia, characteristic face with hypertelorism, wide palpebral fissures, midface hypoplasia and large mouth, and hypogenitalism. Parental consanguinity and the presence of affected individuals in two sibships of common ancestry strongly suggested autosomal recessive inheritance. In 1991, Robinow also had reports of recessive cases from Kuwait (Source: OMIM).

Sabry et al. (1997) reported a child from a Kuwaiti consanguineous family with Robinow syndrome. The index case showed some unusual features including severe associated intrauterine growth retardation (IUGR), laxity of ligaments, hyperextensible joints, redundant skin folds, severe normocytic anemia, and repeated infection associated with increased total T cells and an increased CD4:CD8 ratio.

Soliman et al. (1998) conducted a study on 14 patients from six consanguineous Omani families with the recessive form of Robinow syndrome to analyze their growth patterns and the growth hormone (GH) response to provocation with clonidine and the serum insulin-like growth factor-I (IGF-I) concentration in 12 of these children. A set of 12 normal children with constitutional growth delay were used as a control group for gonadotrophin releasing hormone (GnRH) and human chorionic gonadotrophin (HCG) tests. Children with Robinow syndrome, born at full-term, were short at birth (length, 41.4+/-2.1 cm) and had markedly slow growth velocity (GV) during the first year (13.1+/-2.1 cm/yr); consequently, they were significantly short at the end of the first year of life (length, 54.4+/-2.9 cm). This intrauterine and early extrauterine growth delay reflected low growth potential. During childhood and early adolescence, boys with Robinow syndrome had low basal testosterone and a low testosterone response to HCG stimulation (3,000 IU/m2/d intramuscularly [IM] for 3 days), although they had normal basal and GnRH-stimulated FSH (follicle-stimulating hormone) concentrations. On the other hand, two girls (Tanner II breast development) had a normal serum estradiol (E2) concentration but high LH and FSH responses to GnRH stimulation. This suggested either defective feedback of E2 on the hypothalamic-pituitary axis or hyporesponsiveness of the ovaries to gonadotropin. Three boys received HCG for four weeks and their penile length and testicular volume were increased, reflecting a significant Leydig cell response to prolonged HCG stimulation and the presence of functioning androgen receptors. Soliman et al (1998) suggested that severe micropenis in patients with Robinow syndrome might improve, if they receive HCG and/or testosterone during infancy.

Rajab et al. (2005) undertook a study to estimate the prevalence of commonly diagnosed autosomal recessive diseases in Oman from a hospital-based register in years 1993 to 2002. The study revealed that Robinow syndrome was diagnosed in 12 patients, with an observed incidence of 1 in 35,000 births.

Nazer et al. (1990) reported two children, born to first-cousin Saudi parents, with the 'fetal face syndrome.' Both of the children also had the Crigler-Najjar syndrome, as did two previously born sibs who did not have the fetal face syndrome. Both died at age 4 months. The parents lost two previous children at age 2 months with progressive jaundice but without fetal facial characteristics. Robinow (1991) also had reports of recessive cases from Saudi Arabia (Source: OMIM).